Revision Notes in Psychiatry, Third Edition ( PDFDrive ) (1)

Revision
notes in
PsychiatRy
Third EdiTion
Revision
notes in
PsychiatRy
Third EdiTion
BasanT K. Puri
anniE hall
rogEr ho
The authors acknowledge the following illustrators: Ms. Ja’naed Woods (for Chapter 1, “Descriptive Psychopathology”); Mr. Edwin
Ng (for Chapter 7, “Cognitive Assessment and Neuropsychological Processes”); and Miss Anna Chua (for all other chapters).
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Contents
Preface..................................................................................................................................................................... lxxvii
Authors...................................................................................................................................................................... lxxix
Abbreviations............................................................................................................................................................ lxxxi
Chapter 1 Descriptive Psychopathology.....................................................................................................................1

1.1 Disorders of General Behaviour......................................................................................................1
1.1.1 Underactivity......................................................................................................................1
1.1.1.1 Stupor..................................................................................................................1
1.1.1.2 Depressive Retardation.......................................................................................1
1.1.1.3 Obsessional Slowness.........................................................................................1
1.1.2 Overactivity........................................................................................................................1
1.1.2.1 Psychomotor Agitation.......................................................................................1
1.1.2.2 Hyperkinesis.......................................................................................................1
1.1.2.3 Somnambulism (Sleep Walking)........................................................................1
1.1.2.4 Compulsion (Compulsive Ritual).......................................................................1
1.1.2.5 Abnormal Posture and Movements....................................................................1
1.2 Disorders of Speech.........................................................................................................................3
1.2.1 Disorders of Rate, Quantity, and Articulation...................................................................3
1.2.2 Disorders of the Form of Speech.......................................................................................3
1.2.3 Disorders (Loosening) of Association (Formal Thought Disorder)...................................4
1.3 Disorders of Emotion......................................................................................................................4
1.3.1 Disorders of Affect.............................................................................................................4
1.3.2 Disorders of Mood.............................................................................................................4
1.3.3 Disorders Related to Anxiety.............................................................................................5
1.4 Disorders of Thought Content.........................................................................................................5
1.4.1 Preoccupations...................................................................................................................5
1.4.2 Obsessions..........................................................................................................................5
1.4.3 Phobias...............................................................................................................................5
1.5 Abnormal Beliefs and Interpretations of Events.............................................................................6
1.5.1 Overvalued Ideas................................................................................................................6
1.5.2 Delusions............................................................................................................................6
1.5.3 Passivity Phenomenon........................................................................................................6
1.5.4 Delusional Perception.........................................................................................................7
1.6 Abnormal Experiences....................................................................................................................7
1.6.1 Sensory Distortions............................................................................................................7
1.6.2 Sensory Deceptions............................................................................................................7
1.6.2.1 Illusions...............................................................................................................7
1.6.2.2 Hallucinations.....................................................................................................7
1.6.2.3 Pseudohallucinations (Coined by Kandinsky in 1885).......................................8
1.7 Disorders of Self-Awareness (Ego Disorders).................................................................................9
1.8 Cognitive Disorders.........................................................................................................................9
1.8.1 Disorientation.....................................................................................................................9
1.8.2 Disorders of Attention........................................................................................................9
1.8.3 Disorders of Memory.........................................................................................................9
1.8.4 Disorders of Intelligence..................................................................................................10
v
vi Contents
1.8.5 Disorders of Consciousness..............................................................................................10

1.8.5.1 Levels of Consciousness...................................................................................10
1.8.5.2 Clouding of Consciousness...............................................................................10
1.8.5.3 Delirium............................................................................................................10
1.8.5.4 Fugue................................................................................................................10
1.8.5.5 Aphasias............................................................................................................10
1.9 Dyslexia.........................................................................................................................................10
1.10 Agraphia........................................................................................................................................ 11
1.11 Alexia............................................................................................................................................ 11
1.12 Acalculia........................................................................................................................................ 11
1.13 Apraxias and Agnosias.................................................................................................................. 11
1.13.1 Apraxias........................................................................................................................... 11
1.13.2 Agnosias and Disorders of Body Image...........................................................................12
Bibliography.............................................................................................................................................15
Chapter 2 Classification............................................................................................................................................ 17
2.1 History of Classification Schemes................................................................................................. 17
2.1.1 Ancient Greeks................................................................................................................. 17
2.1.2 Ancient Romans............................................................................................................... 17
2.1.3 Cullen............................................................................................................................... 17
2.2 ICD................................................................................................................................................ 17
2.3 DSM............................................................................................................................................... 17
2.4 ICD-10........................................................................................................................................... 18
2.4.1 Organic, Including Symptomatic, Mental Disorders....................................................... 18
2.4.2 Schizophrenia, Schizotypal, and Delusional Disorders................................................... 18
2.4.3 Mood (Affective) Disorders............................................................................................. 18
2.4.4 Neurotic, Stress-Related, and Somatoform Disorders..................................................... 18
2.4.5 Behavioural Syndromes Associated with Physiological Disturbances and Physical
Factors�� 18
2.4.6 Disorders of Adult Personality and Behaviour.................................................................19
2.4.7 Mental Retardation...........................................................................................................19
2.4.8 Disorders of Psychological Development.........................................................................19
2.4.9 Behavioural and Emotional Disorders with Onset Usually Occurring in
Childhood and Adolescence��19
2.5 DSM-IV-TR and DSM-5...............................................................................................................19
2.5.1 Axis I: Clinical Disorders; Other Conditions That May Be a Focus of Clinical
Attention...........................................................................................................................19
2.5.1.1 DSM-IV-TR and DSM-5: Disorders Usually First Diagnosed in Infancy,
Childhood, or Adolescence (Excluding Mental Retardation Which Is
Diagnosed on Axis II)......................................................................................19
2.5.1.2 DSM-IV-TR and DSM-5: Delirium, Dementia, and Amnestic and Other
Cognitive Disorders..........................................................................................20
2.5.1.3 DSM-IV-TR and DSM-5: Substance-Related Disorders..................................20
2.5.1.4 DSM-IV-TR and DSM-5: Schizophrenia and Other Psychotic Disorders........21
2.5.1.5 DSM-IV-TR and DSM-5: Depressive Disorders..............................................22
2.5.1.6 DSM-IV-TR and DSM-5: Bipolar Disorders....................................................22
2.5.1.7 DSM-IV-TR and DSM-5: Anxiety Disorders...................................................22
2.5.1.8 DSM-IV-TR and DSM-5: Somatoform Disorders............................................22
2.5.1.9 DSM-IV-TR and DSM-5: Factitious Disorders................................................22
2.5.1.10 DSM-IV-TR and DSM-5: Sexual and Gender Identity Disorders....................22
Contents vii
2.5.1.11 DSM-IV-TR and DSM-5: Eating Disorders......................................................23

2.5.1.12 DSM-IV-TR and DSM-5: Sleep Disorders.......................................................23
2.5.1.13 DSM-IV-TR and DSM-5: Impulse-Control Disorders not Elsewhere
Classified..........................................................................................................23
2.5.1.14 Adjustment Disorders.......................................................................................23
2.5.2 AXIS II: Personality Disorders; Mental Retardation.......................................................23
2.5.2.1 Personality Disorders........................................................................................23
2.5.2.2 Mental Retardation...........................................................................................24
2.5.3 Axis III: General Medical Conditions.............................................................................24
2.5.4 Axis IV: Psychosocial and Environmental Problems......................................................24
2.5.5 Axis V: Global Assessment of Functioning.....................................................................24
Bibliography.............................................................................................................................................24
Chapter 3 Basic Psychology......................................................................................................................................25

3.1 Principles of Learning Theory......................................................................................................25
3.1.1 Definition of Learning......................................................................................................25
3.1.2 Classical Conditioning.....................................................................................................25
3.1.2.1 Definition and Introduction..............................................................................25
3.1.2.2 Acquisition Stage..............................................................................................25
3.1.2.3 Delayed Conditioning.......................................................................................25
3.1.2.4 Simultaneous Conditioning..............................................................................25
3.1.2.5 Trace Conditioning...........................................................................................25
3.1.2.6 Backward Conditioning....................................................................................25
3.1.2.7 Higher-Order Conditioning..............................................................................25
3.1.2.8 Extinction..........................................................................................................25
3.1.2.9 Generalization...................................................................................................26
3.1.2.10 Discrimination..................................................................................................26
3.1.2.11 Incubation.........................................................................................................26
3.1.2.12 Stimulus Preparedness......................................................................................26
3.1.2.13 Little Albert......................................................................................................26
3.1.3 Operant Conditioning (Instrumental Learning)...............................................................26
3.1.3.2 Trial-and-Error Learning/Behaviour................................................................26
3.1.3.3 Law of Effect....................................................................................................26
3.1.3.4 Skinner Box......................................................................................................26
3.1.4 Observational Learning (Vicarious Learning/Modelling)..............................................26
3.1.4.2 Bobo Doll Experiments....................................................................................27
3.1.4.3 Optimal Conditions for Observational Learning.............................................27
3.1.4.4 Steps Involved in the Modelling Process..........................................................27
3.1.5 Cognitive Learning..........................................................................................................27
3.1.5.1 Definition..........................................................................................................27
3.1.5.2 Mechanisms......................................................................................................27
3.1.5.3 Assimilation Theory.........................................................................................27
3.1.6 Concepts of Extinction and Reinforcement in Explaining Behaviour.............................28
3.1.6.1 Extinction..........................................................................................................28
3.1.6.2 Reinforcement...................................................................................................28
3.1.6.3 Punishment.......................................................................................................28
3.1.6.4 Primary Reinforcement....................................................................................28
viii Contents
3.1.6.5 Secondary Reinforcement................................................................................28

3.1.6.6 Schedules of Reinforcement.............................................................................28
3.1.6.7 Motivation.........................................................................................................28
3.1.7 Clinical Applications of Behavioural Treatments............................................................28
3.1.7.1 Reciprocal Inhibition........................................................................................28
3.1.7.2 Habituation.......................................................................................................28
3.1.7.3 Chaining...........................................................................................................29
3.1.7.4 Shaping.............................................................................................................29
3.1.7.5 Cueing...............................................................................................................29
3.1.7.6 Escape Conditioning.........................................................................................30
3.1.7.7 Avoidance Conditioning...................................................................................30
3.1.7.8 Self-Control Therapy........................................................................................30
3.1.7.9 Modelling Therapy........................................................................................... 31
3.2 Phenomena of Visual and Auditory Perception............................................................................ 31
3.2.1 Perception......................................................................................................................... 31
3.2.1.1 Definition.......................................................................................................... 31
3.2.1.2 Absolute Threshold........................................................................................... 31
3.2.1.3 Difference Threshold........................................................................................ 31
3.2.1.4 Weber’s Law..................................................................................................... 31
3.2.1.5 Fechner’s Law................................................................................................... 31
3.2.1.6 Signal Detection Theory................................................................................... 31
3.2.2 Perceptual Organization................................................................................................... 31
3.2.2.1 Figure-Ground Differentiation......................................................................... 31
3.2.2.2 Object Constancy..............................................................................................32
3.2.2.3 Depth Perception..............................................................................................32
3.2.2.4 Perceptual Set...................................................................................................32
3.2.3 Relevance of Visual Perceptual Theory to Psychopathology...........................................32
3.2.3.1 Illusions.............................................................................................................32
3.2.3.2 Hallucinations...................................................................................................33
3.2.3.3 Other Psychopathologies..................................................................................33
3.2.4 Development of Visual Perception...................................................................................33
3.2.5 Culturally Sanctioned Distress States..............................................................................33
3.2.5.1 Nocturnal Hallucinations in Ultra-Orthodox Jewish Israeli Men....................33
3.2.5.2 Isolated Sleep Paralysis with Visual Hallucinations among Nigerian Students��34
3.2.5.3 Mu-Ghayeb.......................................................................................................34
3.2.5.4 Auditory and Visual Hallucinations Related to Bereavement in the
Caribbean��34
3.3 Information Processing and Attention..........................................................................................34
3.3.1 Information Processing....................................................................................................34
3.3.1.1 Data-Driven Processing....................................................................................35
3.3.1.2 Conceptually Driven Processing......................................................................35
3.3.2 Attention...........................................................................................................................35
3.4 Factors Affecting Memory............................................................................................................35
3.4.1 Memory............................................................................................................................35
3.4.1.1 Encoding/Registration......................................................................................35
3.4.1.2 Storage..............................................................................................................35
3.4.1.3 Retrieval............................................................................................................35
3.4.2 Influences upon Memory..................................................................................................36
3.4.3 Optimal Conditions for Encoding, Storage, and Retrieval of Information......................36
3.4.3.1 Encoding/Registration......................................................................................36
3.4.3.2 Storage..............................................................................................................37
Contents ix
3.4.3.3 Retrieval............................................................................................................37
3.4.4 Memory Information Processing.....................................................................................37
3.4.4.1 Primary Working Memory Storage Capacity...................................................37
3.4.4.2 Principle of Chunking......................................................................................39
3.4.4.3 Semantic Memory.............................................................................................39
3.4.4.4 Episodic Memory.............................................................................................39
3.4.4.5 Skills Memory..................................................................................................39
3.4.4.6 Other Aspects of Long-Term/Secondary Memory...........................................39
3.4.5 Process of Forgetting and the Influence of Emotional Factors on Retrieval...................39
3.4.5.1 Forgetting..........................................................................................................39
3.4.5.2 Theories of Forgetting......................................................................................39
3.4.5.3 Influence of Emotional Factors on Retrieval....................................................40
3.4.6 Processes of Interference, Schemata, and Elaboration....................................................40
3.4.6.1 Interference.......................................................................................................40
3.4.6.2 Schemata...........................................................................................................40
3.4.6.3 Elaboration........................................................................................................40
3.5 Factors Affecting Thought............................................................................................................40
3.5.1 Relationship of Thought to Language..............................................................................40
3.5.1.1 Concepts...........................................................................................................40
3.5.1.2 Prototypes......................................................................................................... 41
3.5.2 Reasoning......................................................................................................................... 41
3.5.2.1 Deductive Reasoning........................................................................................ 41
3.5.2.2 Inductive Reasoning.........................................................................................42
3.5.3 Problem-Solving Strategies..............................................................................................43
3.5.3.1 Alternative Representations..............................................................................43
3.5.3.2 Expertise...........................................................................................................43
3.5.3.3 Computer Simulation........................................................................................43
3.5.4 Algorithms.......................................................................................................................43
3.5.5 Heuristics..........................................................................................................................43
3.6 Factors Affecting Personality........................................................................................................44
3.6.1 Derivation of Nomothetic and Idiographic Theories.......................................................44
3.6.2 Trait and State Approaches..............................................................................................44
3.6.3 Construct Theory.............................................................................................................46
3.6.4 Humanist Approaches......................................................................................................46
3.6.4.1 Roger’s Self Theory..........................................................................................47
3.6.4.2 Maslow..............................................................................................................47
3.6.5 Psychoanalytic Approaches..............................................................................................47
3.6.5.1 Freud’s Stages of Psychosexual Development..................................................47
3.6.5.2 Erikson’s Stages of Development.....................................................................48
3.6.6 Situationist Approach.......................................................................................................48
3.6.7 Interactionist Approach....................................................................................................48
3.6.8 Inventories........................................................................................................................48
3.6.8.1 16PF..................................................................................................................48
3.6.8.2 MMPI...............................................................................................................48
3.6.8.3 CPI....................................................................................................................49
3.6.8.4 Other Inventories..............................................................................................50
3.6.8.5 Limitations........................................................................................................50
3.6.9 Rating Scales....................................................................................................................50
3.6.9.1 SAP...................................................................................................................50
3.6.9.2 SCID II.............................................................................................................50
3.6.9.3 SIDP..................................................................................................................50
x Contents
3.6.9.4 PAS...................................................................................................................50
3.6.9.5 PDE................................................................................................................... 51
3.6.9.6 IPDE................................................................................................................. 51
3.6.10 Repertory Grid................................................................................................................. 51
3.6.11 Q-Sort Schedule............................................................................................................... 51
3.7 Factors Affecting Motivation........................................................................................................ 51
3.7.1 Extrinsic Theories and Homeostasis................................................................................ 51
3.7.2 Hypothalamic Systems and Satiety.................................................................................. 51
3.7.3 Intrinsic Theories............................................................................................................. 51
3.7.3.1 Optimal Arousal............................................................................................... 51
3.7.3.2 Cognitive Dissonance....................................................................................... 51
3.7.3.3 Attitude-Discrepant Behaviour.........................................................................52
3.7.3.4 Need for Achievement......................................................................................52
3.7.4 Curiosity Drive.................................................................................................................52
3.7.5 Maslow’s Hierarchy of Needs..........................................................................................52
3.8 Factors Affecting Emotion............................................................................................................52
3.8.1 Types of Emotion.............................................................................................................52
3.8.2 Components of Emotional Response...............................................................................52
3.8.3 James–Lange Theory.......................................................................................................52
3.8.4 Cannon–Bard Theory.......................................................................................................53
3.8.5 Schachter’s Cognitive Labelling Theory and Cognitive Appraisal..................................53
3.9 Stress..............................................................................................................................................53
3.9.1 Physiological and Psychological Aspects.........................................................................53
3.9.2 Situational Factors............................................................................................................53
3.9.2.1 Life Events........................................................................................................53
3.9.3 Vulnerability and Invulnerability.....................................................................................53
3.9.4 Coping Mechanisms.........................................................................................................53
3.9.5 Learned Helplessness.......................................................................................................53
3.9.6 Locus of Control...............................................................................................................54
References................................................................................................................................................54
Chapter 4 Social Psychology.....................................................................................................................................57

4.1 Attitudes and How They Are Affected.........................................................................................57
4.1.1 Definition..........................................................................................................................57
4.1.2 Components......................................................................................................................57
4.1.3 Measurement....................................................................................................................57
4.1.3.1 Thurstone Scale................................................................................................57
4.1.3.2 Likert Scale.......................................................................................................57
4.1.3.3 Semantic Differential Scale..............................................................................57
4.1.4 Attitude Change...............................................................................................................57
4.1.5 Persuasive Communication..............................................................................................57
4.1.5.1 Communicator..................................................................................................57
4.1.5.2 Recipient...........................................................................................................58
4.1.5.3 Message............................................................................................................58
4.1.6 Cognitive Consistency and Dissonance...........................................................................58
4.2 Self-Psychology.............................................................................................................................58
4.2.1 Self-Concept.....................................................................................................................58
4.2.1.1 Self-Esteem.......................................................................................................58
4.2.1.2 Self-Image.........................................................................................................58
Contents xi
4.2.2 Self-Perception Theory....................................................................................................58

4.3 Interpersonal Issues.......................................................................................................................58
4.3.1 Interpersonal Attraction...................................................................................................58
4.3.2 Attribution Theory (Heider).............................................................................................59
4.3.2.1 Internal or Dispositional Attribution................................................................59
4.3.2.2 External or Situational Attribution...................................................................59
4.3.2.3 Primary (Fundamental) Attribution Error........................................................59
4.3.3 Theory of Mind................................................................................................................59
4.4 Leadership, Social Influence, Power, and Obedience...................................................................59
4.4.1 Leadership........................................................................................................................59
4.4.2 Social Facilitation.............................................................................................................59
4.4.3 Social Power.....................................................................................................................59
4.4.4 Conformity.......................................................................................................................59
4.4.5 Obedience to Authority....................................................................................................60
4.5 Phenomenon of Aggression...........................................................................................................60
4.5.1 Explanations.....................................................................................................................60
4.5.1.1 Psychoanalytic..................................................................................................60
4.5.1.2 Social Learning Theory....................................................................................60
4.5.1.3 Operant Conditioning.......................................................................................60
4.5.1.4 Ethology............................................................................................................60
4.5.1.5 Frustration–Aggression Hypothesis.................................................................60
4.5.1.6 Arousal.............................................................................................................60
4.5.2 Influence of Television.....................................................................................................60
4.6 Concept of Altruism......................................................................................................................60
Bibliography............................................................................................................................................. 61
Chapter 5 Human Growth and Development............................................................................................................63

5.1 Conceptualizing Development......................................................................................................63
5.1.1 Basic Concepts.................................................................................................................63
5.1.2 Gene–Environment Interactions......................................................................................63
5.1.3 Historical Models.............................................................................................................63
5.2 Attachment and Bonding...............................................................................................................63
5.2.1 Attachment Theory..........................................................................................................63
5.2.2 Attachment Abnormalities...............................................................................................64
5.2.2.1 Insecure Attachment.........................................................................................64
5.2.2.2 Avoidant Attachment........................................................................................64
5.2.3 Separation Anxiety...........................................................................................................64
5.2.4 Acute Separation Reaction...............................................................................................64
5.2.5 Stranger Anxiety..............................................................................................................64
5.2.6 Maternal Deprivation.......................................................................................................64
5.3 Family Relationships and Parenting Practise................................................................................64
5.3.1 Child-Rearing Practise.....................................................................................................64
5.3.2 Family Structure...............................................................................................................65
5.3.3 Ordinal Position in Family...............................................................................................65
5.3.4 Distorted Family Function...............................................................................................65
5.3.5 Impact of Bereavement.....................................................................................................65
5.3.6 Impact of Parental Divorce..............................................................................................65
5.3.7 Impact of Intrafamilial Abuse..........................................................................................65
5.3.7.1 Sexual Abuse....................................................................................................65
xii Contents
5.3.7.2 Physical Abuse/Nonaccidental Injury..............................................................66

5.4 Temperament.................................................................................................................................66
5.4.1 Individual Temperamental Differences............................................................................66
5.4.2 Origins, Typologies, and Stability of Temperament........................................................67
5.5 Piaget’s Model of Cognitive Development....................................................................................68
5.5.1 Sensorimotor Stage..........................................................................................................68
5.5.2 Preoperational Stage........................................................................................................68
5.5.3 Concrete Operational Stage.............................................................................................68
5.5.4 Formal Operational Stage................................................................................................68
5.6 Language Development.................................................................................................................69
5.6.1 Normal Childhood Development.....................................................................................69
5.6.2 Environmental Influences and Communicative Competence..........................................69
5.7 Moral Development.......................................................................................................................69
5.7.1 Kohlberg’s Stage Theory..................................................................................................69
5.7.1.1 Preconventional Morality (Level I)..................................................................69
5.7.1.2 Conventional Morality (Level II).....................................................................69
5.7.1.3 Postconventional Morality (Level III)..............................................................69
5.7.2 Relationship to the Development of Social Perspective Taking.......................................70
5.8 Development of Fears in Childhood and Adolescence.................................................................70
5.8.1 Definition..........................................................................................................................70
5.8.2 Development with Age.....................................................................................................70
5.8.3 Possible Etiological and Maintenance Mechanisms........................................................70
5.8.3.1 Unconscious Conflict........................................................................................70
5.8.3.2 Learned Response.............................................................................................70
5.8.3.3 Lack of Control.................................................................................................70
5.9 Sexual Development......................................................................................................................70
5.9.1 Sex Determination............................................................................................................70
5.9.2 Changes at Puberty..........................................................................................................71
5.9.2.1 Physical Changes..............................................................................................71
5.9.2.2 Onset in Girls....................................................................................................71
5.9.2.3 Onset in Boys....................................................................................................71
5.9.2.4 Physiological Changes......................................................................................71
5.9.3 Gender Identity.................................................................................................................71
5.9.4 Gender/Sex Typing...........................................................................................................71
5.9.5 Gender Role......................................................................................................................71
5.9.6 Sexual Behaviour.............................................................................................................71
5.9.6.1 Sexual Drive.....................................................................................................71
5.9.6.2 Childhood Sexuality.........................................................................................72
5.9.6.3 Masturbation.....................................................................................................72
5.9.7 Sexual Orientation............................................................................................................72
5.9.7.1 Homosexuality..................................................................................................72
5.9.7.2 Modern Arguments in Favor of Biological Determinism................................73
5.9.7.3 Arguments against Biological Determinism.................................................... 74
5.10 Adolescence................................................................................................................................... 74
5.10.1 Conflict with Parents and Authority................................................................................. 74
5.10.1.1 Cognitive Developmental Models.................................................................... 74
5.10.1.2 Erikson’s Stages of Psychosocial Development................................................ 74
5.10.1.3 Ethological and Sociobiological Models.......................................................... 74
5.10.1.4 Social-Learning Theory................................................................................... 74
5.10.1.5 Equity Theory................................................................................................... 74
Contents xiii
5.10.1.6 Separation–Individuation.................................................................................75
5.10.2 Affective Stability and ‘Turmoil’.....................................................................................75
5.10.2.1 Anna Freud.......................................................................................................75
5.10.2.2 Erikson..............................................................................................................75
5.10.2.3 Offer and Offer.................................................................................................75
5.10.3 Normal and Abnormal Adolescent Development............................................................75
5.10.3.1 Offer and Offer.................................................................................................75
5.10.3.2 Block and Haan.................................................................................................75
5.11 Adaptations in Adult Life..............................................................................................................76
5.11.1 Pairing..............................................................................................................................76
5.11.1.1 Homogamous Mate Selection...........................................................................76
5.11.1.2 Reinforcement Theory......................................................................................76
5.11.1.3 Social Exchange Theory...................................................................................76
5.11.1.4 Equity Theory...................................................................................................76
5.11.1.5 Matching Hypothesis........................................................................................76
5.11.1.6 Cultural Differences.........................................................................................76
5.11.1.7 Cross-Cultural Constancies..............................................................................76
5.11.2 Parenting..........................................................................................................................76
5.11.3 Grief, Mourning, and Bereavement..................................................................................76
5.11.3.1 Definitions........................................................................................................76
5.11.3.2 Normal Grief....................................................................................................77
5.11.3.3 Bereavement.....................................................................................................77
5.11.3.4 Morbid Grief Reactions....................................................................................77
5.11.3.5 Differentiating between Bereavement and a Depressive Episode....................77
5.12 Normal Ageing.............................................................................................................................77
5.12.1 Physical Aspects...............................................................................................................77
5.12.1.1 Health................................................................................................................77
5.12.1.2 Cerebral Changes..............................................................................................77
5.12.2 Social Aspects..................................................................................................................78
5.12.2.1 Stereotyping......................................................................................................78
5.12.2.2 Empty Nest Syndrome......................................................................................78
5.12.3 Ego Integrity versus Despair............................................................................................78
5.12.3.1 Ego Integrity.....................................................................................................78
5.12.3.2 Despair..............................................................................................................78
5.12.4 Cognitive Aspects............................................................................................................78
5.13 Death and Dying...........................................................................................................................78
5.13.1 Definitions........................................................................................................................78
5.13.1.1 Timely Death....................................................................................................78
5.13.1.2 Untimely Death.................................................................................................78
5.13.1.3 Unintended Death.............................................................................................78
5.13.1.4 Intended Death..................................................................................................79
5.13.1.5 Subintended Death............................................................................................79
5.13.2 Impending Death..............................................................................................................79
References................................................................................................................................................79
Chapter 6 Description and Measurement.................................................................................................................83

6.1 Description....................................................................................................................................83
6.1.1 Types of Data....................................................................................................................83
6.1.1.1 Qualitative........................................................................................................83
xiv Contents
6.1.1.2 Quantitative......................................................................................................83
6.1.2 Scales of Measurement.....................................................................................................83
6.1.3 Sampling Methods...........................................................................................................83
6.1.3.1 Simple Random Sampling................................................................................83
6.1.3.2 Systematic Sampling........................................................................................83
6.1.4 Frequency Distributions...................................................................................................83
6.1.4.1 Frequency Distribution.....................................................................................83
6.1.4.2 Frequency Table................................................................................................83
6.1.4.3 Relative Frequency...........................................................................................83
6.1.4.4 Cumulative Frequency......................................................................................83
6.1.4.5 Cumulative Frequency Table............................................................................83
6.1.4.6 Cumulative Relative Frequency........................................................................84
6.1.4.7 Cumulative Relative Frequency Table..............................................................84
6.1.5 Discrete Probability Distributions....................................................................................84
6.1.5.1 Bernoulli Trial..................................................................................................84
6.1.5.2 Bernoulli Distribution.......................................................................................84
6.1.5.3 Binomial Distribution.......................................................................................84
6.1.5.4 Poisson Distribution..........................................................................................84
6.1.6 Continuous Probability Distributions...............................................................................84
6.1.6.1 Normal Distribution..........................................................................................84
6.1.6.2 t Distribution.....................................................................................................85
6.1.6.3 χ2 Distribution...................................................................................................85
6.1.6.4 F Distribution...................................................................................................86
6.1.7 Summary Statistics: Measures of Location.....................................................................86
6.1.7.1 Measures of Central Tendency.........................................................................86
6.1.7.2 Quantiles...........................................................................................................86
6.1.8 Summary Statistics: Measures of Dispersion...................................................................86
6.1.8.1 Range................................................................................................................86
6.1.8.2 Measures Relating to Quantiles........................................................................86
6.1.8.3 Standard Deviation...........................................................................................86
6.1.8.4 Variance............................................................................................................87
6.1.9 Graphs..............................................................................................................................87
6.1.9.1 Definition..........................................................................................................87
6.1.9.2 Drawing Graphs................................................................................................87
6.1.9.3 Linear Relationship...........................................................................................87
6.1.9.4 Power Law Relationship...................................................................................87
6.1.9.5 Exponential Relationship..................................................................................87
6.1.9.6 Other Relationships Involving Expressions......................................................88
6.1.10 Outliers.............................................................................................................................88
6.1.10.1 Measures of Central Tendency.........................................................................88
6.1.10.2 Measures of Dispersion....................................................................................88
6.1.10.3 Correlation and Linear Regression...................................................................88
6.1.11 Stem-and-Leaf Plots.........................................................................................................88
6.1.12 Boxplots (Box-and-Whisker Plots)...................................................................................88
6.1.13 Scatter Plot (Scattergrams, Scatter Diagrams, or Dot Graphs)........................................89
6.2 Principles of Measurement............................................................................................................90
6.2.1 Interviews.........................................................................................................................90
6.2.2 Self-Predictions................................................................................................................90
6.2.3 Psychophysiological Techniques......................................................................................90
6.2.4 Naturalistic Observations.................................................................................................90
Contents xv
6.2.5 Scaling..............................................................................................................................90
6.2.6 Norm Referencing............................................................................................................90
6.2.7 Criterion Referencing.......................................................................................................90
6.3 Intelligence....................................................................................................................................90
6.3.1 Aptitude............................................................................................................................90
6.3.2 Attainment........................................................................................................................90
6.3.3 Components of Intelligence..............................................................................................90
6.3.4 Mental Age Scale............................................................................................................. 91
6.3.5 Intelligence Quotient........................................................................................................ 91
6.3.6 Wechsler Adult Intelligence Scale................................................................................... 91
6.3.7 Wechsler Intelligence Scale for Children: Revised.......................................................... 91
6.3.8 Wechsler Preschool and Primary Scale of Intelligence................................................... 91
6.3.9 Group Ability Tests.......................................................................................................... 91
6.3.10 Nature–Nurture................................................................................................................92
6.3.11 Cultural Influences...........................................................................................................92
6.4 Techniques Used in Neuropsychological Assessment...................................................................92
6.4.1 Comprehensive Test Batteries..........................................................................................92
6.4.1.1 Halstead–Reitan Battery...................................................................................92
6.4.1.2 Luria–Nebraska Neuropsychological Battery..................................................92
6.4.1.3 Repeatable Battery for the Assessment of Neuropsychological Status............93
6.4.2 Language Tests.................................................................................................................93
6.4.2.1 Boston Diagnostic Aphasia Examination, 3rd Edition.....................................93
6.4.2.2 Boston Naming Test.........................................................................................93
6.4.2.3 Graded Naming Test.........................................................................................94
6.4.2.4 Token Test.........................................................................................................94
6.4.2.5 Speed and Capacity of Language Processing Test...........................................94
6.4.3 Perception Tests................................................................................................................94
6.4.3.1 Bender–Gestalt Test/Bender Visual Motor Gestalt Test..................................94
6.4.3.2 Visual Object and Space Perception Battery....................................................94
6.4.3.3 Behavioural Inattention Test.............................................................................94
6.4.4 Memory Tests...................................................................................................................94
6.4.4.1 Benton Visual Retention Test...........................................................................94
6.4.4.2 Graham–Kendall Memory for Designs Test....................................................94
6.4.4.3 Rey–Osterrieth Test..........................................................................................94
6.4.4.4 Paired Associate Learning Tests......................................................................95
6.4.4.5 Synonym Learning Test....................................................................................95
6.4.4.6 Object Learning Test........................................................................................95
6.4.4.7 Rey Auditory Verbal Learning Test.................................................................95
6.4.4.8 California Verbal Learning Test.......................................................................95
6.4.4.9 Wechsler Memory Scale-IV.............................................................................95
6.4.4.10 Rivermead Behavioural Memory Test..............................................................95
6.4.4.11 Adult Memory and Information Processing Battery........................................95
6.4.5 Intelligence Tests..............................................................................................................96
6.4.5.1 WAIS and Similar Tests...................................................................................96
6.4.5.2 National Adult Reading Test.............................................................................96
6.4.5.3 Raven’s Progressive Matrices...........................................................................96
6.4.6 Executive Function (Frontal Lobe) Tests.........................................................................96
6.4.6.1 Stroop................................................................................................................96
6.4.6.2 Verbal Fluency..................................................................................................96
6.4.6.3 Tower of London Test.......................................................................................96
xvi Contents
6.4.6.4 Wisconsin Card Sort Test.................................................................................96

6.4.6.5 Cognitive Estimates Test..................................................................................97
6.4.6.6 Six Elements Test..............................................................................................97
6.4.6.7 Multiple Errands Task......................................................................................97
6.4.6.8 Trail Making Test.............................................................................................97
6.4.7 Personality Tests...............................................................................................................97
6.4.7.1 Objective Tests..................................................................................................97
6.4.7.2 Projective Tests.................................................................................................98
6.4.8 Dementia Tests and Related Tests....................................................................................98
6.4.8.1 Mini-Mental State Examination.......................................................................98
6.4.8.2 Cambridge Neuropsychological Test Automated Battery................................98
6.4.8.3 Gresham Ward Questionnaire..........................................................................98
6.4.8.4 Blessed’s Dementia Scale.................................................................................99
6.4.8.5 Information–Memory–Concentration Test.......................................................99
6.4.8.6 Geriatric Mental State Schedule.......................................................................99
6.4.8.7 Cambridge Examination for Mental Disorders................................................99
6.4.8.8 Crichton Geriatric Behaviour Rating Scale......................................................99
6.4.8.9 Clifton Assessment Schedule...........................................................................99
6.4.8.10 Stockton Geriatric Rating Scale.......................................................................99
6.4.8.11 Present Behavioural Examination....................................................................99
6.4.8.12 Manchester and Oxford Universities Scale for the Psychopathological
Assessment of Dementia...................................................................................99
6.4.8.13 Sandoz Clinical Assessment.............................................................................99
6.4.8.14 Vineland Social Maturity Scale......................................................................100
6.4.8.15 Performance Test of Activities of Daily Living..............................................100
References..............................................................................................................................................100
Chapter 7 Cognitive Assessment and Neuropsychological Processes.................................................................... 103

7.1 Memory....................................................................................................................................... 103
7.1.1 Sensory Memory............................................................................................................ 103
7.1.1.1 Short-Term Memory....................................................................................... 103
7.1.1.2 Explicit Memory............................................................................................. 103
7.1.1.3 Implicit Memory............................................................................................. 103
7.2 Amnesia....................................................................................................................................... 103
7.3 Language..................................................................................................................................... 103
7.3.1 Cerebral Dominance...................................................................................................... 103
7.3.1.1 Speech and Language Areas.......................................................................... 103
7.3.1.2 Pathways......................................................................................................... 105
7.3.2 Dysphasias...................................................................................................................... 105
7.3.2.1 Receptive Dysphasia....................................................................................... 105
7.3.2.2 Expressive Dysphasia..................................................................................... 105
7.3.2.3 Conduction Dysphasia.................................................................................... 105
7.3.2.4 Global Dysphasia............................................................................................ 105
7.3.3 Mutism............................................................................................................................ 105
7.4 Perception.................................................................................................................................... 105
7.4.1 Visual Perception........................................................................................................... 105
7.4.1.1 Other Agnosias...............................................................................................106
7.5 Dyslexia and Dysgraphia.............................................................................................................107
7.5.1 Dyslexia..........................................................................................................................107
7.5.2 Dysgraphia.....................................................................................................................107
Contents xvii
7.6 Alexia and Agraphia....................................................................................................................107

7.6.1 Alexia without Agraphia................................................................................................107
7.6.2 Alexia with Agraphia.....................................................................................................108
7.7 Apraxias......................................................................................................................................108
7.7.1 Acalculia and Anarithmetria..........................................................................................108
7.8 Frontal Lobe Functions...............................................................................................................109
7.8.1 Prefrontal Cortex............................................................................................................109
7.8.2 Frontal Eye Fields...........................................................................................................109
7.8.3 Motor and Premotor Cortex........................................................................................... 110
7.8.4 Broca’s Area................................................................................................................... 110
7.8.5 Orbital Cortex................................................................................................................ 110
7.8.6 Frontal Lobe Lesions...................................................................................................... 110
7.8.7 Assessment of Temporal Lobe Functions...................................................................... 110
7.9 Left and Right Cerebral Hemispheres......................................................................................... 110
Bibliography........................................................................................................................................... 114
Chapter 8 Social Sciences and Stigma.................................................................................................................... 115

8.1 Descriptive Terms........................................................................................................................ 115
8.1.1 Social Class.................................................................................................................... 115
8.1.1.1 Determinants.................................................................................................. 115
8.1.1.2 Occupational Classification............................................................................ 115
8.1.2 Socioeconomic Status.................................................................................................... 115
8.1.3 Relevance to Psychiatric Disorder and Health-Care Delivery....................................... 115
8.1.3.1 Psychiatric Disorder........................................................................................ 115
8.1.3.2 Relationship between Social Class and Psychiatric Disorder........................ 115
8.1.3.3 Health-Care Delivery..................................................................................... 116
8.1.3.4 Pathways to Psychiatric Care.......................................................................... 116
8.1.4 Black Report on Socioeconomic Inequalities in Health................................................ 116
8.1.4.1 Explanations................................................................................................... 116
8.1.4.2 Changes after 10 Years................................................................................... 116
8.2 Historical Sociological Theories................................................................................................. 117
8.2.1 Weber............................................................................................................................. 117
8.2.1.1 Bureaucracy.................................................................................................... 117
8.2.1.2 Rationalization................................................................................................ 117
8.2.1.3 Religion........................................................................................................... 117
8.2.2 Marx............................................................................................................................... 117
8.2.2.1 Communism................................................................................................... 117
8.2.2.2 Crime.............................................................................................................. 117
8.2.2.3 Religion........................................................................................................... 117
8.2.3 Durkheim....................................................................................................................... 117
8.2.3.1 Anomie........................................................................................................... 118
8.2.3.2 Suicide............................................................................................................ 118
8.2.4 Foucault.......................................................................................................................... 118
8.2.4.1 Principles of Exclusion................................................................................... 118
8.2.4.2 Sexuality......................................................................................................... 118
8.2.5 Parsons........................................................................................................................... 118
8.2.6 Goffman......................................................................................................................... 118
8.2.7 Habermas....................................................................................................................... 118
8.3 Social Roles of Doctors and Illness............................................................................................. 119
8.3.1 Social Role..................................................................................................................... 119
xviii Contents
8.3.2
Social Role of Doctors................................................................................................... 119
8.3.3
Sick Role......................................................................................................................... 119
8.3.3.1 Rights (Privileges).......................................................................................... 119
8.3.3.2 Obligations...................................................................................................... 119
8.3.4 Illness Behaviour............................................................................................................ 119
8.3.4.1 Stages.............................................................................................................. 119
8.3.4.2 Determinants.................................................................................................. 119
8.4 Family Life in Relation to Major Mental Illness.........................................................................120
8.4.1 Elements of Family Functioning....................................................................................120
8.4.2 Schizophrenia.................................................................................................................120
8.4.2.1 Schizophrenogenic Mother.............................................................................120
8.4.2.2 Double Bind....................................................................................................120
8.4.2.3 Marital Skew and Marital Schism..................................................................120
8.4.2.4 Abnormal Family Communication.................................................................120
8.4.2.5 Expressed Emotion......................................................................................... 121
8.4.3 Mood Disorders.............................................................................................................. 121
8.4.3.1 Expressed Emotion......................................................................................... 121
8.4.3.2 Vulnerability Factors...................................................................................... 121
8.4.4 Problem Drinking and Alcohol Dependence................................................................. 121
8.4.5 Learning Disability/Mental Retardation........................................................................ 121
8.5 Life Events...................................................................................................................................122
8.5.1 Definition........................................................................................................................122
8.5.2 Life-Change Scale..........................................................................................................122
8.5.3 Aetiology of Psychiatric Disorders................................................................................122
8.5.4 Difficulties in the Evaluation of Life Events..................................................................122
8.5.5 Clinical Significance......................................................................................................122
8.5.5.1 Depression......................................................................................................122
8.5.5.2 Schizophrenia.................................................................................................123
8.5.5.3 Anxiety...........................................................................................................123
8.5.5.4 Mania..............................................................................................................123
8.5.5.5 Parasuicide/Deliberate Self-Harm..................................................................123
8.5.5.6 Functional Disorders.......................................................................................123
8.6 Residential Institutions................................................................................................................123
8.6.1 Social Institutions...........................................................................................................123
8.6.1.1 Definition........................................................................................................123
8.6.1.2 Examples.........................................................................................................123
8.6.2 Total Institutions.............................................................................................................123
8.6.2.1 Definition........................................................................................................123
8.6.2.2 Examples.........................................................................................................123
8.6.3 Goffman.........................................................................................................................123
8.6.3.1 Reactions to the Mortification Process...........................................................124
8.6.4 Institutional Neurosis.....................................................................................................124
8.6.5 Secondary Handicap......................................................................................................124
8.6.5.1 Primary Handicap..........................................................................................124
8.6.5.2 Secondary Handicap.......................................................................................124
8.6.6 Three Mental Hospitals Study.......................................................................................124
8.7 Ethnic Minorities, Adaptation, and Mental Health.....................................................................124
8.7.1 Prevalence of Schizophrenia..........................................................................................124
8.7.2 Causes of Different Prevalence Rates............................................................................124
8.7.3 Depression and Anxiety.................................................................................................125
Contents xix
8.8 Professions...................................................................................................................................125
8.8.1 Characteristics of Professions........................................................................................125
8.8.2 Professional Groups Involved in Patient Care................................................................125
8.9 Intergroup Behaviour and Stigma...............................................................................................125
8.9.1 Stereotypes.....................................................................................................................125
8.9.2 Stigma.............................................................................................................................125
8.9.2.1 Definition........................................................................................................125
8.9.2.2 Example..........................................................................................................125
8.9.2.3 Enacted Stigma...............................................................................................125
8.9.2.4 Felt Stigma......................................................................................................125
8.9.2.5 Development...................................................................................................125
8.9.3 Prejudice.........................................................................................................................125
8.9.3.1 Definition........................................................................................................125
8.9.3.2 Example..........................................................................................................126
8.9.3.3 Discrimination................................................................................................126
8.9.3.4 Causes.............................................................................................................126
8.9.3.5 Reducing Prejudice.........................................................................................126
References..............................................................................................................................................126
Chapter 9 Dynamic Psychopathology and Psychoanalytic Theories......................................................................129

9.1 Basic Principles of Dynamic Psychotherapy...............................................................................129
9.2 Sigmund Freud (1856–1939)........................................................................................................129
9.2.1 Early Influences..............................................................................................................129
9.2.2 Protopsychoanalytic Phase (1887 to c.1897)..................................................................129
9.2.2.1 Studies on Hysteria.........................................................................................129
9.2.2.2 Technical Development..................................................................................129
9.2.2.3 Project for a Scientific Psychology.................................................................129
9.2.3 Topographical Model of the Mind.................................................................................130
9.2.3.1 Unconscious....................................................................................................130
9.2.3.2 Preconscious...................................................................................................130
9.2.3.3 Conscious........................................................................................................130
9.2.3.4 Censorship......................................................................................................130
9.2.3.5 Primary Process..............................................................................................130
9.2.3.6 Secondary Process.......................................................................................... 131
9.2.3.7 Pleasure Principle........................................................................................... 131
9.2.3.8 Reality Principle............................................................................................. 131
9.2.4 Dreaming........................................................................................................................ 131
9.2.4.1 Dream Composition........................................................................................ 131
9.2.4.2 Dream Work................................................................................................... 131
9.2.5 Structural Model of the Mind........................................................................................ 131
9.2.5.1 Id..................................................................................................................... 131
9.2.5.2 Ego.................................................................................................................. 131
9.2.5.3 Superego......................................................................................................... 132
9.2.5.4 Relationship between the Id, Ego, and Superego........................................... 132
9.2.6 Resistance....................................................................................................................... 132
9.2.7 Transference................................................................................................................... 132
9.2.8 Countertransference....................................................................................................... 132
9.2.9 Instinctual Drives........................................................................................................... 132
xx Contents
9.2.10 Psychosexual Development............................................................................................ 133

9.2.10.1 Oral Phase....................................................................................................... 133
9.2.10.2 Anal Phase...................................................................................................... 133
9.2.10.3 Phallic Phase................................................................................................... 133
9.2.10.4 Latency Stage.................................................................................................. 133
9.2.10.5 Genital Stage.................................................................................................. 133
9.3 Carl Jung (1875–1961)................................................................................................................. 133
9.3.1 Early Influences.............................................................................................................. 133
9.3.2 Differences between Jungian and Freudian Theory...................................................... 133
9.3.2.1 Libido Theory................................................................................................. 133
9.3.2.2 Nature of the Unconscious.............................................................................. 133
9.3.2.3 Causality......................................................................................................... 133
9.3.2.4 Dreaming........................................................................................................ 133
9.3.3 Archetypes..................................................................................................................... 133
9.3.3.1 Anima............................................................................................................. 133
9.3.3.2 Animus........................................................................................................... 133
9.3.3.3 Persona............................................................................................................134
9.3.3.4 Shadow............................................................................................................134
9.3.3.5 Self..................................................................................................................134
9.3.4 Complexes......................................................................................................................134
9.3.5 Mental Operations..........................................................................................................134
9.3.5.1 Feeling............................................................................................................134
9.3.5.2 Intuition..........................................................................................................134
9.3.5.3 Sensation.........................................................................................................134
9.3.5.4 Thinking.........................................................................................................134
9.3.6 Extroversion and Introversion........................................................................................134
9.3.6.1 Extroversion....................................................................................................134
9.3.6.2 Introversion.....................................................................................................134
9.3.7 Individuation..................................................................................................................134
9.4 Melanie Klein (1882–1960).........................................................................................................134
9.4.1 Background....................................................................................................................134
9.4.2 Differences between Kleinian and Freudian Theory.....................................................134
9.4.2.1 Object Relations..............................................................................................134
9.4.2.2 Paranoid-Schizoid Position.............................................................................134
9.4.2.3 Aggression...................................................................................................... 135
9.4.2.4 Depressive Position......................................................................................... 135
9.4.2.5 Development of the Ego and Superego........................................................... 135
9.4.3 Early Development......................................................................................................... 135
9.4.4 Analytic Play Technique................................................................................................ 135
9.5 Donald Winnicott (1897–1971).................................................................................................... 135
9.5.1 Background.................................................................................................................... 135
9.5.2 Mother–Baby Dyad........................................................................................................ 135
9.5.3 Countertransference....................................................................................................... 135
9.5.3.1 Objective Countertransference....................................................................... 135
9.5.3.2 Countertransference Hate............................................................................... 135
9.5.4 Motherhood.................................................................................................................... 135
9.5.4.1 Good-Enough Mother..................................................................................... 135
9.5.4.2 Pathological Mother........................................................................................ 135
9.5.4.3 Capacity to Be Alone......................................................................................136
9.5.5 Transitional Object.........................................................................................................136
9.5.6 Other Concepts...............................................................................................................136
Contents xxi
9.6 Psychodynamic Theory of Defence Mechanisms.......................................................................136

9.6.1 Repression......................................................................................................................136
9.6.2 Reaction Formation........................................................................................................136
9.6.3 Isolation..........................................................................................................................136
9.6.4 Undoing (What Has Been Done)....................................................................................136
9.6.5 Projection.......................................................................................................................136
9.6.6 Projective Identification.................................................................................................136
9.6.7 Identification...................................................................................................................136
9.6.8 Introjection.....................................................................................................................136
9.6.9 Incorporation..................................................................................................................136
9.6.10 Turning against the Self................................................................................................. 137
9.6.11 Reversal into the Opposite............................................................................................. 137
9.6.12 Rationalization............................................................................................................... 137
9.6.13 Sublimation.................................................................................................................... 137
9.6.14 Idealization..................................................................................................................... 137
9.6.15 Regression...................................................................................................................... 137
9.6.16 Denial............................................................................................................................. 137
9.6.17 Splitting.......................................................................................................................... 137
9.6.18 Distortion........................................................................................................................ 137
9.6.19 Acting Out...................................................................................................................... 137
9.6.20 Displacement.................................................................................................................. 137
9.6.21 Intellectualization........................................................................................................... 137
Bibliography........................................................................................................................................... 137
Chapter 10 History of Psychiatry.............................................................................................................................. 139

10.1 Before Common Era (BCE)........................................................................................................ 139
10.2 Common Era................................................................................................................................ 139
10.3 Middle Ages................................................................................................................................ 139
10.4 1247–1320.................................................................................................................................... 139
10.5 1700s............................................................................................................................................ 139
10.6 1790–1830.................................................................................................................................... 139
10.7 1830–1914.................................................................................................................................... 139
10.8 1830s............................................................................................................................................ 139
10.9 1840s............................................................................................................................................ 139
10.10 1850s............................................................................................................................................ 140
10.11 1860s............................................................................................................................................ 140
10.12 1870s............................................................................................................................................ 140
10.13 1880s and 1890s........................................................................................................................... 140
10.14 1900s........................................................................................................................................... 140
10.15 1910s............................................................................................................................................ 141
10.16 1920s............................................................................................................................................ 141
10.17 1930s............................................................................................................................................ 141
10.18 1940s............................................................................................................................................ 142
10.18.1 Development of Psychotherapies in the 1940s............................................................... 142
10.19 1950s............................................................................................................................................ 143
10.20 1960s............................................................................................................................................ 143
10.21 1970s............................................................................................................................................ 143
10.22 1980s............................................................................................................................................ 143
10.23 1990s............................................................................................................................................ 143
xxii Contents
10.24 2000s...........................................................................................................................................144
Bibliography...........................................................................................................................................144
Chapter 11 Basic Ethics, Principles of Law, and Philosophy of Psychiatry............................................................. 145

11.1 Ethical Standards and Codes of Practise..................................................................................... 145
11.1.1 Hippocratic Oath............................................................................................................ 145
11.1.2 Declaration of Geneva (1948)......................................................................................... 145
11.1.3 Declaration of Madrid.................................................................................................... 145
11.1.4 Royal College of Psychiatrists........................................................................................ 145
11.2 Classical Ethical Theories........................................................................................................... 145
11.2.1 Utilitarian Theories........................................................................................................ 145
11.2.2 Deontological Theories (aka the Kantian Theories)...................................................... 146
11.2.3 Virtue Theories (Plato and Aristotle)............................................................................. 146
11.2.3.1 Ethical Principles............................................................................................ 146
11.2.3.2 Other Ethical Theories................................................................................... 146
11.2.3.3 Confidentiality and Privileges........................................................................ 146
11.2.3.4 Exceptions to Confidentiality......................................................................... 147
11.2.3.5 Approaches to Breach Confidentiality............................................................ 147
11.2.3.6 Confidentiality in Minors............................................................................... 147
11.3 Ethics and Psychiatric Research.................................................................................................. 147
11.3.1 Nuremberg Code (1947)................................................................................................. 147
11.3.2 Declaration of Helsinki (1964)....................................................................................... 148
11.3.3 Belmont Report (1979)................................................................................................... 148
11.4 Competency and Capacity........................................................................................................... 148
11.4.1 Competency.................................................................................................................... 148
11.4.2 Capacity.......................................................................................................................... 148
11.4.2.1 Capacity for Informed Consent...................................................................... 148
11.5 Principles of Law......................................................................................................................... 149
11.5.1 Mental Capacity Act (2005) (England and Wales)........................................................ 149
11.5.1.1 Principles of the Mental Capacity Act (2005)................................................ 151
11.5.1.2 Three Parts of the Mental Capacity Act (2005)............................................. 151
11.5.2 Mental Health Act (MHA, 2007) in England and Wales.............................................. 151
11.6 Philosophy of Psychiatry.............................................................................................................154
11.6.1 Philosophy and Science..................................................................................................154
11.6.2 Formal and Informal Logic............................................................................................154
11.6.3 Philosophy of Anti- and Propsychiatry.......................................................................... 155
11.6.3.1 Philosophy of Antipsychiatry......................................................................... 155
Bibliography........................................................................................................................................... 158
Chapter 12 Neurology and Neurological Examination............................................................................................. 159

12.1 Cranial Nerves (CNs II, III, IV, and VI) and the Visual System................................................ 159
12.1.1 Central Visual Pathway and Visual Field Deficits......................................................... 159
12.1.1.1 Common Lesions in the Central Visual Pathway........................................... 159
12.2 Cranial Nerves (CNs III, IV, and VI) and Double Vision........................................................... 159
12.2.1 Oculomotor Nerve (CN III)............................................................................................ 159
12.2.2 Trochlear Nerve (CN IV)...............................................................................................160
12.2.3 Abducens Nerve (CN VI)...............................................................................................160
Contents xxiii
12.2.4 Medial Longitudinal Fasciculus..................................................................................... 161

12.2.4.1 Examination of the Pupils and Related Conditions........................................ 161
12.2.5 Trigeminal Nerve (CN V).............................................................................................. 162
12.2.6 Facial Nerve................................................................................................................... 163
12.2.7 Vestibulocochlear Nerve (CN VIII)............................................................................... 163
12.2.7.1 Weber’s Test.................................................................................................... 163
12.2.7.2 Rinne’s Test.....................................................................................................164
12.2.7.3 Anatomy of the Auditory System...................................................................164
12.3 Other Cranial Nerves................................................................................................................... 165
12.3.1 Spinal Cord..................................................................................................................... 165
12.3.1.1 Spinothalamic Tracts...................................................................................... 166
12.3.1.2 Second-Order Neurons................................................................................... 166
12.3.1.3 Third-Order Neurons...................................................................................... 166
12.3.2 Dorsal Column............................................................................................................... 166
12.3.2.1 Ascending Dorsal Columns............................................................................ 166
12.3.2.2 Decussation in the Medulla............................................................................ 167
12.3.2.3 Third-Order Neurons...................................................................................... 167
12.3.4 Corticospinal and Corticobulbar Tracts......................................................................... 167
12.4 Myotomes and Neurological Examination in the CASC............................................................ 168
12.4.1 Myotomes of the Upper Limb........................................................................................ 168
12.4.2 Myotomes of the Lower Limb........................................................................................ 169
12.5 Dermatomes................................................................................................................................ 171
12.6 Compression and Entrapment Neuropathies............................................................................... 172
12.7 Other Neurological Conditions.................................................................................................... 172
12.7.1 Headache........................................................................................................................ 172
12.7.1.1 Types of Headache.......................................................................................... 172
12.7.2 Pellagra........................................................................................................................... 172
12.7.3 Blepharospasm............................................................................................................... 172
12.7.4 Other Dystonia............................................................................................................... 172
12.7.4.1 Gait Abnormalities......................................................................................... 174
12.7.4.2 Ekbom’s Syndrome (Restless Leg Syndrome)................................................ 174
12.7.4.3 Peripheral Neuropathies................................................................................. 174
12.7.4.4 Guillain–Barré Syndrome.............................................................................. 174
Acknowledgments.................................................................................................................................. 174
Bibliography........................................................................................................................................... 174
Chapter 13 Neuroanatomy........................................................................................................................................ 175

13.1 Organization of the Nervous System........................................................................................... 175
13.1.1 Structural Organization.................................................................................................. 175
13.1.1.1 Central Nervous System................................................................................. 175
13.1.1.2 Peripheral Nervous System............................................................................. 175
13.1.2 Functional Organization................................................................................................. 175
13.1.2.1 Somatic Nervous System................................................................................ 175
13.1.2.2 Autonomic Nervous System........................................................................... 175
13.1.3 Developmental Organization.......................................................................................... 175
13.2 Types of Nervous System Cell.................................................................................................... 176
13.2.1 Neurons.......................................................................................................................... 176
13.2.1.1 Classification by Morphology......................................................................... 176
13.2.1.2 Classification by Size...................................................................................... 176
xxiv Contents
13.2.2 Neuroglia........................................................................................................................ 176

13.2.2.1 Relative Numbers............................................................................................ 176
13.2.2.2 Central Nervous System................................................................................. 176
13.2.2.3 Peripheral Nervous System............................................................................. 176
13.2.2.4 Astrocytes....................................................................................................... 176
13.2.2.5 Oligodendrocytes............................................................................................ 177
13.2.2.6 Microglia........................................................................................................ 177
13.2.2.7 Ependymal Cells............................................................................................. 177
13.2.2.8 Schwann Cells................................................................................................ 177
13.2.2.9 Satellite Cells.................................................................................................. 177
13.3 Frontal Lobes............................................................................................................................... 177
13.3.1 Frontal Operculum......................................................................................................... 177
13.3.1.1 Broca’s Area................................................................................................... 177
13.3.1.2 Right Side....................................................................................................... 177
13.3.2 Superior Mesial Region.................................................................................................. 177
13.3.3 Inferior Mesial Region................................................................................................... 177
13.3.3.1 Orbital Cortex................................................................................................. 177
13.3.3.2 Basal Forebrain............................................................................................... 177
13.3.4 Dorsolateral Prefrontal Cortex....................................................................................... 177
13.4 Temporal Lobes........................................................................................................................... 178
13.4.1 Superior Temporal Gyrus............................................................................................... 178
13.4.2 Posterior Inferolateral Region........................................................................................ 179
13.4.3 Anterior Inferolateral Region......................................................................................... 179
13.4.4 Mesial Temporal Region................................................................................................ 179
13.5 Parietal Lobes.............................................................................................................................. 179
13.5.1 Temporoparietal Junction............................................................................................... 179
13.5.2 Inferior Parietal Lobule.................................................................................................. 180
13.6 Occipital Lobes........................................................................................................................... 180
13.7 Basal Ganglia.............................................................................................................................. 180
13.7.1 Components.................................................................................................................... 180
13.7.2 Connections of the Lentiform Nucleus.......................................................................... 180
13.7.2.1 Afferents......................................................................................................... 180
13.7.2.2 Efferents.......................................................................................................... 181
13.7.3 Frontal–Subcortical Circuits.......................................................................................... 181
13.7.3.1 Motor Circuit.................................................................................................. 181
13.7.3.2 Oculomotor Circuit......................................................................................... 181
13.7.3.3 Dorsolateral Prefrontal Circuit....................................................................... 181
13.7.3.4 Lateral Orbitofrontal Circuit.......................................................................... 181
13.7.3.5 Anterior Cingulate Circuit.............................................................................. 181
13.8 Limbic System............................................................................................................................. 181
13.8.1 Limbic Lobe................................................................................................................... 181
13.8.1.1 Cortical Areas................................................................................................. 181
13.8.1.2 Nuclei.............................................................................................................. 181
13.8.2 Components.................................................................................................................... 181
13.8.2.1 Cortical Areas................................................................................................. 181
13.8.2.2 Nuclei.............................................................................................................. 182
13.8.2.3 Connecting Pathways...................................................................................... 182
13.9 Internal Anatomy of the Temporal Lobes................................................................................... 182
13.9.1 Hippocampal Formation................................................................................................ 182
13.9.1.1 Dentate Gyrus................................................................................................. 182
Contents xxv
13.9.1.2 Hippocampus.............................................................................................. 182

13.9.1.3 Parahippocampal Gyrus............................................................................. 182
13.9.2 Amygdala..................................................................................................................... 182
13.9.2.1 Afferent Connections................................................................................. 182
13.9.2.2 Efferent Connections.................................................................................. 183
13.10 Major White Matter Pathways..................................................................................................... 183
13.10.1 Corpus Callosum......................................................................................................... 183
13.10.1.1 Divisions..................................................................................................... 183
13.10.2 Fornix.......................................................................................................................... 183
13.10.2.1 Destination of Fibres in the Fornix............................................................ 183
13.10.3 Papez Circuit............................................................................................................... 183
13.10.4 Arcuate Bundle............................................................................................................ 184
13.10.5 Anterior Commissure.................................................................................................. 184
13.11 Cranial Nerves............................................................................................................................. 184
13.11.1 Olfactory Nerve........................................................................................................... 184
13.11.2 Optic Nerve................................................................................................................. 184
13.11.3 Oculomotor Nerve....................................................................................................... 184
13.11.4 Trochlear Nerve........................................................................................................... 184
13.11.5 Trigeminal Nerve......................................................................................................... 184
13.11.5.1 Nuclei......................................................................................................... 185
13.11.5.2 Sensory Components.................................................................................. 185
13.11.5.3 Motor Component...................................................................................... 185
13.11.6 Abducens Nerve.......................................................................................................... 185
13.11.7 Facial Nerve................................................................................................................. 185
13.11.7.1 Nuclei......................................................................................................... 185
13.11.7.2 Main Motor Nucleus.................................................................................. 185
13.11.7.3 Parasympathetic Nuclei.............................................................................. 186
13.11.7.4 Sensory Nucleus......................................................................................... 186
13.11.7.5 Chorda Tympani......................................................................................... 186
13.11.8 Vestibulocochlear Nerve............................................................................................. 186
13.11.8.1 Cochlear Nerve........................................................................................... 186
13.11.8.2 Vestibular Nerve......................................................................................... 186
13.11.9 Glossopharyngeal Nerve............................................................................................. 186
13.11.9.1 Nuclei......................................................................................................... 186
13.11.9.3 Parasympathetic Nucleus........................................................................... 186
13.11.9.4 Sensory Nucleus......................................................................................... 186
13.11.10 Vagus Nerve................................................................................................................ 186
13.11.10.1 Nuclei......................................................................................................... 186
13.11.10.3 Parasympathetic Nucleus........................................................................... 187
13.11.10.4 Sensory Nucleus......................................................................................... 187
13.11.11 Accessory Nerve.......................................................................................................... 187
13.11.11.1 Cranial Root............................................................................................... 187
13.11.11.2 Spinal Root................................................................................................. 187
13.11.12 Hypoglossal Nerve...................................................................................................... 187
13.12 Spinal Cord.................................................................................................................................. 187
13.12.1 Divisions...................................................................................................................... 187
13.12.2 Ascending White Column Tracts................................................................................ 187
13.12.2.1 Anterior...................................................................................................... 188
xxvi Contents
13.12.2.2 Lateral........................................................................................................ 188

13.12.2.3 Posterior..................................................................................................... 188
13.12.3 Descending White Column Tracts................................................................................ 188
13.12.3.1 Anterior...................................................................................................... 189
13.12.3.2 Lateral........................................................................................................ 189
13.13 Major Neurochemical Pathways.................................................................................................. 189
13.13.1 Nigrostriatal Dopaminergic Pathway............................................................................ 189
13.13.2 Mesolimbic–Mesocortical Dopaminergic Pathway......................................................190
13.13.3 Ascending Noradrenergic Pathway from the Locus Coeruleus....................................190
13.13.4 Basal Forebrain Cholinergic Pathway........................................................................... 191
13.13.5 Brain Stem Cholinergic Pathway.................................................................................. 191
13.13.6 Glutamate System......................................................................................................... 193
13.13.7 Ascending Serotonin System........................................................................................ 193
Bibliography........................................................................................................................................... 193
Chapter 14 Neuropathology...................................................................................................................................... 195

14.1 Dementias.................................................................................................................................... 195
14.1.1 Alzheimer’s Disease...................................................................................................... 195
14.1.1.1 Macroscopic Neuropathology.................................................................... 195
14.1.1.2 Histopathology........................................................................................... 195
14.1.1.3 Ultrastructural Pathology........................................................................... 195
14.1.1.4 Neurochemical Pathology.......................................................................... 195
14.1.2 Pick’s Disease................................................................................................................ 195
14.1.2.1 Macroscopic Neuropathology.................................................................... 195
14.1.2.2 Histopathology........................................................................................... 195
14.1.2.3 Ultrastructural Pathology...........................................................................196
14.1.3 Multi-Infarct Dementia.................................................................................................196
14.1.3.1 Macroscopic Neuropathology....................................................................196
14.1.3.2 Histopathology...........................................................................................196
14.1.4 Lewy Body Disease......................................................................................................196
14.1.4.1 Histopathology...........................................................................................196
14.1.4.2 Ultrastructural Pathology...........................................................................196
14.1.5 Creutzfeldt–Jakob Disease............................................................................................196
14.1.5.2 Histopathology...........................................................................................196
14.1.6 Punch-Drunk Syndrome...............................................................................................197
14.1.6.2 Histopathology...........................................................................................197
14.2 Cerebral Tumours........................................................................................................................197
14.2.1 Types.............................................................................................................................197
14.2.2 Gliomas.........................................................................................................................197
14.2.3 Metastases.....................................................................................................................197
14.2.4 Meningeal Tumours......................................................................................................197
14.2.5 Pituitary Adenomas.......................................................................................................197
14.2.6 Neurilemmomas............................................................................................................197
14.2.7 Haemangioblastomas....................................................................................................197
14.2.8 Medulloblastomas.........................................................................................................197
14.3 Schizophrenia.............................................................................................................................. 198
14.3.1 Gross Neuropathology.................................................................................................. 198
14.3.1.1 Brain Mass................................................................................................. 198
Contents xxvii
14.3.1.2 Brain Length................................................................................................... 198

14.3.1.3 Cerebral Volumes........................................................................................... 198
14.3.1.4 Hippocampus and Parahippocampal Gyrus................................................... 198
14.3.1.5 Ventricular Volume......................................................................................... 198
14.3.1.6 Temporal Lobe................................................................................................ 198
14.3.2 Morphometric Studies.................................................................................................... 198
14.3.2.1 Temporal Lobe................................................................................................ 198
14.3.2.2 Other Cortical Areas......................................................................................199
14.3.2.3 Other Brain Regions.......................................................................................199
14.3.3 Synaptic Pathology.........................................................................................................199
14.3.3.1 Synaptic Vesicles............................................................................................199
14.3.3.2 Synaptophysin.................................................................................................199
14.3.4 Gliosis.............................................................................................................................199
14.3.5 Antipsychotic Medication..............................................................................................199
14.4 Autism.........................................................................................................................................200
14.4.1 Histological Changes......................................................................................................200
14.4.2 Cerebellar Pathology......................................................................................................200
14.4.2.1 Reduced Purkinje Cell Count.........................................................................200
14.4.2.2 Neocerebellar Abnormality............................................................................200
14.5 Movement Disorders...................................................................................................................200
14.5.1 Parkinson’s Disease........................................................................................................200
14.5.1.1 Macroscopic Neuropathology.........................................................................200
14.5.1.2 Histopathology................................................................................................200
14.5.1.3 Neurochemical Pathology...............................................................................201
14.5.2 Huntington’s Disease (Chorea).......................................................................................201
14.5.2.1 Macroscopic Neuropathology.........................................................................201
14.5.2.2 Histopathology................................................................................................201
14.5.2.3 Neurochemical Pathology...............................................................................201
14.5.3 Tardive Dyskinesia.........................................................................................................201
14.5.3.1 Dopamine Hypersensitivity Hypothesis.........................................................201
14.5.3.2 Free-Radical-Induced Neurotoxicity..............................................................202
14.5.3.3 GABA Insufficiency.......................................................................................202
14.5.3.4 Noradrenergic Dysfunction............................................................................203
References..............................................................................................................................................203
Chapter 15 Neuroimaging Techniques.....................................................................................................................205

15.1 X-Ray...........................................................................................................................................205
15.1.1 Basis...............................................................................................................................205
15.1.2 Type of Imaging.............................................................................................................205
15.1.3 Neuropsychiatric Applications.......................................................................................205
15.2 CT................................................................................................................................................205
15.2.1 Basis...............................................................................................................................205
15.2.2 Type of Imaging.............................................................................................................205
15.3 PET..............................................................................................................................................205
15.3.1 Basis...............................................................................................................................205
15.3.2 Type of Imaging.............................................................................................................206
15.4 SPECT.........................................................................................................................................206
15.4.1 Basis...............................................................................................................................206
xxviii Contents
15.4.2 Type of Imaging.............................................................................................................206

15.5 MRI.............................................................................................................................................206
15.5.1 Basis...............................................................................................................................206
15.5.2 Type of Imaging.............................................................................................................208
Bibliography...........................................................................................................................................208
Chapter 16 Neurophysiology.....................................................................................................................................209
16.1 Physiology of Neurons, Synapses, and Receptors.......................................................................209
16.1.1 Neurons..........................................................................................................................209
16.1.1.1 Resting Membrane Ion Permeabilities...........................................................209
16.1.1.2 Resting Membrane Potential..........................................................................209
16.1.1.3 Changes in Membrane Ion Permeabilities......................................................209
16.1.1.4 Action Potential..............................................................................................209
16.1.1.5 Propagation of Action Potential......................................................................209
16.1.1.6 All-or-None Phenomenon...............................................................................209
16.1.1.7 Absolute Refractory Period............................................................................209
16.1.1.8 Relative Refractory Period..............................................................................209
16.1.1.9 Conduction in Unmyelinated Fibres...............................................................209
16.1.1.10 Conduction in Myelinated Fibres...................................................................209
16.1.2 Synapses.........................................................................................................................209
16.1.2.1 Synaptic Cleft.................................................................................................209
16.1.2.2 Location..........................................................................................................209
16.1.2.3 Types............................................................................................................... 210
16.1.2.4 Synaptic Transmission.................................................................................... 210
16.1.2.5 Excitatory Postsynaptic Potentials.................................................................. 210
16.1.2.6 Inhibitory Postsynaptic Potentials.................................................................. 210
16.1.2.7 Summation...................................................................................................... 210
16.1.3 Receptors........................................................................................................................ 210
16.1.3.1 Sensory Receptors.......................................................................................... 210
16.1.3.2 Adaptation....................................................................................................... 210
16.2 Pituitary Hormones..................................................................................................................... 211
16.2.1 Anterior Pituitary Hormones......................................................................................... 211
16.2.1.1 ACTH............................................................................................................. 211
16.2.1.2 FSH................................................................................................................. 211
16.2.1.3 LH................................................................................................................... 211
16.2.1.4 MSH................................................................................................................ 212
16.2.1.5 Prolactin.......................................................................................................... 212
16.2.1.6 GH................................................................................................................... 212
16.2.1.7 TSH................................................................................................................. 212
16.2.2 Posterior Pituitary Hormones......................................................................................... 212
16.2.2.1 AVP or ADH................................................................................................... 212
16.2.2.2 Oxytocin......................................................................................................... 212
16.3 Integrated Behaviours.................................................................................................................. 212
16.3.1 Regulatory Behaviour.................................................................................................... 212
16.3.2 Pain................................................................................................................................. 212
16.3.3 Motor Function............................................................................................................... 212
16.3.4 Arousal........................................................................................................................... 213
16.3.5 Sexual Behaviour........................................................................................................... 213
Contents xxix
16.3.6 Hunger............................................................................................................................ 213

16.3.6.1 Insulin............................................................................................................. 213
16.3.6.2 Satiety Signals................................................................................................ 214
16.3.6.3 Hypothalamus................................................................................................. 214
16.3.6.4 Ghrelin............................................................................................................ 214
16.3.6.5 Cognitive Factors............................................................................................ 214
16.3.7 Thirst.............................................................................................................................. 214
16.3.7.1 Osmotic Thirst................................................................................................ 215
16.3.7.2 Hypovolaemic Thirst...................................................................................... 215
16.4 Arousal and Sleep........................................................................................................................ 216
16.4.1 Sleep Architecture.......................................................................................................... 216
16.4.1.1 REM and NREM Sleep.................................................................................. 216
16.4.1.2 Stages of Sleep................................................................................................ 216
16.4.2 Physiological Correlates of Sleep................................................................................... 216
16.4.2.1 REM Sleep...................................................................................................... 216
16.4.2.2 NREM Sleep................................................................................................... 216
16.4.3 Causes of the Sleeping–Waking Cycle........................................................................... 216
16.4.3.1 Monoaminergic Model................................................................................... 216
16.4.3.2 Cellular Model................................................................................................ 216
16.5 EEG............................................................................................................................................. 217
16.5.1 Recording Techniques.................................................................................................... 217
16.5.1.1 Conventional................................................................................................... 217
16.5.1.2 Specialized...................................................................................................... 217
16.5.2 Normal EEG Rhythms................................................................................................... 217
16.5.2.1 Classification according to Frequency Band.................................................. 217
16.5.2.2 Lambda Activity............................................................................................. 217
16.5.2.3 Mu Activity..................................................................................................... 217
16.5.3 Spikes and Waves........................................................................................................... 217
16.5.3.1 Spikes.............................................................................................................. 217
16.5.3.2 Sharp Waves................................................................................................... 217
16.5.4 Effect of Drugs............................................................................................................... 217
16.5.4.1 Antidepressants............................................................................................... 217
16.5.4.2 Antipsychotics................................................................................................ 217
16.5.4.3 Anxiolytics...................................................................................................... 217
16.5.4.4 Lithium........................................................................................................... 217
Bibliography........................................................................................................................................... 217
Chapter 17 Neurochemistry...................................................................................................................................... 219

17.1 Transmitter Synthesis, Storage, and Release............................................................................... 219
17.1.1 Transmitter Synthesis..................................................................................................... 219
17.1.2 Transmitter Storage........................................................................................................ 219
17.1.3 Transmitter Release........................................................................................................ 219
17.2 Ion Channels................................................................................................................................ 219
17.2.1 6-Transmembrane (TM) Family.................................................................................... 219
17.2.2 2-TM Family.................................................................................................................. 219
17.2.3 4-TM or 8-TM Family.................................................................................................... 219
17.2.4 Ionotropic Glutamate Receptors..................................................................................... 219
17.2.5 Nicotinic ACh and Related Receptors........................................................................... 219
17.2.6 Intracellular Calcium Ion Channels...............................................................................220
17.2.7 Chloride Ion Channels....................................................................................................220
xxx Contents
17.3 Receptors.....................................................................................................................................220
17.3.1 Structure.........................................................................................................................220
17.3.2 Function..........................................................................................................................220
17.3.2.1 G Proteins.......................................................................................................220
17.3.2.2 Second Messengers.........................................................................................220
17.3.2.3 Acetylcholine..................................................................................................220
17.3.3 Cholinergic Receptors.................................................................................................... 221
17.3.3.1 Muscarinic Receptors..................................................................................... 221
17.3.3.2 Nicotinic Receptors........................................................................................222
17.3.3.3 Dopamine.......................................................................................................222
17.3.3.4 Disease Processes Involving DA....................................................................223
17.3.3.5 Dopamine Receptors......................................................................................224
17.3.3.6 Noradrenaline.................................................................................................224
17.3.3.7 NA and Psychiatric Disorders........................................................................226
17.3.4 Adrenoceptors................................................................................................................226
17.3.4.1 α-Adrenoceptors.............................................................................................226
17.3.4.2 β-Adrenoceptors.............................................................................................227
17.3.4.3 Serotonin (5-HT)............................................................................................228
17.3.4.4 Serotonin and Psychiatric Disorders..............................................................228
17.3.5 Serotonergic Receptors..................................................................................................229
17.3.5.1 γ-Aminobutyric Acid (GABA).......................................................................229
17.3.5.2 GABA and Disease Processes........................................................................229
17.3.5.3 GABA Receptors............................................................................................229
17.3.5.4 Glutamate........................................................................................................232
17.3.5.5 Clinical Relevance of Glutamate....................................................................232
17.3.6 Glutamate Receptors......................................................................................................232
17.3.6.1 NMDA Receptors...........................................................................................232
17.3.6.2 AMPA Receptors............................................................................................232
17.3.6.3 KA Receptors.................................................................................................232
17.3.6.4 mGluRs...........................................................................................................233
17.3.6.5 Neuropeptides.................................................................................................233
17.3.7 Endogenous Opioids.......................................................................................................234
Acknowledgments..................................................................................................................................234
References..............................................................................................................................................234
Chapter 18 General Principles of Psychopharmacology..........................................................................................237

18.1 Historical Overview....................................................................................................................237
18.1.1 Antidepressants..............................................................................................................237
18.1.1.1 Tricyclic Antidepressants and MAOIs............................................................237
18.1.1.2 SSRIs..............................................................................................................237
18.1.1.3 RIMA, SNRI, NARI, and NaSSA..................................................................237
18.1.2 Lithium...........................................................................................................................237
18.1.3 Antipsychotics................................................................................................................237
18.1.3.1 Reserpine........................................................................................................237
18.1.3.2 Typical Antipsychotics....................................................................................237
18.1.3.3 Clozapine........................................................................................................237
18.1.4 Anxiolytics.....................................................................................................................238
18.1.4.1 Barbiturates.....................................................................................................238
18.1.4.2 Benzodiazepines.............................................................................................238
Contents xxxi
18.2 Classification...............................................................................................................................238
18.2.1 Antipsychotics (Neuroleptics)........................................................................................238
18.2.1.1 First-Generation (Typical) Antipsychotics.....................................................238
18.2.1.2 Second-Generation (Atypical) Antipsychotics...............................................238
18.2.2 Antimuscarinics (Anticholinergics)...............................................................................238
18.2.3 Prophylaxis of Bipolar Mood Disorder..........................................................................238
18.2.4 Antidepressants..............................................................................................................238
18.2.4.1 Tricyclic Antidepressants...............................................................................238
18.2.4.2 Tricyclic-Related Antidepressants..................................................................238
18.2.4.3 Tetracyclic Antidepressants............................................................................238
18.2.4.4 MAOIs............................................................................................................239
18.2.4.5 SSRIs..............................................................................................................239
18.2.4.6 RIMA..............................................................................................................239
18.2.4.7 SNRI...............................................................................................................239
18.2.4.8 NARI..............................................................................................................239
18.2.4.9 NaSSA............................................................................................................239
18.2.4.10 Others.............................................................................................................239
18.2.5 Nonbenzodiazepine Hypnotics.......................................................................................239
18.2.6 Benzodiazepines.............................................................................................................239
18.2.7 Other Anxiolytics...........................................................................................................239
18.2.8 Drugs Used in Alcohol Dependence..............................................................................239
18.2.9 Drugs Used in Opioid Dependence................................................................................239
18.2.10 Antiandrogens................................................................................................................239
18.2.11 Drugs for Alzheimer’s Disease......................................................................................239
18.3 Optimizing Patient Compliance..................................................................................................240
18.4 Placebo Effect..............................................................................................................................240
18.4.1 Definition........................................................................................................................240
18.4.2 Mechanisms of the Placebo Effect.................................................................................240
18.4.3 Pill Factors.....................................................................................................................240
18.4.4 Controlling for the Placebo Effect.................................................................................240
18.5 Prescribing for Psychiatric Patients.............................................................................................240
18.6 Pharmacokinetics........................................................................................................................ 241
18.6.1 Absorption......................................................................................................................241
18.6.1.1 Routes of Administration............................................................................... 241
18.6.1.2 Rate of Absorption.......................................................................................... 241
18.6.1.3 Oral Administration........................................................................................241
18.6.1.4 Rectal Administration.................................................................................... 241
18.6.1.5 Intramuscular Administration........................................................................241
18.6.1.6 Intravenous Administration............................................................................242
18.6.2 Distribution.....................................................................................................................242
18.6.2.1 Lipid Solubility...............................................................................................242
18.6.2.2 Plasma–Protein Binding.................................................................................242
18.6.2.3 Volume of Distribution...................................................................................242
18.6.2.4 Blood–Brain Barrier and Brain Distribution..................................................243
18.6.2.5 Placenta...........................................................................................................243
18.6.3 Metabolism.....................................................................................................................243
18.6.3.1 Hepatic Phase I Metabolism (Biotransformation)..........................................243
18.6.3.2 Hepatic Phase II Metabolism (Biotransformation).........................................244
18.6.3.3 First-Pass Effect..............................................................................................244
18.6.4 Elimination.....................................................................................................................244
xxxii Contents
18.7 Pharmacodynamics.....................................................................................................................244
18.7.1 Antipsychotics................................................................................................................244
18.7.1.1 First-Generation Antipsychotics.....................................................................244
18.7.1.2 Second-Generation Antipsychotics................................................................245
18.7.2 Drugs Used in the Treatment of Mood Disorder............................................................245
18.7.2.1 Lithium...........................................................................................................245
18.7.2.2 Tricyclic Antidepressants...............................................................................245
18.7.2.3 SSRIs..............................................................................................................245
18.7.2.4 MAOIs............................................................................................................245
18.7.2.5 RIMA..............................................................................................................246
18.7.2.6 SNRI...............................................................................................................246
18.7.2.7 NARI..............................................................................................................246
18.7.2.8 NaSSA............................................................................................................246
18.7.2.9 Asenapine.......................................................................................................246
18.7.2.10 Agomelatine....................................................................................................246
18.7.3 Anxiolytics and Hypnotics.............................................................................................246
18.7.3.1 Benzodiazepines.............................................................................................246
18.7.3.2 Buspirone........................................................................................................246
18.7.3.3 β-Adrenoceptor Blocking Drugs....................................................................246
18.7.3.4 Zopiclone........................................................................................................247
18.7.3.5 Zolpidem.........................................................................................................247
18.7.3.6 Zaleplon..........................................................................................................247
18.7.4 Drugs for Alzheimer’s Disease......................................................................................247
18.7.5 Antiepileptic Agents.......................................................................................................247
18.7.5.1 Carbamazepine...............................................................................................247
18.7.5.2 Sodium Valproate...........................................................................................247
18.7.5.3 Phenytoin........................................................................................................247
18.7.5.4 Phenobarbitone...............................................................................................247
18.7.5.5 Gabapentin......................................................................................................247
18.7.5.6 Vigabatrin.......................................................................................................247
18.7.5.7 Lamotrigine....................................................................................................247
18.7.5.8 Levetiracetam.................................................................................................247
18.7.5.9 Lacosamide.....................................................................................................247
18.7.6 Neurochemical Effects of ECT......................................................................................248
18.7.6.1 Noradrenaline.................................................................................................248
18.7.6.2 Serotonin.........................................................................................................248
18.7.6.3 Dopamine.......................................................................................................248
18.7.6.4 GABA.............................................................................................................248
18.7.6.5 Acetylcholine..................................................................................................248
18.7.6.6 Endogenous Opioids.......................................................................................248
18.7.6.7 Adenosine.......................................................................................................248
Bibliography...........................................................................................................................................248
Chapter 19 Psychotropic Drugs and Adverse Drug Reactions................................................................................. 251

19.1 Do Psychotropic Drugs Work?.................................................................................................... 251
19.1.1 CATIE and CUtLASS.................................................................................................... 251
19.1.1.1 CATIE............................................................................................................. 251
19.1.1.2 CUtLASS........................................................................................................ 251
19.2 Types of Adverse Drug Reactions............................................................................................... 251
19.2.1 Classification.................................................................................................................. 251
Contents xxxiii
19.2.2
Causal Relationship........................................................................................................ 251
19.2.3
Intolerance......................................................................................................................252
19.2.4
Idiosyncratic Reactions..................................................................................................252
19.2.5
Allergic Reactions..........................................................................................................252
19.2.6
Drug Interactions............................................................................................................252
19.2.6.1 Pharmacokinetic Interactions.........................................................................252
19.2.6.2 Pharmacodynamic Interactions......................................................................252
19.3 Psychotropic Medication.............................................................................................................252
19.3.1 First-Generation Antipsychotics.....................................................................................252
19.3.1.1 Photosensitization...........................................................................................252
19.3.1.2 Hypothermia or Pyrexia.................................................................................252
19.3.1.3 Allergic (Sensitivity) Reactions......................................................................253
19.3.1.4 Neuroleptic Malignant Syndrome..................................................................253
19.3.1.5 Chronic Pharmacotherapy..............................................................................253
19.3.2 Second-Generation Antipsychotics................................................................................253
19.3.2.1 Clozapine........................................................................................................253
19.3.2.2 General Side Effects.......................................................................................253
19.3.3 Antimuscarinic Drugs....................................................................................................253
19.3.4 Lithium...........................................................................................................................253
19.3.4.1 Renal Function................................................................................................253
19.3.4.2 Plasma Levels.................................................................................................253
19.3.4.3 Side Effects.....................................................................................................253
19.3.4.4 Intoxication.....................................................................................................254
19.3.4.5 Severe Overdosage..........................................................................................254
19.3.4.6 Chronic Therapy.............................................................................................254
19.3.5 Carbamazepine...............................................................................................................254
19.3.6 Tricyclic Antidepressants...............................................................................................254
19.3.6.1 Blockade of Muscarinic Receptors.................................................................254
19.3.6.2 Blockade of Histamine H1 Receptors.............................................................254
19.3.6.3 Blockade of α1-Adrenoceptors........................................................................254
19.3.6.4 Blockade of 5-HT2/1c Receptors......................................................................254
19.3.6.5 Membrane Stabilization..................................................................................254
19.3.6.6 Cardiovascular Side Effects............................................................................255
19.3.6.7 Allergic and Haematological Reactions.........................................................255
19.3.6.8 Endocrine Side Effects...................................................................................255
19.3.6.9 Others.............................................................................................................255
19.3.7 SSRIs..............................................................................................................................255
19.3.8 MAOIs............................................................................................................................255
19.3.8.1 Dangerous Food Interactions..........................................................................255
19.3.8.2 Dangerous Drug Interactions..........................................................................255
19.3.8.3 Other Side Effects...........................................................................................255
19.3.10 Buspirone.......................................................................................................................256
19.3.11 Disulfiram.......................................................................................................................256
19.3.12 Cyproterone Acetate.......................................................................................................256
19.4 Official Guidance........................................................................................................................256
19.4.1 Antipsychotic Doses above the BNF Upper Limit.........................................................256
19.4.3 Prevention of Adverse Drug Reactions..........................................................................257
19.5 Reporting.....................................................................................................................................257
19.5.1 Britain.............................................................................................................................257
xxxiv Contents
19.6 ADROIT....................................................................................................................................257
19.6.1 Newer Drugs...............................................................................................................257
19.6.2 Established Drugs......................................................................................................257
Bibliography...........................................................................................................................................258
Chapter 20 Genetics..................................................................................................................................................259
20.1 DNA and the Double Helix.......................................................................................................259
20.2 Chromosomes............................................................................................................................259
20.2.1 Number.......................................................................................................................259
20.2.2 Karyotype...................................................................................................................259
20.2.3 Centromere.................................................................................................................259
20.2.4 Telomere.....................................................................................................................259
20.2.5 Metacentric Chromosomes........................................................................................259
20.2.6 Acrocentric Chromosomes.........................................................................................259
20.2.7 Chromosomal Map.....................................................................................................259
20.3 Autosomal Abnormalities..........................................................................................................260
20.3.1 Down’s Syndrome......................................................................................................260
20.3.2 Edward’s Syndrome................................................................................................... 261
20.3.3 Patau’s Syndrome....................................................................................................... 261
20.3.4 Cri-du-Chat Syndrome............................................................................................... 261
20.4 Sex Chromosome Abnormalities............................................................................................... 261
20.4.1 Klinefelter’s Syndrome............................................................................................... 261
20.4.2 XYY Syndrome.......................................................................................................... 261
20.4.3 Triple-X Syndrome..................................................................................................... 261
20.4.4 Tetra-X Syndrome...................................................................................................... 261
20.4.5 Turner Syndrome........................................................................................................ 261
20.4.6 Alzheimer’s Disease................................................................................................... 261
20.5 Cell Division.............................................................................................................................. 261
20.5.1 Mitosis........................................................................................................................ 261
20.5.2 Meiosis....................................................................................................................... 261
20.6 Gene Structure........................................................................................................................... 261
20.7 DNA Replication.......................................................................................................................262
20.7.1 Transcription..............................................................................................................262
20.7.2 Translation..................................................................................................................263
20.8 Posttranslational Modification...................................................................................................263
20.9 Mutations...................................................................................................................................263
20.10 Techniques in Molecular Genetics............................................................................................263
20.10.1 Restriction Enzymes..................................................................................................263
20.10.2 Gene Library..............................................................................................................263
20.10.3 Molecular Cloning......................................................................................................264
20.10.4 Gene Probes...............................................................................................................264
20.10.5 Oligonucleotide Probes..............................................................................................264
20.11 Polymerase Chain Reaction.......................................................................................................264
20.12 Separating and Visualizing Different DNA Sequences............................................................264
20.13 Restriction Fragment Length Polymorphism............................................................................264
20.14 Gel Electrophoresis...................................................................................................................265
20.14.1 Southern Blotting.......................................................................................................265
20.15 Genome-Wide Studies Using Microarray Technology..............................................................266
20.15.1 Recombination...........................................................................................................266
20.15.2 Maximum Likelihood Score......................................................................................266
Contents xxxv
20.16 Linkage Analysis.......................................................................................................................266

20.16.1 Genetic Markers.........................................................................................................266
20.16.2 Linkage.......................................................................................................................266
20.16.3 Linkage Phases...........................................................................................................266
20.16.4 Linkage Analysis........................................................................................................266
20.17 Quantitative Genetics................................................................................................................267
20.18 Basic Concepts of Quantitative Genetics..................................................................................267
20.18.1 Pattern of Inheritance.................................................................................................267
20.18.1.1 Law of Uniformity...................................................................................268
20.18.1.2 Mendel’s First Law...................................................................................268
20.18.1.3 Mendel’s Second Law..............................................................................268
20.19 Autosomal Dominant Inheritance.............................................................................................268
20.20 Autosomal Dominant Disorders................................................................................................268
20.20.1 Huntington’s Disease..................................................................................................268
20.20.2 Phacomatoses.............................................................................................................268
20.20.3 Early-Onset Alzheimer’s Disease..............................................................................269
20.20.4 Other Autosomal Dominant Disorders......................................................................269
20.21 Autosomal Recessive Inheritance.............................................................................................269
20.22 X-Linked Recessive Inheritance...............................................................................................269
20.23 Autosomal Recessive Disorders................................................................................................269
20.23.1 Disorders of Protein Metabolism...............................................................................269
20.23.2 Disorders of Carbohydrate Metabolism and Lysosomal Storage...............................270
20.23.3 Other Disorders.......................................................................................................... 271
20.24 X-Linked Dominant Inheritance............................................................................................... 271
20.24.1 X-Linked Dominant Disorders................................................................................... 271
20.24.2 X-Linked Recessive Disorders................................................................................... 271
20.25 Other Concepts of Inheritance.................................................................................................. 271
20.25.1 Anticipation................................................................................................................ 271
20.25.2 Mosaicism.................................................................................................................. 271
20.25.3 Uniparental Disomy................................................................................................... 271
20.25.4 Genomic Imprinting................................................................................................... 271
20.25.5 Mitochondrial Inheritance......................................................................................... 271
20.26 Family Studies........................................................................................................................... 271
20.26.1 Difficulties..................................................................................................................272
20.27 Morbid Risk...............................................................................................................................272
20.28 Twin Studies..............................................................................................................................272
20.28.1 Methodology..............................................................................................................273
20.28.2 Difficulties.................................................................................................................. 274
20.29 Adoption Studies....................................................................................................................... 274
20.29.1 Methodology.............................................................................................................. 274
20.29.2 Difficulties.................................................................................................................. 274
Acknowledgments.................................................................................................................................. 275
Bibliography........................................................................................................................................... 275
Chapter 21 Psychiatric Epidemiology.......................................................................................................................277

21.1 Disease Frequency....................................................................................................................277
21.1.1 Incidence....................................................................................................................277
21.1.1.1 Units.........................................................................................................277
21.1.2 Prevalence..................................................................................................................277
21.1.2.1 Units.........................................................................................................277
xxxvi Contents
21.1.3 Population at Risk..........................................................................................................277

21.1.4 Chronicity.......................................................................................................................277
21.1.5 Steady-State Relationship between Point Prevalence and Incidence.............................277
21.2 Case Identification, Case Registers, and Mortality and Morbidity Statistics..............................278
21.2.1 Case Identification..........................................................................................................278
21.2.1.1 Caseness......................................................................................................278
21.2.1.2 Classification...............................................................................................278
21.2.1.3 Screening.....................................................................................................278
21.2.1.4 Likelihood Ratio..........................................................................................279
21.2.1.5 Pretest Odds.................................................................................................279
21.2.1.6 Posttest Odds...............................................................................................279
21.2.2 Case Registers................................................................................................................279
21.2.2.1 Mortality Statistics......................................................................................279
21.2.2.2 Life Expectancy...........................................................................................279
21.3 Measurements of Risk.................................................................................................................280
21.3.1 Relative Risk..................................................................................................................280
21.3.2 Attributable Risk............................................................................................................ 281
21.3.3 Relative Risk Increase.................................................................................................... 281
21.3.4 Absolute Risk Reduction................................................................................................ 281
21.3.5 Relative Risk Reduction................................................................................................. 281
21.3.6 Number Needed to Treat................................................................................................281
21.3.7 Odds Ratio...................................................................................................................... 281
21.4 Study Design...............................................................................................................................282
21.4.1 Hierarchy of Research Methods.....................................................................................282
21.4.2 Confounding...................................................................................................................282
References..............................................................................................................................................303
Chapter 22 Biostatistics............................................................................................................................................305
22.1 Descriptive and Inferential Statistics...........................................................................................305
22.1.1 Descriptive Statistics......................................................................................................305
22.1.2 Inferential Statistics........................................................................................................305
22.1.3 Hypothesis Testing: Significance Tests..........................................................................305
22.1.3.1 Null Hypothesis...........................................................................................305
22.1.3.2 Alternative Hypothesis................................................................................305
22.1.3.3 Simple Hypothesis.......................................................................................305
22.1.3.4 Composite Hypothesis.................................................................................305
22.1.3.5 One-Sided Significance Test........................................................................305
22.1.3.6 Two-Sided Significance Test.......................................................................305
22.1.3.7 Critical Region.............................................................................................305
22.1.3.8 Critical Value...............................................................................................305
22.1.3.9 Significance Level.......................................................................................305
22.1.3.10 Steps in Carrying Out a Significance/Hypothesis Test...............................306
22.1.4 Estimation: Confidence Intervals...................................................................................306
22.1.5 Advantages of Confidence Intervals Over p Values.......................................................306
22.2 Specific Biostatistical Tests.........................................................................................................307
22.2.1 t-Test...............................................................................................................................307
22.2.1.1 Independent Samples t-Test.........................................................................307
22.2.1.2 Paired Samples t-Test...................................................................................307
22.2.2 Chi-Square Test..............................................................................................................307
22.2.2.1 Null Hypothesis...........................................................................................307
Contents xxxvii
22.2.2.2 Calculation of χ2.............................................................................................307

22.2.2.3 2 × 2 Contingency Table.................................................................................308
22.2.2.4 Small Expected Values...................................................................................308
22.2.2.5 Goodness of Fit...............................................................................................308
22.2.3 Fisher’s Exact Probability Test.......................................................................................308
22.2.4 Mann–Whitney U Test...................................................................................................308
22.2.5 Confidence Interval for the Difference between Two Means........................................309
22.2.6 Confidence Interval for the Difference between Two Proportions................................309
22.2.7 Confidence Interval for the Difference between Two Medians.....................................309
22.2.7.1 Two Unpaired Samples...................................................................................309
22.2.7.2 Two Paired Samples........................................................................................309
22.3 More Complex Methods..............................................................................................................309
22.3.1 Factor Analysis...............................................................................................................309
22.3.2 Principal Components Analysis.....................................................................................309
22.3.3 Correspondence Analysis............................................................................................... 310
22.3.4 Discriminant Analysis.................................................................................................... 310
22.3.5 Cluster Analysis............................................................................................................. 310
22.3.6 Multivariate Regression Analysis.................................................................................. 310
22.3.7 Path Analysis.................................................................................................................. 310
22.3.8 Canonical Correlation Analysis..................................................................................... 310
22.4 Meta-Analysis, Survival Analysis, and Logistic Regression...................................................... 310
22.4.1 Meta-Analysis................................................................................................................ 310
22.4.1.1 Definition........................................................................................................ 310
22.4.1.2 Difficulties...................................................................................................... 310
22.4.2 Survival Analysis........................................................................................................... 310
22.4.2.1 Survival Function........................................................................................... 311
22.4.2.2 Survival Curve................................................................................................ 311
22.4.2.3 Hazard Function............................................................................................. 311
22.4.3 Logistic Regression........................................................................................................ 311
Bibliography........................................................................................................................................... 311
Chapter 23 Research Methodology and Critical Appraisal...................................................................................... 313

23.1 Research Study Design................................................................................................................ 313
23.1.1 Types.............................................................................................................................. 313
23.1.2 Hierarchy of Evidence.................................................................................................... 313
23.1.3 Selection Process............................................................................................................ 313
23.2 Clinical Trials.............................................................................................................................. 313
23.2.1 Definition........................................................................................................................ 313
23.2.2 Classification.................................................................................................................. 314
23.2.3 Advantages of Randomized Trials................................................................................. 314
23.2.4 Disadvantages of Non-randomized Trials...................................................................... 315
23.2.4.1 Concurrent Controls....................................................................................... 315
23.2.4.2 Historical Controls.......................................................................................... 315
23.3 Problems of Measurement in Psychiatry..................................................................................... 316
23.3.1 Aims of Measurement.................................................................................................... 316
23.3.2 Problems of Measurement.............................................................................................. 316
23.3.3 Measurement Methods................................................................................................... 316
23.3.4 Latent Traits (Constructs)............................................................................................... 316
23.3.5 Reliability....................................................................................................................... 316
xxxviii Contents
23.3.5.1 Definition................................................................................................... 316

23.3.5.2 Interrater Reliability.................................................................................. 316
23.3.5.3 Intrarater Reliability.................................................................................. 316
23.3.5.4 Test–Retest Reliability............................................................................... 316
23.3.5.5 Alternative Forms Reliability.................................................................... 317
23.3.5.6 Split-Half Reliability................................................................................. 317
23.3.6 Statistical Tests of Reliability...................................................................................... 317
23.3.6.1 Percentage Agreement............................................................................... 317
23.3.6.2 Product–Moment Correlation Coefficient................................................. 317
23.3.6.3 Kappa Statistic........................................................................................... 317
23.3.6.4 Intraclass Correlation Coefficient.............................................................. 317
23.3.6.5 Cronbach’s Alpha...................................................................................... 318
23.3.7 Validity........................................................................................................................ 318
23.3.7.1 Definition................................................................................................... 318
23.3.7.2 Face Validity.............................................................................................. 318
23.3.7.3 Content Validity......................................................................................... 318
23.3.7.4 Predictive Validity..................................................................................... 318
23.3.7.5 Concurrent Validity................................................................................... 318
23.3.7.6 Criterion Validity....................................................................................... 318
23.3.7.7 Incremental Validity.................................................................................. 318
23.3.7.8 Cross-Validity............................................................................................ 318
23.3.7.9 Convergent Validity................................................................................... 318
23.3.7.10 Divergent Validity..................................................................................... 318
23.3.7.11 Construct Validity..................................................................................... 318
23.3.8 Type I Error................................................................................................................. 318
23.3.9 Type II Error................................................................................................................ 318
23.3.10 Power........................................................................................................................... 318
23.3.11 Sensitivity.................................................................................................................... 318
23.3.12 Specificity.................................................................................................................... 319
23.3.13 ROC Curve.................................................................................................................. 319
23.3.14 Predictive Values......................................................................................................... 319
23.3.15 Likelihood Ratios........................................................................................................ 319
23.3.16 Bias.............................................................................................................................. 319
23.3.16.1 Selection Bias............................................................................................ 319
23.3.16.2 Observer Bias............................................................................................ 319
23.3.16.3 Recall Bias................................................................................................. 319
23.3.16.4 Information bias........................................................................................320
23.3.16.5 Confounding bias.......................................................................................320
Bibliography...........................................................................................................................................320
Chapter 24 Physical Therapies.................................................................................................................................. 321

24.1 Neurostimulation Therapies........................................................................................................ 321
24.2 Electroconvulsive Therapy.......................................................................................................... 321
24.2.1 ECT Indications and Contraindications...................................................................... 321
24.2.1.1 Indications for ECT................................................................................... 321
24.2.1.2 Contraindications against ECT................................................................. 321
24.2.1.3 Medications to Avoid before ECT.............................................................322
24.3 Preparation for ECT....................................................................................................................322
24.4 Administration of ECT................................................................................................................322
24.4.1 Side Effects of ECT.....................................................................................................325
Contents xxxix
24.5 Complications of ECT.................................................................................................................326

24.6 Mortality......................................................................................................................................327
24.7 Repetitive Transcranial Magnetic Stimulation............................................................................327
24.7.1 Indications for rTMS.....................................................................................................327
24.7.2 Mechanisms of rTMS....................................................................................................327
24.7.3 Efficacy of rTMS...........................................................................................................327
24.8 Side Effects..................................................................................................................................327
24.8.1 ECT versus rTMS/MST................................................................................................327
24.9 Vagal Nerve Stimulation.............................................................................................................328
24.9.1 Indications for VNS......................................................................................................328
24.9.2 Mechanisms of Actions.................................................................................................328
24.9.3 Efficacy of VNS............................................................................................................328
24.9.4 Side Effects....................................................................................................................328
24.10 Deep Brain Stimulation...............................................................................................................328
24.11 Other Physical Therapies.............................................................................................................328
24.11.1 Light Therapy/Phototherapy.........................................................................................328
24.11.1.1 Administration.............................................................................................329
24.11.1.2 Efficacy........................................................................................................329
24.11.1.3 Side Effects..................................................................................................329
24.11.2 Sleep Deprivation..........................................................................................................329
24.11.2.1 Indications...................................................................................................329
24.11.2.2 Administration.............................................................................................329
24.11.3 Psychosurgery...............................................................................................................329
24.11.3.1 Indications for Psychosurgery.....................................................................329
24.11.3.2 Psychosurgery Practise................................................................................329
References..............................................................................................................................................329
Chapter 25 Advanced Psychological Process and Treatment................................................................................... 331

25.1 Supportive Psychotherapy........................................................................................................... 331
25.1.1 Objectives...................................................................................................................... 331
25.1.2 Historical Development................................................................................................. 331
25.1.3 Characteristics............................................................................................................... 331
25.1.4 Indications..................................................................................................................... 331
25.1.5 Contraindications.......................................................................................................... 331
25.1.6 Techniques..................................................................................................................... 331
25.2 Brief Dynamic Psychotherapy..................................................................................................... 333
25.2.1 Historical Development................................................................................................. 333
25.2.2 Objectives...................................................................................................................... 333
25.2.3 Indications..................................................................................................................... 333
25.2.4 Contraindications.......................................................................................................... 333
25.2.5 General Techniques....................................................................................................... 333
25.2.6 Subtypes of Brief Dynamic Psychotherapy.................................................................. 333
25.2.7 Negative Reactions During Brief Dynamic Psychotherapy.......................................... 333
25.2.8 Structure........................................................................................................................334
25.2.8.1 Initial Phase.................................................................................................334
25.2.8.2 Middle Phase...............................................................................................334
25.2.8.3 Terminal Phase............................................................................................334
25.2.9 Case Vignette................................................................................................................334
25.2.10 Psychodynamic Formulation.........................................................................................334
25.2.11 CASC Preparation: Explain Brief Dynamic Psychotherapy to a Client.......................334
xl Contents
25.2.12 Research and Brief Psychodynamic Therapy................................................................ 335

25.2.12.1 Structural Aspects........................................................................................ 335
25.2.12.2 Methodological Aspects...............................................................................336
25.2.12.3 Measurement of Outcomes...........................................................................336
25.3 CBT.............................................................................................................................................336
25.3.1 Historical Development of CBT.....................................................................................336
25.3.1.1 Cognitive Therapy........................................................................................336
25.3.1.2 Behaviour Therapy.......................................................................................336
25.3.2 Objectives.......................................................................................................................336
25.3.3 Characteristics................................................................................................................336
25.3.4 Indications......................................................................................................................336
25.3.5 Contraindications...........................................................................................................336
25.3.6 Techniques...................................................................................................................... 337
25.3.6.1 Cognitive Techniques................................................................................... 337
25.3.6.2 Behavioural Techniques................................................................................ 337
25.3.7 Socratic Questioning...................................................................................................... 337
25.3.8 During Each Session...................................................................................................... 337
25.3.9 Structure......................................................................................................................... 337
25.3.9.1 Early Phase (Session 1–4)............................................................................. 337
25.3.9.2 Middle Phase (Session 5–12)........................................................................ 337
25.3.9.3 Termination (Session 13–16)........................................................................ 337
25.4 DBT.............................................................................................................................................338
25.4.1 Historical Background...................................................................................................338
25.4.2 Objectives.......................................................................................................................338
25.4.3 Indications......................................................................................................................338
25.4.4 Contraindications...........................................................................................................338
25.4.5 Components of DBT.......................................................................................................338
25.4.6 Techniques......................................................................................................................338
25.5 Mentalization-Based Treatment.................................................................................................. 339
25.5.1 Historical Development.................................................................................................. 339
25.5.2 Objectives....................................................................................................................... 339
25.5.3 Indications...................................................................................................................... 339
25.5.4 Techniques...................................................................................................................... 339
25.6 Cognitive Analytic Therapy........................................................................................................ 339
25.6.1 Historical Background................................................................................................... 339
25.6.2 Objectives....................................................................................................................... 339
25.6.3 Indications...................................................................................................................... 339
25.6.4 Techniques...................................................................................................................... 339
25.7 Interpersonal Therapy.................................................................................................................340
25.7.1 Historical Background...................................................................................................340
25.7.2 Objectives....................................................................................................................... 341
25.7.3 Indications...................................................................................................................... 341
25.7.4 Techniques...................................................................................................................... 341
25.7.4.1 Structure....................................................................................................... 341
25.7.5 CASC Preparation: Explain IPT to a Client..................................................................342
25.8 Family Therapy...........................................................................................................................343
25.8.1 Historical Perspectives...................................................................................................343
25.8.2 Indications......................................................................................................................343
25.8.2.1 External Indicators for Family Therapy.......................................................343
25.8.2.2 Internal Indicators for Family Therapy........................................................343
25.8.3 Assessment Techniques..................................................................................................343
Contents xli
25.8.4 Types of Family Therapy.............................................................................................343

25.8.4.1 Structural Family Therapy (Minuchin)......................................................343
25.8.4.2 Systemic Family Therapy...........................................................................344
25.8.4.3 Strategic Family Therapy...........................................................................344
25.8.4.4 Eclectic Family Therapy.............................................................................345
25.9 Group Therapy............................................................................................................................345
25.9.1 Historical Development................................................................................................345
25.9.2 Indications....................................................................................................................345
25.9.3 Contraindications.........................................................................................................345
25.9.4 Types of Group Therapy..............................................................................................346
25.9.4.1 Classification Based on Service Administration........................................346
25.9.4.2 Classification Based on Technique.............................................................346
25.10 Therapeutic Process.....................................................................................................................346
25.10.1 Pregroup Therapy Assessment.....................................................................................346
25.10.2 Yalom’s 11 Therapeutic Factors...................................................................................346
25.10.2.1 Early Stages................................................................................................346
25.10.2.2 Middle Stage...............................................................................................347
25.10.2.3 End Stage....................................................................................................347
25.10.3 Role of the Therapist....................................................................................................347
25.10.4 Advantages of Group Therapy.....................................................................................347
25.10.5 Countertherapeutic Process..........................................................................................347
25.11 Couple Therapy...........................................................................................................................347
25.11.1 Objectives.....................................................................................................................347
25.11.2 Indications....................................................................................................................347
25.11.3 Contraindications.........................................................................................................347
25.11.4 Issues to Be Considered Before Arranging Couple Therapy.......................................347
25.11.5 Types of Couple Therapy.............................................................................................348
25.11.6 Techniques of Couple Therapy.....................................................................................348
25.12 Motivational Interviewing...........................................................................................................348
25.12.1 Indications....................................................................................................................348
25.12.2 Techniques....................................................................................................................348
25.12.3 Eye Movement and Desensitization Reprocessing.......................................................348
25.12.4 Grief Counselling.........................................................................................................349
25.12.5 Approach to This CASC Station..................................................................................349
25.12.5.1 Issues the Candidate Needs to Explore......................................................349
25.13 Brief Insight-Oriented Therapy...................................................................................................349
25.14 Art Therapies...............................................................................................................................349
25.14.1 Types of Art Therapy...................................................................................................349
References..............................................................................................................................................350
Chapter 26 Schizophrenia and Delusional Disorders............................................................................................... 351

26.1 Schizophrenia.............................................................................................................................. 351
26.1.1 History.......................................................................................................................... 351
26.2 Classification of Schizophrenia................................................................................................... 351
26.2.1 Schneiderian First-Rank Symptoms............................................................................ 351
26.2.2 St. Louis Criteria.......................................................................................................... 352
26.2.3 Catego........................................................................................................................... 352
26.2.4 Research Diagnostic Criteria....................................................................................... 352
26.2.5 International Classification of Diseases, Tenth Revision: ICD-10............................... 352
26.2.5.1 Subtypes...................................................................................................... 352
xlii Contents
26.2.6
Type 1 and Type 2 Schizophrenia................................................................................ 355
26.2.7
SAPS and SANS........................................................................................................... 355
26.2.8
Liddle’s Syndromes...................................................................................................... 355
26.2.8.1 Psychomotor Poverty Syndrome................................................................... 355
26.2.8.2 Disorganization Syndrome........................................................................... 355
26.2.8.3 Reality Distortion Syndrome........................................................................ 355
26.2.9 Neurodevelopmental Classification..............................................................................356
26.3 Epidemiology of Schizophrenia.................................................................................................. 358
26.3.1 Statistics........................................................................................................................ 358
26.3.2 Theories........................................................................................................................ 358
26.4 Aetiology of Schizophrenia......................................................................................................... 358
26.4.1 Genetics in Schizophrenia............................................................................................ 358
26.4.1.1 Family Studies.............................................................................................. 358
26.4.1.2 Twin Studies.................................................................................................. 358
26.4.1.3 Adoption Studies........................................................................................... 359
26.4.1.4 Linkage Studies............................................................................................ 359
26.4.2 Prenatal Factors in Schizophrenia................................................................................ 359
26.4.3 Personality in Schizophrenia........................................................................................360
26.4.4 Social Factors in Schizophrenia...................................................................................360
26.4.4.1 Rural or Urban Setting..................................................................................360
26.4.4.2 Ethnicity........................................................................................................360
26.4.4.3 Expressed Emotion.......................................................................................360
26.4.5 CASC Station on Schizophrenia and Cannabis........................................................... 361
26.4.5.1 Approach to This Station.............................................................................. 361
26.4.6 Neurotransmitters in Schizophrenia............................................................................. 361
26.4.6.1 Dopamine...................................................................................................... 361
26.4.6.2 Serotonin (5-HT)...........................................................................................362
26.4.6.3 Glutamate......................................................................................................362
26.4.7 Structural Cerebral Abnormalities in Schizophrenia...................................................362
26.4.8 Neuropathological Abnormalities in Schizophrenia....................................................363
26.4.8.1 Postmortem Studies......................................................................................363
26.4.8.2 Histological Studies......................................................................................363
26.4.9 Functional Brain Abnormalities in Schizophrenia.......................................................363
26.4.10 Deficits in Cognition in Schizophrenia........................................................................363
26.5 Management of Schizophrenia....................................................................................................364
26.5.1 Physical Examination...................................................................................................364
26.5.2 Investigations................................................................................................................364
26.5.3 General Management Strategies (Scottish Schizophrenia Guidelines and NICE
Guidelines)...................................................................................................................364
26.5.4 Promoting Recovery.....................................................................................................365
26.5.4.1 Primary Care................................................................................................365
26.5.4.2 Secondary Care.............................................................................................365
26.5.5 Service Interventions....................................................................................................365
26.5.6 Hospitalization..............................................................................................................365
26.5.7 Drug Treatments for Schizophrenia.............................................................................365
26.5.8 Use of Atypical Neuroleptics.......................................................................................366
26.5.8.1 NICE Guidelines on Atypical Antipsychotics..............................................366
26.5.9 Treatment-Resistant Schizophrenia..............................................................................366
26.5.9.1 Past Psychiatric History................................................................................366
Contents xliii
26.5.9.2 Cross Sectional Measures............................................................................366

26.5.9.3 Prospective Trials........................................................................................366
26.5.9.4 Clozapine Patient Management System......................................................366
26.6 Medication Adherence.................................................................................................................366
26.6.1 Psychosocial Treatments for Schizophrenia...................................................................367
26.6.1.1 General Principles.......................................................................................367
26.6.1.2 Psychoeducation..........................................................................................367
26.6.1.3 Social Milieu...............................................................................................368
26.6.1.4 Grief Work on Losses..................................................................................368
26.6.1.5 Supportive Psychotherapy...........................................................................369
26.6.1.6 Cognitive Behavioural Therapy...................................................................369
26.6.1.7 Expressed Emotion......................................................................................369
26.6.1.8 Family Intervention.....................................................................................369
26.6.1.9 Art Therapy.................................................................................................369
26.6.1.10 Rehabilitation..............................................................................................369
26.6.2 Prognosis for Schizophrenia..........................................................................................370
26.6.2.1 Sociodemographics......................................................................................370
26.6.2.2 Past History.................................................................................................370
26.6.2.3 Pathology.....................................................................................................370
26.6.2.4 Course of Illness..........................................................................................370
26.6.2.5 Symptoms....................................................................................................370
26.6.2.6 Treatment.....................................................................................................370
26.6.2.7 Suicide.........................................................................................................370
26.6.2.8 Violence.......................................................................................................370
26.6.3 Prodrome of Schizophrenia............................................................................................370
26.6.3.1 Attenuated Positive Symptoms....................................................................370
26.6.3.2 Negative Symptoms..................................................................................... 371
26.6.3.3 Cognitive Symptoms................................................................................... 371
26.6.3.4 General Symptoms...................................................................................... 371
26.6.3.5 Interventions for Prodrome......................................................................... 371
26.6.3.6 Prognosis..................................................................................................... 371
26.6.3.7 Predictors for Further Progression to Psychosis or Schizophrenia............. 371
26.7 Catatonia...................................................................................................................................... 371
26.7.1 Aetiology........................................................................................................................ 371
26.7.2 Clinical Features............................................................................................................ 371
26.7.3 Management................................................................................................................... 371
26.7.3.1 Investigations............................................................................................... 371
26.7.4 Medications.................................................................................................................... 371
26.7.5 Prognosis........................................................................................................................372
26.8 Delusional (Paranoid) Disorders.................................................................................................372
26.8.1 ICD-10 Issues.................................................................................................................372
26.8.2 Epidemiology of Delusional Disorders..........................................................................372
26.8.3 Specific Delusional (Paranoid) Disorders......................................................................372
26.8.3.1 Pathological (Delusional) Jealousy..............................................................372
26.8.3.2 Erotomania (De Clérambault’s Syndrome).................................................372
26.8.3.3 Cotard’s Syndrome......................................................................................372
26.8.3.4 Capgras Syndrome......................................................................................372
26.8.3.5 Fregoli Syndrome........................................................................................373
26.8.3.6 Induced Psychosis (Folie À Deux)..............................................................373
xliv Contents
26.9 Schizoaffective Disorders............................................................................................................373

26.9.1 Types of Disorder...........................................................................................................373
26.9.2 Relationship between Affective and Schizophrenic Components.................................373
26.9.3 Prognosis for Schizoaffective Disorders........................................................................373
References.............................................................................................................................................. 374
Chapter 27 Mood Disorders, Suicide, and Parasuicide............................................................................................377

27.1 History.........................................................................................................................................377
27.2 Classifications of Mood Disorders..............................................................................................377
27.2.1 ICD-10 Classifications....................................................................................................377
27.2.1.1 F30 Manic Episode.........................................................................................377
27.2.1.2 F31 Bipolar Affective Disorder......................................................................377
27.2.2 DSM-5............................................................................................................................377
27.2.2.1 ICD-10 Criteria for Depressive Episode (F32)...............................................378
27.2.2.2 ICD-10 Criteria for Recurrent Depressive Disorder (F33).............................379
27.2.2.3 ICD-10 Criteria for Dysthymia (F34).............................................................379
27.2.3 Other Classifications of Depression...............................................................................380
27.2.3.1 Endogenous versus Reactive Depression........................................................380
27.2.3.2 Unipolar versus Bipolar Depression...............................................................380
27.2.3.3 Rapid-Cycling Bipolar Disorder.....................................................................380
27.2.3.4 Other Classes..................................................................................................380
27.3 Epidemiology of Mood Disorders...............................................................................................383
27.3.1 Depressive Episodes.......................................................................................................383
27.3.2 Bipolar Mood Disorder..................................................................................................384
27.4 Aetiology of Mood Disorders......................................................................................................384
27.4.1 Genetic Factors...............................................................................................................384
27.4.1.1 Family Studies................................................................................................384
27.4.1.2 Twin Studies...................................................................................................384
27.4.1.3 Adoption Studies.............................................................................................384
27.4.1.4 Molecular Genetics.........................................................................................384
27.4.2 Personality Factors in Mood Disorder...........................................................................385
27.4.2.1 Cyclothymic Personality Disorder..................................................................385
27.4.2.2 Depressive Personality Disorder.....................................................................385
27.4.3 Psychosocial Stressors in Mood Disorder......................................................................385
27.4.3.1 Childhood Factors..........................................................................................385
27.4.3.2 Adulthood Factors..........................................................................................385
27.4.3.3 Recent Life Events..........................................................................................385
27.4.4 Physical Illness in Mood Disorder.................................................................................386
27.4.5 Psychological Factors in Mood Disorder.......................................................................386
27.4.6 Neurotransmitters in Mood Disorder.............................................................................388
27.4.6.1 Serotonin (5-HT)............................................................................................388
27.4.6.2 Adaptive Changes in Receptors......................................................................389
27.4.6.3 Brain-Derived Neurotropic Factor..................................................................389
27.4.7 Neuroendocrine Factors in Mood Disorder...................................................................389
27.4.7.1 Brain–Steroid Axis.........................................................................................389
27.4.7.2 Brain–Thyroid Axis........................................................................................389
27.4.7.3 Melatonin........................................................................................................389
27.4.7.4 Water and Electrolyte Changes......................................................................390
27.4.8 Neuroanatomy and Imaging...........................................................................................390
27.4.8.1 Structural Imaging..........................................................................................390
Contents xlv
27.4.8.2 Bipolar Disorder.............................................................................................390

27.4.8.3 Functional Imaging.........................................................................................390
27.4.8.4 Bipolar Disorder.............................................................................................390
27.5 Management of Depressive Disorder..........................................................................................390
27.5.1 Investigations..................................................................................................................390
27.5.2 Pharmacotherapy: NICE Guidelines..............................................................................390
27.5.2.1 Unipolar Depression.......................................................................................390
27.5.2.2 Sequenced Treatment Alternatives to Relieve Depression Trial....................392
27.5.2.3 Atypical Depression........................................................................................392
27.5.2.4 Psychotic Depression......................................................................................392
27.5.2.5 Resistant Major Depression............................................................................392
27.5.3 Electroconvulsive Therapy and Physical Therapies in Mood Disorder.........................394
27.5.4 Psychosocial Treatments................................................................................................394
27.5.4.1 Psychotherapies...............................................................................................394
27.5.4.2 CASC Preparation: Explain CBT to a Depressed Person..............................394
27.5.4.3 NICE Guidelines Recommendations on CBT and Depressive
Disorder............................................................................................. 395
27.5.5 Management of Bipolar Disorder (NICE Guidelines Recommendations).....................395
27.5.5.1 Investigations..................................................................................................395
27.5.5.2 Pharmacotherapy............................................................................................396
27.5.5.3 Psychotherapy.................................................................................................396
27.5.5.4 Relapse Prevention..........................................................................................396
27.5.6 Management of Rapid Cycling.......................................................................................397
27.5.6.1 Prognosis for Mood Disorders........................................................................397
27.6 Persistent Mood Disorders..........................................................................................................397
27.6.1 Cyclothymia...................................................................................................................397
27.6.2 Dysthymia......................................................................................................................397
27.7 Suicide and Parasuicide (Deliberate Self-Harm).........................................................................398
27.7.1 Suicide............................................................................................................................398
27.7.1.1 Epidemiology..................................................................................................398
27.7.1.2 Aetiology of Suicide.......................................................................................398
27.7.1.3 Assessment of the Individual for Suicide.......................................................399
27.7.1.4 Management of Suicidal Ideation...................................................................399
27.7.2 Parasuicide.....................................................................................................................399
27.7.2.1 Epidemiology..................................................................................................399
27.7.2.2 Aetiology of Parasuicide.................................................................................400
27.7.2.3 Assessment of the Individual for Suicide.......................................................400
27.7.2.4 Assessment of Risk Factors for Subsequent Completion of Suicide..............401
27.7.2.5 Management of Parasuicide............................................................................401
References..............................................................................................................................................401
Chapter 28 Neurotic and Stress-Related Disorders..................................................................................................405

28.1 History.........................................................................................................................................405
28.2 Classifications of Neurosis..........................................................................................................405
28.3 General Issues..............................................................................................................................405
28.3.1 Effect of Childhood Neurosis.........................................................................................405
28.3.2 Effect of Personality Disorder........................................................................................405
28.3.3 Mortality.........................................................................................................................405
28.4 Phobic Anxiety Disorders...........................................................................................................405
28.4.1 Epidemiology of Phobic Anxiety Disorder....................................................................405
28.4.2 Aetiology of Phobic Anxiety Disorder...........................................................................407
xlvi Contents
28.4.2.1 Genetic Factors...............................................................................................407

28.4.2.2 Psychological Factors.....................................................................................407
28.4.2.3 Comorbidity....................................................................................................407
28.4.3 Management of Phobic Anxiety Disorder......................................................................407
28.4.3.1 Psychological Approaches..............................................................................407
28.4.3.2 Pharmacological Approaches.........................................................................407
28.4.4 Specific Phobic Disorders..............................................................................................407
28.4.4.1 Agoraphobia....................................................................................................407
28.4.4.2 Social Phobias.................................................................................................408
28.4.4.3 Isolated Phobias..............................................................................................408
28.5 Generalized Anxiety Disorder....................................................................................................409
28.5.1 Epidemiology of Generalized Anxiety Disorder...........................................................409
28.5.2 Aetiology of Generalized Anxiety Disorder..................................................................409
28.5.2.1 Genetic Factors...............................................................................................409
28.5.2.2 Neurochemistry..............................................................................................409
28.5.2.3 Endocrinology................................................................................................409
28.5.2.4 Imaging...........................................................................................................409
28.5.2.5 Cognitive Theories.........................................................................................409
28.5.2.6 Psychoanalytic Theories.................................................................................409
28.5.2.7 Environmental Factors....................................................................................409
28.5.3 Diagnostic Criteria.........................................................................................................409
28.5.4 Medical Differential Diagnosis...................................................................................... 410
28.5.5 Management of Generalized Anxiety Disorder............................................................. 410
28.5.5.1 Psychological Therapies................................................................................. 410
28.6 Panic Disorder............................................................................................................................. 413
28.6.1 Epidemiology of Panic Disorder.................................................................................... 413
28.6.2 Aetiology of Panic Disorder........................................................................................... 413
28.6.2.1 Genetic Factors............................................................................................... 413
28.6.2.2 Cognitive Theories......................................................................................... 413
28.6.2.3 Psychoanalytic Theories................................................................................. 413
28.6.2.4 Neurochemistry.............................................................................................. 413
28.6.2.5 Neuroimaging................................................................................................. 414
28.6.2.6 Comorbidity.................................................................................................... 414
28.6.2.7 Life Events...................................................................................................... 414
28.6.2.8 Physiological Factors...................................................................................... 414
28.6.3 Diagnostic Criteria......................................................................................................... 415
28.6.3.1 Diagnostic Criteria.......................................................................................... 415
28.6.4 Differential Diagnosis.................................................................................................... 415
28.6.4.1 Hyperventilation Syndrome............................................................................ 415
28.6.4.2 Medical Differential Diagnosis...................................................................... 415
28.6.5 Management of Panic Disorder...................................................................................... 415
28.6.5.1 Pharmacotherapy............................................................................................ 415
28.6.5.2 Psychological Treatment................................................................................. 416
28.7 OCD............................................................................................................................................. 416
28.7.1 Epidemiology of OCD.................................................................................................... 416
28.7.2 Aetiology of OCD.......................................................................................................... 416
28.7.2.1 Genetic Factors............................................................................................... 416
28.7.2.2 Neuroimaging................................................................................................. 417
28.7.2.3 Neurological Factors....................................................................................... 417
Contents xlvii
28.7.2.4 Psychological Factors.................................................................................. 417

28.7.3 Diagnostic Criteria....................................................................................................... 417
28.7.3.1 ICD-10 (F42)............................................................................................... 417
28.7.3.2 DSM-5......................................................................................................... 417
28.7.4 Management of OCD................................................................................................... 418
28.7.4.1 Pharmacotherapy........................................................................................ 418
28.7.4.2 Psychological Treatments............................................................................ 418
28.7.4.3 Physical Treatments.................................................................................... 418
28.7.5 Course.......................................................................................................................... 418
28.8 OCD-Spectrum Disorders...........................................................................................................422
28.8.1 Body Dysmorphic Disorder.........................................................................................422
28.8.1.1 Historical Development...............................................................................422
28.8.1.2 Epidemiology..............................................................................................422
28.8.1.3 Aetiology.....................................................................................................422
28.8.1.4 Clinical Features.........................................................................................422
28.8.1.5 Differential Diagnosis.................................................................................423
28.8.1.6 Comorbidity................................................................................................423
28.8.1.7 Management................................................................................................423
28.9 Hoarding......................................................................................................................................425
28.9.1.1 Epidemiology..............................................................................................425
28.9.1.2 Aetiology.....................................................................................................425
28.9.1.3 Clinical Features.........................................................................................426
28.9.1.4 Questionnaires............................................................................................426
28.9.1.5 Differential Diagnosis.................................................................................426
28.9.1.6 Psychiatric Comorbidity..............................................................................426
28.10 Treatment.....................................................................................................................................426
28.10.1 Psychological Treatment..............................................................................................426
28.10.1.1 Cognitive Behaviour Therapy.....................................................................426
28.10.2 Pharmacological Treatment..........................................................................................426
28.10.3 Trichotillomania...........................................................................................................426
28.10.3.1 ICD-10 Criteria...........................................................................................426
28.10.3.2 DSM-5 Criteria (312.39).............................................................................426
28.10.4 Skin Picking Disorder..................................................................................................426
28.11 Acute Stress Reaction..................................................................................................................426
28.11.1 ICD-10..........................................................................................................................427
28.11.2 DSM-5 (308.3)..............................................................................................................427
28.11.3 Management.................................................................................................................427
28.12 PTSD...........................................................................................................................................427
28.12.1 Aetiology of PTSD.......................................................................................................427
28.12.1.1 General Factors............................................................................................427
28.12.1.2 Biological Factors........................................................................................427
28.12.1.3 Psychosocial Factors...................................................................................427
28.12.2 Diagnostic Criteria.......................................................................................................427
28.12.2.1 ICD-10 (F43.1)............................................................................................427
28.12.2.2 DSM-5 (309.81)..........................................................................................428
28.12.3 Management of PTSD..................................................................................................428
28.12.3.1 Psychological Therapy................................................................................428
xlviii Contents
28.12.3.2 Pharmacotherapy...........................................................................................428
28.12.3.3 Eye Movement Desensitization Reprocessing..............................................428
28.12.4 Course............................................................................................................................428
28.13 Adjustment Disorders.................................................................................................................. 432
28.13.1 ICD-10 (F43.2)................................................................................................................ 432
28.13.2 DSM-5 (APA 2013)........................................................................................................ 432
28.14 Dissociative (Conversion) Disorders........................................................................................... 433
28.14.1 ICD-10............................................................................................................................ 433
28.14.2 Specific Dissociative Conditions.................................................................................... 433
28.14.2.1 Dissociative Amnesia.................................................................................... 433
28.14.2.2 Dissociative Fugue........................................................................................ 433
28.14.2.3 Dissociative Stupor........................................................................................ 433
28.14.2.4 Trance and Possession Disorders.................................................................. 433
28.14.2.5 Dissociative Disorders of Movement and Sensation..................................... 433
28.14.2.6 Dissociative Convulsions.............................................................................. 433
28.14.2.7 Dissociative Anaesthesia and Sensory Loss..................................................434
28.14.2.8 Other Dissociative Disorders.........................................................................434
28.14.3 Epidemiology of Dissociative Disorder.........................................................................434
28.14.4 Aetiology of Dissociative Disorder................................................................................434
28.14.5 Management of Dissociative Disorder...........................................................................434
28.14.6 Course............................................................................................................................434
28.15 Depersonalization–Derealization................................................................................................ 435
28.15.1 DSM-5 (300.6)................................................................................................................ 435
References.............................................................................................................................................. 435
Chapter 29 Personality Disorders............................................................................................................................. 437

29.1 History......................................................................................................................................... 437
29.2 Classification and Measurement.................................................................................................. 437
29.2.1 Dimensional Approach................................................................................................... 437
29.2.1.1 Cattell’s Trait Theory.................................................................................... 437
29.2.1.2 Eysenck’s Theory.......................................................................................... 437
29.2.1.3 Minnesota Multiphasic Personality Inventory.............................................. 437
29.2.1.4 Rorschach Inkblot Test.................................................................................. 437
29.2.1.5 Rotter’s Internal–External Locus of Control................................................ 437
29.2.2 Categorical Approach.....................................................................................................438
29.3 ICD-10 and Proposed DSM-5 Classifications.............................................................................438
29.4 Statistics....................................................................................................................................... 438
29.5 Cluster A Personality Disorders.................................................................................................. 439
29.5.1 Schizoid Personality Disorder........................................................................................ 439
29.5.1.1 Epidemiology................................................................................................ 439
29.5.1.2 Aetiology....................................................................................................... 439
29.5.1.3 Diagnostic Criteria........................................................................................440
29.5.1.4 Elicit Schizoid Personality in CASC............................................................440
29.5.1.5 Differential Diagnosis...................................................................................440
29.5.1.6 Management..................................................................................................440
29.5.1.7 Course...........................................................................................................440
29.5.2 Schizotypal Disorder......................................................................................................440
Contents xlix
29.5.2.1 Epidemiology..................................................................................................440
29.5.2.2 Aetiology........................................................................................................440
29.5.2.3 Clinical Features.............................................................................................441
29.5.2.4 Elicit Schizotypal Disorder in CASC.............................................................441
29.5.2.5 Differential Diagnosis.....................................................................................441
29.5.2.6 Management...................................................................................................441
29.5.2.7 Course and Prognosis.....................................................................................442
29.5.3 Paranoid Personality Disorder.......................................................................................442
29.5.3.1 Epidemiology..................................................................................................442
29.5.3.2 Aetiology........................................................................................................442
29.5.3.4 Elicit Paranoid Personality Disorder in CASC...............................................442
29.5.3.6 Management...................................................................................................443
29.6 Cluster B Personality Disorders..................................................................................................443
29.6.1 Borderline Personality Disorder.....................................................................................443
29.6.1.1 Epidemiology..................................................................................................443
29.6.1.2 Aetiology........................................................................................................443
29.6.1.4 Elicit Borderline Personality Disorder in CASC............................................444
29.6.2 Management...................................................................................................................445
29.6.2.1 Inpatient Treatment and Therapeutic Communities.......................................445
29.6.2.2 Psychotherapy.................................................................................................446
29.6.2.3 Pharmacotherapy............................................................................................446
29.6.3 Dissocial Personality Disorder.......................................................................................447
29.6.3.1 Epidemiology..................................................................................................447
29.6.3.2 Aetiology........................................................................................................447
29.6.3.4 Elicit Dissocial Personality Disorder in CASC..............................................448
29.6.3.6 Comorbidity....................................................................................................449
29.6.3.7 Management...................................................................................................449
29.6.4 Narcissistic Personality Disorder...................................................................................450
29.6.4.1 Epidemiology..................................................................................................450
29.6.4.2 Aetiology........................................................................................................450
29.6.4.4 Elicit Narcissistic Personality Disorder in CASC..........................................450
29.6.4.5 Differential Diagnosis..................................................................................... 451
29.6.4.6 Comorbidity.................................................................................................... 451
29.6.4.7 Treatment........................................................................................................ 451
29.6.4.8 Course and Prognosis..................................................................................... 451
29.6.5 Histrionic Personality Disorder...................................................................................... 451
29.6.5.1 Epidemiology.................................................................................................. 451
29.6.5.2 Aetiology........................................................................................................ 451
29.6.5.3 Clinical Features............................................................................................. 451
l Contents
29.6.5.4 Elicit Histrionic Personality Disorder in CASC............................................. 451

29.6.5.6 Comorbidity.................................................................................................... 452
29.6.5.7 Treatment........................................................................................................ 452
29.7 Cluster C Personality Disorders.................................................................................................. 452
29.7.1 Anankastic Personality Disorder................................................................................... 452
29.7.1.1 Epidemiology.................................................................................................. 452
29.7.1.2 Aetiology........................................................................................................ 452
29.7.1.4 Elicit Anankastic Personality Disorder in CASC........................................... 453
29.7.1.6 Comorbidity.................................................................................................... 453
29.7.1.7 Management................................................................................................... 453
29.7.2 Anxious (Avoidant) Personality Disorder...................................................................... 453
29.7.2.1 Epidemiology.................................................................................................. 453
29.7.2.2 Aetiology........................................................................................................454
29.7.2.4 Elicit Anxious (Avoidant) Personality Disorder in CASC..............................454
29.7.2.6 Comorbidity....................................................................................................454
29.7.2.7 Treatment........................................................................................................ 455
29.7.3 Dependent Personality Disorder.................................................................................... 455
29.7.3.1 Epidemiology.................................................................................................. 455
29.7.3.2 Aetiology........................................................................................................ 455
29.7.3.4 Elicit Dependent Personality Disorder in CASC............................................ 455
29.7.3.6 Treatment........................................................................................................456
Bibliography........................................................................................................................................... 457
Chapter 30 Cross-Cultural Psychiatry...................................................................................................................... 459

30.1 Basic Concepts............................................................................................................................ 459
30.1.1 Cultural Assessment....................................................................................................... 459
30.2 International Comparisons.......................................................................................................... 459
30.2.1 Schizophrenia................................................................................................................. 459
30.2.1.1 International Pilot Study of Schizophrenia....................................................460
30.2.1.2 Determinants of Outcome Study....................................................................460
30.2.2 Neurosis..........................................................................................................................460
30.2.2.1 New Cross-Cultural Psychiatry...................................................................... 461
30.2.2.2 Translation and Validity of Rating Scales...................................................... 461
30.2.2.3 Classificatory Systems.................................................................................... 461
30.2.2.4 Culture-Bound Syndromes............................................................................. 461
30.3 Culture-Bound Syndromes in Asia............................................................................................. 461
30.3.1 Amok.............................................................................................................................. 461
30.3.2 Latah...............................................................................................................................462
30.3.3 Koro................................................................................................................................462
30.3.4 Dhat................................................................................................................................462
Contents li
30.3.5 Frigophobia....................................................................................................................462
30.3.6 Taijinkyofusho................................................................................................................462
30.4 Culture-Bound Syndromes in America.......................................................................................462
30.4.1 Piblokto..........................................................................................................................462
30.4.2 Susto...............................................................................................................................462
30.4.3 Windigo..........................................................................................................................463
30.4.4 Uqamairineq...................................................................................................................463
30.5 Culture-Bound Syndromes in Africa..........................................................................................463
30.5.1 Bouffee Delirante...........................................................................................................463
30.5.2 Brain Fag Syndrome.......................................................................................................463
30.5.3 Ufufuyane.......................................................................................................................463
30.5.4 Nerfiza............................................................................................................................463
30.6 Psychiatry and Black and Ethnic Minorities in Britain..............................................................463
30.6.1 Immigrants.....................................................................................................................463
30.6.1.1 Types of Migrants...........................................................................................463
30.6.1.2 Stresses Involved in Migration.......................................................................464
30.6.2 Mental Illness among Ethnic Minorities........................................................................464
30.6.2.1 Schizophrenia.................................................................................................464
30.6.2.2 Suicide............................................................................................................464
30.6.2.3 Other Countries..............................................................................................465
30.6.2.4 Child and Adolescent Psychiatric Presentations............................................465
30.6.3 Use of Psychiatric Services by Ethnic Minorities..........................................................465
30.6.3.1 Approaches to Management...........................................................................466
References..............................................................................................................................................466
Chapter 31 Liaison, Organic, and Neuropsychiatry.................................................................................................469

31.1 Liaison Psychiatry.......................................................................................................................469
31.1.1 Somatization Disorder....................................................................................................469
31.1.1.1 Epidemiology..................................................................................................469
31.1.1.2 Aetiology........................................................................................................469
31.1.2 Somatoform Autonomic Dysfunction............................................................................ 470
31.1.3 Persistent Somatoform Pain Disorder............................................................................ 470
31.1.4 Hypochondriacal Disorder............................................................................................. 470
31.1.4.1 Epidemiology.................................................................................................. 470
31.1.4.2 Aetiology........................................................................................................ 471
31.1.4.3 DSM-5............................................................................................................. 471
31.1.4.4 Management................................................................................................... 471
31.1.4.6 Conversion Disorder and Body Dysmorphic Disorder................................... 471
31.2 Factitious Disorder and Malingering........................................................................................... 471
31.2.1 Factitious Disorder......................................................................................................... 471
31.2.2 Factitious Disorder by Proxy.......................................................................................... 471
31.2.3 Malingering.................................................................................................................... 471
31.3 Cardiology and Psychiatry.......................................................................................................... 472
31.3.1 Antidepressant Trials in Patients Suffering from IHD.................................................. 472
31.4 Nephrology and Psychiatry......................................................................................................... 473
31.4.1 Psychiatric Aspects of Chronic Renal Failure............................................................... 473
31.4.2 Psychiatric Aspects of Dialysis...................................................................................... 473
lii Contents
31.5 Hepatology and Psychiatry.......................................................................................................... 475

31.5.1 Hepatic Encephalopathy............................................................................................... 475
31.5.2 Wilson’s Disease........................................................................................................... 475
31.5.3 Use of Psychotropic Drugs for Patients Suffering from Liver Diseases...................... 475
31.6 Endocrinology and Psychiatry.................................................................................................... 476
31.6.1 Hyperthyroidism........................................................................................................... 476
31.6.2 Hypothyroidism............................................................................................................ 476
31.6.2.1 Aetiology....................................................................................................... 476
31.6.2.2 Neuropsychiatric Symptoms......................................................................... 476
31.6.2.3 Investigations................................................................................................ 476
31.6.2.4 Treatment...................................................................................................... 476
31.6.3 Cushing’s Syndrome..................................................................................................... 476
31.6.4 Addison’s Disease.........................................................................................................477
31.6.5 Syndrome of Inappropriate Antidiuretic Hormone Hypersecretion............................477
31.6.6 Psychogenic Polydipsia.................................................................................................477
31.6.7 Diabetes Mellitus..........................................................................................................477
31.6.8 Diabetes Insipidus........................................................................................................477
31.6.9 Hyperparathyroidism.................................................................................................... 478
31.6.10 Hypoparathyroidism..................................................................................................... 478
31.7 Oncology and Psychiatry............................................................................................................. 478
31.7.1 Side Effects of Chemotherapeutic Agents.................................................................... 479
31.7.2 Chronic Fatigue Syndrome........................................................................................... 479
31.7.2.1 Epidemiology................................................................................................ 479
31.7.2.2 Aetiology....................................................................................................... 479
31.7.2.3 Pathology...................................................................................................... 479
31.7.2.4 Diagnostic Criteria........................................................................................ 479
31.7.2.5 Investigations................................................................................................ 479
31.7.2.6 Management..................................................................................................480
31.7.2.7 Prognosis.......................................................................................................480
31.8 Organic Psychiatry...................................................................................................................... 481
31.8.1 Organic Mental Disorders............................................................................................ 481
31.8.1.1 Organic Hallucinosis....................................................................................482
31.8.1.2 Organic Mood Disorder................................................................................482
31.8.1.3 Organic Anxiety Disorder............................................................................482
31.8.1.4 Organic Catatonic Disorder..........................................................................483
31.8.1.5 Organic Delusional or Schizophrenia-Like Disorder...................................483
31.8.1.6 Organic Personality Disorder.......................................................................483
31.9 Neuropsychiatric Aspects of Human Immunodeficiency Virus Infection and Acquired
Immunodeficiency Syndrome......................................................................................................484
31.9.1 Introduction..................................................................................................................484
31.9.1.1 Epidemiology of HIV/AIDS in the United Kingdom...................................484
31.9.2 Human Immunodeficiency Virus.................................................................................484
31.9.3 Diagnosis of HIV Infection and Counseling................................................................484
31.9.4 Antiretroviral Treatment..............................................................................................485
31.9.5 Psychiatric Disorders and HIV Infection.....................................................................485
31.9.5.1 Acute Stress Reaction...................................................................................485
31.9.5.2 Adjustment Disorder.....................................................................................485
31.9.5.3 Depressive Disorder......................................................................................485
31.9.5.4 Mania............................................................................................................486
31.9.5.5 Cognitive Impairment and Dementia...........................................................487
31.9.6 Differential Diagnosis..................................................................................................488
Contents liii
31.9.7 Management................................................................................................................488
31.9.7.1 Investigations.............................................................................................488
31.9.7.2 Treatment...................................................................................................488
31.10 Neuropsychiatric Aspects of Parkinson’s Disease....................................................................488
31.10.1 Introduction.................................................................................................................488
31.10.1.1 Pathophysiology of Parkinson’s Disease....................................................488
31.10.1.2 Clinical Features of PKD...........................................................................488
31.10.1.3 Treatment of PKD......................................................................................489
31.10.2 Psychiatric Disorders and PKD..................................................................................489
31.10.2.1 Depression..................................................................................................489
31.10.2.2 Mania.........................................................................................................490
31.10.2.3 Anxiety......................................................................................................490
31.10.2.4 Psychosis....................................................................................................490
31.10.2.5 Sleep Disturbances..................................................................................... 491
31.10.2.6 Cognitive Impairment and Dementia........................................................ 491
31.11 Neuropsychiatric Aspects of Cerebrovascular Accident........................................................... 491
31.11.1 Introduction................................................................................................................. 491
31.11.1.1 Types of Cerebrovascular Accident........................................................... 491
31.11.1.2 Psychiatric Disorders and Cerebrovascular Accident................................ 491
31.12 Neuropsychiatric Aspects of Epilepsy......................................................................................494
31.12.1 Introduction.................................................................................................................494
31.12.1.1 Classification of Epilepsy...........................................................................494
31.13 Psychiatric Aspects of Epilepsy................................................................................................496
31.13.1 Epidemiology..............................................................................................................496
31.13.1.1 Psychiatric Comorbidity of Epilepsy.........................................................496
31.13.1.2 Psychiatric Conditions and Epilepsy.........................................................496
31.13.2 Psychotropic Medications and Epilepsy.....................................................................496
31.14 Neuropsychiatric Aspects of Head Injury.................................................................................496
31.14.1 Epidemiology..............................................................................................................496
31.14.1.1 Head Injury................................................................................................496
31.14.1.2 Neuropsychiatric Sequelae of Head Injury................................................498
31.14.1.3 Aetiological Factors and Severity of Head Injury.....................................498
31.14.1.4 Mild Head Injury.......................................................................................499
31.14.1.5 Moderate Head Injury................................................................................499
31.14.1.6 Severe Head Injury....................................................................................499
31.14.2 Postconcussion Syndrome...........................................................................................499
31.14.3 Posttraumatic Amnesia...............................................................................................499
31.14.3.1 Intracranial Pressure and Head Injury.......................................................499
31.14.3.2 Imaging and Head Injury...........................................................................500
31.14.3.3 Neuropsychiatric Sequelae of Frontal Lobe Injury...................................500
31.15 Neuropsychiatric Sequelae of Haematoma...............................................................................500
31.15.1 Rehabilitation of Patients Suffering from Head Injury.............................................. 501
31.16 Neuropsychiatric Aspects of Brain Tumour.............................................................................. 501
31.16.1 Multiple Sclerosis........................................................................................................ 501
31.16.1.1 Epidemiology............................................................................................. 501
31.16.1.2 Pathology................................................................................................... 501
31.16.1.3 Clinical Features........................................................................................502
31.16.1.4 Psychiatric Manifestations.........................................................................502
31.16.1.5 Cognitive Impairments..............................................................................502
31.16.1.6 Management of Neuropsychiatric Conditions Associated with MS..........502
liv Contents
31.17 Neuropsychiatric Aspects of Lyme Disease..............................................................................502

31.17.1 Neurosyphilis..............................................................................................................503
31.18 Paediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal
Infections...................................................................................................................................503
31.18.1 Epidemiology..............................................................................................................503
31.18.2 Pathophysiology..........................................................................................................503
31.18.3 Clinical Features.........................................................................................................503
31.18.4 Investigations..............................................................................................................504
31.18.5 Treatment....................................................................................................................504
References..............................................................................................................................................506
Chapter 32 Addiction and Psychoactive Substance Use Disorders..........................................................................507

32.1 Classification and Definitions....................................................................................................507
32.1.1 DSM-5.........................................................................................................................507
32.1.2 Acute Intoxication.......................................................................................................507
32.1.3 Harmful Use...............................................................................................................507
32.1.4 Dependence Syndrome...............................................................................................508
32.1.5 Withdrawal State.........................................................................................................508
32.1.6 Withdrawal State with Delirium.................................................................................508
32.1.7 Psychotic Disorder......................................................................................................509
32.1.8 Amnesic Syndrome.....................................................................................................509
32.1.9 Residual and Late-Onset Psychotic Disorder.............................................................509
32.2 Alcohol: The Chemical and Pharmacological Properties.........................................................509
32.2.1 Unit of Alcohol...........................................................................................................509
32.2.2 Levels of Consumption............................................................................................... 510
32.2.3 Mechanism of Action.................................................................................................. 510
32.2.4 Adverse Effects of Alcohol on Physical Health.......................................................... 512
32.2.4.1 Nervous System......................................................................................... 513
32.2.4.2 Cardiovascular System............................................................................... 513
32.2.4.3 Gastrointestinal Disorders......................................................................... 513
32.2.4.4 Malnutrition............................................................................................... 513
32.2.4.5 Liver........................................................................................................... 513
32.2.4.6 Pancreas..................................................................................................... 514
32.2.4.7 Electrolyte Disturbance............................................................................. 514
32.2.4.8 Endocrine and Sexual Disorders................................................................ 514
32.2.4.9 Blood.......................................................................................................... 514
32.2.4.10 Infections................................................................................................... 514
32.2.4.11 Metabolism................................................................................................ 515
32.2.4.12 Neoplasms.................................................................................................. 515
32.2.4.13 Early Death................................................................................................ 515
32.2.4.14 Trauma....................................................................................................... 515
32.2.4.15 Pregnancy.................................................................................................. 515
32.2.5 Adverse Effects of Alcohol on Mental Health............................................................ 516
32.2.5.1 Organic Brain Syndromes......................................................................... 516
32.2.6 Adverse Effect of Alcohol on Social Functions.......................................................... 519
32.3 Alcohol Consumption and Misuse............................................................................................ 519
32.3.1 Epidemiology of Alcohol Consumption and Misuse.................................................. 519
32.3.2 Aetiology of Alcohol Consumption and Misuse........................................................ 519
Contents lv
32.3.2.1 Genetic Factors............................................................................................... 519

32.3.2.2 Biological Factors...........................................................................................520
32.3.2.4 Psychiatric Illness...........................................................................................520
32.3.2.5 Personality Factors.........................................................................................520
32.3.2.6 Social Factors..................................................................................................520
32.3.2.7 Cultural Factors.............................................................................................. 521
32.3.2.8 Religion........................................................................................................... 521
32.3.3 Diagnosis of Alcohol Intoxication and Dependence...................................................... 521
32.3.4 Management................................................................................................................... 521
32.3.4.1 Clinical Assessment........................................................................................ 521
32.3.4.2 Investigations.................................................................................................. 521
32.3.5 Management on Withdrawal and Detoxification............................................................523
32.3.6 Maintenance of Abstinence............................................................................................524
32.4 Pharmacological Treatments.......................................................................................................524
32.4.1 Disulfiram.......................................................................................................................524
32.4.1.1 Mechanism of Action.....................................................................................524
32.4.1.2 Aversive Effects with Ingestion of Alcohol....................................................525
32.4.1.3 Dosage............................................................................................................525
32.4.1.4 Side Effects.....................................................................................................525
32.4.1.5 Drug Interactions and Contraindication.........................................................525
32.4.2 Acamprosate...................................................................................................................525
32.4.2.2 Dosage............................................................................................................525
32.4.2.3 Side Effects.....................................................................................................526
32.4.2.4 Drug Interactions and Contraindications.......................................................526
32.4.3 Naltrexone......................................................................................................................526
32.4.3.1 Medical Use....................................................................................................526
32.4.3.3 Dosage............................................................................................................526
32.5 Psychological Treatments............................................................................................................526
32.5.1 Alcoholics Anonymous..................................................................................................526
32.5.2 Other Psychological Treatments.....................................................................................527
32.5.3 Clinical Trials.................................................................................................................527
32.5.3.1 Prognosis.........................................................................................................527
32.6 Nonalcoholic Psychoactive Substances: Legal Aspects in the United Kingdom........................ 529
32.6.1 Misuse of Drug Regulations 2001.................................................................................. 529
32.6.2 Misuse of Drugs Act 1971 (Modification) Order 2003 and Misuse of Drugs
Regulations 2003............................................................................................................ 529
32.6.3 Prescribing Controlled Drugs........................................................................................530
32.6.4 Opioids...........................................................................................................................530
32.6.4.1 Heroin (Gear, Smack, Scag)........................................................................... 531
32.6.4.2 Epidemiology.................................................................................................. 531
32.6.4.3 Drug Action.................................................................................................... 531
32.6.4.4 Effects of Opioid Withdrawal......................................................................... 531
32.6.4.5 Harmful Effects.............................................................................................. 531
32.6.5 Codeine.......................................................................................................................... 533
32.6.5.1 Management of Opiate/Opioid Dependence................................................... 533
32.6.6 Methadone...................................................................................................................... 535
32.6.6.1 Indications...................................................................................................... 535
lvi Contents
32.6.6.2 Contraindications......................................................................................... 535

32.6.6.3 Properties of Methadone.............................................................................. 535
32.6.6.4 Administration............................................................................................. 535
32.6.6.5 Dose............................................................................................................. 535
32.6.6.6 Duration of Maintenance Treatment............................................................ 535
32.6.6.7 Treatment Setting......................................................................................... 536
32.6.6.8 Management of Methadone Overdose......................................................... 536
32.6.6.9 Cardiovascular Risks................................................................................... 536
32.6.6.10 Management of Pain.................................................................................... 536
32.6.7 Buprenorphine.............................................................................................................. 536
32.6.7.1 Indications.................................................................................................... 536
32.6.7.2 Pharmacodynamics...................................................................................... 536
32.6.7.3 Pharmacokinetics......................................................................................... 536
32.6.7.4 Dosage.......................................................................................................... 537
32.6.7.5 Side Effects.................................................................................................. 537
32.6.7.6 Contraindications......................................................................................... 537
32.6.7.7 Withdrawal of Buprenorphine..................................................................... 537
32.6.7.8 Diversion...................................................................................................... 537
32.6.7.9 Antagonist Treatment................................................................................... 538
32.6.7.10 Psychosocial Intervention............................................................................ 538
32.6.7.11 Psychological Methods................................................................................. 538
32.6.7.12 Motivational Interviewing............................................................................ 538
32.6.7.13 Relapse Prevention....................................................................................... 538
32.6.7.14 Prognosis...................................................................................................... 538
32.6.8 Cannabis (Grass, Hash, Ganja, Pot)............................................................................. 538
32.6.8.1 Mechanism of Actions................................................................................. 538
32.6.8.2 Cannabinoid Receptors................................................................................ 538
32.6.8.3 Clinical Features.......................................................................................... 539
32.6.8.4 Drug Withdrawal.........................................................................................540
32.6.8.5 Harmful Effects...........................................................................................540
32.6.8.6 Treatment.....................................................................................................540
32.6.9 Stimulants.....................................................................................................................540
32.6.9.1 Cocaine (Coke, Snow, Crack).......................................................................540
32.6.9.2 Epidemiology...............................................................................................540
32.6.9.3 Drug Action..................................................................................................540
32.6.9.4 Routes of Administration............................................................................. 541
32.6.9.6 Cocaine Withdrawal..................................................................................... 541
32.6.9.7 Harmful Effects........................................................................................... 541
32.6.9.8 Pharmacological Treatment.........................................................................542
32.6.9.9 Prognosis......................................................................................................542
32.6.10 Course..........................................................................................................................542
32.6.10.1 Amphetamines (Speed, Whizz, Sulphate)...................................................542
32.6.10.2 Clinical Features..........................................................................................542
32.6.10.3 Treatment.....................................................................................................542
32.6.11 3,4-Methylenedioxymethamphetamine (MDMA, Ecstasy, XTC, E, Adam)..............543
32.6.11.1 Background..................................................................................................543
32.6.11.2 Chemical Properties.....................................................................................543
32.6.11.3 Administration.............................................................................................543
32.6.11.4 Clinical Effects............................................................................................543
Contents lvii
32.6.11.5 Other Harmful Effects.................................................................................543

32.6.11.6 Management.................................................................................................544
32.6.12 Caffeine........................................................................................................................544
32.6.12.2 Mechanisms of Actions of Caffeine.............................................................544
32.6.12.3 Dose and Clinical Effects............................................................................544
32.6.12.4 Other Systemic Effects of Caffeine.............................................................544
32.6.12.5 Dependence and Withdrawal.......................................................................544
32.6.13 Hallucinogens...............................................................................................................544
32.6.13.1 Epidemiology...............................................................................................545
32.6.13.2 Route of Administration..............................................................................545
32.6.13.4 Treatment.....................................................................................................545
32.6.14 Lysergic Acid Diethylamide (LSD, Trips, Acid, Microdots, Supermans)...................545
32.6.14.2 Route of Administration..............................................................................545
32.6.14.3 Drug Action..................................................................................................545
32.6.14.4 Drug Withdrawal.........................................................................................546
32.6.14.5 Harmful Effects...........................................................................................546
32.6.15 Hallucinogenic Mushrooms (Magic Mushrooms).......................................................546
32.6.16 Mescaline.....................................................................................................................546
32.6.17 Phencyclidine (PCP, Angle Dust).................................................................................546
32.6.17.2 Neurochemical Effects.................................................................................546
32.6.18 Ketamine (K)...............................................................................................................547
32.6.19 Sedatives.......................................................................................................................547
32.6.20 Benzodiazepines...........................................................................................................547
32.6.20.1 Epidemiology...............................................................................................547
32.6.20.2 Drug Action..................................................................................................547
32.6.20.3 Drug Withdrawal.........................................................................................547
32.6.20.4 Harmful Effects...........................................................................................548
32.6.20.5 Management.................................................................................................548
32.6.21 Barbiturates..................................................................................................................548
32.6.21.1 Drug Action..................................................................................................548
32.6.21.2 Drug Withdrawal.........................................................................................548
32.6.21.3 Harmful Effects...........................................................................................548
32.6.21.4 Management.................................................................................................548
32.6.22 Nicotine........................................................................................................................548
32.6.22.1 Epidemiology...............................................................................................548
32.6.22.2 Pharmacodynamics......................................................................................549
32.6.22.3 Pharmacokinetics.........................................................................................549
32.6.22.5 Tobacco Withdrawal Syndrome...................................................................549
32.6.22.6 Pharmacological Treatment.........................................................................549
32.6.22.7 Nicotine Replacement Therapy....................................................................549
32.6.22.8 Prognosis......................................................................................................550
32.6.23 Volatile Solvents...........................................................................................................550
32.6.23.1 Drug Action..................................................................................................550
lviii Contents
32.6.23.2 Drug Withdrawal...........................................................................................550

32.6.23.3 Harmful Effects.............................................................................................550
32.6.23.4 Management..................................................................................................550
32.6.23.5 Khat...............................................................................................................550
32.6.23.6 Anabolic Steroid............................................................................................550
32.7 Addiction without Substances.....................................................................................................550
32.7.1 Pathological Gambling...................................................................................................550
32.7.1.1 Epidemiology.................................................................................................550
32.7.1.2 Aetiology and Risk Factors........................................................................... 551
32.7.1.3 Clinical Features........................................................................................... 551
32.7.1.4 Management.................................................................................................. 551
32.8 Internet Addiction........................................................................................................................ 552
32.8.1 Historical Development.................................................................................................. 552
32.8.2 Epidemiology................................................................................................................. 552
32.8.3 Aetiology and Risk Factors............................................................................................ 552
32.8.3.1 Biological Theories........................................................................................ 552
32.8.3.2 Psychological Theories.................................................................................. 552
32.8.4.1 Young’s Definition......................................................................................... 552
32.8.4.2 Proposed Criteria........................................................................................... 552
32.8.5 Subtype of Internet Addiction........................................................................................ 553
32.8.6 Psychiatric Comorbidity................................................................................................. 553
32.8.7 Medical Complications.................................................................................................. 553
32.8.8 Management................................................................................................................... 553
32.8.8.1 Psychological Treatment................................................................................ 553
32.8.8.2 Pharmacological Treatment........................................................................... 553
32.8.8.3 Prognosis....................................................................................................... 553
References.............................................................................................................................................. 553
Chapter 33 Disorders Specific to Women and Perinatal Psychiatry......................................................................... 557

33.1 Premenstrual Syndrome.............................................................................................................. 557
33.1.1 Epidemiology of PMS.................................................................................................... 557
33.1.2 Aetiology of PMS........................................................................................................... 557
33.1.2.1 Genetic Factors.............................................................................................. 557
33.1.2.2 Neuroendocrine Factors................................................................................ 557
33.1.2.3 Neurophysiological Factors........................................................................... 557
33.1.2.4 Personality Factors........................................................................................ 558
33.1.2.5 Psychological Factors.................................................................................... 558
33.1.3 Symptoms of PMS.......................................................................................................... 558
33.1.4 Management of PMS...................................................................................................... 558
33.1.4.1 Nonpharmacological Treatment.................................................................... 558
33.1.4.2 Pharmacological Treatment........................................................................... 558
33.2 Cyclic Psychosis.......................................................................................................................... 559
33.3 Pregnancy.................................................................................................................................... 559
33.3.1 Miscarriage.................................................................................................................... 559
33.3.1.1 Consequences of Miscarriage....................................................................... 559
33.3.2 Termination of Pregnancy..............................................................................................560
33.3.3 Mental Disorders in Pregnancy......................................................................................560
33.3.3.1 Minor Mental Illness.....................................................................................560
33.3.3.2 Major Mental Illness.....................................................................................560
Contents lix
33.4 Puerperal Disorders.....................................................................................................................566

33.4.1 General Issues................................................................................................................566
33.4.2 Postnatal Blues...............................................................................................................566
33.4.2.1 Epidemiology..................................................................................................566
33.4.2.2 Aetiology........................................................................................................566
33.4.2.4 Management...................................................................................................567
33.4.3 Postnatal Depression......................................................................................................567
33.4.3.1 Epidemiology..................................................................................................567
33.4.3.2 Aetiology........................................................................................................567
33.4.3.4 Management...................................................................................................568
33.4.3.5 Outcome..........................................................................................................568
33.4.4 Puerperal Psychosis........................................................................................................568
33.4.4.1 Epidemiology..................................................................................................568
33.4.4.2 Aetiology........................................................................................................569
33.4.4.3 Management...................................................................................................569
33.4.4.4 Course............................................................................................................. 570
33.4.5 Breast-Feeding and Psychotropic Medication................................................................ 570
33.5 Menopause................................................................................................................................... 573
33.5.1 Aetiology........................................................................................................................ 573
33.5.1.1 Biological Factors........................................................................................... 573
33.5.1.2 Psychological Factors..................................................................................... 573
33.5.1.3 Social Factors.................................................................................................. 573
33.5.3 Management................................................................................................................... 573
References.............................................................................................................................................. 573
Chapter 34 Eating Disorders and Metabolic Syndrome........................................................................................... 575

34.1 Anorexia Nervosa........................................................................................................................ 575
34.1.1 Epidemiology................................................................................................................. 575
34.1.2 Aetiology........................................................................................................................ 575
34.1.2.1 Genetic Factors............................................................................................... 575
34.1.2.2 Biological Factors........................................................................................... 575
34.1.2.3 Psychological Factors..................................................................................... 576
34.1.2.4 Environmental Factors.................................................................................... 576
34.1.3 Classification..................................................................................................................577
34.1.3.1 ICD-10 (F50.0 Anorexia Nervosa)..................................................................577
34.1.3.2 DSM-5 (Anorexia Nervosa)............................................................................577
34.1.4 Differential Diagnosis of Anorexia Nervosa..................................................................577
34.1.5 Clinical Features............................................................................................................577
34.1.5.1 Psychological Symptoms and Signs...............................................................577
34.1.5.2 Physical Signs and Complications.................................................................. 578
34.1.6 Baseline Monitoring and Investigations......................................................................... 578
34.1.6.1 Baseline Monitoring....................................................................................... 578
34.1.6.2 Full Blood Count............................................................................................ 578
34.1.6.3 Electrolyte Disturbances................................................................................. 579
34.1.6.4 Arterial Blood Gas......................................................................................... 579
34.1.6.5 Renal Function Tests....................................................................................... 579
lx Contents
34.1.6.6 Liver Function Tests.................................................................................... 579

34.1.6.7 Fasting Blood............................................................................................... 579
34.1.6.8 Others.......................................................................................................... 579
34.1.6.9 Hormones....................................................................................................579
34.1.6.10 Imaging........................................................................................................ 579
34.1.7 Management................................................................................................................... 579
34.1.7.1 Treatment Setting........................................................................................ 579
34.1.7.2 Weight Restoration...................................................................................... 579
34.1.7.3 Feeding........................................................................................................580
34.1.7.4 Managing Risk............................................................................................580
34.1.7.5 Psychotherapy..............................................................................................580
34.1.7.6 Pharmacotherapy......................................................................................... 581
34.1.8 Prognosis........................................................................................................................ 581
34.2 Bulimia Nervosa..........................................................................................................................584
34.2.1 Epidemiology.................................................................................................................584
34.2.2 Aetiology of Bulimia Nervosa.......................................................................................584
34.2.2.1 Genetic Factors............................................................................................584
34.2.2.2 Biological Factors........................................................................................584
34.2.2.3 Psychological Factors..................................................................................584
34.2.2.4 Environmental Factors................................................................................584
34.2.3 Classification..................................................................................................................585
34.2.3.1 ICD-10 (F50.2 Bulimia Nervosa)................................................................585
34.2.3.2 DSM-5 (Bulimia Nervosa)..........................................................................585
34.2.3.3 DSM-5 (Binge-Eating Disorder).................................................................585
34.2.4 Differential Diagnosis of Bulimia Nervosa...................................................................585
34.2.5 Clinical Features of Bulimia Nervosa............................................................................585
34.2.5.1 Psychological Symptoms and Signs............................................................585
34.2.5.2 Physical Signs and Complications...............................................................586
34.2.6 Management...................................................................................................................586
34.2.6.1 Psychotherapy..............................................................................................586
34.2.6.2 Cognitive–Behavioural Therapy for BN.....................................................586
34.2.6.3 Interpersonal Therapy.................................................................................587
34.2.6.4 Pharmacotherapy.........................................................................................587
34.2.7 Prognosis........................................................................................................................587
34.3 Metabolic Syndrome ..................................................................................................................587
34.3.1 Epidemiology.................................................................................................................587
34.3.2 Psychiatric Diseases and MetS.......................................................................................587
34.3.2.1 Schizophrenia..............................................................................................587
34.3.2.2 Depressive Disorder....................................................................................587
34.3.2.3 Bipolar Disorder..........................................................................................587
34.3.3 Classification..................................................................................................................588
34.3.4 Management...................................................................................................................589
34.4 DSM-5.........................................................................................................................................589
References..............................................................................................................................................589
Chapter 35 Sexual Disorders.................................................................................................................................... 591

35.1 History......................................................................................................................................... 591
35.1.1 British Sexual Behaviour and Attitudes......................................................................... 591
35.1.2 First Heterosexual Intercourse....................................................................................... 591
Contents lxi
35.1.3 Heterosexual Partnerships.............................................................................................. 591

35.1.4 Heterosexual Practices................................................................................................... 591
35.1.5 Sexual Diversity and Homosexual Behaviour................................................................592
35.1.6 Sexual Attitudes.............................................................................................................592
35.1.7 Physical Health...............................................................................................................592
35.1.8 Perceived Risk................................................................................................................592
35.2 Sexual Response Cycle................................................................................................................592
35.3 Sexual Dysfunction.....................................................................................................................593
35.3.1 ICD-10 Classification.....................................................................................................593
35.3.2 DSM-5 Classification.....................................................................................................593
35.3.3 Sensate-Focus Therapy..................................................................................................593
35.4 Erectile Dysfunction....................................................................................................................594
35.4.1 Normal Physiology.........................................................................................................594
35.4.2 Epidemiology of Erectile Dysfunction...........................................................................594
35.4.3 Aetiology of Erectile Dysfunction.................................................................................594
35.4.3.1 Organic Causes...............................................................................................594
35.4.3.2 Pharmacological Factors.................................................................................595
35.4.4 Assessment of Erectile Dysfunction..............................................................................595
35.4.5.1 DSM-5 Criteria: 302.72 Erectile Disorder......................................................596
35.4.6 Investigations..................................................................................................................596
35.4.7 Management of Erectile Dysfunction............................................................................596
35.4.7.1 Objectives.......................................................................................................596
35.4.7.2 First-Line Treatment.......................................................................................596
35.4.7.3 Second-Line Treatment..................................................................................598
35.4.7.4 Third-Line Treatment.....................................................................................599
35.5 Failure of Genital Responses for Women....................................................................................599
35.6 Lack of Sexual Drive or Sexual Enjoyment................................................................................599
35.6.1 Aetiology and Risk Factors............................................................................................599
35.6.2.1 ICD-10 Criteria...............................................................................................599
35.6.2.2 DSM-5 Criteria...............................................................................................599
35.6.3 Treatment........................................................................................................................600
35.7 Premature Ejaculation.................................................................................................................600
35.7.2 Epidemiology of Premature Ejaculation........................................................................600
35.7.3 Aetiology of Premature Ejaculation...............................................................................600
35.7.3.1 Nonphysical Factors........................................................................................600
35.7.3.2 Physical Factors..............................................................................................600
35.7.4.1 ICD-10 Criteria: F52.4 Premature Ejaculation...............................................600
35.7.4.2 DSM-5 Criteria: 302.75 Early Ejaculation......................................................600
35.7.5 Management of Premature Ejaculation..........................................................................601
35.8 Anorgasmia.................................................................................................................................601
35.8.2 Epidemiology of Anorgasmia........................................................................................601
35.8.3 Aetiology of Anorgasmia...............................................................................................601
35.8.3.1 Physical Factors..............................................................................................601
lxii Contents
35.8.4.1 ICD-10 Criteria: F52.3 Orgasmic Dysfunction...........................................601

35.8.4.2 DSM-5 Criteria............................................................................................601
35.8.5 Management of Anorgasmia..........................................................................................602
35.9 Vaginismus and Dyspareunia......................................................................................................602
35.9.2 Epidemiology of Vaginismus.........................................................................................602
35.9.3 Aetiology of Vaginismus................................................................................................602
35.9.4.1 ICD-10 Criteria............................................................................................602
35.9.5 Management of Vaginismus...........................................................................................603
35.10 Disorders of Gender Identity.......................................................................................................603
35.10.1 Classification..................................................................................................................603
35.10.1.1 Transsexualism............................................................................................603
35.10.1.2 Dual-Role Transvestism..............................................................................603
35.10.1.3 Gender Identity Disorder of Childhood......................................................603
35.10.2.1 ICD-10...........................................................................................................603
35.10.3 Treatment of Disorders of Gender Identity....................................................................604
35.11 Sexual Deviation.........................................................................................................................604
35.11.1 Classification..................................................................................................................604
35.11.1.1 ICD-10 F65.0 Fetishism/DSM-5 302.81 Fetishistic Disorder.....................604
35.11.1.2 ICD-10 F65.1 Fetishistic Transvestism/DSM-5 302.3 Transvestic
Disorder��604
35.11.1.3 F64.1 Dual-Role Transvestism....................................................................604
35.11.1.4 ICD-10 F65.2 Exhibitionism/DSM-5 302.4 Exhibitionistic Disorder.........605
35.11.1.5 ICD-10 F65.3 Voyeurism/DSM-5 302.82 Voyeuristic Disorder.................605
35.11.1.6 ICD-10 F65.4 Paedophilia/DSM-5 302.2 Paedophilic Disorder.................605
35.11.1.7 ICD-10 F65.5 Sadomasochism/DSM-5 302.83 Sexual Masochism
Disorder and 302.84 Sexual Sadism Disorder��605
35.11.1.8 DSM-5 302.89 Frotteuristic Disorder..........................................................605
35.11.2 Multiple Disorders of Sexual Preference.......................................................................605
35.11.3 Other Disorders of Sexual Preference............................................................................605
35.12 Sexual Orientation.......................................................................................................................606
35.13 Antisocial Sexual Behaviour.......................................................................................................606
35.13.1 Specific Antisocial Sexual Behaviours..........................................................................606
35.13.1.1 Rape.............................................................................................................606
35.13.1.2 Paedophilia..................................................................................................606
35.13.1.3 Incest...........................................................................................................606
35.13.1.4 Indecent Exposure.......................................................................................607
35.13.1.5 Others..........................................................................................................607
35.13.2 Treatment of Antisocial Sexual Behaviour....................................................................607
35.14 Sex Offender Treatment Programme..........................................................................................607
35.15 Pharmacological Treatment.........................................................................................................607
References.............................................................................................................................................. 610
Chapter 36 Sleep Disorders...................................................................................................................................... 613
36.1 Classification............................................................................................................................... 613
36.2 Dyssomnias................................................................................................................................. 613
36.2.1 Insomnia......................................................................................................................... 613
36.2.1.1 Epidemiology............................................................................................... 613
36.2.1.2 Aetiology..................................................................................................... 613
Contents lxiii

36.2.1.6 Management................................................................................................... 614
36.2.2 Hypersomnia.................................................................................................................. 615
36.2.2.1 Epidemiology.................................................................................................. 615
36.2.2.2 Aetiology........................................................................................................ 615
36.2.2.6 Assessment and Investigations....................................................................... 615
36.2.2.7 Management................................................................................................... 616
36.2.3 Narcolepsy (Hypocretin Deficiency).............................................................................. 616
36.2.3.1 Epidemiology.................................................................................................. 616
36.2.3.2 Aetiology........................................................................................................ 616
36.2.3.4 Management................................................................................................... 616
36.2.3.5 Course............................................................................................................. 617
36.3 Breathing-Related Sleep Disorder............................................................................................... 617
36.3.1 Obstructive Sleep Apnoea.............................................................................................. 617
36.3.1.1 Epidemiology.................................................................................................. 617
36.3.1.2 Risk Factors.................................................................................................... 617
36.3.1.3 Other Clinical Features.................................................................................. 617
36.3.1.4 Management................................................................................................... 617
36.3.2 Central Sleep Apnoea..................................................................................................... 617
36.3.2.1 Epidemiology.................................................................................................. 617
36.3.2.2 Risk Factors.................................................................................................... 617
36.3.2.4 Management................................................................................................... 617
36.3.3 Disorders of the Sleep–Wake Cycle............................................................................... 618
36.3.3.1 Epidemiology.................................................................................................. 618
36.3.3.2 Aetiology........................................................................................................ 618
36.3.3.4 Management................................................................................................... 618
36.3.4 Restless Leg Syndrome.................................................................................................. 618
36.3.4.1 Epidemiology.................................................................................................. 618
36.3.4.2 Aetiology........................................................................................................ 618
36.3.4.3 DSM-5 Criteria............................................................................................... 618
36.3.4.5 Management................................................................................................... 619
36.3.5 Parasomnias................................................................................................................... 619
36.4 Non-REM Parasomnias............................................................................................................... 619
36.4.1 Somnambulism (Sleepwalking)..................................................................................... 619
36.4.1.1 Epidemiology.................................................................................................. 619
36.4.1.2 Aetiology and Risk Factors............................................................................. 619
36.4.1.3 ICD-10 Criteria............................................................................................... 619
36.4.1.4 DSM-5 Criteria............................................................................................... 619
lxiv Contents

36.4.1.7 Management...................................................................................................620
36.4.2 Sleep Terrors (Night Terrors).........................................................................................620
36.4.2.1 Epidemiology..................................................................................................620
36.4.2.2 Aetiology........................................................................................................620
36.4.2.3 ICD-10 Criteria...............................................................................................620
36.4.2.4 DSM-5 Criteria...............................................................................................620
36.4.2.5 Other Clinical Features..................................................................................620
36.4.2.7 Management...................................................................................................620
36.5 REM Parasomnias.......................................................................................................................620
36.5.1 Nightmares.....................................................................................................................620
36.5.1.1 Epidemiology..................................................................................................620
36.5.1.2 Aetiology........................................................................................................ 621
36.5.1.3 ICD-10 Criteria............................................................................................... 621
36.5.1.4 DSM-5 Criteria............................................................................................... 621
36.5.1.7 Management................................................................................................... 621
36.5.2 REM Sleep Behaviour Disorder..................................................................................... 621
36.5.2.1 Epidemiology.................................................................................................. 621
36.5.2.2 Aetiology........................................................................................................ 621
36.5.2.3 DSM-5 Criteria............................................................................................... 621
36.5.2.4 Management................................................................................................... 621
References..............................................................................................................................................622
Chapter 37 Child and Adolescent Psychiatry...........................................................................................................623

37.1 Epidemiology...............................................................................................................................623
37.1.1 Preschool........................................................................................................................623
37.1.2 Middle Childhood..........................................................................................................623
37.1.3 Adolescence....................................................................................................................623
37.2 Assessment..................................................................................................................................623
37.3 Pervasive Developmental Disorders............................................................................................623
37.3.1 Childhood Autism (ICD-10 F84.0)/Autistic Disorder (DSM-5 299.0)...........................623
37.3.1.1 Historical Development..................................................................................623
37.3.1.2 Epidemiology..................................................................................................623
37.3.1.3 Aetiology........................................................................................................623
37.3.1.4 Pathogenesis and Neurobiology......................................................................624
37.3.1.5 Theory of Mind..............................................................................................624
37.3.1.6 ICD-10 Diagnostic Criteria and Clinical Characteristics...............................624
37.3.1.7 Differences between the ICD-10 and DSM-5 Criteria...................................625
37.3.2 NICE Guidelines............................................................................................................625
37.3.2.1 Neurodevelopmental Disorders......................................................................625
37.3.2.2 Mental and Behavioural Disorders.................................................................625
37.3.2.3 Other Conditions.............................................................................................626
37.3.2.4 Physical Examination.....................................................................................626
37.3.2.5 Investigations..................................................................................................626
37.3.2.6 Comorbidity....................................................................................................626
Contents lxv
37.3.2.7 Treatment.....................................................................................................627
37.3.2.8 Course of Illness..........................................................................................628
37.3.2.9 Prognosis......................................................................................................628
37.4 Asperger’s Syndrome (ICD-10 F84.5).........................................................................................628
37.4.2 Epidemiology................................................................................................................628
37.4.3 Clinical Features..........................................................................................................628
37.4.4 Differences between Childhood Autism and Asperger’s Syndrome............................628
37.4.5 Comorbidity..................................................................................................................628
37.4.6 Treatment......................................................................................................................628
37.4.7 Prognosis......................................................................................................................628
37.5 Rett’s Syndrome (ICD-10 F84.2).................................................................................................629
37.5.2 Epidemiology................................................................................................................629
37.5.3 Inheritance....................................................................................................................629
37.5.4 Clinical Features and Course of Illness.......................................................................629
37.5.5 Treatment......................................................................................................................630
37.6 Childhood Disintegrative Disorder (ICD-10 F84.3)....................................................................630
37.6.1 Epidemiology................................................................................................................630
37.6.3 Comorbidity..................................................................................................................630
37.6.4 Course of Illness...........................................................................................................630
37.7 Hyperkinetic Disorder (ICD-10 F90)..........................................................................................630
37.7.1 Attention Deficit and Hyperactivity Disorder (DSM-5 314).........................................630
37.7.1.1 Terminology.................................................................................................630
37.7.1.2 Epidemiology...............................................................................................630
37.7.1.3 Aetiology.....................................................................................................630
37.7.1.4 Genetics.......................................................................................................630
37.7.1.5 Neurodevelopment....................................................................................... 631
37.7.1.6 Neurochemistry........................................................................................... 631
37.7.1.8 Rating Scales and Cognitive Assessment....................................................632
37.7.1.9 Further Investigations..................................................................................632
37.7.1.10 Differential Diagnosis..................................................................................632
37.7.1.11 Comorbidity.................................................................................................632
37.7.1.12 Treatment.....................................................................................................632
37.7.1.13 Psychosocial Treatment...............................................................................633
37.7.2 Multimodal Treatment Study.......................................................................................634
37.7.2.1 Prognosis......................................................................................................635
37.8 Conduct Disorder (ICD-10 F91.0-F91.2/DSM-5 312) and Oppositional Defiant Disorder
(ICD-10 F91.3/DSM-5 313).........................................................................................................635
37.8.1 Epidemiology................................................................................................................635
37.8.2 Aetiology......................................................................................................................635
37.8.3 Clinical Features .........................................................................................................636
37.8.4 DSM-5 Criteria.............................................................................................................636
37.8.5 Sex Differences............................................................................................................638
37.8.6 Differential Diagnosis..................................................................................................638
37.8.7 Comorbidities...............................................................................................................638
37.8.8 Management of Conduct Disorder...............................................................................638
37.8.9 Management of Oppositional Defiant Disorder...........................................................639
37.8.10 Prognosis......................................................................................................................639
lxvi Contents
37.9 Elective Mutism (ICD-10 F94.0)...............................................................................................639

37.9.1 Epidemiology..............................................................................................................639
37.9.2 Aetiology.....................................................................................................................639
37.9.3 Diagnosis....................................................................................................................639
37.9.5 Management................................................................................................................639
37.9.6 Course and Prognosis.................................................................................................640
37.10 Tic Disorders and Gilles de la Tourette’s Syndrome (ICD-10F 95.2; DSM-5 A11)..................640
37.10.1 Epidemiology..............................................................................................................640
37.10.2 Age of Onset...............................................................................................................640
37.10.3 Aetiology.....................................................................................................................640
37.10.4 Pathophysiology..........................................................................................................640
37.10.6 Investigations..............................................................................................................641
37.10.7 Differential Diagnosis.................................................................................................641
37.10.8 Comorbidity................................................................................................................641
37.10.9 Management................................................................................................................641
37.10.10 Course of Illness...........................................................................................................................642
37.11 Pica (ICD-10 F98.3)...................................................................................................................642
37.12 Stammering (ICD-10 F98.5).....................................................................................................642
37.13 Cluttering (ICD-10 F98.6).........................................................................................................642
37.14 Communication Disorders (DSM-5).........................................................................................642
37.15 Nonorganic Enuresis (ICD-10 F98.0; DSM-5 307.6)................................................................642
37.15.1 Definition....................................................................................................................642
37.15.2 Epidemiology..............................................................................................................642
37.15.4 Aetiology.....................................................................................................................643
37.15.5 Management................................................................................................................643
37.16 Nonorganic Encopresis (ICD-10 F98.1) (DSM 5 307.7)............................................................643
37.16.1 Definition....................................................................................................................643
37.16.2 Epidemiology..............................................................................................................643
37.16.4 Aetiology.....................................................................................................................643
37.16.5 Management................................................................................................................643
37.17 School Refusal...........................................................................................................................644
37.17.1 Epidemiology..............................................................................................................645
37.17.2 Differences from Truancy..........................................................................................645
37.17.3 Management................................................................................................................645
37.17.5 Disorders in Scholastic Skills ....................................................................................646
37.18 Other Psychiatric Disorders in Childhood (0–11 Years) and Adolescence
(12–17 Years). . ............................................................................................................ 646
37.19 Substance Misuse in Adolescence.............................................................................................646
37.19.1 Type of Substance Misuse..........................................................................................646
37.19.2 Aetiology.....................................................................................................................647
37.19.3 Smoking......................................................................................................................647
37.19.4 Alcohol Abuse in Adolescence...................................................................................649
37.19.5 Volatile Substances.....................................................................................................649
Contents lxvii
37.19.6 Cannabis.....................................................................................................................649
37.19.7 Other Substances........................................................................................................649
37.19.8 Treatment....................................................................................................................649
37.19.9 Prognosis.....................................................................................................................649
37.19.10 Legal Aspects of the Child and Adolescent Psychiatry...........................................................649
37.20 Physical and Sexual Abuse in Children and Adolescents......................................................... 653
37.20.1 Epidemiology.............................................................................................................. 653
37.20.2 Assessment.................................................................................................................. 653
37.20.3 Management................................................................................................................657
References..............................................................................................................................................660
Chapter 38 Learning Disability................................................................................................................................663

38.1 Classification of Mental Retardation.........................................................................................663
38.1.1 DSM-5 Adopts Similar Classification........................................................................663
38.2 Epidemiology of Learning Disability........................................................................................663
38.3 Aetiology of Learning Disability..............................................................................................663
38.4 Down Syndrome........................................................................................................................663
38.4.1 Clinical Case...............................................................................................................663
38.4.2 Epidemiology..............................................................................................................664
38.4.3 Genetic Mechanism....................................................................................................664
38.4.4 Intelligence..................................................................................................................665
38.4.5 Growth........................................................................................................................665
38.4.6 Behavioural Features..................................................................................................665
38.4.7 Comorbidity................................................................................................................665
38.5 Learning Disability and Genetic Defects in Sex Chromosomes...............................................665
38.6 Fragile X (Martin-Bell) Syndrome............................................................................................665
38.6.1 Clinical Case...............................................................................................................665
38.6.2 Epidemiology..............................................................................................................665
38.6.3 Mode of Inheritance...................................................................................................665
38.6.4 Intelligence..................................................................................................................666
38.6.6 Other Clinical Features...............................................................................................666
38.6.7 Psychiatric Features....................................................................................................666
38.6.8 Management................................................................................................................666
38.7 Turner’s (XO) Syndrome...........................................................................................................666
38.7.1 Epidemiology..............................................................................................................666
38.7.2 Mode of Inheritance...................................................................................................666
38.7.4 Intelligence..................................................................................................................667
38.7.5 Comorbidity................................................................................................................667
38.7.6 Treatment....................................................................................................................667
38.8 Klinefelter’s Syndrome (XXY).................................................................................................667
38.8.1 Case Example.............................................................................................................667
38.8.2 Epidemiology..............................................................................................................667
38.8.3 Genetic Mechanisms...................................................................................................667
38.8.5 Intelligence..................................................................................................................667
38.8.6 Treatment....................................................................................................................668
38.9 Other X-Linked Syndromes......................................................................................................668
lxviii Contents
38.10 XYY Syndrome.........................................................................................................................668

38.10.1 Epidemiology............................................................................................................668
38.10.2 Mode of Inheritance.................................................................................................668
38.10.3 Clinical Features......................................................................................................668
38.10.4 Intelligence...............................................................................................................668
38.11 Learning Disability and Inborn Error of Metabolism...............................................................668
38.12 Lesch–Nyhan Syndrome...........................................................................................................668
38.12.1 Clinical History........................................................................................................668
38.12.2 Epidemiology............................................................................................................669
38.12.4 Error in Metabolism.................................................................................................669
38.12.6 Behavioural Features................................................................................................669
38.12.7 Intelligence...............................................................................................................669
38.12.8 Medical Comorbidity................................................................................................669
38.12.9 Treatment..................................................................................................................669
38.13 Hurler’s Syndrome.....................................................................................................................669
38.13.1 Case History.............................................................................................................669
38.13.2 Epidemiology............................................................................................................669
38.13.4 Error in Metabolism.................................................................................................669
38.13.6 Psychiatric Features..................................................................................................669
38.13.7 Intelligence...............................................................................................................669
38.13.8 Causes of Death........................................................................................................669
38.13.9 Treatment.................................................................................................................. 670
38.14 Phenylketonuria......................................................................................................................... 670
38.14.1 Epidemiology............................................................................................................ 670
38.14.2 Mode of Inheritance................................................................................................. 670
38.14.3 Error in Metabolism................................................................................................. 670
38.14.4 Clinical Features...................................................................................................... 670
38.14.5 Behavioural Features................................................................................................ 670
38.14.6 Intelligence............................................................................................................... 670
38.14.7 Screening Test.......................................................................................................... 670
38.14.8 Treatment.................................................................................................................. 670
38.15 Sanfilippo Syndrome................................................................................................................. 670
38.15.1 Case History............................................................................................................. 670
38.15.2 Metabolic Problems.................................................................................................. 670
38.15.3 Intelligence............................................................................................................... 670
38.15.4 Cause of Death......................................................................................................... 670
38.15.5 Galactosaemia.......................................................................................................... 670
38.15.6 Epidemiology............................................................................................................ 670
38.15.8 Metabolic Problems.................................................................................................. 670
38.15.10 Behavioural Features................................................................................................ 671
38.15.11 Intelligence............................................................................................................... 671
38.16 Metachromatic Leukodystrophy................................................................................................ 671
38.16.2 Error of Metabolism................................................................................................. 671
Contents lxix

38.17 Tay–Sachs Disease.................................................................................................................... 671
38.17.2 Error of Metabolism................................................................................................. 671
38.17.3 Course of Illness....................................................................................................... 671
38.18 Learning Disability and Neurocutaneous Syndromes.............................................................. 671
38.19 Tuberous Sclerosis..................................................................................................................... 671
38.19.1 Case History............................................................................................................. 671
38.19.2 Epidemiology............................................................................................................ 671
38.19.5 Psychiatric Features.................................................................................................. 671
38.19.6 Intelligence............................................................................................................... 672
38.19.7 Comorbidity..............................................................................................................672
38.20 Neurofibromatosis Type 1 (Von Recklinghausen Disease).......................................................672
38.20.1 Epidemiology............................................................................................................672
38.20.3 Intelligence............................................................................................................... 672
38.21 Learning Disability and Microdeletion Syndromes..................................................................672
38.22 Prader–Willi Syndrome.............................................................................................................672
38.22.1 Case History............................................................................................................. 672
38.22.2 Epidemiology............................................................................................................ 673
38.22.5 Intelligence............................................................................................................... 675
38.22.6 Comorbidity.............................................................................................................. 675
38.22.7 Treatment.................................................................................................................. 675
38.23 Angelman Syndrome................................................................................................................. 675
38.23.1 Case History............................................................................................................. 675
38.23.2 Epidemiology............................................................................................................ 675
38.23.4 Intelligence............................................................................................................... 676
38.23.6 Psychiatric Features.................................................................................................. 676
38.24 Williams Syndrome................................................................................................................... 676
38.24.1 Case Scenario........................................................................................................... 676
38.24.2 Epidemiology............................................................................................................ 676
38.24.4 Physical Features......................................................................................................677
38.24.6 Intelligence...............................................................................................................677
38.24.7 Association...............................................................................................................677
38.25 DiGeorge (Velo–Cardio–Facial) Syndrome.............................................................................677
38.25.1 Epidemiology............................................................................................................677
38.25.2 Genetic Defect..........................................................................................................677
38.25.3 Intelligence...............................................................................................................677
lxx Contents
38.26 Rubinstein—Taybi Syndrome......................................................................................................677

38.26.1 Epidemiology...............................................................................................................677
38.26.2 Mode of Inheritance..................................................................................................... 678
38.26.3 Clinical Features.......................................................................................................... 678
38.26.4 Psychiatric Features..................................................................................................... 678
38.26.5 Intelligence................................................................................................................... 678
38.27 Smith–Magenis Syndrome.......................................................................................................... 678
38.27.1 Case History................................................................................................................. 678
38.27.2 Epidemiology............................................................................................................... 678
38.27.3 Genetic Defect.............................................................................................................. 678
38.27.4 Clinical Features.......................................................................................................... 678
38.27.5 Psychiatric Features.....................................................................................................679
38.27.6 Intelligence................................................................................................................... 679
38.27.7 Treatment......................................................................................................................679
38.28 Cornelia de Lange Syndrome...................................................................................................... 679
38.28.1 Epidemiology...............................................................................................................679
38.28.2 Genetic Mechanism......................................................................................................679
38.28.5 Intelligence................................................................................................................... 679
38.28.6 Comorbidity..................................................................................................................679
38.29 Fetal Alcohol Syndrome..............................................................................................................679
38.29.1 Epidemiology...............................................................................................................679
38.29.2 Pathogenesis.................................................................................................................679
38.29.5 Intelligence...................................................................................................................680
Bibliography...........................................................................................................................................680
Chapter 39 Old-Age Psychiatry................................................................................................................................ 681

39.1 Epidemiology............................................................................................................................... 681
39.2 Physical Processes of Ageing...................................................................................................... 681
39.2.1 Theories of Ageing....................................................................................................... 681
39.2.2 Genetic Factors............................................................................................................. 681
39.2.3 Nongenetic Theories.................................................................................................... 681
39.2.4 Neurobiology of Ageing............................................................................................... 681
39.2.5 Changes in Sleep Architecture.....................................................................................683
39.3 Psychology of Ageing..................................................................................................................683
39.3.1 Cognition......................................................................................................................683
39.3.1.1 Intellectual Functioning................................................................................683
39.3.2 Psychomotor Speed......................................................................................................683
39.3.3 Memory........................................................................................................................683
39.3.4 Importance of Loss......................................................................................................684
39.3.5 Personality Changes.....................................................................................................684
39.4 Social and Economic Factors in Old Age....................................................................................684
39.4.1 Attitudes.......................................................................................................................684
39.4.2 Status............................................................................................................................684
39.4.3 Retirement....................................................................................................................684
39.4.4 Accommodation...........................................................................................................684
39.4.5 Sociocultural Differences.............................................................................................685
Contents lxxi
39.4.5.1 Social Class................................................................................................685

39.4.5.2 Ethnicity....................................................................................................685
39.5 Psychopharmacology of Old Age..............................................................................................685
39.5.1 Pharmacokinetics and Pharmacodynamics................................................................685
39.5.1.1 Absorption.................................................................................................685
39.5.1.2 Clearance...................................................................................................685
39.5.1.3 Metabolism................................................................................................685
39.5.1.4 Distribution................................................................................................685
39.5.2 Drug Interactions........................................................................................................686
39.5.3 Side Effects.................................................................................................................686
39.5.4 Practical Considerations.............................................................................................686
39.6 District Service Provision..........................................................................................................686
39.6.1 Principles of Service Provision..................................................................................686
39.6.2 Needs of Carers..........................................................................................................686
39.7 Assessment of a Referral...........................................................................................................686
39.7.1 Psychiatric Assessment...............................................................................................686
39.7.1.1 Mental State Examination.........................................................................687
39.7.2 Investigations..............................................................................................................688
39.7.3 Structural Imageing....................................................................................................689
39.7.4 Electroencephalography.............................................................................................690
39.7.4.1 Dementias..................................................................................................690
39.7.4.2 Delirium.....................................................................................................690
39.7.5 Psychological Assessment.......................................................................................... 691
39.7.5.1 Psychometric Testing and Measures of Function...................................... 691
39.7.5.2 Experiential Assessment and Analysis of Function.................................. 691
39.8 Psychological Reactions to Physical Disease............................................................................692
39.8.1 Adjusting to Physical Illness......................................................................................692
39.8.2 Responses to Physical Illness.....................................................................................692
39.8.3 Psychiatric Consequences of Specific Physical Disorders.........................................692
39.8.3.1 Cerebrovascular Disease............................................................................692
39.8.3.2 Sensory Impairment..................................................................................692
39.9 Mild Cognitive Impairment.......................................................................................................692
39.9.1 Epidemiology..............................................................................................................692
39.9.2 Pathology....................................................................................................................692
39.9.3 Clinical Features........................................................................................................692
39.9.4 Treatment....................................................................................................................693
39.10 Dementia in Old Age.................................................................................................................693
39.10.1 Risk and Protective Factors for Dementia..................................................................694
39.10.2 Alzheimer’s Disease...................................................................................................694
39.10.2.1 Aetiology...................................................................................................694
39.10.2.2 Neuropathology.........................................................................................694
39.10.2.4 Diagnostic Criteria.....................................................................................695
39.10.2.5 Investigations.............................................................................................696
39.10.2.6 Management..............................................................................................696
39.10.2.7 Management of Behavioural and Psychological Symptoms of Dementia.....698
39.10.2.8 Prognosis....................................................................................................698
39.10.3 Vascular Dementia.....................................................................................................699
39.10.3.1 Aetiology...................................................................................................699
lxxii Contents
39.10.3.4 Investigation...............................................................................................700
39.10.3.5 Management..............................................................................................700
39.10.3.6 Prognosis....................................................................................................700
39.10.4 Frontotemporal Lobe Dementias................................................................................700
39.10.4.1 Epidemiology.............................................................................................700
39.10.4.2 Aetiology and Classification......................................................................700
39.10.4.3 Neurochemistry.........................................................................................700
39.10.4.5 Investigations............................................................................................. 701
39.10.4.6 Management.............................................................................................. 701
39.10.4.7 Prognosis.................................................................................................... 701
39.10.4.8 Diogenes Syndrome................................................................................... 701
39.11 Dementia with Movement Disorders.........................................................................................702
39.11.1 Dementia with Lewy Bodies......................................................................................702
39.11.1.1 Epidemiology.............................................................................................702
39.11.1.2 Neuropathology.........................................................................................702
39.11.1.3 Neurochemistry.........................................................................................702
39.11.1.4 Clinical Features (McKeith’s Criteria)......................................................702
39.11.1.5 Investigations.............................................................................................702
39.11.1.6 Management..............................................................................................703
39.11.2 Parkinson’s Disease Dementia...................................................................................703
39.11.2.1 Aetiology...................................................................................................703
39.11.2.3 Management..............................................................................................703
39.11.3 Normal-Pressure Hydrocephalus................................................................................704
39.11.3.2 Aetiology...................................................................................................704
39.11.3.3 Management..............................................................................................704
39.11.3.4 Prognosis....................................................................................................704
39.11.4 Creutzfeldt–Jakob Disease.........................................................................................704
39.11.4.1 Epidemiology.............................................................................................704
39.11.4.2 Aetiology...................................................................................................704
39.11.4.3 Pathology...................................................................................................705
39.11.4.5 Investigations.............................................................................................705
39.11.4.6 Management..............................................................................................705
39.11.4.7 Prognosis....................................................................................................705
39.11.5 Human Immunodeficiency Virus Dementia...............................................................705
39.11.5.1 Epidemiology.............................................................................................705
39.11.5.2 Aetiology...................................................................................................705
39.11.5.3 Pathology...................................................................................................705
39.11.5.5 Classification..............................................................................................706
39.11.5.6 Differential Diagnosis................................................................................706
39.11.5.7 Investigations.............................................................................................706
39.11.5.8 Management and Prognosis.......................................................................706
39.11.6 Huntington’s Disease (Chorea)...................................................................................706
39.11.6.1 Epidemiology.............................................................................................706
39.11.6.2 Aetiology...................................................................................................706
Contents lxxiii
39.11.6.4 Investigation...............................................................................................706
39.11.6.5 Management..............................................................................................707
39.11.6.6 Prognosis....................................................................................................707
39.11.7 General Paralysis of the Insane..................................................................................707
39.11.7.1 Aetiology...................................................................................................707
39.11.7.3 Management and Prognosis.......................................................................707
39.12 Delirium in Old Age..................................................................................................................707
39.12.1 Aetiology....................................................................................................................707
39.12.3 Classification..............................................................................................................708
39.12.4 Investigation...............................................................................................................708
39.12.5 Management...............................................................................................................708
39.12.5.1 Nonpharmacological Treatment................................................................708
39.12.5.2 Pharmacological Treatment.......................................................................708
39.12.6 Prognosis....................................................................................................................709
39.13 Depression in Old Age...............................................................................................................709
39.13.1 Epidemiology..............................................................................................................709
39.13.2 Aetiology....................................................................................................................709
39.13.2.1 Genetic Factors..........................................................................................709
39.13.2.2 Neurobiological Factors.............................................................................709
39.13.2.3 Physical Illness..........................................................................................709
39.13.2.4 Personality.................................................................................................709
39.13.2.5 Environmental Factors...............................................................................709
39.13.4 Diagnosis.................................................................................................................... 710
39.13.5 Management............................................................................................................... 710
39.13.6 Prognosis.................................................................................................................... 711
39.14 Mania in Old Age...................................................................................................................... 711
39.14.1 Aetiology.................................................................................................................... 711
39.14.1.1 Genetic Factors.......................................................................................... 711
39.14.1.2 Organic Factors.......................................................................................... 711
39.14.2 Clinical Features........................................................................................................ 712
39.14.3 Management............................................................................................................... 712
39.14.4 Prognosis.................................................................................................................... 712
39.15 Paraphrenia or Psychosis in Old Age........................................................................................ 712
39.15.1 Explanatory Note........................................................................................................ 712
39.15.2 Epidemiology.............................................................................................................. 712
39.15.3 Aetiology.................................................................................................................... 712
39.15.3.1 Genetic Factors.......................................................................................... 712
39.15.3.2 Personality................................................................................................. 712
39.15.3.3 Sensory Impairment.................................................................................. 712
39.15.3.4 Brain Disease............................................................................................. 713
39.15.5 Management............................................................................................................... 713
39.15.5.1 Pharmacological Treatment....................................................................... 713
39.15.5.2 Nonpharmacological Treatment................................................................ 713
39.15.6 Prognosis.................................................................................................................... 713
39.16 Anxiety in Old Age................................................................................................................... 713
39.16.1 Epidemiology.............................................................................................................. 713
lxxiv Contents
39.16.1.1 Phobias....................................................................................................... 713

39.16.1.2 Generalized Anxiety Disorder.................................................................. 714
39.16.1.3 Panic Disorder........................................................................................... 714
39.16.2 Aetiology.................................................................................................................... 714
39.16.2.1 Environmental Factors............................................................................... 714
39.16.2.2 Physical Illness.......................................................................................... 714
39.16.2.3 Comorbidity............................................................................................... 714
39.16.4 Management............................................................................................................... 714
39.17 Further Considerations in Old-Age Psychiatry......................................................................... 714
39.17.1 Suicide and Attempted Suicide.................................................................................. 714
39.17.2 Alcohol and Drug Abuse............................................................................................ 715
39.17.2.1 Alcohol...................................................................................................... 715
39.17.2.2 Drugs......................................................................................................... 715
39.17.3 Somatization and Somatoform Disorders................................................................... 715
39.17.4 Sexual Activity........................................................................................................... 715
39.17.4.1 Normal Sexual Behaviour in Old Age....................................................... 715
39.17.4.2 Physiological Changes with Ageing.......................................................... 715
39.17.4.3 Sexual Problems in Old Age...................................................................... 716
39.17.5 Sleep Disorders........................................................................................................... 716
39.17.5.1 Primary Sleep Disorders........................................................................... 716
39.17.5.2 Secondary Sleep Disorders........................................................................ 716
39.17.6 Bereavement............................................................................................................... 717
39.18 Psychotherapy with Older Adults.............................................................................................. 717
39.18.1 Individual Psychodynamic Therapy........................................................................... 717
39.18.2 Adaptations in Therapy.............................................................................................. 717
39.18.3 Transference and Countertransference....................................................................... 717
39.18.4 Common Themes....................................................................................................... 717
39.19 Medicolegal Issues in Old-Age Psychiatry................................................................................ 717
39.19.1 Elder Abuse................................................................................................................ 717
39.19.2 Management of Financial Affairs.............................................................................. 718
References..............................................................................................................................................720
Chapter 40 Forensic Psychiatry................................................................................................................................723

40.1 Epidemiology of Offending.......................................................................................................723
40.1.1 Relationship with Age................................................................................................723
40.1.2 Sex Ratio.....................................................................................................................723
40.2 Juvenile Delinquency................................................................................................................723
40.2.1 Aetiology....................................................................................................................723
40.2.2 Management and prognosis........................................................................................723
40.3 Mentally Abnormal Offenders..................................................................................................723
40.3.1 Epidemiology..............................................................................................................723
40.3.2 Mental Disorders........................................................................................................723
40.4 Psychiatric Aspects of Offences................................................................................................723
40.4.1 Shoplifting..................................................................................................................723
40.4.2 Kleptomania...............................................................................................................724
40.4.3 Fire Setting.................................................................................................................725
40.5 Dangerousness...........................................................................................................................725
40.5.1 Multiagency Public Protection Arrangements...........................................................725
Contents lxxv
40.6 Risk Assessment........................................................................................................................728

40.6.1 Actuarial and Clinical Risk Assessment......................................................................728
40.7 Legal Systems in the United Kingdom ..................................................................................... 731
40.8 Criminal Responsibility in the United Kingdom...................................................................... 731
40.8.1 Definitions.................................................................................................................... 731
40.8.2 Forensic Psychiatric Assessment and Court Reports................................................... 731
40.8.3 Classification of Homicide........................................................................................... 732
40.8.4 McNaughton Rules.......................................................................................................734
40.8.4.1 Diminished Responsibility...........................................................................734
40.8.5 Automatism.................................................................................................................. 735
40.8.6 Outcome of Sentencing................................................................................................ 735
40.9 Civil Aspects............................................................................................................................. 735
40.9.1 Testamentary Capacity................................................................................................. 735
40.9.2 Tort............................................................................................................................... 735
40.9.3 Contracts...................................................................................................................... 735
40.9.4 Marriage....................................................................................................................... 735
40.10 Prison Psychiatry.......................................................................................................................739
References..............................................................................................................................................739
Chapter 41 Preparation for Psychiatric Examinations.............................................................................................. 741

Preface
The preparation of the third edition of this book has references. Finally, we have included many more figures.
involved a number of major changes. First, we have taken As with previous editions, we believe the third edition of
on a new co-author, Roger Ho. Roger has relatively recent Revision Notes in Psychiatry should prove useful not only
experience of preparing for and sitting the examinations for the membership of the Royal College of Psychiatrists
of the membership of the Royal College of Psychiatrists but also for similar postgraduate examinations in psychia-
and is actively involved in teaching candidates based in try in other parts of the English-speaking world.
Singapore. Second, we have added new chapters and,
within existing chapters, we have included new mate- Basant K. Puri
rial (including NICE guidelines), updated the DSM- Annie Hall
IV-TR criteria to the new DSM-5, and cited more recent Roger Ho
lxxvii
Authors
Basant K. Puri, MA, PhD, MB, BChir, BSc (Hons) College, Oxford, and completed her clinical training at the
MathSci, DipStat, PG Dip Maths, MMath, FRCPsych, Welsh National School of Medicine. She works in a busy
FSB, is based at Hammersmith Hospital and Imperial NHS inner-city psychiatric service as a consultant general
College London, United Kingdom. He read medicine adult psychiatrist.
at St. John’s College, University of Cambridge. He
also trained in molecular genetics at the MRC MNU, Dr. Roger Ho, MBBS, DPM, DCP, Gdip Psychotherapy,
Laboratory of Molecular Biology, Cambridge. He has MMed (Psych), MRCPsych, FRCPC, is an assistant pro-
authored or co-authored more than 40 books, includ- fessor and consultant psychiatrist at the Department of
ing the second edition of Drugs in Psychiatry (Oxford Psychological Medicine, National University of Singapore.
University Press, 2013), the third edition of Textbook He graduated from the University of Hong Kong and
of Psychiatry with Dr. Ian Treasaden (Churchill received his training in psychiatry from the National
Livingstone, 2011) and, with the publisher of the pres- University of Singapore. He is a general adult psychia-
ent volume, the third edition of Textbook of Clinical trist and in charge of the Mood Disorder Clinic, National
Neuropsychiatry and Neuroscience Fundamentals University Hospital, Singapore. He is a member of the
with Professor David Moore (2012). editorial board of Advances of Psychiatric Treatment,
an academic journal published by the Royal College of
Annie Hall, BA, MB BCh, MRCPsych is a consultant psy- Psychiatrists. His research focuses on mood disorders, psy-
chiatrist at South Kensington and Chelsea Mental Health choneuroimmunology, and liaison psychiatry. He is one
Centre and Chelsea and Westminster Hospital, London, of the key authors for the revision website, Exam doctor
United Kingdom. She read medicine at St Catherines’ MRCPsych Paper 1 questions (http://examdoctor.co.uk/).
lxxix
Abbreviations
5-HIAA 5-Hydroxyindoleacetic acid CBT Cognitive behavioural therapy

5-HT Serotonin CBT-Gp Group-based CBT
5-HTT Serotonin transporter CBT-Mb Mindfulness-based CBT
Aβ Beta-amyloid CBT-Tf Trauma-focused CBT
AA Alcoholics anonymous CCBT Computerized CBT
ACA Anterior cerebral artery CCK Cholecystokinin
ACh Acetylcholine CD Cluster of differentiation
AChE Acetylcholinesterase ChAT Choline acetyltransferase
AChEI Acetylcholinesterase inhibitor CJD Creutzfeldt–Jakob disease
ACT Assertive community treatment CK Creatinine kinase
ACTH Adrenocorticotrophic hormone CMHT Community mental health team
ADH Antidiuretic hormone CMV Cytomegalovirus
ADHD Attention-deficit hyperactivity CN Cranial nerve
disorder CNS Central nervous system
ADL Activities of daily living COMT Catechol-O-methyl transferase
AED Accident and emergency department CPA Care programme approach
AF Atrial fibrillation CPMS Clozaril Patient Management System
ALDH Acetaldehyde dehydrogenase CPN Community psychiatric nurse
AN Anorexia nervosa CR Chronic release
APA American Psychiatric Association CRF Chronic renal failure
ASPD Antisocial personality disorder CRP C-reactive protein
ATP Adenosine triphosphate CSF Cerebrospinal fluid
BCh Butyrylcholinesterase CT Computed tomography
BDD Body dysmorphic disorder CVA Cerebrovascular accident
BDNF Brain-derived neurotrophic factor CVS Cardiovascular system
BMI Body mass index DBT Dialectical behaviour therapy
BN Bulimia nervosa DDX Differential diagnosis
BNF British National Formulary DLPFC Dorsolateral prefrontal cortex
BPSD Behavioural and psychological DM Diabetes mellitus
symptoms in dementia DSH Deliberate self-harm
BZD Benzodiazepine DST Dexamethasone suppression test
CADASIL Cerebral autosomal dominant arte- DT Delirium tremens
riopathy with subcortical infarcts DVLA Drive and Vehicle Licensing Agency
and leukoencephalopathy (United Kingdom)
CAMCOG Cambridge Cognitive Examination DZ Dizygotic
CAMDEX Cambridge Examination for Mental ECG Electrocardiogram
Disorder of the Elderly ECT Electroconvulsive therapy
CAMHS Child and Adolescent Mental ED Erectile dysfunction
Health Services EE Expressed emotion
cAMP Cyclic adenosine monophosphate EEG Electroencephalogram
CASC Clinical Assessment of Skills & EPI Eysenck Personality Inventory
Competencies EPSE Extrapyramidal side effects
CAT Cognitive analytic therapy ERP Exposure and response prevention
CBF Cerebral blood flow ESR Erythrocyte sedimentation rate
lxxxi
lxxxii Abbreviations
FAS Foetal alcohol syndrome MDMA Methylenedioxymethamphetamine

FBC Full blood count MDT Multidisciplinary team
FRS First-rank symptoms Mg Magnesium
FSH Follicle-stimulating hormone MHA Mental Health Act
FTD Fronto-temporal dementia MI Myocardial infarction
GA General anaesthesia MLF Medial longitudinal fasciculus
GABA γ-Aminobutyric acid MMR Measles, mumps, and rubella
GAD Generalized anxiety disorder MMSE Mini-mental state examination
GAF Global assessment of functioning MRCPsych Member of the Royal College of
GDS Geriatric Depression Scale Psychiatrists
GFR Glomerular filtration rate MRI Magnetic resonance imaging
GH Growth hormone MS Multiple sclerosis
GI/GIT Gastrointestinal/gastrointestinal tract MSE Mental state examination
GMC General Medical Council MSU Midstream urine
GP General practitioner MSW Medical social worker
HCG Human chorionic gonadotropin 99mTc-HMPAO Tc99m hexamethylpropyleneamine
HMSN Hereditary motor and sensory oxime

neuropathies MVP Mitral valve prolapse
HPA Hypothalamic–pituitary–adrenal MZ Monozygotic
HSV Herpes simplex virus NA Noradrenaline
HVA Homovanillic acid NAI Nonaccidental injury
HVS Hyperventilation syndrome NART National Adult Reading Test
IBS Irritable bowel syndrome NAS Neonate abstinence syndrome
ICP Intracranial pressure NF Neurofibromatosis
IDDM Insulin-dependent diabetes mellitus NFT Neurofibrillary tangle
IHD Ischaemic heart disease NHS National Health Service (United
IM Intramuscular Kingdom)
IMR Inmate record NICE National Institute for Health and
IPT Interpersonal therapy Care Excellence (United Kingdom)
IUGR Intrauterine growth retardation NMDA N-methyl-D-aspartate
IV Intravenous nocte Every night
K Potassium NPH Normal pressure hydrocephalus
K-SADS-PL Kiddie-Schedule for Affective NRT Nicotine replacement therapy
Disorders and Schizophrenia- NSAID Nonsteroidal anti-inflammatory
Present and Lifetime Version drug
LBD Lewy body dementia OCD Obsessive–compulsive disorder
LC Locus coeruleus OCPD Obsessive–compulsive personality
LD Learning disability disorder
LFT Liver function test ODD Oppositional defiant disorder
LH Luteinizing hormone OM Every morning
LMBBS Laurence–Moon–Biedl syndrome OT Occupational therapist
LMNL Lower motor neurone lesion PANDAS Paediatric autoimmune neuropsy-
LOC Loss of consciousness chiatric disorders associated with
LOCF Last observation carried forward streptococcal infections
LP Lumbar puncture PANSS Positive and Negative Syndrome
LTM Long-term memory Scale
MAOI Monoamine oxidase inhibitor PCA Posterior cerebral artery
MCA Middle cerebral artery PCOS Polycystic ovary syndrome
MCQ Multiple-choice question PCP Phencyclidine
MCI Mild cognitive impairment PCS Postconcussion syndrome
M:F Male-to-female ratio PDD Pervasive development disorder
Abbreviations lxxxiii
PE Physical examination SNRI Serotonin–noradrenaline reuptake

PFC Prefrontal cortex inhibitor
PI Projective identification SPECT Single-proton emission computed
PK Pharmacokinetics tomography
PKD Parkinson’s disease SSRI Selective serotonin reuptake inhibitor
PKU Phenylketonuria STD Sexually transmitted disease
PMC Premotor cortex STM Short-term memory
PMH Past medical history SWS Slow-wave sleep
PMS Premenstrual syndrome t1/2 Half-life
PNS Peripheral nervous system TCA Tricyclic antidepressant
PPG Penile plethysmography TD Tardive dyskinesia
PPH Past psychiatric history TFT Thyroid function test
PROM Premature rupture of membrane TI Therapeutic index
PrP Prion protein TIA Transient ischaemic attack
PSP Progressive supranuclear palsy TLE Temporal lobe epilepsy
PT Physiotherapist TMS Transcranial magnetic stimulation
PTA Posttraumatic amnesia TNF Tumour necrosis factor
PTSD Posttraumatic stress disorder TNR Trinucleotide repeat
PWS Prader–Willi syndrome TRD Treatment-resistant depression
QoL Quality of life TRH Thyrotropin-releasing hormone
RCT Randomized controlled trial TRS Treatment-resistant schizophrenia
RFLP Restriction fragment length TSH Thyroid-stimulating hormone
polymorphism U&E Urea and electrolytes
RFT Renal function test UMNL Upper motor neurone lesion
RTA Road traffic accident UTI Urinary tract infection
SDH Subdural haemorrhage VaD Vascular dementia
SIDS Sudden infant death syndrome VDRL Venereal Disease Research
SLE Systemic lupus erythematosus Laboratory
SMR Standardized mortality ratio VIP Vasoactive intestinal peptide
SMS Smith–Magenis syndrome VNS Vagus nerve stimulation
SNECO Special education needs WBC White blood cell
coordinator WCST Wisconsin card sorting test
1 Descriptive Psychopathology
1.1 DISORDERS OF GENERAL BEHAVIOUR 1.1.2.2 Hyperkinesis

In hyperkinesis, which may be seen in children and ado-
1.1.1 Underactivity lescents, the following features occur:
1.1.1.1 Stupor
The key features of stupor, when the term is used in its • Overactivity
psychiatric sense, include • Distractibility
• Impulsivity
• Mutism • Excitability
• Immobility
• Occasional periods of excitement and overactivity 1.1.2.3 Somnambulism (Sleep Walking)
A complex sequence of behaviours is carried out by a per-
Stupor is seen in son who rises from sleep and is not fully aware of his or
her surroundings.
• Catatonic stupor
• Depressive stupor 1.1.2.4 Compulsion (Compulsive Ritual)
• Manic stupor This is a repetitive and stereotyped seemingly purposeful
• Epilepsy behaviour. It is the motor component of an obsessional
• Hysteria thought. Examples of compulsions include
In neurology, the term ‘stupor’ refers to a person who • Checking rituals

responds to pain and loud sounds and may exhibit brief • Cleaning rituals
monosyllabic utterances, and some spontaneous motor • Counting rituals
activity takes place. • Dipsomania: a compulsion to drink alcohol
• Dressing rituals
• Kleptomania: a compulsion to steal
1.1.1.2 Depressive Retardation • Nymphomania: a compulsive need in the female
This is a lesser form of psychomotor retardation occur- to engage in sexual intercourse
ring in depression that, in its extreme form, merges with • Polydipsia: a compulsion to drink water
depressive stupor. • Satyriasis: a compulsive need in the male to
engage in sexual intercourse
• Trichotillomania: a compulsion to pull out one’s
1.1.1.3 Obsessional Slowness hair
This may occur secondary to repeated doubts and com-
pulsive rituals. 1.1.2.5 Abnormal Posture and Movements
Particularly in schizophrenia, but sometimes also in
other disorders such as catatonia and some learning dis-
1.1.2 Overactivity abilities, the following abnormal movements may occur:
ambitendency, echopraxia, mannerisms, negativism, pos-
1.1.2.1 Psychomotor Agitation turing, stereotypies, and waxy flexibility.
A person with psychomotor agitation manifests
• Ambitendency. The person makes a series of
• Excessive overactivity, which is usually tentative incomplete movements when expected
unproductive to carry out a voluntary action. For example, a
• Restlessness woman offers a handshake, then withdraws and
1
2 Revision Notes in Psychiatry
2 1
3 4 Slight pressure
FIGURE 1.1 Ambitendency. FIGURE 1.2 Mitgehen.
then offers again for 10 times. The examiner person’s arm upward and asks the person to
cannot make a handshake with her at the end resist movement. Even with a slight touch, the
(Figure 1.1). person continues to move his or her arm upward
• Automatic obedience. This refers to a condition and then returns to the original position after the
where the person follows the examiner’s instruc- test (Figure 1.2).
tions blindly without judgement and resistance. • Mitmachen. This refers to the limb movement in
For example, the examiner asks the person to response to an applied force to any direction with-
move his or her arm in different direction, and out resistance. For example, the examiner wants
the person is unable to resist even if it is against to move the person’s arm upward and asks the
his or her will. person not to move his or her limb and resist. The
• Catalepsy. This refers to abnormal maintenance person’s arm moves upward. When the examiner
of postures. For example, a person holds his or wants to move his or her arm downward, the per-
her arm in the air for a long time like a wax statue. son’s arm moves downward without any resis-
• Cataplexy. This refers to the temporary loss of tance. At the end of examination, his or her arm
muscle tone in narcolepsy. For example, a per- returns to the original position (Figure 1.3).
son develops temporary paralysis after emo- • Negativism. This is a motiveless resistance
tional excitement. to commands and to attempts to be moved.
• Echopraxia. This refers to the automatic imi-
tation by the person of another person’s move-
ments. It occurs even when the person is asked
1
not to. For example, when the consultant touches
his or her spectacles with his or her right hand,
the patient performs the same action even if he
or she does not wear spectacles.
• Mannerisms. These are repeated involuntary
movements that appear to be goal directed. For 2
example, a person repeatedly moving his or her
hand when he or she talks and tries to convey his
or her message to the examiner. 2
• Mitgehen. This is the excessive limb movement
1
in response to slight pressure of an applied force
even when the person is told to resist movement.
For example, the examiner wants to move the FIGURE 1.3 Mitmachen.
Descriptive Psychopathology 3
For example, the examiner asks the person 1.2 DISORDERS OF SPEECH
to open his or her fist but he closes it tightly
instead. 1.2.1 Disorders of Rate, Quantity,
• Posturing. The person adopts an inappropriate and Articulation
or bizarre bodily posture continuously for a long
• Dysarthria. This is difficulty in the articulation
time.
of speech.
• Stereotypies. These are repeated regular fixed
• Dysprosody. This is speech with the loss of its
patterns of movement (or speech) that are not
normal melody.
goal directed. For example, a person keeps on
• Logorrhoea (volubility). The speech is fluent
rubbing his or her right elbow with his or her left
and rambling with the use of many words.
hand during the interview.
• Mutism. This is the complete loss of speech.
• Waxy flexibility (cerea flexibilitas). There is
• Poverty of speech. There is a restricted amount
a feeling of plastic resistance resembling the
of speech. If the person replies to questions, he
bending of a soft wax rod as the examiner
or she may do so with monosyllabic answers.
moves part of the person’s body; that body part
• Pressure of speech. There is an increase in both
then remains ‘moulded’ by the examiner in the
the quantity and rate of speech, which is diffi-
new position. For example, the examiner wants
cult to interrupt.
to move the person’s arm upward. The person’s
• Stammering. The flow of speech is broken by
arm moves in upward direction but stays in the
pauses and the repetition of parts of words.
same position for 3 h after the examination
• Verbigeration. This refers to a form of stereo-
(Figure 1.4).
typy consisting of morbid repetition of words,
• Tics. These are repeated irregular movements
phrases, or sentences.
involving a muscle group and may be seen fol-
lowing encephalitis, for example, in Huntington’s
disease and in Gilles de la Tourette’s syndrome. 1.2.2 Disorders of the Form of Speech
• Parkinsonism. The features of parkinsonism • Approximate answer (vorbeireden). This refers
include to an approximate answer that, although clearly
• A resting tremor incorrect, demonstrates the answer is known.
• Cogwheel rigidity For example, when asked ‘how many legs does a
• Postural abnormalities duck have?’ the person may reply ‘three legs’. It
• A festinant gait is seen in the Ganser syndrome, first described
in criminals awaiting trial.
• Cryptolalia. The speech is in a language that no
one can understand.
• Circumstantiality. Thinking appears slow with
the incorporation of unnecessary trivial details.
Stays in The goal of thought is finally reached, however.
this • Echolalia. This is the automatic imitation by
position
the person of another person’s speech. It occurs
1 even when the person does not understand the
speech (which may be in e.g. another language).
• Flight of ideas. The speech consists of a stream
of accelerated thoughts with abrupt changes
from topic to topic and no central direction.
The connections between the thoughts may be
based on the following:
• Chance relationships.
• Clang associations. A syllable of one word
is associated with another word by sound
FIGURE 1.4 Waxy flexibility. (e.g. manic, garlic).
• Distracting stimuli.
• Punning. A humorous play of words.
• Verbal associations (e.g. alliteration and
assonance).
• Metonym. Approximate but related term is used
in an idiomatic way. For example, a person with
schizophrenia refers cloud as ‘sky sheep’.
• Neologism. A new word is constructed by the
person or an everyday word used in a special
way by the person.
• Passing by the point (vorbeigehen). The answers to
questions, although clearly incorrect, demonstrate
that the questions are understood. For example,
when asked ‘what colour is grass?’ the person may FIGURE 1.5 Knight’s move thinking.
reply ‘blue’. It is seen in the Ganser syndrome.
• Perseveration. In perseveration (of both speech • Derailment. The thought derails onto a subsid-
and movement), mental operations are contin- iary thought.
ued beyond the point at which they are relevant. • Drivelling. There is a disordered intermixture
Particular types of perseveration of speech are of the constituent parts of one complex thought.
• Palilalia. The person repeats a word with • Fusion. Heterogeneous elements of thought are
increasing frequency. interwoven with each other.
• Logoclonia. The person repeats the last syl- • Omission. A thought or part of a thought is
lable of the last word. senselessly omitted.
• Thought blocking. There is a sudden interruption • Substitution. A major thought is substituted by a
in the train of thought, before it is completed, subsidiary thought.
leaving a ‘blank’. After a period of silence, the
person cannot recall what he or she had been
saying or had been thinking of saying. 1.3 DISORDERS OF EMOTION
1.3.1 Disorders of Affect
1.2.3 Disorders (Loosening) of Association
Affect is a pattern of observable behaviours that is the
(Formal Thought Disorder)
expression of a subjectively experienced feeling state
These occur particularly in schizophrenia and may be (emotion) and is variable over time, in response to chang-
considered to be a schizophrenic language disorder. ing emotional states (DSM-IV-TR).
Examples include knight’s move thinking. The knight
can go two squares forward, backward, left, or right and • Blunted affect. In a person with a blunted affect,
turn at a right angle. If the knight is blocked by another the externalized feeling tone is severely reduced.
piece, the knight can jump over, and this refers to the • Flat affect. This consists of a total or almost
abrupt change in schizophrenia speech (Figure 1.5). total absence of signs of expression of affect.
In schizophrenia, there are odd tangential associations • Inappropriate affect. This is an affect that
between ideas, leading to disruptions in the smooth con- is inappropriate to the thought or speech it
tinuity of the speech. Schizophasia, is, also called ‘word accompanies.
salad’ or ‘speech confusion’, in which the speech is an • Labile affect. A person with a labile affect has
incoherent and incomprehensible mixture of words and a labile externalized feeling tone that is not
phrases. Schneider described the following features of related to environmental stimuli.
formal thought disorder:
1.3.2 Disorders of Mood
• Asyndesis. Juxtaposition of elements without
adequate linkage between them. Mood is a pervasive and sustained emotion that, in the
• Condensation. Combining ideas to make it extreme, markedly colours the person’s perception of the
incomprehensible. world (DSM-IV-TR).
• Dysphoria. This is an unpleasant mood. an unrealistic interpretation of physical signs or

• Depression. This is a low or depressed mood. It sensations as being abnormal.
may be accompanied by anhedonia, in which the • Monomania. This is a pathological preoccupa-
ability to enjoy pleasurable activities is lost. In tion with a single object.
normal grief or mourning, the sadness is appro- • Egomania. This is a pathological preoccupation
priate to the loss. with oneself.
• Elation. This is an elevated mood or exagger-
ated feeling of well-being that is pathological. It
is seen in mania. 1.4.2 Obsessions
• Euphoria. This is a personal and subjective feeling
of unconcern and contentment, usually seen after Obsessions are repetitive senseless thoughts that are rec-
taking opiates or as a late sequel to head injury. ognized as irrational by the person and that are unsuc-
• Irritability. This is a liability to outbursts cessfully resisted. Themes include
or a state of reduced control over aggressive
impulses towards others. It may be a personality • Aggression
trait or may accompany anxiety. It also occurs in • Dirt and contamination
premenstrual syndrome. • Fear of causing harm
• Apathy. There is a loss of emotional tone and the • Religion
ability to feel pleasure, associated with detach- • Sex
ment or indifference.
• Alexithymia. This is difficulty in the awareness
1.4.3 Phobias
of or description of one’s emotions.
A phobia is a persistent irrational fear of an activity,
object, or situation leading to avoidance. The fear is out
1.3.3 Disorders Related to Anxiety
of proportion to the real danger and cannot be reasoned
• Anxiety. This is a feeling of apprehension, ten- away, being out of voluntary control. Some types of pho-
sion, or uneasiness owing to the anticipation of bia are as follows:
an external or internal danger. Types of anxiety
include • Acrophobia. The fear of heights.
• Phobic anxiety. The focus of the anxiety is • Agoraphobia. This literally means the fear of
avoided (phobias are a disorder of thought the marketplace. It is a syndrome with a gener-
content). alized high anxiety level about, or avoidance of,
• Free-floating anxiety. The anxiety is perva- places or situations from which escape might be
sive and unfocused. difficult, or embarrassing, or in which help may
• Panic attacks. Anxiety is experienced in not be available in the event of having a panic
acute, episodic, intense attacks and may be attack or panic-like symptoms. Objects of fear
accompanied by physiological symptoms. may include crowds, open and closed spaces,
• Fear. This is anxiety caused by a realistic shopping, social situations, and travelling by
danger that is recognized at a conscious level. public transport.
• Agitation. There is excessive motor activity • Algophobia. The fear of pain
associated with a feeling of inner tension. • Claustrophobia. The fear of closed spaces
• Tension. There is an unpleasant increase in • Social phobia. The fear of personal interactions
psychomotor activity. in a public setting, such as public speaking, eat-
ing in public, and meeting people
• Specific (simple) phobia. The fear of discrete
1.4 DISORDERS OF THOUGHT CONTENT objects (e.g. snakes) or situations
• Xenophobia. The fear of strangers
1.4.1 Preoccupations
• Zoophobia. The fear of animals
• Hypochondriasis. This is a preoccupation with • Phobias of internal stimuli. These include
a fear of having a serious illness that is not obsessive phobias and illness phobias, which
based on real organic pathology but instead on overlap with hypochondriasis
1.5 ABNORMAL BELIEFS AND to a delusion that a person known to the patient

INTERPRETATIONS OF EVENTS has been in disguise of different people.
• Delusion of infestation (Ekbom’s syndrome).
1.5.1 Overvalued Ideas A delusion that one is infested by parasites.
• Delusion of poverty. A delusion that one is in
An overvalued idea is an unreasonable and sustained
poverty.
intense preoccupation maintained with less than delu-
• Delusion of pregnancy (couvade syndrome).
sional intensity, that is, the person is able to acknowledge
A delusion that one is pregnant (usually the hus-
the possibility that the belief may not be true. The idea
band of a pregnant wife).
or belief held is demonstrably false and is not one that is
• Delusion of reference. The theme is that events,
normally held by others of the person’s subculture. There
objects, or other people in one’s immediate envi-
is a marked associated emotional investment.
ronment have a particular and unusual signifi-
cance. These delusions are usually of a negative
or pejorative nature but also may be grandiose
1.5.2 Delusions
in content (DSM-IV). When similar thoughts
A delusion is a false belief based on incorrect inference are held with less than delusional intensity, they
about external reality that is firmly sustained despite are ideas of reference.
what almost everyone else believes and despite what con- • Delusion of self-accusation. A delusion of one’s
stitutes incontrovertible and obvious proof or evidence to own guilt.
the contrary. The belief is not one ordinarily accepted by • Doppelganger. A delusion that a double of a per-
other members of the person’s culture or subculture (e.g. son or place exists somewhere else.
it is not an article of religious faith). When a false belief • Erotomania (de Clérambault’s syndrome).
involves a value judgement, it is regarded as a delusion A delusion that another person, usually of higher
only when the judgement is so extreme as to defy cred- status, is deeply in love with the individual.
ibility (DSM-IV-TR). • Grandiose delusion. A delusion of inflated
worth, power, knowledge, identity, or special
• Mood-congruent delusion. The content of the relationship to a deity or famous person.
delusion is appropriate to the mood of the person. • Nihilistic delusion (Cotard’s syndrome). A delu-
• Mood-incongruent delusion. The content of the sion of death, disintegration of organs, and
delusion is not appropriate to the mood of the nonexistence.
person. • Persecutory (querulant) delusion. The central
• Primary delusion. A delusion that arises fully theme is that one (or someone to whom one is
formed without any discernible connection with close) is being attacked, harassed, cheated, per-
previous events. It may be preceded by a delu- secuted, or conspired against (DSM-IV-TR).
sional mood in which the person is aware of • Somatic delusion. A delusion whose main con-
something strange and threatening happening. tent pertains to the appearance or functioning of
• Bizarre delusion. A delusion involving a phe- one’s body (DSM-IV-TR).
nomenon that the person’s culture would regard
as totally implausible.
• Delusional jealousy (pathological jealousy,
1.5.3 Passivity Phenomenon
Othello syndrome, delusion of infidelity). A This is a delusional belief that an external agency is control-
delusion that one’s sexual partner is unfaithful. ling aspects of the self that are normally entirely under one’s
• Delusion of being controlled. Feelings, own control. Passivity phenomena include the following:
impulses, thoughts, or actions of the person are
experienced as being under the control of some • Thought alienation. The person believes that
external force rather than under his or her own his or her thoughts are under the control of an
control. outside agency or that others are participating in
• Delusion of doubles (l’illusion de sosies). A his or her thinking. This includes the following:
delusion that a person known to the person has • Thought insertion. The delusion that certain of
been replaced by a double. It is seen in Capgras’ one’s thoughts are not one’s own but rather are
syndrome. In contrast, l’illusion de Fregoli refers inserted into one’s mind by an external agency.
• Thought withdrawal. The delusion that one’s

thoughts are being removed from one’s mind
by an external agency.
• Thought broadcasting. The delusion that
one’s thoughts are being broadcast out loud
so that they can be perceived by others.
• Made feelings. This is the delusional belief
that one’s own free will has been removed and
that an external agency is controlling one’s
feelings.
• Made impulses. This is the delusional belief
that one’s own free will has been removed and FIGURE 1.6 Afterimage.
that an external agency is controlling one’s
impulses. 1.6.2 Sensory Deceptions
• Made actions. This is the delusional belief that
one’s own free will has been removed and that 1.6.2.1 Illusions
an external agency is controlling one’s actions. An illusion is a false perception of a real external stimulus.
• Somatic passivity. This is the delusional belief
that one is a passive recipient of somatic or • Afterimage. A visual illusion that refers to an
bodily sensations from an external agency. image continuing to appear in one’s vision after
the exposure to the original image has ceased.
Afterimage occurs after prolonged exposure to
1.5.4 Delusional Perception an unchanging visual stimulus such as inverted
In a delusional perception, the person attaches a new and colour American flag due to the fatigue of cone
delusional significance to a familiar real perception with- cells in the retina (Figure 1.6).
out any logical reason. • Palinopia. Prolonged afterimage.
1.6.2.2 Hallucinations
1.6 ABNORMAL EXPERIENCES A hallucination is a false sensory perception in the
absence of a real external stimulus. A hallucination is
1.6.1 Sensory Distortions
perceived as being located in objective space and as hav-
• Hyperesthesias. These are changes in sensory ing the same realistic qualities as normal perceptions. It is
perception in which there is an increased inten- not subject to conscious manipulation and only indicates a
sity of sensation. Hyperacusis is an increased psychotic disturbance when there is also impaired reality
sensitivity to sounds. testing. Hallucinations can be mood congruent or mood
• Hypoesthesias. These are changes in sensory incongruent. Types of hallucination include the following:
perception in which there is a decreased inten-
sity of sensation. Hypoacusis is a decreased sen- • Auditory.
sitivity to sounds. • Simple auditory. Sounds or musical.
• Changes in quality. Changes in quality of sen- • Mood congruent complex auditory hallucination:
sations occur particularly with visual stimuli, Stating depressive or manic themes in second
giving rise to visual distortions. Colourings of person, for example, ‘You are useless’.
visual perceptions include Command hallucination: ‘Since you are useless,
• Chloropsia—green you should hurt yourself’.
• Erythropsia—red • Mood incongruent complex auditory
• Xanthopsia—yellow hallucination:
• Dysmegalopsia. Changes in spatial form include Voices discussing the person in third person.
• Macropsia. Objects are seen larger or nearer Voices giving a running commentary on a per-
than is actually the case. son’s behaviour.
• Micropsia. Objects are seen smaller or far- Thoughts spoken out loud (thought echo/écho de
ther away than is actually the case. la pensée).
real stimulus; these include the sensa-

tion of insects crawling under the skin
( formication).
• Visceral. Hallucinations of deep sensations.
• Trailing phenomenon. Moving objects are
seen as a series of discrete discontinuous
images.
• Visual. Simple (e.g. flashlight) or complex
(e.g. Charles de Bonnet syndrome). Charles de
Bonnet syndrome refers to vivid and persisting
hallucinations in people with central or periph-
eral reduction in vision.
FIGURE 1.7 Negative autoscopy. 1.6.2.3 Pseudohallucinations (Coined

by Kandinsky in 1885)
A pseudohallucination is a form of imagery arising in
• Autoscopy (phantom mirror image). The person the subjective inner space of the mind. It lacks the sub-
sees himself or herself and knows that it is he or stantiality of normal perceptions and occupies subjec-
she. Negative autoscopy occurs when a person tive space rather than objective space. It is not subject
looks into the mirror and cannot see one’s image to conscious manipulation. An eidetic image is a vivid
(Figure 1.7). and detailed reproduction of a previous perception. In
• Cenesthesia. The person feels that there is a pareidolia, vivid imagery occurs without conscious
change in tone in a part of the body. effort while looking at a poorly structured background
• Extracampine. The hallucination occurs outside (Figure 1.8 and Table 1.1).
the person’s sensory field.
• Functional. The stimulus causing the hallucina-
tion is experienced in addition to the hallucination
itself.
• Gustatory. Taste hallucination.
• Hallucinosis. Hallucinations (usually auditory)
occur in clear consciousness.
• Hypnagogic. The hallucination (usually visual
or auditory) occurs while falling asleep.
• Hypnopompic. The hallucination (usually visual
or auditory) occurs while waking from sleep.
• Kinesthetic. The hallucination occurs when
there is a false sensation of body movement.
• Lilliputian hallucination (usually visual).
Hallucinated objects appear greatly reduced in
size.
• Olfactory.
• Peduncular. Vivid hallucinations (usually
visual) in organic diseases.
• Reflex. A stimulus in one sensory field leads to a
hallucination in another sensory field.
• Somatic. Somatic hallucinations include
• Tactile (haptic) hallucinations. Superficial
and usually involving sensations on or FIGURE 1.8 Pareidolia: seeing a woman’s face when looking
just under the skin in the absence of a at the tree.
TABLE 1.1
Characteristics of Sensory Deceptions
Characteristics Imagination (Fantasy) Illusion Pseudohallucination Hallucination Real Perception
Voluntary or Voluntary Involuntary Involuntary (except Involuntary Involuntary
involuntary eidetic imagery)
Vividness Not vivid Vivid Vivid Vivid Vivid
Space Inner subjective space Inner subjective space Inner subjective space Outer space Outer space
Insight Intact Intact Intact Impaired Intact
Examples Normal experience Delirium Depression Schizophrenia Normal experience
1.7 DISORDERS OF SELF-AWARENESS • Psychogenic amnesia. This is a part of the

(EGO DISORDERS) dissociative disorder consisting of a sudden
inability to recall important personal data. It
These include disturbances of is associated with ‘la belle indifference’ (lack
of concerns) with highly unpredictable course.
• Awareness of self-activity, including • Retrograde amnesia. This refers to loss of
• Depersonalization. One feels that one is memory for events that occurred prior to the
altered or not real in some way event (e.g. intoxication and head injury). It
• Derealization. The surroundings do not tends to improve with more distant events in
seem real the past recover first. In general, the retrograde
• The immediate awareness of self-unity amnesia is shorter than posttraumatic amnesia.
• The continuity of self • Transient global amnesia. The person pres-
• The boundaries of the self ents with abrupt onset of disorientation, loss
of ability to encode recent memories, and ret-
1.8 COGNITIVE DISORDERS rograde amnesia for variable durations. This
episode usually lasts for a few hours and is
1.8.1 Disorientation never repeated. The aetiology is due to tran-
sient ischaemia of the hippocampus–fornix–
This is a disturbance of orientation in time, place, or person.
hypothalamus system.
• Hypermnesia. In hypermnesia, the degree of
1.8.2 Disorders of Attention retention and recall is exaggerated.
• Distractibility. A distractible subject’s attention • Paramnesia. A paramnesia is a distorted recall
is drawn too frequently to unimportant or irrel- leading to falsification of memory. Paramnesias
evant external stimuli. include the following:
• Selective inattention. In selective inattention, • Confabulation. Gaps in memory are uncon-
anxiety-provoking stimuli are blocked out. sciously filled with false memories.
• Déjà vu. The subject feels that the cur-
rent situation has been seen or experienced
1.8.3 Disorders of Memory
before.
• Amnesia. This is the inability to recall past • Déjà entendu. The illusion of auditory
experiences. recognition.
• Anterograde amnesia. This refers to inabil- • Déjà pensé. The illusion of recognition of a
ity to form new memories due to failure to new thought.
consolidate or inability to retrieve. • Jamais vu. The illusion of failure to recog-
• Posttraumatic amnesia. This refers to mem- nize a familiar situation.
ory loss from the time of accident to the time • Retrospective falsification. False details are
that the person can give a clear account of the added to the recollection of an otherwise
recent events. It tends to remain unchanged. real memory.
1.8.4 Disorders of Intelligence • Oneiroid state. A dreamlike state in a person

who is not asleep
• Learning disability (mental retardation). • Torpor. The person is drowsy and easily falls
Learning difficulty or mental retardation is clas- asleep
sified by DSM-IV-TR and ICD-10 according to • Twilight state: A prolonged oneiroid state of dis-
the intelligence quotient (IQ) of the subject: turbed consciousness with hallucinations
50 ≤ IQ ≤ 70 (50 ≤ IQ ≤ 69 in ICD-10): mild
mental retardation 1.8.5.4 Fugue
35 ≤ IQ ≤ 49: moderate mental retardation This is a state of wandering from the usual surroundings
20 ≤ IQ ≤ 34: severe mental retardation in which there is also loss of memory.
IQ ≤ 20: profound mental retardation
• Dementia. This is a global organic impairment 1.8.5.5 Aphasias
of intellectual functioning without impairment • Receptive (sensory) aphasia (Wernicke’s fluent
of consciousness. aphasia). Difficulty is experienced in compre-
• Pseudodementia. This resembles dementia clin- hending the meaning of words. Types include
ically, but is not organic in origin. the following:
Agnostic alexia: Words can be seen but cannot
1.8.5 Disorders of Consciousness be read.
Pure word deafness: Words that are heard and
1.8.5.1 Levels of Consciousness cannot be comprehended.
The neurological terms used to describe progressively Visual asymbolia: Words can be transcribed but
more unconscious levels are as follows: cannot be read.
• Intermediate aphasia. Types of intermediate
• Somnolence (drowsiness). A subject who is aphasia include
drowsy or somnolent can be awoken by mild Central (syntactical) aphasia: There is difficulty
stimuli and will be able to speak comprehensi- in arranging words in their proper sequence.
bly, albeit perhaps for only a little while before Nominal aphasia (anomia): There is difficulty
falling asleep again. in naming objects. The person may use cir-
• Stupor. A stuporous person responds to pain cumlocutions (speaking in a roundabout way)
and loud sounds. Brief monosyllabic utter- to express certain words (e.g. the person can-
ances and some spontaneous motor activity not name the ‘clock’ but labels the clock as ‘the
may occur. thing which tells time’).
• Semicoma. A semicomatose person will with- • Expressive (motor) aphasia (Broca’s nonfluent
draw from the source of pain, but spontaneous aphasia). This refers to difficulty in expressing
motor activity does not take place. thoughts in words while comprehension remains.
• Deep coma. No response can be elicited, and • Global aphasia. Both receptive aphasia and
there is no response to deep pain nor is there expressive aphasia are present at the same time.
any spontaneous movement. Tendon, pupillary, • Jargon aphasia: The person utters incoherent
and corneal reflexes are usually absent. meaningless neologistic speech.
• Death. • Semantic aphasia. This refers to errors in using the
target words due to deficits in semantic memory. It
1.8.5.2 Clouding of Consciousness is associated with left temporal lobe tumours (e.g.
The person is drowsy and does not react completely to orange is named as apple) (Table 1.2).
stimuli. There is a disturbance of attention, concentra-
tion, memory, orientation, and thinking.
1.9 DYSLEXIA
1.8.5.3 Delirium Dyslexia refers to pure word blindness. Developmental dys-
The person is bewildered, disoriented, and restless. There lexia involves difficulty in reading, erratic spelling, and lack
may be associated fear and hallucinations. Variations of capacity to apply written language. Half of the people
include the following: with dyslexia also have achromatopsia (colour blindness).
TABLE 1.2
Summary of Aphasic Syndromes
Types of Aphasia Fluency Repetition Comprehension Naming
Anomic Fluent ✔ ✔ ✘
Conduction Fluent ✘ ✔ ✘
Broca’s Nonfluent ✘ ✔ ✘
Lesion in arcuate fasciculus Fluent ✘ ✔ ✘
Wernicke’s Fluent ✘ ✘ ✘
Transcortical motor Nonfluent ✔ ✔ ✘
Transcortical sensory Fluent ✔ ✘ ✘
Global Nonfluent ✘ ✘ ✘
✔ : Intact ✘ : Impaired
• Surface dyslexia. This is due to lesions in left defective copying although the person can spell
temporoparietal region. The person breaks correctly. The person has difficulty in writ-
down the whole word (lexical reading) and ing the smooth part of a letter. Letter may be
has difficulty to deal with the irregularly spelt inverted or reversed (e.g. ‘A’ is written as ‘∀’).
words. Reliance is placed on subword corre-
spondence between letters and sounds but not
1.11 ALEXIA
the normal way: spelling to sound (e.g. big is
read as dig). Alexia refers to reading disorder that affects learning and
• Deep dyslexia. This is due to extensive left hemi- academic skills.
sphere lesions. This occurs when the person
produces verbal response based on the meaning • Alexia with agraphia. The person cannot read,
of the word but not based on sound-based read- write, or connect letters due to lesions of the
ing (e.g. sister is read as auntie). angular or supramarginal gyrus.
• Neglect dyslexia. This usually occurs when the • Alexia without agraphia. The person cannot
left half of the word is being ignored due to right comprehend any written material but he can
parietal lobe lesion (e.g. bicycle is read as cycle). write. This is due to occlusion of left poste-
If the lesion is found in the left hemisphere, then rior cerebral artery leading to infarction of the
the right half of the word is affected. medial aspect of the left occipital lobe and the
splenium of the corpus callosum.
1.10 AGRAPHIA 1.12 ACALCULIA

Agraphia refers to impaired writing ability. Acalculia refers to a disturbance in the ability to compre-
hend or write numbers properly. This is due to lesion in
• Lexical agraphia. This is due to lesions in the the left angular gyrus.
left temporoparietal region. The person breaks
down the word’s spelling and has difficulty in
writing irregular words (e.g. ‘cough’ is written 1.13 APRAXIAS AND AGNOSIAS
as ‘coff’ as phonologically similar).
1.13.1 Apraxias
• Neglect agraphia. This is due to the right hemi-
spheric lesions and leads to misspelling of the Apraxia is an inability to perform purposive volitional
initial part of a word. acts, which does not result from paresis, incoordination,
• Dyspraxic agraphia. This is due to dominant sensory loss, or involuntary movements. It may be con-
frontal or parietal lobe lesions. This leads to sidered to be the motor equivalent of agnosia.
• Constructional apraxia. There is difficulty in • Apperceptive visual agnosia. The person is

constructing objects or copying drawings (e.g. unable to copy shapes or discriminate two ver-
double pentagon). It is associated with non- sions of the same object. Further details are con-
dominant parietal lobe. This is closely asso- sidered in Chapter 7.
ciated with visuospatial agnosia, with some • Associative visual agnosia. The person is unable
authorities treating the two as being essen- to recognize visually presented objects but able
tially the same. to copy objects that they cannot recognize.
• Dressing apraxia. There is difficulty in putting Further details are considered in Chapter 7.
on one’s clothes correctly. It is associated with • Prosopagnosia. This is an inability to rec-
nondominant parietal lobe. ognize faces. In the mirror sign, which may
• Ideomotor apraxia. There is difficulty in car- occur in advanced Alzheimer’s disease, a per-
rying out progressively more difficult tasks, for son may misidentify his or her own mirrored
example, involving touching parts of the face reflection.
with specified fingers and in demonstrating the • Agnosia for colours. The person is unable cor-
use of household items (e.g. toothbrush). It is rectly to name colours, although colour sense is
associated with left parietal and frontal lobe still present.
lesions. • Simultanagnosia. The person is unable to recog-
• Ideational apraxia. There is difficulty in car- nize the overall meaning of a picture, whereas
rying out a coordinated sequence of actions, its individual details are understood.
but the individual components of the sequence • Agraphognosia or agraphesthesia. The person
can be successfully performed (e.g. a person is unable to identify, with closed eyes, numbers
cannot work in a café as he or she cannot or letters traced on his or her palm.
make tea and serve the others. If you ask him • Anosognosia. There is a lack of awareness of
or her to put a tea bag into the cup, he or she disease, particularly of hemiplegia (most often
is able to do it). It is associated with lesions in following a right parietal lesion).
corpus callosum. • Coenestopathic state. There is a localized dis-
• Orobuccal apraxia. There is difficulty in per- tortion of body awareness.
forming skilled movements of the face, lips, • Autotopagnosia. This is an inability to name, rec-
tongue, cheek, larynx, and pharynx (e.g. when ognize, or point on command to parts of the body.
a person is asked to pretend to blow out a match • Astereognosia. Objects cannot be recognized by
or suck a straw, he or she makes incorrect move- palpation.
ments). It is associated with lesions in left infe- • Finger agnosia. The person is unable to recog-
rior frontal lobe and insula. nize individual fingers, be they his or her own or
those of another person.
• Topographical disorientation. This can be
1.13.2 Agnosias and Disorders of Body Image
tested by using a locomotor map-reading task in
Agnosia is an inability to interpret and recognize the which the person is asked to trace out a given
significance of sensory information, which does not route by foot.
result from impairment of the sensory pathways, men- • Distorted awareness of size and shape. For
tal deterioration, disorders of consciousness and atten- example, a limb may be felt to be growing
tion, or, in the case of an object, a lack of familiarity larger.
with the object. • Hemisomatognosis or hemidepersonalization.
The person feels that a limb (which in fact is
• Visuospatial agnosia. See ‘constructional apraxia’ present) is missing.
earlier. • Phantom limb. The continued awareness
• Visual (object) agnosia. A familiar object, which occurs of the presence of a limb that has been
can be seen though not recognized by sight, can removed.
be recognized through another modality such as • Reduplication phenomenon. The person feels
touch or hearing. that part or all of the body has been duplicated.
CLINICAL ASSESSMENT OF SKILLS AND COMPETENCIES (CASC)

STATION 1: A MAN WITH VISUAL HALLUCINATIONS
A 60-year-old man admitted to the orthopaedic ward was found to have a fractured tibia. He was brought in
by the police prior to admission and told them he saw Spanish guerrillas. He also complains of seeing small
animals and spiders around him.
Tasks: Assess his psychopathology and perform a risk assessment.
CASC Grid
The person can be frightened by his seeing Spanish guerrilla and be anticipated that your interview will be
disrupted. Candidates are required to empathize with his fear from time to time.
A. Visual A1. ‘Have you A2. ‘What do you A3. ‘How long have A4. ‘How do you feel A5. ‘Do you have
hallucinations seen things that see? Can you you been seeing when you see them?’ any explanation of
other people can’t give me an those things? Empathize with the above experience?
see?’ example? Are When do those things patient: ‘I can Do you need help?’
they very small?’ you saw appear? Do imagine that this is a
they usually come at frightening
night?’ experience for you’.
‘Do you feel that they
are real? Can you
stop them?’
B. Auditory B1. ‘Do you hear B2. If there are B3. ‘What do they B4. ‘How do you feel B5. ‘Are you alert at
hallucinations sounds or voices voices, then ask say?’ when you hear that time when you
others do not ‘How many voices them?’ hear those voices?’
hear?’ are there?’
C. Other C1. Olfactory: C2. Gustatory: C3. Somatic: C4. Persecutory C5. Jealousy:
hallucinations, ‘Is there anything ‘Have you noticed ‘Have you had any ideas: ‘Can you tell me
persecutory wrong about the that food or drink strange feelings in ‘Do you think about your
ideas, and way you smell? seems to have a your body? someone is trying to relationship? Do
jealousy Can you tell me different taste How about people harm you? How you feel that your
more about it? recently?’ touching you? about watching or partner is
Who sent the gas How about insects spying on you?’ unfaithful? If so,
to you?’ crawling?’ what’s your
evidence?’
D. Alcohol and D1. ‘Do you drink D2. ‘When did D3. ‘When was your D4. ‘Have you tried D5. ‘Do you use
drug history alcohol? If so, you start to last drink? to quit alcohol? other drugs? Do
how often do you drink? Have you You have told me that What was the you have other
drink?’ increased your you started to see outcome?’ medical problems
alcohol intake those things for such as fit or head
recently?’ 2 days. Did you drink injury?’
a lot on that day?’
E. Risk/ E1. Suicide risk: E2. Risk on E3. Comorbidity: E4. Forensic history: E5. Social history:
comorbidity/ ‘I can imagine that others: ‘Some people started ‘Have you been ‘Where do you stay
social support you are frightened ‘How about taking to drink to overcome involved with the at this moment?’
and stressed? revenge on those depression and justice system? ‘Are you staying
Some people may small people? anxiety. Do you have Do you drive? Can alone?’
want to give up. How about the such problems? you tell me more ‘Do you get any
Do you have other people?’ How is your sleep at about your driving support from
thought of ending night?’ record?’ others?’
your life?’
CASC STATION 2: A PATIENT WITH DELUSION OF LOVE

Mr. P comes to the clinic and requests to see a female psychiatric trainee called Eva. He came to the clinic
1 week ago and she treated him. He firmly believes Eva is in love with him and he wants to make love with her.
He hid a knife in his bag and prepared to attack someone if he is not allowed to see Eva.
Task: (1) Explore his belief and psychopathology. (2) Assess his risks.
CASC Grid
The patient may be aggressive and hostile. You need to spend time to build rapport. Be prepared that he will shout for
the name of his love, ‘Eva, Eva, Eva’. Pay attention to nonverbal cues as the patient may hold a bag with a knife in it.
Inform the examiner that you will disarm the patient in real practice.
A. Establish A1. ‘What is A2. ‘She is off duty A3. Acknowledge his A4. ‘In the meantime, I A5. ‘I am here to
rapport your now. Can I pass a eagerness to see was asked by Eva to help you. I want to
relationship message to her?’ Eva but no false talk to you?’ hear your views in
with Eva?’ promise. your own words.’
B. Delusion of B1. Onset: B2. Precipitant: B3. Evidence: ‘How B4. Intensity: ‘From a B5. Shake his
love ‘When did Eva ‘What happened do you know that scale of 1–10 (1 = delusion: ‘Based
start to love before that?’ Eva loves you?’ unlikely, 10 = very on the information
you?’ likely), can you tell provided, Eva only
me how likely that met you once.
Eva loves you?’ How can you be so
certain that she
likes you? Is there
any other
explanation?’
C. Other C1. Mood: ‘How C2. Biological C3. Grandiose C4. Hallucinations/ C5. Substance
symptoms do you feel at symptoms: thought: passivity: misuse:
and this moment? Sleep ‘When compared to ‘Do you hear voices? ‘Do you use any
substance Can you tell me Appetite sexual the others, are you Are you in control in recreational drugs?
misuse more about drive, sexual superior? How yourself?’ How about
your mood?’ activity, and would you feel if alcohol?’
unprotected sex Eva rejects you?’
‘Besides Eva, have
you made a lot of
new friends lately?’
D. Risk D1. Explore the D2. ‘What are you D3. Risk on Eva: D4. Self-harm: D5. Risk to others:
assessment bag: going to do with the ‘Do you know where ‘Do you have thought ‘If someone stops
‘What is inside knife?’ Inform the Eva stays? of harming yourself?’ you from seeing
your bag?’ examiner that you Have you followed Eva, what would
Mr. P: ‘There is will call in the her before? you do?’
a knife inside’. security to disarm Have you sent e-mail
the patient. to her?’
E. Background E1. Forensic E2. Occupational E3. Social history: E4. Relationship E5. Willingness for
history history: history: ‘Where do you stay history: treatment:
‘Were you ‘Are you employed at this moment?’ ‘Can you tell me more ‘I can imagine that
involved with at this moment?’ ‘Are you staying about your you are quite
the justice ‘May I know the alone?’ relationship in the stressed when
system before?’ nature of your past?’ searching for Eva,
work?’ can I offer you
some help such as
medication?’
BIBLIOGRAPHY Institute of Psychiatry. 1973: Notes on Eliciting and

Recording Clinical Information. Oxford, U.K.: Oxford
American Psychiatric Association. 2000: DSM-IV-TR: Diagnostic University Press.
and Statistical Manual of Mental Disorders, 4th edn, text Leff JP and Isaacs AD. 1990: Psychiatric Examination in
revision. Washington, DC: American Psychiatric Association Clinical Practice, 3rd edn. Oxford, U.K.: Blackwell
Publishing Inc. Scientific.
Campbell RJ. 1996: Psychiatric Dictionary. Oxford, U.K.: Sadock BJ and Sadock VA. 2007: Kaplan & Sadock’s
Oxford University Press. Synopsis of Psychiatry. Behavioural Sciences/Clinical
Hamilton M. (ed.) 1985: Fish’s Clinical Psychopathology, 2nd Psychiatry, 10th edn. Philadelphia, PA: Lippincott
edn. Bristol, U.K.: Wright. Williams & Wilkins.
Hodges J. 2002: Cognitive Assessment for Clinicians. Oxford, Sims ACP. 1985: Symptoms in the Mind. London, U.K.:
U.K.: Oxford University Press. Baillière Tindall.
2 Classification
The main classification systems in use at the time of writing • Black bile. melancholic (considerate, creative,
are as follows: kind)—cold and dry
• Phlegm. phlegmatic (affectionate, dependable,
• Mental and behavioural disorders of the kind)—cold and moist
International Classification of Diseases, 10th
edn. (ICD-10) of the World Health Organization
(WHO), published in 1992 2.1.3 Cullen
• The Diagnostic and Statistical Manual of
William Cullen (1710–1790) of Edinburgh published a clas-
Mental Disorders, 4th edn., text revision (DSM-
sification of diseases that was widely used in the English-
IV-TR) of the American Psychiatric Association
speaking world (Doig et al., 1993). His classification of the
(APA), published in 2000
neuroses was fourfold:
2.1 HISTORY OF CLASSIFICATION SCHEMES • Adynamias

2.1.1 Ancient Greeks • Coma
• Spasms
The classification of mental illness proposed by Hippocrates • Vesanias, which included amentia, mania, mel-
(circa 460 BCE to circa 370 BCE) and his Hippocratic ancholia, and oneirodynia
School of Medicine included the following categories:
• Mania 2.2 ICD

• Melancholia
• Paranoia A classification section for mental disorders first
• Phobias appeared in ICD-6 (1949) (WHO, 1990). At the time
• Scythian disease (i.e. transvestism) of writing, ICD-11 is being prepared and parts of it are
undergoing field testing. It is probably due to be pub-
These were believed to be based on abnormalities in the lished by 2015.
levels and balance of the following four humours or cambia:
• Blood 2.3 DSM

• Yellow bile DSM-I (1952) was essentially based on the mental disor-
• Black bile ders section of ICD-6 (Grob, 1991). There was a strong
• Phlegm psychodynamic influence evident in DSM-I; for example,
the widespread use of the term ‘reaction’ was based on
2.1.2 Ancient Romans Adolf Meyer’s psychobiological viewpoint. The term
reaction was removed from DSM-II (1968) (Kirk and
An ancient Roman (of Greek ancestry), Galen of
Kutchins, 1994).
Pergamon (CE 129 to circa 216), identified the follow-
ing human temperaments based on the aforementioned
humours or cambia, in which combinations of four quali- 1. DSM-III (1980) was an innovative psychi-
ties (warm, cold, moist, and dry) were said to occur: atric classification system that tried not to
appear favourably disposed to competing
• Blood. sanguine (extroverted, social)—warm etiological theories and that introduced the
and moist following (APA, 1985):
• Yellow bile. choleric (charismatic, passionate, a. Operational diagnostic criteria
energy)—warm and dry b. A multiaxial classification
17
DSM-III was revised (and corrected) and pub- 2.4.2 Schizophrenia, Schizotypal,

lished as DSM-III-R in 1987 (Wilson, 1993). and Delusional Disorders
2. DSM-IV and DSM-IV-TR was published in
1994 and 2000 respectively. DSM-5 is essen- F20 Schizophrenia
tially the version in use at the time of writing. F21 Schizotypal disorder
F22 Persistent delusional disorders
F23 Acute and transient psychotic disorders
2.4 ICD-10 (WHO, 1992) F24 Induced delusional disorder
F25 Schizoaffective disorders
2.4.1 Organic, Including Symptomatic, F28 Other nonorganic psychotic disorders
Mental Disorders F29 Unspecified nonorganic psychosis
F00 Dementia in Alzheimer’s disease

F01 Vascular dementia 2.4.3 Mood (Affective) Disorders
F02 Dementia in other diseases classified elsewhere F30 Manic episode
F03 Unspecified dementia F31 Bipolar affective disorder
F04 Organic amnesic syndrome, not induced by F32 Depressive episode
alcohol and other psychoactive substances F33 Recurrent depressive disorder
F05 Delirium, not induced by alcohol and other psy- F34 Persistent mood (affective) disorders
choactive substances F35 Other mood (affective) disorders
F06 Other mental disorders caused by brain damage F39 Unspecified mood (affective) disorder
and dysfunction and by physical disease
F07 Personality and behavioural disorders caused by
brain disease, damage, and dysfunction 2.4.4 Neurotic, Stress-Related,
F09 Unspecified organic or symptomatic mental and Somatoform Disorders
disorder
Mental and behavioural disorders caused by F40 Phobic anxiety disorders
psychoactive substance use F41 Other anxiety disorders
F10 Mental and behavioural disorders caused by the F42 Obsessive–compulsive disorder
use of alcohol F43 Reaction to severe stress and adjustment disorders
F11 Mental and behavioural disorders caused by the F44 Dissociative (conversion) disorders
use of opioids F45 Somatoform disorders
F12 Mental and behavioural disorders caused by the F48 Other neurotic disorders
use of cannabinoids
F13 Mental and behavioural disorders caused by the 2.4.5 Behavioural Syndromes Associated
use of sedatives or hypnotics with Physiological Disturbances
F14 Mental and behavioural disorders caused by the
and Physical Factors
use of cocaine
F15 Mental and behavioural disorders caused by the F50 Eating disorders
use of other stimulants, including caffeine F51 Nonorganic sleep disorders
F16 Mental and behavioural disorders caused by the F52 Sexual dysfunction, not caused by organic dis-
use of hallucinogens order or disease
F17 Mental and behavioural disorders caused by the F53 Mental and behavioural disorders associated
use of tobacco with the puerperium, not elsewhere classified
F18 Mental and behavioural disorders caused by the F54 Psychological and behavioural factors associated
use of volatile solvents with disorders or diseases classified elsewhere
F19 Mental and behavioural disorders caused by F55 Abuse of nondependence-producing substances
multiple drug use and the use of other psychoac- F59 Unspecified behavioural syndromes associated
tive substances with physiological disturbances and physical factors
Classification 19
2.4.6 Disorders of Adult Personality F98

Other behavioural and emotional disorders
and Behaviour with onset usually occurring in childhood and
adolescence
F60 Specific personality disorders Unspecified mental disorder
F61 Mixed and other personality disorders F99 Mental disorder, not otherwise specified
F62 Enduring personality changes, not attributable
to brain damage and disease 2.5 DSM-IV-TR AND DSM-5
F63 Habit and impulse disorders
F64 Gender identity disorders This is a multiaxial classification with the following five
F65 Disorders of sexual preference axes:
F66 Psychological and behavioural disorders associ-
ated with sexual development and orientation Axis I Clinical disorders and other conditions that
F68 Other disorders of adult personality and may be a focus of clinical attention
behaviour Axis II Personality disorders and mental retardation
F69 Unspecified disorder of adult personality and Axis III General medical conditions
behaviour Axis IV Psychosocial and environmental problems
Axis V Global assessment of functioning
2.4.7 Mental Retardation
In the following summary, NOS stands for ‘not other-
F70 Mild mental retardation wise specified’.
F71 Moderate mental retardation
F72 Severe mental retardation
F73 Profound mental retardation 2.5.1 Axis I: Clinical Disorders; Other
F78 Other mental retardation Conditions That May Be a Focus
F79 Unspecified mental retardation of Clinical Attention
2.5.1.1 DSM-IV-TR and DSM-5: Disorders Usually

2.4.8 Disorders of Psychological Development First Diagnosed in Infancy, Childhood,
F80 Specific developmental disorders of speech and or Adolescence (Excluding Mental
language Retardation Which Is Diagnosed on Axis II)
F81 Specific developmental disorders of scholastic skills Learning disorder
F82 Specific developmental disorder of motor Motor skills disorder
function Communication disorders
F83 Mixed specific developmental disorders Pervasive developmental disorders
F84 Pervasive developmental disorders
F88 Other disorders of psychological development • Autistic disorder
F89 Unspecified disorder of psychological development • Rett’s disorder
• Childhood disintegrative disorder
• Asperger’s disorder
2.4.9 Behavioural and Emotional Disorders
• NOS
with Onset Usually Occurring in
Childhood and Adolescence Attention-deficit and disruptive behaviour disorders
Feeding and eating disorders of infancy and early childhood
F90 Hyperkinetic disorders
Tic disorders
F91 Conduct disorders
Elimination disorders
F92 Mixed disorders of conduct and emotions
F93 Emotional disorders with onset specific to childhood • Encopresis
F94 Disorders of social functioning with onset spe- • Enuresis
cific to childhood and adolescence
F95 Tic disorders Other disorders of infancy, childhood, or adolescence
DSM-5 (APA, 2013) Subtypes of major and mild neurocognitive disorders

Intellectual developmental disorders
• 305 Neurocognitive disorder due to Alzheimer’s
• 319 Intellectual developmental disorder (mild, disease
moderate, severe, and profound) • 306 Frontotemporal neurocognitive disorder
• 315.8 Global developmental delay • 310 Neurocogntive disorder due to traumatic
brain injury
Communication disorders • 308 Neurocognitive disorder due to Lewy body
dementia
• 315.39 Language disorder • 316 Neurocognitive disorder due to Parkinson’s
• 315.39 Speech disorder disease
• 315.39 Social communication disorder • 315 Neurocognitive disorder due to HIV
• 315.35 Childhood-onset fluency disorder infection
• 311 Substance-induced neurocognitive disorder
299 Autism spectrum disorder • 317 Neurocognitive disorder due to Huntington’s
314 Attention deficit/hyperactivity disorder disease
• 316 Neurocognitive disorder due to prion
• 314.00 Attention deficit/hyperactivity disorder/
disease
combined type
• 318 Neurocognitive disorder due to another
• 314.01 Attention deficit/hyperactivity disorder
medical condition
not elsewhere classified
• 320 Neurocognitive disorder not elsewhere
classified
315 Specific learning disorder (reading, writing, and
mathematics)
2.5.1.3 DSM-IV-TR and DSM-5:
Motor disorders Substance-Related Disorders
• Alcohol-related disorders
• 315.4 Developmental coordination disorder • Amphetamine (or amphetamine-like)-related
• 307.3 Stereotypic movement disorder disorders
• 307.33 Tourette’s disorder • Caffeine-related disorders
• 307.22 Chronic motor or vocal tic disorder • Cannabis-related disorders
• 307.21 Provisional tic disorder • Cocaine-related disorders
• 307.20 Tic disorder not elsewhere classified • Hallucinogen-related disorders
• Inhalant-related disorders
• Nicotine-related disorders
2.5.1.2 DSM-IV-TR and DSM-5: Delirium, • Opioid-related disorders
Dementia, and Amnestic and • Phencyclidine (or phencyclidine-like)-related
Other Cognitive Disorders disorders
• Delirium • Sedative-, hypnotic-, or anxiolytic-related disorders
• Dementia • Polysubstance-related disorders
• Amnestic disorders • Other (or unknown) substance-related disorders
• Other cognitive disorders
DSM-5 (APA, 2013)
DSM-5 (APA, 2013) Alcohol-related disorders
292 Delirium
• 305 Alcohol use disorder
• Substance-induced delirium • 303 Alcohol intoxication
• Delirium not elsewhere classified • 291.81 Alcohol withdrawal
• 291.9 Alcohol-induced disorder not elsewhere
Mild and major neurocognitive disorder classified
Classification 21
Caffeine-related disorders Stimulant-related disorders
• 305.9 Caffeine intoxication • 305.7 Stimulant use disorder

• 292.0 Caffeine withdrawal • 292.89 Stimulant intoxication
• 292.9 Caffeine-induced disorder not elsewhere • 292.0 Stimulant withdrawal
classified • 292.9 Stimulant-induced disorders not else-
where classified
Cannabis-related disorders Tobacco-related disorders
• 305.2 Cannabis use disorder • 305.1 Tobacco use disorder

• 292.89 Cannabis intoxication • 292.0 Tobacco withdrawal
• 292.0 Cannabis withdrawal
• 292.9 Cannabis-induced disorder not elsewhere Unknown substance disorders
classified
• 305.9 Unknown substance use disorder
Hallucinogen-related disorders • 292.89 Unknown substance intoxication
• 292.0 Unknown substance withdrawal
• 305.9 Hallucinogen use disorder • 292.9 Unknown substance-induced disorder not
• 292.89 Hallucinogen intoxication elsewhere classified
• 292.89 Hallucinogen persisting perception
disorder 312.31 Gambling disorder
• 292.9 Hallucinogen-induced disorder not else-
where classified Recommended for further study by DSM-5
• Caffeine use disorder

Inhalant-related disorders • Internet use disorder
• Neurobehavioural disorder associated with pre-
• 305.9 Inhalant use disorder natal alcohol exposure
• 292.89 Inhalant intoxication
• 292.9 Inhalant-induced disorder not elsewhere 2.5.1.4 DSM-IV-TR and DSM-5: Schizophrenia
classified and Other Psychotic Disorders
• Schizophrenia
Opioid-related disorders • Schizophreniform disorder
• Schizoaffective disorder
• Delusional disorder
• 305.5 Opioid use disorder • Brief psychotic disorder
• 292.89 Opioid intoxication • Shared psychotic disorder
• 292.0 Opioid withdrawal • Psychotic disorder caused by a general medical
• 292.9 Opioid-induced disorder not elsewhere condition
classified • Substance-induced psychotic disorder
• Psychotic disorder
Sedative/hypnotic-related disorders • NOS
• 305.4 Sedative/hypnotic use disorder DSM-5 (APA, 2013)

• 292.89 Sedative/hypnotic intoxication 301.22 Schizotypal personality disorder
• 292.0 Sedative/hypnotic withdrawal 297.1 Delusional disorder
• 292.9 Sedative/hypnotic-induced disorder not 298.8 Brief psychotic disorder
elsewhere classified Substance-induced psychotic disorder
sychotic disorder associated with another

P 300.01 Panic disorder
medical condition 300.22 Agoraphobia
293.89 Catatonic disorder associated with another 300.29 Specific phobia
medical condition 300.23 Social anxiety disorder (social phobia)
295.40 Schizophreniform disorder 300.02 Generalized anxiety disorder
295.70 Schizoaffective disorder Substance-induced anxiety disorder
295.90 Schizophrenia 293.84 Anxiety disorder attributable to another medi-
Psychotic disorder not elsewhere classified cal condition
Catatonic disorder not elsewhere classified 300.00 Anxiety disorder not elsewhere classified
• Mood disorders 2.5.1.8 DSM-IV-TR and DSM-5:

Somatoform Disorders
2.5.1.5 DSM-IV-TR and DSM-5: Depressive Disorders Somatization disorder
DSM-5 (APA, 2013)
296.99 Disruptive mood dysregulation disorder • Undifferentiated somatoform disorder
296.2 Major depressive disorder, single episode • Conversion disorder
296.3 Major depressive disorder, recurrent • Pain disorder
300.4 Dysthymic disorder • Hypochondriasis
625.4 Premenstrual dysphoric disorder • Body dysmorphic disorder
Substance-induced depressive disorder • NOS
293.83 Depressive disorder associated with another
medical condition DSM-5 (APA, 2013)
311 Depressive disorder not elsewhere classified 300.82 Somatic symptom disorder
300.7 Illness anxiety disorder
2.5.1.6 DSM-IV-TR and DSM-5: Bipolar Disorders 300.11 Conversion disorder (functional neurological
DSM-5 (APA, 2013) symptom disorder)
296.4 Bipolar I disorder 316 Psychological factors affecting medical condition
296.89 Bipolar II disorder 300.19 Factitious disorder
301.13 Cyclothymic disorder 300.82 Somatic symptom disorder not elsewhere classified
Substance-induced bipolar disorder
2.5.1.9 DSM-IV-TR and DSM-5: Factitious Disorders
293.83 Bipolar disorder associated with another medi-
cal condition Dissociative disorders
296.80 Bipolar disorder not elsewhere classified
• Dissociative amnesia
2.5.1.7 DSM-IV-TR and DSM-5: Anxiety Disorders • Dissociative fugue
• Dissociative identity disorder
• Panic disorder without agoraphobia
• Depersonalization disorder
• Panic disorder with agoraphobia
• NOS
• Agoraphobia without history of panic disorder
• Specific phobia DSM-5 (APA, 2013)
• Social phobia 300.6 Depersonalization–derealization disorder
• Obsessive–compulsive disorder 300.12 Dissociative amnesia
• Posttraumatic stress disorder 300.14 Dissociative identity disorder
• Acute stress disorder 300.15 Dissociative disorder not elsewhere classified
• Generalized anxiety disorder
• Anxiety disorder caused by a general medical 2.5.1.10 DSM-IV-TR and DSM-5: Sexual
condition and Gender Identity Disorders
• Substance-induced anxiety disorder Sexual dysfunctions
• NOS
• Sexual desire disorders
DSM-5 (APA, 2013) • Sexual arousal disorders
309.21 Separation anxiety disorder • Orgasmic disorders
Classification 23
• Sexual pain disorders Sleep disorders related to another medical disorder

• Sexual dysfunction caused by a general medical Other sleep disorders
condition
DSM-5 (APA, 2013)
Paraphilias 780.52 Insomnia disorder
780.54 Hypersomnolence disorders
• Exhibitionism 347.00 Narcolepsy/hypocretin deficiency
• Fetishism 327.23 Obstructive sleep apnea hypopnea syndrome
• Frotteurism Central sleep apnea
• Pedophilia Sleep-related hypoventilation
• Sexual masochism Circadian rhythm sleep-wake disorder
• Sexual sadism 307.46 Sleepwalking disorder
• Transvestic fetishism 307.46 Sleep terror disorder
• Voyeurism 307.47 Nightmare disorder
• NOS 327.42 Rapid eye movement sleep behaviour disorder
333.94 Restless legs syndrome
Gender identity disorders Substance-induced sleep disorder
DSM-5 (APA, 2013) 2.5.1.13 DSM-IV-TR and DSM-5: Impulse-Control
302.72 Erectile disorder
Disorders not Elsewhere Classified
302.73 Female orgasmic disorder
302.74 Delayed ejaculation DSM-5 (APA, 2013)
302.75 Early ejaculation Disruptive, impulse-control, and conduct disorders
302.73 Female orgasmic disorder 313.81 Oppositional defiant disorder
302.72 Female sexual interest/arousal disorder 312.34 Intermittent explosive disorder
302.71 Male hypoactive sexual desire disorder 312.81 Conduct disorder
302.76 Genito-pelvic pain/penetration disorder 312.33 Pyromania
Substance/medication-induced sexual dysfunction 312.32 Kleptomania
302.80 Sexual dysfunction not elsewhere classified 312.9 Unspecified disruptive, impulse-control, and
302.6 Gender dysphoria in children conduct disorders
302.85 Gender dysphoria in adolescents or adults 2.5.1.14 Adjustment Disorders
Other conditions that may be a focus of clinical attention.
2.5.1.11 DSM-IV-TR and DSM-5: Eating Disorders
Anorexia nervosa 2.5.2
AXIS II: Personality Disorders;
Bulimia nervosa Mental Retardation
NOS
2.5.2.1 Personality Disorders
DSM-5 (APA, 2013) • Paranoid personality disorder
307.52 Pica • Schizoid personality disorder
307.53 Rumination disorder • Schizotypal personality disorder
307.59 Avoidant/restrictive food intake disorder • Antisocial personality disorder
307.1 Anorexia nervosa • Borderline personality disorder
307.51 Bulimia nervosa • Histrionic personality disorder
307.51 Binge eating disorder • Narcissistic personality disorder
307.50 Feeding or eating disorder not elsewhere • Avoidant personality disorder
classified • Dependent personality disorder
• Obsessive–compulsive personality disorder
2.5.1.12 DSM-IV-TR and DSM-5: Sleep Disorders
• NOS
Primary sleep disorders
DSM-5 (2013)
• Dyssomnias Cluster A Personality disorders
• Parasomnias 301.0 Paranoid personality disorder
301.2 Schizoid personality disorder 2.5.4 Axis IV: Psychosocial and

301.22 Schizotypal personality disorder Environmental Problems
Cluster B Personality disorders Problems with primary support group
301.7 Antisocial personality disorder Problems related to the social environment
301.83 Borderline personality disorder Educational problems
301.5 Histrionic personality disorder Occupational problems
301.81 Narcissistic personality disorder Housing problems
Economic problems
Cluster C Personality disorders Problems with access to health-care services
301.82 Avoidant personality disorder Problems related to interaction with the legal system/
301.6 Dependent personality disorder crime
301.4 Obsessive–compulsive personality disorder Other psychosocial and environmental problems
Other personality disorders

310.1 Personality change due to another medical condition 2.5.5 Axis V: Global Assessment of Functioning
301.89 Other personality disorder The fifth axis allows for a global assessment of function-
ing of the individual.
2.5.2.2 Mental Retardation
Mild mental retardation
Moderate mental retardation REFERENCES
Severe mental retardation American Psychiatric Association. 1985: DSM III: Diagnostic
Profound mental retardation Statistical Manual, 3rd edn., Washington, DC: American
Mental retardation, severity unspecified Psychiatric Association Press.
American Psychiatric Association. 2000: Diagnostic and
Statistical Manual of Mental Disorders, 4th edn., Text
2.5.3 Axis III: General Medical Conditions Revision (DSM-IV-TR). Washington, DC: American
Psychiatric Association.
Infectious and parasitic diseases American Psychiatric Association. 2013: Desk Reference to
Neoplasms the Diagnostic Criteria from DSM-5. Washington, DC:
Endocrine, nutritional, and metabolic diseases and American Psychiatric Association Press.
immunity disorders Doig A, Ferguson JPS, Milne IA, and Passmore R. 1993:
Diseases of the blood and blood-forming organs William Cullen and the Eighteenth Century Medical
Diseases of the nervous system and sensory organs World, pp. 34–55. Edinburgh University Press.
Grob GN. 1991: Origins of DSM-I: A study in appear-
Diseases of the circulatory system
ance and reality. American Journal of Psychiatry
Diseases of the respiratory system 148(4):421–431.
Diseases of the digestive system Kirk SA and Kutchins H. 1994: The myth of the reliability of
Diseases of the genitourinary system DSM. Journal of Mind and Behavior 15:1–2.
Complications of pregnancy, childbirth, and the puerperium Wilson M. 1993: DSM-III and the transformation of American
Diseases of the skin and subcutaneous tissue psychiatry: A history. American Journal of Psychiatry
Diseases of the musculoskeletal system and connective 150(3):399–410.
World Health Organization. 1990: History of the development
tissue
of the ICD. http://www.who.int/classifications/icd/en/
Congenital anomalies HistoryOfICD.pdf
Certain conditions originating in the perinatal period World Health Organization. 1992: The ICD-10 Classification of
Symptoms, signs, and ill-defined conditions Mental and Behavioural Disorders. Geneva, Switzerland:
Injury and poisoning World Health Organization.
3 Basic Psychology
3.1 PRINCIPLES OF LEARNING THEORY 3.1.2.2 Acquisition Stage

The acquisition stage of conditioning is the period during
3.1.1 Definition of Learning which the association is being acquired between the CS
Learning is a change in behaviour as a result of prior and the US with which it is being paired.
experience. It does not include behaviour change caused
by maturation or temporary conditions (e.g. drug effects 3.1.2.3 Delayed Conditioning
or fatigue). In delayed conditioning, the onset of the CS precedes that
Learning may occur through associations being made of the US, and the CS continues until the response occurs.
between two or more phenomena. Two forms of such Delayed conditioning is optimal when the delay between
associative learning are recognized: classical condition- the onsets of the two stimuli is around half a second.
ing and operant conditioning. Cognitive learning is a
more complex process in which current perceptions are 3.1.2.4 Simultaneous Conditioning
interpreted in the context of previous information in order In simultaneous conditioning, the onset of both stim-
to solve unfamiliar problems. Evidence that learning can uli is simultaneous, and the CS continues until the
also take place through the observation and imitation of response occurs. It is less successful than delayed
others has led to the development of the observational conditioning.
learning theory.
3.1.2.5 Trace Conditioning
3.1.2 Classical Conditioning In trace conditioning, the CS ends before the onset of the
US, and the conditioning becomes less effective as the
3.1.2.1 Definition and Introduction delay between the two increases.
Classical conditioning (respondent learning) was first
described by the Russian physiologist Ivan Petrovich 3.1.2.6 Backward Conditioning
Pavlov (1849–1936) in 1927. (Although Pavlov was In backward conditioning, the presentation of the CS
awarded a Nobel Prize, this was in 1904 for his work occurs after that of the US.
on digestion.) Following several repetitions of pairing
of light (or a bell sounding) followed by the presenta- 3.1.2.7 Higher-Order Conditioning
tion of food to a dog, it was found that just switch- In higher-order conditioning, the CS is paired with a sec-
ing on the light led to salivation. The dog had been ond (or third) CS, which on presentation by itself elicits
conditioned to associate the light with food. Food was the original CR. In other words, the original CS now acts
acting as the unconditioned stimulus (US), eliciting as the US in the new pairing. If there is just a second CS,
the reflex response of salivation without new learning then this gives rise to second-order conditioning. A third
being involved. The response to the US is known as CS gives rise to third-order conditioning. Higher-order
the unconditioned response (UR). The light would not (i.e. second-order or above) conditioning is weaker than
normally have elicited the response of salivation but first-order conditioning; in general, the higher the order,
was now a conditioned stimulus (CS) that had elicited the weaker the conditioning.
the response through its association with a US. The
conditioned response (CR) is the learned or acquired 3.1.2.8 Extinction
response to a CS. This is shown diagrammatically in Extinction is the gradual disappearance of a CR and
Figure 3.1. Thus, in Pavlov’s experiments, salivation occurs when the CS is repeatedly presented without the
was both a UR before conditioning and a CR after US. It does not entail the complete loss of the condi-
conditioning. tion stimulus. Following extinction, if an experimental
25
US UR 1969) although much of the groundwork for the under-

lying theory was carried out by Thorndike (1911);
Burrhus Frederic Skinner (1904–1990) and Edward
Lee Thorndike (1874–1949) were American psycholo-
gists. A voluntary behaviour is engaged in because
CS CR
its occurrence is reinforced by being rewarded. Such
behaviour is independent of stimuli and was termed
FIGURE 3.1 Diagram showing the processes associated operant behaviour by Skinner. An alternative type of
with classical conditioning. US, unconditioned stimulus; UR, behaviour termed respondent behaviour by Skinner
unconditioned response; CS, conditioned stimulus; CR, condi- refers to behaviour that is dependent on known stimuli.
tioned response.
3.1.3.2 Trial-and-Error Learning/Behaviour
animal is allowed to rest, a weaker CR reemerges; this
Thorndike described experiments in which hungry
is known as partial recovery.
cats were placed in puzzle boxes. By chance, in time,
3.1.2.9 Generalization a cat would effect an escape, for example, by press-
ing on a lever, and reach some visible food outside the
Generalization is the process whereby once a CR has been
box. Less time would be needed to carry out the same
established to given stimulus, that response can also be
behaviour in later trials. This is trial-and-error learn-
evoked by other stimuli that are similar to the original CS.
ing or behaviour.
3.1.2.10 Discrimination
Discrimination is the differential recognition of and 3.1.3.3 Law of Effect
response to two or more similar stimuli. Thorndike’s law of effect holds that voluntary behaviour
that is paired with subsequent reward is strengthened.
3.1.2.11 Incubation
Incubation is the increase in strength of CRs resulting 3.1.3.4 Skinner Box
from repeated brief exposure to the CS. Skinner developed the experimental procedures of
Thorndike, creating the Skinner box. Operant condi-
3.1.2.12 Stimulus Preparedness tioning can be demonstrated using a Skinner box in
Stimulus preparedness refers to the fact that some stimuli are which, for example, every time the animal presses a
more likely to become conditioned stimuli than are others. lever, a pellet of food is released. If hungry rats are
placed in it, random trial-and-error learning leads to
3.1.2.13 Little Albert the lever being pressed, the CR, to obtain the rein-
In 1920, the American psychologist John Broadus Watson forcing stimulus of the reward of food pellets. If, after
(1878–1958) and his research assistant Rosalie Rayner many repetitions of this pairing, the CR is no longer
described the experimental induction of a phobia, using reinforced, then the CR abates, that is, extinction
classical conditioning, in an 11-month-old boy known as occurs. Following extinction, if the animal is allowed
Little Albert. Following several episodes of pairing in to rest, a weaker CR can reemerge; this is partial recov-
which the presentation of a white rat was accompanied ery. Discrimination (see preceding text) can also occur.
by a loud noise caused by striking a steel bar, the boy
developed a fear of the rat in the absence of the frighten-
ing noise. This was then repeated with a rabbit and then
3.1.4 Observational Learning (Vicarious
generalized to any furry mammal. Learning/Modelling)
3.1.4.1 Definition and Introduction
3.1.3 Operant Conditioning Observational learning (or modelling), also known as
(Instrumental Learning) vicarious learning (or modelling), is the learning of
behaviours and skills that can occur by observation with-
3.1.3.1 Definition and Introduction out direct reinforcement. The occurrence of the obser-
Operant conditioning, or instrumental learning, is par- vational learning of aggressive behaviour in humans has
ticularly associated with Skinner (see Skinner, 1953, been demonstrated by Bandura.
Basic Psychology 27
3.1.4.2 Bobo Doll Experiments e. A model who appears to be like the observer
Albert Bandura (1925–present) is a Canadian psychol- In contrast, unsuccessful observational learning
ogist (working at Stanford, United States) who carried is more likely to occur in association with the
out the Bobo doll experiments. (Bobo dolls are inflat- following factors:
able, balloon-like objects, shaped like eggs, which a. Low arousal (e.g. sleepiness)
bob back up after being knocked down, owing to the b. Overarousal
presence of extra weighting in the dolls’ ‘bottoms’.) c. The presence of distracting stimuli
Bandura made a film of one of his female students ver- 2. Retention.
bally and physically attacking a Bobo doll, including 3. Reproduction. The translation of what has been
hitting it with a hammer. This film was then shown to remembered into behaviour.
groups of kindergartners. The children liked the film 4. Motivation. See Section 3.1.6.
and when let out to play in an area containing a new
Bobo doll and some toy hammers, they proceeded ver-
bally and physically to imitate the actions of the young
3.1.5 Cognitive Learning
woman in Bandura’s film. 3.1.5.1 Definition
Bandura pointed out that a change in behaviour The notion of a mental model of reality is central to the
in the children had occurred without rewards being cognitive approach to psychology. Cognition involves the
received for approximations to the new behaviour. He reception, organization, and utilization of information.
termed this phenomenon, which was clearly differed Cognitive learning is an active form of learning in which
from classical and operant learning, observational mental cognitive structures (cognitive maps) are formed.
learning or modelling; his theory is referred to as These allow mental images to be formed, which allow
social learning theory. meaning and structure to be given to the internal and
To deal with the criticism that a Bobo doll is made external environment.
to be hit, Bandura repeated the Bobo doll experiments,
this time substituting a live clown for the doll. Again, the 3.1.5.2 Mechanisms
children imitated the actions of the young woman, to the
Cognitive learning can occur in the following ways:
extent of kicking and punching a live clown and hitting
him with (toy) hammers.
• Insight learning—the learning occurs appar-
ently out of the blue, because of an understand-
3.1.4.3 Optimal Conditions for ing of the relationship between various elements
Observational Learning relevant to a problem.
1. The subject sees that the behaviour observed is • Latent learning—cognitive learning takes
being reinforced. place but is not manifested except in certain
2. Perceived similarity—the subject must believe circumstances such as the need to satisfy a
that they can emit the response necessary to basic drive.
obtain reinforcement (self-efficacy).
3.1.5.3 Assimilation Theory
The assimilation theory of cognitive learning is based on
3.1.4.4 Steps Involved in the Modelling Process the following concepts:
According to Bandura (1973), the following steps are
involved in the modelling process: 1. Learning in humans is influenced by prior
knowledge.
1. Attention. Successful observational learning is 2. Human learning is manifested by a change in
more likely to occur in association with the fol- the meaning of experience rather than a purely
lowing factors: behavioural change.
a. Optimal arousal 3. Those involved in teaching should help their
b. An attractive model students reflect on their experiences.
c. A prestigious model 4. Those involved in teaching should construct
d. A colourful and dramatic model new meanings.
3.1.6 Concepts of Extinction and Reinforcement In a fixed ratio schedule, reinforcement occurs

in Explaining Behaviour after a fixed number of responses. It is good
at maintaining a high response rate.
3.1.6.1 Extinction In a variable ratio schedule, reinforcement occurs
Extinction has been defined earlier. after a variable number of responses. It is very
good at maintaining a high response rate.
3.1.6.2 Reinforcement
A positive reinforcer is a reinforcing reward stimulus (e.g. 3.1.6.7 Motivation
food and water, money in humans), which increases the In observational learning theory, Bandura has put for-
probability of occurrence of the operant behaviour, while ward the following motives that encourage observational
a negative reinforcer is an aversive stimulus (e.g. an elec- learning:
tric shock, fear) whose removal increases the probability
of occurrence of the operant behaviour. For example, a • Past reinforcement. This is similar to the types
Skinner box may be arranged so that in order to avoid an of reinforcement that are recognized in classical
aversive stimulus, the animal must press a lever. Learning and operant learning theory.
this response is called avoidance conditioning. Escape • Promised reinforcements. These are incentives
conditioning is a variety of negative reinforcement in that can be imagined.
which the response learnt provides complete escape from • Vicarious reinforcement. This refers to the
the aversive stimulus (very resistant to extinction). sight and recollection of the model that is being
reinforced.
3.1.6.3 Punishment
Punishment is the situation that occurs if an aversive Negative motivations that inhibit observational learning
stimulus is presented whenever a given behaviour occurs, include
thereby reducing the probability of occurrence of this
response. The removal of the aversive stimulus then allows • Past punishment
it to act as a negative reinforcer rather than a punisher. • Promised punishment, that is, threats
• Vicarious punishment
3.1.6.4 Primary Reinforcement
This is reinforcement that is occurring through reduction Bandura contends that punishment is less effective than
of needs deriving from basic drives (e.g. food and drink). reinforcement.
3.1.6.5 Secondary Reinforcement
This is reinforcement deriving from association with pri- 3.1.7 Clinical Applications of
mary reinforcers (e.g. money, tokens). Behavioural Treatments
3.1.6.6 Schedules of Reinforcement 3.1.7.1 Reciprocal Inhibition
Different schedules of reinforcement can be used: This holds that relaxation inhibits anxiety so that the two
are mutually exclusive (Wolpe, 1958) and in fact does not
• In continuous reinforcement, reinforcement takes hold true. It can be used in treating conditions associated
place following every CR. This leads to the maxi- with anticipatory anxiety (e.g. phobias). Patients identify
mum response rate. increasingly greater anxiety-evoking stimuli, to form an
• In partial reinforcement, only some of the CRs anxiety hierarchy. During systematic desensitization, the
are reinforced. patient is successfully exposed (in reality or in imagina-
In a fixed interval schedule, reinforcement tion) to these stimuli in the hierarchy, beginning with the
occurs after a fixed interval of time. It is least anxiety-evoking one, each exposure being paired
poor at maintaining the CR; the maximum with relaxation.
response rate typically occurs only when the
reinforcement is expected. 3.1.7.2 Habituation
In a variable interval schedule, reinforcement Habituation is an important component of the behav-
occurs after variable intervals. It is very ioural treatment of obsessive–compulsive disorder using
good at maintaining the CR. exposure and response prevention. The ultimate aim of
Basic Psychology 29
exposure techniques is to reduce the discomfort associ- difficulties and in the therapy of patients suffering from
ated with the eliciting stimuli through habituation. psychoactive substance use disorder.
For example, Vaughan and Tarrier (1992) have For example, Preston et al. (2001) have used shaping to
described the use of image habituation training in the attempt to bring about cocaine abstinence by successive
therapy of patients suffering from post-traumatic stress approximation. Cocaine-using methadone-maintenance
disorder. Image habituation training involved the genera- patients were randomized to standard contingency man-
tion by the patient of verbal descriptions of the traumatic agement (abstinence group of size 49) or to a contingency
event, which were recorded onto audiotape. After the designed to increase contact with reinforcers (shap-
initial training session with the therapist, homework ses- ing group of size 46). For 8 weeks, both groups earned
sions of self-directed exposure in which the patient visu- escalating-value vouchers based on thrice-weekly urinaly-
alized the described event in response to listening to the ses: the abstinence group earned vouchers for cocaine-
audiotape recordings were carried out. There were sig- negative urines only; the shaping group earned vouchers
nificant decreases in anxiety between and within home- for each urine specimen with a 25% or greater decrease in
work sessions, suggesting that habituation did occur and cocaine metabolite (during the first 3 weeks) and then for
was responsible for improvement. Treatment gains were negative urines only (during the final 5 weeks). Cocaine
maintained at 6 month follow-up. use was found to be lower in the shaping group but only
in the last 5 weeks, when the response requirement was
3.1.7.3 Chaining identical. Thus, the shaping contingency appeared to bet-
In (response) chaining, the components of a more com- ter prepare patients for abstinence. (A second phase of the
plex desired behaviour are first taught and then connected study showed that abstinence induced by escalating-value
in order to teach the latter. Chaining may be conceptual- vouchers can be maintained by a nonescalating schedule,
ized in the following two different ways: suggesting that contingency management can be practical
as a maintenance treatment.)
1. Responses function as discriminative stimuli for
subsequent responses. 3.1.7.5 Cueing
2. Responses produce stimuli that function as dis- Cueing is the process of helping the learner to focus their
criminative stimuli for subsequent responses. attention on the important or relevant stimuli to render
the essential learning characteristics distinct from the
Chaining can be used in, for example, people with learning other stimuli; it consists of any action that separates fig-
difficulties. Thvedt et al. (1984) described studied stimu- ure from ground (see succeeding text). The use of cue-
lus functions in chaining. Twenty-four adults with learning can decrease learning times. For example, in reading
ing difficulties learned a chain of circuit board assembly matter and pictorial presentations, visual cues can be
responses consisting of placing resistors in the board and given using any of the following strategies:
pressing switches. Lights came on after switch responses.
After learning the chain, each subject was exposed to • Highlighting
three experimental conditions (counterbalanced): • Underlining
• Arrows
• Altered stimulus location • Contrasting colours
• Altered stimulus sequence • Animation
• Missing stimulus • Explosions
• Implosions
This study lent some support for the second conceptual • Bordering
position given earlier (i.e. that responses produce stimuli • Texture
that function as discriminative stimuli for subsequent • Novelty
responses). • Size
• Labelling
3.1.7.4 Shaping
In shaping, successively closer approximations to the A famous example is that of Clever Hans. Hans was
desired behaviour are reinforced in order to achieve the a horse, belonging to Mr. Wilhelm von Osten, which
latter. It finds application clinically in the management appeared capable of carrying out a range of intellec-
of behavioural disturbances in people with learning tual tasks normally associated with humans, such as the
arithmetic operations of addition, subtraction, multipli- better prognosis was associated with higher social class
cation, and division of natural numbers and fractions; and older age, and poorer prognosis with single marital
reading; and spelling. Answers were communicated by status. There were no variations in outcome for age in the
means of tapping out the answer with one of his feet. For control group. In the age range 20–40 years, escape con-
example, if asked to calculate ‘2 + 3’, Clever Hans would ditioning did not show better results than conventional
tap his foot five times and then stop. Pfungst (1907/1911), therapies, but with subjects above this age range, it was
in conjunction with the Berlin psychologist Carl Stumpf, significantly superior.
designed a set of experiments that showed that Clever
Hans was, in fact, being cued to give the correct answer 3.1.7.7 Avoidance Conditioning
by the questioner. The questioner, consciously or uncon- As mentioned earlier, in avoidance conditioning, the ani-
sciously, would provide Clever Hans with visual cues, mal learns to avoid an unpleasant or punishing stimulus
such as subtle changes in facial expression and posture. by making a new response. For example, rodents can be
For example, in the earlier example, as Clever Hans trained to avoid electric shocks by pressing a button.
reached five foot taps, he could pick up visual cues show- Like escape conditioning, avoidance conditioning is a
ing how the tension in the questioner was rising. As soon form of negative reinforcement, in which the reinforce-
as the fifth tap was executed, the sense of relief in the ment is getting away from an aversive stimulus. Avoidance
questioner was also apparent in visual cues, and the horse conditioning may be considered to be a special case of
knew this was when to stop tapping. operant conditioning under intermittent reinforcement.
A clinical example of the therapeutic use of cueing is in Avoidance conditioning, and indeed also escape con-
unilateral neglect, following a cerebral lesion. Robertson ditioning, may be used in the treatment of enuresis. For
et al. (1992) based their therapeutic intervention on the example, Hansen (1979) described a twin-signal device
experimental finding that limb activation contralateral to that provided both escape and avoidance conditioning in
a cerebral lesion appears to reduce visual neglect. (There enuresis control.
is controversy as to whether this is the result of percep-
tual cueing or of hemispheric activation.) In the treatment 3.1.7.8 Self-Control Therapy
of unilateral left neglect, Robertson et al. (1992) found Bandura helped to develop the therapeutic technique of
that treatment focused on cueing for left arm activation, self-control therapy, based on concepts of self-regulation.
without explicit instructions for perceptual anchoring, It may be used as part of a treatment package for the ces-
gave positive results. sation of smoking, in countering overeating, and in help-
ing students to improve their ability to study.
3.1.7.6 Escape Conditioning The components are as follows:
As mentioned earlier, in escape conditioning, the animal
learns to escape from an unpleasant or punishing stimu- 1. Behavioural charts. This involves keeping a
lus by making a new response. For example, rodents can record of one’s behaviour based on self-obser-
be trained to escape from electric shocks by pressing vation. For example, in attempting to improve
a button. study habits prior to an examination, a student
It is a form of negative reinforcement, in which the may make a record of how much time is spent
reinforcement is getting away from an aversive stimulus. studying each day, how many books are (re)
It is a special form of operant conditioning, consisting read, and how many past or sample examina-
of a conditioning procedure in which successive occur- tion papers are fully attempted. Such a record
rences of a response repeatedly terminate a negative rein- could be graphical or in the form of a behav-
forcing stimulus. ioural diary. In the case of the latter, further rel-
Escape conditioning may be used in the treatment evant details should be noted, which may offer
of alcoholism. For example, Glover and McCue (1977) insight into cues associated with the desired
found that a group of patients with alcoholism, when (or undesired) behaviour, for example, the stu-
treated with partially reinforced electric escape condi- dent may find that they accomplish more when
tioning, had a significantly better outcome on follow-up in a library compared with being at home and
than a control group who showed a parallel level of moti- accomplish least when in a room with a televi-
vation and were treated by conventional methods. No sex sion switched on.
differences in outcome were found for either group. In 2. Environmental planning. Based on the behavioural
the experimental group treated with escape conditioning, chart and diary, changes to one’s environment
Basic Psychology 31
can be planned. For example, to continue with 3.2.1.5 Fechner’s Law

the example of the student, he or she may plan to Weber’s law is only an approximation that fails to hold
spend more time in a library and in study groups over a large range of stimulus intensity. A better, though
with others also sitting the same examination and again not perfect, approximation is provided by Fechner’s
less time at home with the television switched on. law that holds that sensory perception is a logarithmic
3. Self-contracts. A contract can be written function of stimulus intensity.
down (perhaps witnessed by the therapist),
stipulating the reward to oneself for accom- 3.2.1.6 Signal Detection Theory
plishing certain tasks and the punishment for This holds that perception does not depend solely on
not doing so. For example, in the case of the stimulus intensity but is also a function of biophysical
student, their contract might state ‘If I fully factors and psychological factors such as motivation, pre-
revise chapters 1 to 4 from my revision book vious experiences, and expectations.
next week, then I shall reward myself by buy-
ing my favourite recording of Beethoven’s 5th 3.2.2 Perceptual Organization
Piano Concerto; if I fail to achieve this goal,
then I shall …[state some unpleasant but nec- Perception is an active process in which there is a search
essary task or chore]’. for meaning. A number of perceptual phenomena are
described in Gestalt psychology:
3.1.7.9 Modelling Therapy
Bandura also developed modelling therapy. Here, a • The whole perception is different from the sum
patient suffering from a difficulty coping with a certain of its parts.
situation watches somebody else cope perfectly easily • Law of simplicity—the percept corresponds to
with the same situation and then in turn is able to cope by the simplest stimulation interpretation.
means of observational learning. An example of the use • Law of continuity—for example, interrupted
of modelling therapy is in the treatment of phobias. lines seen as continuous.
• Law of similarity—like items are grouped together.
• Law of proximity—adjacent items are grouped
3.2 PHENOMENA OF VISUAL together.
AND AUDITORY PERCEPTION • Figure-ground differentiation.
3.2.1 Perception Note that gestalt is a German word meaning shape or form.

3.2.1.1 Definition 3.2.2.1 Figure-Ground Differentiation
Perception is an active process involving the awareness Patterns are perceived as figures differentiated from their
and interpretation of sensations received through sensory background with contours and boundaries, thus simulat-
organs. ing objects. Thus, the relevant perceptual system needs
to make a ‘decision’ as to how to differentiate correctly
3.2.1.2 Absolute Threshold
between the figure that is being perceived and its back-
This is the minimum energy required to activate the sen- ground. In doing so, the following features characterize
sory organ. figure and ground, particularly in respect of visual stimuli:
3.2.1.3 Difference Threshold • The figure is more conspicuous than the ground.
The difference threshold of two sources of a sensory • The figure appears more like an object in its
modality is the minimum difference that has to exist own right.
between the intensities of the two sources to allow them • The ground does not appear to be an object but
to be perceived separately. rather generally formless.
• The ground extends past the figure.
3.2.1.4 Weber’s Law • The perception is of the figure being ‘in front
The increase in stimulus intensity needed to allow two of’ the ground.
sources of intensity to be perceived as being differ- • The contour or outline that differentiates figure
ent is directly proportional to the value of the baseline from ground is perceived as belonging to the fig-
intensity. ure rather than the ground.
• Lightness/colour constancy—the perception of

an object’s shade/colour is constant regardless
of the lighting conditions.
FIGURE 3.2 Visual example of a figure-ground relationship.
• Location constancy—the perception of an
object’s spatial position is constant regardless of
the viewer’s movement.
For example, when walking or running through a room,

all the walls and the ceiling and floor are perceived as
each having a rectangular shape, in spite of the fact that
the shapes projected on the retina are those of nonstatic
nonrectangles.
3.2.2.3 Depth Perception

A 3D visual perception is formed from 2D retinal images
as a result of multiple cues such as binocular vision and
convergence, relative size and brightness, motion paral-
lax, object interposition, and linear perspective.
FIGURE 3.3 Visual example of a reversible figure-ground 3.2.2.4 Perceptual Set
relationship—the Rubin vase.
Perceptual set is a motivational state of mind in which
certain aspects of stimuli are perceived according to
An example of a visual figure-ground relationship is expectation. This can be associated with a change in the
shown in Figure 3.2. (It may not be obvious, the first perception threshold. The way in which stimuli are per-
time it is looked at, what information it conveys. In fact, ceived is influenced by personality and individual values
the figure consists of the spaces between the objects [the and past experiences. Perceptual set was described in his
ground]. Armed with this knowledge, it is immediately book Becoming in 1955 by the American psychologist
clear that a word of importance to examination candi- Gordon Willard Allport (1897–1967).
dates is depicted.)
An example of an ambiguous, reversible, visual
figure-ground relationship is that of the Rubin vase,
3.2.3 Relevance of Visual Perceptual
shown in Figure 3.3. (This was devised by the Danish Theory to Psychopathology
psychologist Edgar Rubin.) Here, the figure may be the 3.2.3.1 Illusions
face and the ground the vases. Alternatively, the two
Illusions are misperceptions of real stimuli that are influ-
vases may be considered to be the figure and the facial
enced by the perceptual set and suggest an active search
shape in between them the ground.
for meaning. With respect to visual perceptual theory,
Figure-ground differentiation is not confined to
illusions can arise from the following phenomena:
visual stimuli. An example involving auditory stimuli
is that of hearing a particular conversation over back-
• Difficulties in figure-ground differentiation—for
ground noise.
example, ambiguous figures such as the Rubin vase.
• Changes in object constancy—for example,
3.2.2.2 Object Constancy perceptual constancy may change as a result
This is the tendency to perceive objects as unchanged of different lighting conditions, giving rise to
under different conditions: visual illusions.
• Difficulties in depth perception—for example,
• Shape constancy—the perception of an object’s owing to ocular problems, abnormal ocular lens
shape is constant regardless of the viewing angle. accommodation can give rise to abnormalities
• Size constancy—the perception of an object’s in monocular cueing, while defects in the abil-
size is constant regardless of the viewing ity of the eyes properly to converge can cause
distance. abnormalities in binocular cueing.
Basic Psychology 33
3.2.3.2 Hallucinations • 2 months—depth perception (as evidenced by

Hallucinations are false sensory perceptions occurring in visual cliff experiments).
the absence of real external stimuli. They are perceived • 4 months—accommodation and colour vision.
as being located in objective space and as having the • 6 months—6:6 acuity.
same realistic qualities as normal perceptions.
According to visual perceptual theory, the majority of the The following visual processes appear to be innate:
processing that comprises perception takes place within the
brain rather than in the sense organs themselves. Therefore, • Visual scanning
any factors that adversely affect neuronal processing within • Tracking
the brain may cause the subject to experience hallucinations. • Fixating
Such factors (described in Chapters 31 and 32) include cere- • Figure-ground discrimination
bral lesions, psychoactive substances, and toxic states.
Furthermore, on the basis of visual perceptual theory, In contrast, the following visual processes appear to be
it would also be predicted that abnormalities in the sense learnt:
organs themselves or in primary perceptual functioning
could also give rise to hallucinations. Evidence exists to • Size constancy
support this contention. For instance, visual hallucina- • Shape constancy
tions, in the absence of other psychopathology, have been • Depth perception
reported in association with ocular disease with visual loss • Shape discrimination
in Charles Bonnet syndrome (‘visual hallucinations of the
blind’). An auditory analogue to visual perceptual theory
also exists; an example of auditory impairment being asso- 3.2.5 Culturally Sanctioned Distress States
ciated with auditory hallucinations is the report of the asso- Reports of cultural and ethnic variation in the experience
ciation of musical hallucinations with hearing impairment. of hallucinations (Al-Issa, 1977; Schwab, 1977) suggest
that hallucinations are not necessarily pathological phe-
3.2.3.3 Other Psychopathologies nomena, while reports of hallucinatory experiences in
An agnosia is an inability to interpret and recognize the the general population provide additional evidence that
significance of sensory information, which does not result psychosis is on a continuum with normality (Johns et al.,
from impairment of the sensory pathways, mental dete- 2002); cognitive psychological models have attempted
rioration, disorders of consciousness and attention, or, in to explain how anomalous experiences are transformed
the case of an object, a lack of familiarity with the object. into psychotic symptoms (Garety et al., 2001). Visual and
Abnormalities in the way in which visual perceptual sys- auditory phenomena can occur in culturally sanctioned
tems (functioning according to visual perceptual theory) distress states without necessarily being pathognomonic
interact with systems of the brain associated with functions of mental disorder. A few examples follow.
such as learning and memory can give rise to agnosias.
In schizophrenia, depersonalization, derealization, 3.2.5.1 Nocturnal Hallucinations in
temporal lobe epilepsy, and acute brain syndromes, there Ultra-Orthodox Jewish Israeli Men
is disturbance of perception, particularly depth percep- Greenberg and Brom (2001) reported that hallucinations
tion and perceptual constancy. that occur predominantly at night were found in 122 out of
a sample of 302 ultra-orthodox Jewish Israeli men referred
for psychiatric evaluation. Most of those with nocturnal
3.2.4 Development of Visual Perception
hallucinations were in their late teens, were seen only once
The development of human visual perception is an illus- or twice, were brought in order to receive an evaluation
tration of a constitutional–environmental interaction. In letter for the Israeli army, and had a reported history of
general complex, visual stimuli, such as human faces, are serious learning difficulties. The nocturnal hallucinatory
preferred. The early developmental stages are as follows: experiences were predominantly visual, and the images
were frightening figures from daily life or from folklore.
• Birth—there is the ability to discriminate Many of the subjects were withdrawn, monosyllabic,
brightness and to carry out eye tracking; visual reluctant interviewees. Greenberg and Brom suggested
acuity is impaired and focusing is fixed at 0.2 m. that this cultural group’s value on study at Yeshivas away
from home places significant pressure on teenage boys 3.2.5.4 Auditory and Visual Hallucinations
with mild or definite subnormality, possibly precipitating Related to Bereavement in the Caribbean
the phenomenon at this age in this sex. Although malin- Long-lasting auditory and visual hallucinations may occur in
gering had to be considered as a possible explanation in individuals living in, or originally from, the Caribbean, follow-
many cases owing to the circumstances of the evaluation, ing the death of a relative, such that these auditory and visual
short-term and long-term follow-up on a limited sample phenomena may not be pathognomonic of mental disorder. An
allowed this explanation to be dismissed in a significant example is given in a case report by Boran and Viswanathan
number of cases. They therefore suggested that these noc- (2000) relating to an American patient originally from Jamaica:
turnal hallucinations are a culture-specific phenomenon.
Mrs. G, a 28-year-old woman who was eight weeks preg-
nant, was hospitalized on an obstetrics-gynaecology unit of
3.2.5.2 Isolated Sleep Paralysis with Visual a university hospital with a diagnosis of mild hyperemesis
Hallucinations among Nigerian Students gravidarum. The patient had no prior psychiatric history,
Ohaeri et al. (1992) reported the results of a cross-sectional including no history of alcohol or substance abuse, and no
study of the pattern of isolated sleep paralysis among the significant medical history. She lived with her mother and
sister. A psychiatric consultation was requested because
entire population of nursing students at the Neuropsychiatric
the patient had auditory and visual hallucinations.
Hospital in Abeokuta, Nigeria, consisting of 58 males and
37 females. Forty-four percentage of the students (both male The patient was hearing someone knocking at the door
and female) admitted having experienced this phenomenon. and was seeing a man sitting in the chair next to her bed
when there was nobody else in the room. When asked
The findings largely supported the results of a similar study
about the hallucinations, she said that she and her family
of Nigerian medical students, except that there was a slight believed that after death the spirit of the dead person was
male preponderance among those who had the experience. still among them. If the dead one was somebody who
Visual hallucination was the most common perceptual prob- had always helped them in difficult moments of their
lem associated with the episodes, and all the affected sub- life, then he or she continued to do so by ‘showing up’
jects were most distressed by the experience. The popular, and being of comfort. Such was ‘Uncle Pete’, the man the
culturally sanctioned, view in Africa is that this distress state patient saw when she was admitted, and who appeared to
associated with visual phenomena is caused by witchcraft. the family on several other difficult occasions.
Mrs. G’s mental status examination was unremarkable
3.2.5.3 Mu-Ghayeb except for the hallucinations. The medical workup did not
reveal any organic causes for her symptoms. She showed
Mu-Ghayeb is a traditional bereavement reaction that no distress or impairment of functioning as a result of the
occurs in Oman following a sudden unexpected death. The belief. With the patient’s permission, we spoke to her mother
deceased relative or friend may be seen as an unearthly and sister by telephone. They reported that Uncle Pete had
figure at night. During the daytime, the deceased may be also appeared to them and confirmed that neither Mrs. G
seen, normally clothed, in circumstances that are difficult nor others in the family had any prior psychiatric history.
to authenticate, for instance, sitting in a motor vehicle The nurse assigned by the medical staff to watch the
that passes by at speed. These visual phenomena are con- patient in the hospital also told the psychiatric consultant
sistent with the belief in traditional Omani society that about her own family spirit, who was similar to Uncle
after such a sudden untimely ‘death’, the ‘deceased’ con- Pete in many ways. The patient and the nurse were both
tinue to be alive; they are expected to be resurrected to from Jamaica and came to the United States with their
a strange, ghostly existence, with nocturnal wanderings families as children. The patient’s symptoms were deter-
mined to be culturally based beliefs, and there was no
and interleaved episodes of sleeping naked in caves dur-
evidence of psychosis. No psychiatric sequelae appeared
ing the day. This belief in the return of the dead persists in the patient’s subsequent hospital course.
even after an elaborate ritual of burial and a prescribed
period of mourning. The deceased are expected to leave
the grave after burial and join their families when the 3.3 INFORMATION PROCESSING
spell placed on them by a sorcerer is broken or counter- AND ATTENTION
acted. Although the Mu-Ghayeb belief is inconsistent
3.3.1 Information Processing
with their Islamic religion, this culture-specific response
to bereavement may be explained in terms of sudden and Information processing is concerned with the way in
untimely death, which used to be rife in the seafaring which external signals arriving at the sense organs are
Omani society (Al-Adawi et al., 1997). converted into meaningful perceptual experiences.
Basic Psychology 35
3.3.1.1 Data-Driven Processing • Controlled attention—effort is required. It has

The processing is initiated by the arrival of data. The been suggested that a defect of controlled atten-
simplest scheme for classifying and recognizing pat- tion might underlie symptoms of schizophrenia.
terns is template matching, in which recognition is • Automatic attention—the subject becomes
achieved by matching the external signal against the skilled at a task, and therefore little conscious
internal template. effort is required.
• Stroop effect—automatic process is so ingrained
3.3.1.2 Conceptually Driven Processing that it interferes with controlled processing.
This applies when data input is incomplete. The pro-
cessing starts with the conceptualization of what might
be present and then looks for confirmatory evidence, 3.4 FACTORS AFFECTING MEMORY
thereby biasing the processing mechanisms to give the 3.4.1 Memory
expected results. Conceptually driven data (schema)
are essential to perception. However, they can lead to Memory comprises encoding/registration, storage, and
misperceptions. retrieval of information.
3.4.1.1 Encoding/Registration
3.3.2 Attention
This is the transformation of physical information into a
Attention is an intensive process in which information code that memory can accept.
selection takes place. Types include the following:
3.4.1.2 Storage
• Selective/focused attention—one type of infor-
mation is attended to while additional distract- This is the retention of encoded information. According
ing information is ignored, for example, cocktail to the multistore model of Atkinson and Shriffrin (1968),
party effect. In dichotic listening studies in which has now been superseded, memory storage can be
which subjects attend to one channel, evidence considered to be made up of
indicates that the unattended channel is still
being processed and the listener can switch rap- • Sensory memory
idly if appropriate. • Short-term memory
• Divided attention—at least two sources of infor- • Long-term memory
mation are attended simultaneously. Performance
is inefficient. Loss of performance is called dual- This modal model is shown in Figure 3.4.
task interference.
• Sustained attention—the environment is moni- 3.4.1.3 Retrieval
tored over a long period of time. Performance This is the recovery of information from memory when
deteriorates with time. needed.
Iconic Rehearsal/
Environmental transfer
Echoic
input Recoding Short-term Long-term
. .
. . process memory memory
. . Retrieval
Haptic response
control
Sensory
registers
FIGURE 3.4 The multistore modal model of memory. (After Atkinson, R.C. and Shriffrin, R.M., Human memory: A proposed
system and its control processes, in Spence, K.W. and Spence, J.T. (eds.), The Psychology of Learning and Memory, Vol. 2,
Academic Press, New York, 1968, pp. 90–191.)
3.4.2 Influences upon Memory effortful than for short-term memory. Some motivation is
required to encode information into long-term memory.
According to the multistore modal model, sensory mem- Schizophrenia and depression affect memory at this level.
ory has a large capacity; sensory information is retained
here in an unprocessed form in peripheral receptors.
Sensory memory is a very short-lived (fade time 0.5 s) 3.4.3 Optimal Conditions for Encoding,
trace of the sensory input. Visual input is briefly retained Storage, and Retrieval of Information
as a mental image called an icon; this is known as an
iconic memory. The sensory memory for auditory infor- 3.4.3.1 Encoding/Registration
mation is called an echoic memory, while that for infor- Conrad (1964) showed that confusion occurs between
mation from touch is called a haptic memory. Sensory acoustically similar letters presented against background
memory is considered to give an accurate account of the noise. For example, the letter P is more likely to be incor-
environment as experienced by the sensory system. It rectly recalled as V (which is acoustically similar) than as
holds a representation of the stimulus so that parts of it the letter R (which is visually similar). Baddeley (1966a)
can be attended to, processed, and transferred into more then went on to demonstrate that acoustically similar
permanent memory stores. words are also more difficult to recall immediately (a
Those aspects of sensory information that are the test of short-term memory) than are semantically simi-
object of active attention are transferred into a tempo- lar words. For example, the sequence rat, mat, cat, cap
rary working memory called the short-term memory. (which is acoustically similar) is more difficult to recall
Encoding is mainly acoustic; visual encoding rapidly immediately than the sequence large, big, huge, grand
fades. This is the memory used temporarily to hold a (which is semantically similar). However, in a test of long-
telephone number, for example, until dialled. It is lost in term memory, Baddeley (1966b) found a semantic simi-
20 s unless rehearsed. Short-term (primary or working) larity effect rather than a phonological similarity effect.
memory consists of a small finite number (seven ± two) of So, in terms of the parameters studied, it appeared that
registers that can be filled only by data entering one at a encoding or registration for short-term memory is better
time. According to the displacement principle, when the for semantically similar word sequences than for phono-
registers are full, the addition of a new datum leads to the logically (acoustically) similar words, while encoding or
displacement and loss of an existing one. The probability registration for long-term memory is better for phono-
of correctly recalling an item of information is greater if logically (acoustically) similar word sequences than for
it is one of the first items to be encountered, even if more semantically similar words.
than seven items have been presented; this is known as Semantic encoding has been shown to aid short-term
the primacy effect. Similarly, the recency effect refers to memory in respect of trigrams (three-letter sequences).
the finding that the probability of correctly recalling an Increased memory span has been demonstrated for
item of information is increased if it is one of the most meaningful trigrams, such as CNN, CIA, NBC, than for
recent items to be encountered. Those items having an meaningless trigrams, such as AUM, GLB, CDX (Bower
intermediate serial position are least likely to be recalled and Springston, 1970).
accurately, and this overall phenomenon is referred to With respect to iconic memory encoding, a preced-
as the serial position effect. Whereas the recency effect ing or subsequent visual sensory presentation of data at a
can be accounted for in terms of the comparatively short similar energy level (i.e. brightness) to that of the index
interval of time elapsing before recall, the primary effect presentation leads to a masking of the index presentation
is more difficult to explain and may be caused by greater so that it is not registered. The term for this phenomenon
rehearsal of these first items. Retrieval from short-term is energy masking and occurs at the level of the retina.
memory is considered to be effortless and error free. Another form of masking that has been described is pat-
Rehearsal is not as necessary in approximately 5% of tern masking, in which the preceding or subsequent visual
children possessing a photographic memory, known in presentation is of data visually similar to that of the index
psychology as eidetic imagery, in whom a detailed visual presentation. Pattern masking occurs at a deeper level of
image can be retained for over half a minute. visual information processing than the retinal level. The
Long-term memory stores information more or deduction of the relative depth of level of visual process-
less permanently and theoretically may have unlim- ing at which energy masking and pattern masking occur
ited capacity, although there may be limitations on followed from the finding that whereas the former can
retrieval. Input and retrieval take longer and are more only take place when the index presentation and the
Basic Psychology 37
masking presentation are both to the same eye, the latter According to the model, a continuous distraction pro-
can take place even when the index presentation is to one cedure, such as counting backward between the presen-
eye and the corresponding masking presentation is to the tation of items such as unrelated words, should prevent
other eye (Turvey, 1973). With respect to rapidly chang- the subject from rehearsing the items and should replace
ing picture presentations, it appears to take about 100 ms these items in short-term memory. However, in practice,
for a scene to be understood and no longer be susceptible the serial position curve shows both a primacy effect
to ordinary visual masking and a further 300 ms or so to and a recency effect under such circumstances (Tzeng,
no longer be susceptible to conceptual masking (e.g. from 1973). There also does not appear to be a positive (or
a succeeding picture representation) (Potter, 1976). negative) relationship between the amount of rehearsal
So far, as the registration of two auditory stimuli is of presented items and how well they are recalled from
concerned, experiments in which two sounds are pre- short-term memory (Craik and Watkins, 1973; Glenberg
sented to subjects and in which the just noticeable inter- et al., 1977).
val between noise pulses is compared with the level of Gillund and Shiffrin (1981) found that the free recall
second noise pulse demonstrate that confusion occurs of complex pictures was better than that of words. Many
between the echoic image of the first auditory presenta- further studies have confirmed a picture superiority
tion and the onset of the second auditory presentation, effect. In general, pictures are remembered and recalled
unless either a sufficient time interval is allowed for the better than words, and nonverbal information storage of
echoic image of the first presentation to fade before pre- pictures and designs is found to be more stable over a
senting the second stimulus or increasing the volume of period of hours and days than is the storage of words (e.g.
the second stimulus (Plomp, 1964). Hart and O’Shanick, 1993). Simple pictures appear to be
As with visual masking (see aforementioned), bin- better remembered than complex pictures; the asymmet-
aural masking has also been demonstrated. A masking ric confusability effect is manifested in the finding that
sound presented soon after an index sound interferes with there is a greater accuracy in recognition testing of same
detection; this interference is greater when both stimuli versus changed stimulus in simple rather than complex
are presented to the same ear than when the masking pictures (Pezdek and Chen, 1982).
sound is presented to the contralateral ear following the
presentation of the index auditory stimulus (Deatherage 3.4.3.3 Retrieval
and Evans, 1969). Retrieval of information from the long-term memory
In studies of auditory encoding of stimuli and their is error prone but is improved if the information being
serial position, a suffix effect occurs. This refers to the audi- stored is organized. Hierarchical organization is particu-
tory encoding error that occurs when there is a categorical larly useful in this regard, perhaps because it improves
similarity between the penultimate and ultimate speech- the search process within long-term memory (Bower
like sounds heard (Crowder, 1971; Ayres et al., 1979). et al., 1969).
Elaborating meaning appears to improve encoding of Another optimal condition for retrieval of information
the written word. For instance, your encoding of the text is to arrange that the context within which the informa-
of each of the remaining chapters of this book is likely to tion is to be retrieved is similar to that within which it
be better if you look at some questions specifically related was encoded (Estes, 1972).
to these chapters before reading each of them. (Suitable
questions may be found in the companion books of mul-
tiple choice questions [MCQs] and extended matching 3.4.4 Memory Information Processing
items [EMIs].) When you read the actual chapters after 3.4.4.1 Primary Working Memory
being primed with the need to search for the answers, Storage Capacity
you are more likely to elaborate parts of each of these
Working memory refers to the temporary storage of
chapters and encode the information better (Frase, 1975;
information in connection with performing other, more
Anderson, 1980).
complex, tasks (Baddeley, 2007). In the multistore
modal model of memory, it is the short-term memory (or
3.4.3.2 Storage short-term store) that acts as a key working memory sys-
One of many examples of findings that are not consistent tem to allow information to transfer into the long-term
with the multistore modal model of memory is that of the memory (or long-term store) and thereby allow learning
finding of positive recency effects in delayed free recall. to take place.
As mentioned earlier, a number of findings, such as

the lack of a positive (or negative) relationship between
the amount of rehearsal of presented items and how well Central
they are recalled from short-term memory (Craik and executive
Watkins, 1973), cast doubt on the validity of the multi-
store modal model of memory and in particular on the
assumption implicit in this model that holding infor- Visuospatial Articulatory or
scratch pad phonological
mation in short-term memory (or the short-term store) or sketch pad loop
necessarily leads to information transfer into long-term
memory (or the long-term store). Furthermore, since in FIGURE 3.5 The working memory model of Baddeley and
this modal model the short-term memory (store) acts Hitch. (After Baddeley, A.D. and Hitch, G., Working memory, in
Bower, G.A. (ed.), The Psychology of Learning and Motivation,
as the working memory that is essential for learning, it
Vol. 8, Academic Press, New York, 1974, pp. 47–89.)
would be expected that patients with short-term memory
(store) impairment should manifest impaired long-term
learning. However, Shallice and Warrington (1970) visuospatial task concurrently (Baddeley and Lieberman,
described the case of a patient with a severely affected 1980). Again, a patient with gross impairment of digit
short-term memory (store) who nonetheless had a normal span would be hypothesized to have a defect of their pho-
long-term learning capacity; this patient had a memory nological loop functioning; if there were no coexistent
span of just two digits and almost no recency effect in the impairment of the functioning of the central executive or
free recall task (in which the subject is asked to recall as visuospatial sketchpad, then normal learning would still
many of a previously presented list of unrelated words be possible.
as they can, in any order). Moreover, when a short-term Working memory capacity can be measured using a
memory (store) deficit is experimentally induced in nor- task in which, after reading a series of sentences, the sub-
mal subjects by giving them digits to rehearse concur- ject is required to recall the last word of each of these
rently with a grammatical reasoning task, even with eight sentences (Daneman and Carpenter, 1980). This task
digits, the reasoning time only increases by around 50% therefore requires both comprehension and recall (as
and the error rate remains around 5% (the same as with opposed to just recall in the simple word span task).
fewer digits to rehearse) (Baddeley and Hitch, 1974), and There is a strong positive correlation between work-
this in spite of the fact that a digit load of eight should ing memory tests and intelligence quotient (IQ) tests.
have totally filled the short-term memory (store) accord- Furthermore, standard IQ appear to be more susceptible
ing to the multistore modal model. Tasks using a similar to the subject’s previous knowledge, whereas working
digit load concurrent with comprehension and free recall memory tests appear to have a greater relationship to the
learning also show that the long-term memory (store) can speed of processing (Kyllonen and Christal, 1990).
be impaired but that the recency effect still occurs, again In terms of the model of working memory of Baddeley
contrary to the modal model prediction. and Hitch (1974), the central executive is a limited-
In response to these difficulties, Baddeley and Hitch capacity system, which provides the link between the
formulated the working memory model shown diagram- two slave systems (see Figure 3.5) and long-term mem-
matically in Figure 3.5. The central executive is an atten- ory; it is responsible for planning and selecting strategies
tional controller, which is supported by two active slave (Baddeley, 2007). The visuospatial scratchpad or sketch-
systems, the articulatory or phonological loop, responsi- pad appears to have a visual component, which is con-
ble for the maintenance of speech-based information, and cerned with such factors as shape and colour, and a spatial
the visuospatial scratchpad or sketchpad, which can hold component, which is concerned with location (Baddeley
and manipulate information in the visuospatial domain. and Lieberman, 1980; Baddeley, 2007). The articulatory
This model was compatible with the findings mentioned or phonological loop also appears to be made up of two
in the previous paragraph. For example, concurrent verbal components: a memory store that can hold phonological
(articulatory) activity and visual or spatial activity appear information for 1–2 s and an articulatory control process
to interfere with two different systems; subjects using a (or processor) (Paulesu et al., 1993; Baddeley, 2007).
mnemonic based on spatial location to remember word Memory traces in the phonological loop can be refreshed
lists have better recall of the lists than those who use a by means of subvocal articulation. (Subvocal or vocal
simple rote rehearsal procedure, but this advantage dis- articulation may also be used to provide an input into this
appears if the former subjects are required to carry out a slave system upon the visual presentation of objects by
Basic Psychology 39
the subject articulating the names of those objects.) The 3.4.4.4 Episodic Memory
phonological loop is held to provide the basis for digit Episodic memory is an aspect of long-term/secondary
span. In particular, the number of items retained in the memory that refers to the memory for events. It provides
digit span is believed to be a function of both the rate of a continually changing and updated record of autobio-
fading of the memory trace in the phonological loop and graphical material (Tulving, 1972).
the rate of refreshing of memory traces by means of sub-
vocal articulation. The size of the storage capacity can be 3.4.4.5 Skills Memory
reduced in the following ways:
Skills memory, or procedural memory, is an aspect
of long-term/secondary memory that supports skilled
• The phonological similarity effect—trying to
performance.
remember items with similar sounding names.
• Presenting irrelevant spoken material—this
gains access to the store and corrupts the mem- 3.4.4.6 Other Aspects of Long-Term/
ory trace. Secondary Memory
• The word length effect—as the length of the Ryle (1949) distinguished between procedural knowl-
words increases, the memory span decreases, edge and declarative knowledge; whereas the former
presumably because of the longer time required referred to knowledge that supported the perfor-
for longer words to be rehearsed, leading to a mance of tasks, the latter referred to factual knowl-
greater probability of memory trace decay. edge. Tulving (1985) distinguished between autonoetic
• Articulatory suppression—requiring a subject awareness (or remembering) and noetic awareness (or
repeatedly to articulate an irrelevant speech knowing).
sound that interferes with subvocal rehearsal.
3.4.4.2 Principle of Chunking 3.4.5 Process of Forgetting and the Influence

Chunking increases the amount of information stored in of Emotional Factors on Retrieval
‘short-term memory registers’ (in the multimodal model)
3.4.5.1 Forgetting
by allowing one entry to cover several items. While
the number of chunks is restricted, their content is not. Forgetting from long-term/secondary memory is usu-
With the help of long-term memory, new material can be ally the result of retrieval failure rather than storage
recoded, thereby increasing the content of chunks. failure. This explains why forgotten memories can be
For example, British trainee and qualified psychia- recovered under hypnosis and also the ‘tip of the tongue’
trists are unlikely to require eight ‘registers’ in order to experience.
remember the letters MRCPSYCH. Similarly, the string
DSMIVTRICDEEG can readily be split into the chunks 3.4.5.2 Theories of Forgetting
DSM-IV-TR, ICD, and EEG. Under the multimodal model of memory, forgetting from
It has been suggested that the acquisition of skills long-term memory could be caused by interference or
through practice may involve the grouping of sets of trace decay.
mental entities (be they motor or perceptual) as chunks According to the interference theory, forgetting by
(Newell and Rosenbloom, 1981). interference is item dependent. There are two main
types:
3.4.4.3 Semantic Memory
Semantic memory refers to the subject’s knowledge of • Proactive interference/inhibition—previous learn-
facts, language, concepts, and the like and is an aspect of ing is likely to impair subsequent learning.
long-term/secondary memory that is consistent with the • Retroactive interference/inhibition—new learn-
finding that verbal information is stored in terms of meaning is likely to impair previous learning.
ing rather than exact words (Tulving, 1972). It is easier to
remember words paired with meanings (Bower, 1972) and According to the decay theory, memories fade with time.
to recall words synonymous to those in a given list (Sachs, The longer the item remains in the memory system, the
1967). Therefore, semantic encoding is a more efficient weaker is its strength. New material has a high trace
way than simple rehearsal of transferring information from strength, while older has a low trace strength. Forgetting
the ‘short-term memory’ to the long-term/secondary one. by decay is time dependent.
3.4.5.3 Influence of Emotional inability of humans to access their early childhood mem-

Factors on Retrieval ories (Schachtel, 1947). In contrast, the organization of
Emotional factors can influence retrieval from long-term retrieval cues into stable retrieval schemata has been put
memory in the following ways: forward as being part of the explanation of the occur-
rence of exceptional memory performance, in the skilled
• Emotionally charged situations are rehearsed memory theory (Ericsson and Kintsch, 1995).
and organized more than nonemotionally
3.4.6.3 Elaboration
charged ones. Retrieval is facilitated.
• Negative emotions and anxiety hinder retrieval. As mentioned in Section 3.4, elaboration appears to
• Retrieval of events and emotions is more likely improve encoding of new information. Methods of elabo-
to be successful if it occurs in the same context ration include
as that in which the original events and emo-
tions occurred; this is known as state-dependent • Semantic processing
learning. • Forming complex images
• Repression of emotionally charged material hin- • Attempting to answer questions based on the
ders retrieval. material to be learned
3.4.6 Processes of Interference, 3.5 FACTORS AFFECTING THOUGHT

Schemata, and Elaboration 3.5.1 Relationship of Thought to Language
3.4.6.1 Interference Early work in psychology suggested that thought could
Retroactive interference refers to the negative effect of not occur independently of language. It was held that
new learning on retrieval of prior knowledge. It has been children, on learning to speak, simply articulated their
demonstrated in many experimental trials, for example, thoughts until they learned to suppress the vocaliza-
by Slamecka (1960). In contrast, proactive interference tion, whence thought simply became concealed speech.
refers to the negative effect of prior knowledge on new Watson (1913) argued that (unarticulated) thought
learning. consisted of laryngeal motor habits. This gained sup-
port from the electrophysiological finding of Jacobsen
3.4.6.2 Schemata (1932) that mental activities (‘thought’) were accom-
A schema (plural schemata) may be defined as a men- panied by electric activity in the musculature of the
tal model or representation, built up through experi- throat.
ence, about a person, an object, a situation, or an event There is much evidence that stands in opposition to
(Searleman and Herrmann, 1994). The roles of schemata this early theory. The following two examples are;
include (Morton and Bekerian, 1986)
• Many infrahuman animals appear to be able to
• Interpretation of sensory data think but do not appear to possess language.
• Retrieval of information from memory • Temporary paralysis of all voluntary muscles
• Organization of actions with d-tubocurarine is not associated with an
• Determination of goals inability to think (Smith et al., 1947).
• Determination of behaviour
• Allocation of processing resources 3.5.1.1 Concepts
• Directing overall processing in attentional, per- Concepts are the properties or relationships that given
ceptual, and memory systems object classes or ideas have in common. They constitute a
means of grouping what otherwise would form too wide
They help to integrate information that is currently being a variety of disparate items or ideas for efficient thought
experienced with the subject’s long-term past in a single and communication.
representation (Groeger, 1997). Concrete concepts refer to objects. For example, the
It has been suggested that their lack of the sche- concept ‘book’ refers to objects having properties shared
mata needed to help organize episodic memory may by most books, such as having pages, containing infor-
help explain the origin of infantile amnesia, that is, the mation, having a title, and having authors.
Basic Psychology 41
Abstract concepts refer to abstract ideas, such as hon- Syllogisms are based on pairs of statements or prem-
esty, integrity, and justice. Concepts of activities include ises, each of which contains one quantifier, such as
drinking, walking, and cycling.
• The universal quantifier (‘for all’), denoted by ∀
3.5.1.2 Prototypes • Some
Prototypes are idealized forms. For instance, the proto- • The existential quantifier (‘there exist(s)’),
typical book might be considered to have the shape of denoted by ∃
this book with a front cover having a title; a back cover;
multiple pages in between the covers mostly containing Multiply quantified inferences are based on statements or
printed words arranged into sentences, paragraphs, sub- premises that contain more than quantifier. (Such state-
sections, sections, and chapters; some diagrams inter- ments in turn can be converted into sets of statements
spersed among the words; a title page and list of contents that each contain only one quantifier.)
at the beginning; and an index at the end of the pages. The arithmetic symbols used in formal reasoning
According to the prototype theory, the acquisition of pro- statements can be reduced to just three:
totypes occurs through repeated exposure.
• The zero symbol, denoted by 0
3.5.2 Reasoning • The successor symbol, denoted by ′
• The addition symbol, denoted by +
3.5.2.1 Deductive Reasoning
This is reasoning based on deduction, the domains of
In addition, it is convenient to include
which include
• Relational inferences • The multiplication symbol, denoted by ·

• Propositional inferences
• Syllogisms For example, the statement that every (real) number pos-
• Multiply quantified inferences sesses a square root may be formally stated as
Relational inferences are based on relations such as ∀x0 ∃x1 (x1 · x1) = x0
• Is equal to, denoted by =

• Is greater than, denoted by > Some have argued that human cerebral deductive reason-
• Is less than, denoted by < ing is dependent on the formal rules of inference, as used
• Is greater than or equal to, denoted by ≥ in formal logic (e.g. Braine et al., 1984); these are known
• Is less than or equal to, denoted by ≤ as formal rule theories. In contrast, other cognitive sci-
• After entists such as Johnson-Laird (1993) have argued that
• Before deductive reasoning (and indeed also inductive reason-
• To the right of ing) is a semantic process rather similar to that carried
• To the left of out when searching for counterexamples; this is known
as the mental model theory.
Propositional inferences are based on relations such as As an example, suppose that we consider the follow-
ing deductive reasoning problem relating to the relative
• Negation, denoted by – positions of various chapters of this book:
• Conjunction, denoted by &
• Disjunction, denoted by ∨ • The chapter on schizophrenia comes after the
• Implication, denoted by → chapter on social sciences.
• Bi-implication, denoted by ↔ • The chapter on social psychology comes before
the chapter on social sciences.
(Note that these are the symbols used in logic; in ordinary • What is the positional relationship between the
mathematics, other symbols are often used, for instance chapter on schizophrenia and the chapter on
⇒ for implication.) social psychology?
The only model containing all three chapters that is con- Consider the following (correct) equations:
sistent with these statements is
• 1=1
Social psychology • 1+2=3
Social sciences • 1 + 2 + 22 = 7
Schizophrenia • 1 + 2 + 22 + 23 = 15
• 1 + 2 + 22 + 23 + 24 = 31
So the answer to the question is that the chapter on • 1 + 2 + 22 + 23 + 24 + 25 = 63
schizophrenia comes after the chapter on social psychol-
ogy. There is just one model corresponding to the state- Consider the values of the positive integers (whole num-
ments, and the problem has a valid answer, and so this bers) on the right-hand side of each equation. We have
is known as a one-model problem with a valid answer.
Now, consider the following problem: • 1 = 2 − 1 = 21 − 1
• 3 = 22 − 1
• The chapter on schizophrenia comes after the • 7 = 23 − 1
chapter on social psychology. • 15 = 24 − 1
• The chapter on social sciences comes after the • 31 = 25 − 1
chapter on social psychology. • 63 = 26 − 1
• What is the positional relationship between the
chapter on schizophrenia and the chapter on So here we have the following pattern that appears to be
social sciences? emerging:
There are now two models containing all three chapters 1 + 2 + 22 + 23 + + 2 n −1 = 2 n − 1 (3.1)
that are consistent with these statements:
Social psychology (This may also be written as 20 + 21 + 22 + 23 + ⋯ +

Social sciences 2n−1 = 2n − 1.)
Schizophrenia We have six instances in which Equation 3.1 is true.
What we shall now do is use inductive reasoning to prove
and that the general statement, Equation 3.1, is itself true.
Let S represent the set of positive integers (positive whole
Social psychology numbers, such as 1, 2, and 3) for which the formula given in
Schizophrenia Equation 3.1 is correct. Now, when n = 1, the left-hand side of
Social sciences this formula is 1, while the right-hand side is 21 − 1 = 2 − 1 = 1.
Since 1 = 1, the formula is correct for n = 1. Therefore, the
In this particular case, there are two models, and there is
integer 1 belongs to the set S. Assume now that Equation 3.1
no positional relationship between the chapter on schizo-
is true for a fixed positive integer k. Then we have
phrenia and the chapter on social sciences that is common
to both models. We say that there is no valid answer. This
case is a multiple-model problem with no valid answers. 1 + 2 + 22 + + 2 k −1 = 2 k − 1 (3.2)
Formal rule theories predict that one-model problems
are more difficult than multiple-model problems with valid Now we need to show that our formula holds for the posi-
answers. In contrast, the mental model theory predicts that tive integer k + 1. If we add 2k to each side of Equation 3.2,
multiple-model problems with no valid answers are more we obtain
difficult than multiple-model problems with valid answers,
1 + 2 + 22 + + 2 k −1 + 2 k = 2 k − 1 + 2 k
which in turn are themselves more difficult than one-model
problems. Experimental evidence supports the mental = 2k + 2k − 1
model theory (e.g. Byrne and Johnson-Laird, 1989).
= 2 ⋅ 2k − 1
3.5.2.2 Inductive Reasoning
In inductive reasoning, a general statement is derived by = 21 ⋅ 2 k − 1
inductive arguments from many instances. An elementary
example is given from number theory in mathematics. = 2 k +1 − 1
Basic Psychology 43
So this means that Equation 3.1 is true when n = k + 1. to precise instructions in order to solve a given problem.
Therefore, k + 1 belongs to S. Hence, whenever the posi- For example, suppose you were to stop reading right now
tive integer k belongs to S, then k + 1 belongs to S. But we and take a pencil and paper and calculate the value of 22
know that 1 belongs to S. Hence, by inductive reasoning, divided by 7 to 3 decimal places, using long division. The
it follows that S must contain all positive integers. So the correct answer is 3.143. The method you used to carry out
formula shown in Equation 3.1, initially hypothesized on this calculation involved a mechanical use of the rules
just six instances, has been shown to hold for all positive of long division; no deep thought is required but, rather,
integers (infinite in number) by inductive reasoning. a simple adherence to the simple rules of this method
of problem solving. This is a characteristic feature of
algorithms.
3.5.3 Problem-Solving Strategies More precisely, an algorithm is any process that can
3.5.3.1 Alternative Representations be carried out by a Turing machine. A Turing machine
is a simple, mechanical calculating device invented by
One method of problem solving is to represent the given
the British mathematician Alan Turing (1912–1954).
data in a different way. For example, we have seen two
At its most basic, a Turing machine can be imagined
different representations in the last two examples. In the
to be an infinitely long tape segmented into squares.
first of these, in which a problem relating to the rela-
Starting at any one square, the Turing machine can do
tive order of chapters of this book was set, a diagram-
the following:
matic representation was used, in which the data were,
as it were, visualized. In the most recent example, on the
1. Stop the computation
other hand, in which inductive reasoning was being used,
2. Move one square to the right
it was more convenient to use symbolic representation. In
3. Move one square to the left
a similar fashion, in elementary mathematics, problem-
4. Write S 0 to replace whatever is in the square
solving can also sometimes be carried out using a more
being scanned
geometric approach or a more algebraic approach.
5. Write S1 to replace whatever is in the square
being scanned
3.5.3.2 Expertise
.
The way in which problems are represented by experts .
tends to differ from the representations used by inexperi- .
enced people. For instance, the way in which the reader n + 4. Write Sn to replace whatever is in the square
(assumed to be clinically competent and qualified) might being scanned
diagnose a central nervous system lesion in a patient would
likely be different and more efficient (and more likely to be This may seem, at first sight, to be a rather primitive
correct) than the methods employed by relatively inexperi- machine that can only handle addition and subtraction,
enced third-year medical students; the recall of the patient say. In fact, however, it can carry out multiplication, divi-
symptoms and signs would also tend to be better for the sion, and the calculation of square roots and other power
reader. In particular, compared with a beginner, an expert’s functions. Indeed, it may be the case that, in principle, a
memory would tend to have more potential representations Turing machine can carry out any calculation that a pow-
of the problem that he or she can draw upon to solve it. erful modern supercomputer can.
Experts are also more likely to be able to invoke heuristics
(see succeeding text) that are not available to novices.
3.5.5 Heuristics
3.5.3.3 Computer Simulation As mentioned earlier, heuristics are strategies that can
Computer simulations may be used to study the way in be applied to problems and that often give the correct
which representations and heuristics are employed in answer (or ‘goal state’) more quickly than simple algo-
problem solving. rithms; they are not guaranteed to work, however. Such
heuristic techniques are not usually available to nov-
ices, whereas experts can access these during problem-
3.5.4 Algorithms
solving. As an example, at one stage of his career, the
In a general sort of way, an algorithm consists of a specific author of this chapter had cause to devise a method of
sequence of steps that need to be carried out according accurately quantifying cerebral ventricular volumes in
serial magnetic resonance scans that had been accu- The study of traits has a long history. Aristotle (in his
rately matched using a subvoxel registration, a feat Nicomachean Ethics of the fourth century BCE) regarded
that had not hitherto been accomplished. A heuristic determinants of moral and immoral behaviour to include the
of the type ‘consider an analogous problem that you following phenomena, which we might regard as being traits:
know you can solve’ was used first, and then this solu-
tion was generalized to allow the required equations to • Cowardice
be arrived at. • Modesty
• Vanity
3.6 FACTORS AFFECTING PERSONALITY As mentioned in Chapter 2, the Greek physician Galen
3.6.1 Derivation of Nomothetic of Pergamum (Greek: Claudios Galenos; Latin: Claudius
Galenus) regarded the four Hippocratic humours as form-
and Idiographic Theories
ing the basis for his four temperaments:
The terms nomothetic and idiographic in respect of the
study of people were introduced by Wilhelm Windelband, • Choleric
the German philosopher who taught at Heidelberg and initi- • Melancholic
ated axiological neo-Kantianism. He distinguished between • Phlegmatic
the study of whole populations (the nomothetic approach) • Sanguine
and the study of individuals (the idiographic approach).
The nomothetic approach to personality considers that The German philosopher Immanuel Kant (1724–1804)
personality theory should be at least partly based on the placed these four temperaments along the following two
study of the common features and differences between dimensions:
people. For instance, personality has been defined by
Wiggins (1979) as being • Activity
• Feelings
…that branch of psychology which is concerned with
providing a systematic account of the ways in which Thus, a choleric temperament corresponded to strong
individuals differ from one another. activity, and a phlegmatic temperament corresponded to
weak activity. Similarly, a sanguine temperament corre-
In contrast, the idiographic approach attempts to gain sponded to strong feelings, and a melancholic tempera-
an understanding of personality in the context of each ment corresponded to weak feelings.
individual’s unique existence. According to Tyrer and The German physiologist and psychologist Wilhelm
Ferguson (2000), Wundt (1832–1920), whom most regard as the father of
experimental psychology, superimposed the following
The idiographic approach focuses on the uniqueness of
two dimensions on the four temperaments:
the individual and as such can provide a rich, multifac-
eted description of subtle areas of personal attributes
and behaviour. Numerous strands are brought together • Strong versus weak emotions
to build up a portrait which cannot be confused with any • Changeable (or rapid changes) versus unchange-
other. The case history is the most obvious example and able activity (or slow changes)
has been used with effect to describe processes, which
can then be generalized to explain similar psychological Thus, a choleric temperament was unstable (strong emotion)
mechanisms in others. and changeable (rapid changes); a melancholic tempera-
ment was unstable and unchangeable; a phlegmatic tem-
An influential early proponent of the idiographic approach perament was stable (weak emotions) and unchangeable;
was Gordon Willard Allport (1937), but the nomothetic and a sanguine temperament was stable and changeable.
approach has prevailed. A major impetus was given to the scientific study of
the trait approach to personality research by develop-
ments in statistical techniques, particularly the use of
3.6.2 Trait and State Approaches
systematic collection of data and the discovery of cor-
Traits are ‘broad, enduring, relatively stable characteristics relational and factor analytic techniques. Cattell et al.
used to assess and explain behaviour’ (Hirschberg, 1978). (1970) have developed the Sixteen Personality Factor
Basic Psychology 45
Questionnaire (16PF) that measures 16 primary factors • Dominant

along 16 dimensions. These are as follows: • Carefree
• Active
• Trait A: Outgoing/warmhearted versus reserved/ • Assertive
detached • Sensation seeking
• Trait B: Intelligence • Venturesome
• Trait C: Unemotional/calm versus emotional/ • Surgent
changeable
• Trait E: Assertive/dominant versus humble/ Introversion is associated with the opposite traits.
cooperative Neuroticism is associated with traits such as
• Trait F: Cheerful/lively versus sober/taciturn
• Trait G: Conscientious/persistent versus
expedient/undisciplined • Anxious
• Trait H: Venturesome/socially bold versus shy/ • Depressed
retiring • Emotional
• Trait I: Tough minded/self-reliant versus tender • Guilt feelings
minded/sensitive • Irrational
• Trait L: Suspicious/sceptical versus trusting/ • Low self-esteem
accepting • Moody
• Trait M: Imaginative/Bohemian versus • Shy
practical/conventional • Tense
• Trait N: Shrewd/discreet versus forthright/
straightforward
• Trait O: Guilt prone/worrying versus resilient/ Psychoticism, which is orthogonal to (and therefore inde-
self-assured pendent of) extraversion and neuroticism in the revised
• Trait Q1: Radical/experimental versus Eysenck factor analysis-based model of personality, is
conservative/traditional associated with traits such as
• Trait Q2: Self-sufficient/resourceful versus
group dependent/affiliative • Aggressive
• Trait Q3: Controlled/compulsive versus • Antisocial
undisciplined/lax • Cold
• Trait Q4: Tense/driven versus relaxed/tranquil • Creative
• Egocentric
In contrast, Hans Eysenck’s rating studies initially only • Impersonal
yielded two dimensions and more recently the following • Impulsive
three dimensions (following a factor analysis of items) • Tough minded
(see Eysenck and Eysenck, 1991): • Unempathetic
• Extraversion (i.e. extraversion vs. introversion) In contrast to traits, which refer to stable phenomena
• Neuroticism related to behaviour and ideas relating to enduring dis-
• Psychoticism positions, states are unstable short-term features of the
individual. An example of a state variable is a temporary
The first two of these dimensions were derived by Eysenck short-term feeling of anxiety in someone who normally
(1944) following the study of 700 soldiers in a military hos- scores highly on the extraversion dimension.
pital suffering from various ‘neurotic’ disorders and com- Trait and state approaches can be combined. For
plaints (such as ‘headaches’, ‘sex anomalies’, and ‘narrow example, Figure 3.6 shows a model (based on Michael
interests’). Extraversion is associated with traits such as Eysenck, 1982) of the adverse effects of anxiety
on information processing and performance; this
• Sociable model in turn is based on the more complex model of
• Lively Spielberger (1962).
Trait anxiety
External
State anxiety Processing Performance
stressors
Subjective feelings of
apprehension
Autonomic nervous system
arousal
FIGURE 3.6 Eysenck’s state–trait model showing the effects of anxiety on performance. (After Eysenck, M.W., Attention and
Arousal: Cognition and Performance, Springer, New York, 1982.)
3.6.3 Construct Theory construct system in this regard would be chal-

lenged. In these circumstances, you could alter
The personal construct theory of George Kelly (an your construct system in one of following ways:
American engineer who went on to become a clinical a. Adaptation. Your construct system could be
psychologist) is based on the proposition that behaviour in changed to reflect your new experience.
humans is anticipatory rather than reactive (Kelly, 1955). b. Immunization. You could try to maintain
Kelly considered every man to be a scientist, interpreting your belief system by having thoughts such
the world on the basis of past experience. Constructs are as ‘There must be some important reason
created and predictions made accordingly. A system of that I am not privy to which explains why
constructs results, unique in each individual, existing at they seemed to act in such an evil way’.
various levels of consciousness, those formed at earlier 3. The construct system of an individual represents
developmental stages being unconscious. Each construct the truth as uniquely understood and experi-
has a range of convenience; some are specific, for example, enced by that person.
chewy versus tender; and others have a wider range of 4. A construct system is not necessarily internally
convenience. Constructs are arranged into hierarchies. consistent.
Superordinate constructs are central to the individual’s 5. Since construct systems are partly a function of prior
sense of identity, and subordinate constructs less so. experience, they affect expectations and behaviour.
According to this theory, anxiety results when the 6. Constructs representing core values and the
individual is presented with events outside their range of most important relationships of a person are
personal constructs. Hostility comprises imposition of more firmly held and of greater importance that
constructs upon another. those related to less important matters.
The main points relating to construct systems are as 7. The degree to which one individual can relate to
follows: and understand the construct system of another
person is a function to their empathy with the latter.
1. Individuals’ construct systems make the world
more predictable and thereby make it easier to
3.6.4 Humanist Approaches
negotiate one’s way around.
2. Individuals’ construct systems are not static but Humanistic approaches pay particular attention to those
may grow and be modified in response to circum- qualities that differentiate humans from nonhuman ani-
stances. For example, suppose you were under the mal species. The Association for Humanistic Psychology
impression that professors of psychiatry are hon- lists the following five basic postulates:
est, intelligent people of integrity who care deeply
about the need to help discover the aetiology of • Man, as man, supersedes the sum of his parts.
various types of mental illness and who wish to • Man has his being in a human context.
help find the best treatments for such illnesses. If • Man is aware.
you were then to discover that a couple of such • Man has choice.
professors were in fact utterly dishonest, cruel, • Man is intentional.
selfish, and psychopathic, with little or no real
commitment to academic excellence but ready to Self-actualization is held to be a core individual motiva-
steal the fruits of the work of others, then your tional force.
Basic Psychology 47
3.6.4.1 Roger’s Self Theory • Working hard at the tasks decided upon
Each individual has a drive to fulfil themselves and develop • Become fully absorbed and concentrate fully,
an ideal self within a phenomenal field of subjective experi- experiencing life as a child does
ence. The most important aspect of personality is the con- • Identifying one’s defences and giving them up
gruence between the individual’s view of himself or herself • Being prepared to try new things
and reality and their view of themselves compared with • Evaluate experiences personally without being
the ideal self. If an individual acts at variance to their own swayed by the opinions of others
self-image, anxiety, incongruence, and denial result. The • Being willing to be unpopular
congruent individual is able to grow (self-actualization) and
achieve their potential both internally and socially. 3.6.5 Psychoanalytic Approaches
3.6.4.2 Maslow Behaviour and feelings are explained by unconscious
Abraham Maslow is considered to be another leading drives and conflicts. The id is held to be derived from
founder of the humanist approach. Maslow’s hierarchy of the libido. Irrational, impulsive instincts are unable to
needs is considered in Section 3.7.5. Transient episodes of postpone gratification and are present at birth. The ego
self-actualization have been termed peak experiences by develops as the child grows. A conscious mind bal-
Maslow (1970); they are described in terms such as ances the demands of the id with the realities of the
outside world. Anxiety results if ego is unable to con-
• Aliveness trol the energies of id. The superego comprises the
• Beauty internalization of the views of parents and society, like
• Effortlessness a conscience. The id, ego, and superego are in balance
• Goodness with each other.
• Perfection
• Self-sufficiency 3.6.5.1 Freud’s Stages of Psychosexual
• Truth
Development
• Uniqueness
• Wholeness Oral stage
Characteristics of self-actualizers according to Maslow • Age 0–1 year.

(1967) include the following: • Gratification through sucking, biting.
• Failure to negotiate leads to oral personality
• They accept themselves and other people for traits: moodiness, generosity, depression and
what they are. elation, talkativeness, greed, optimism, pessi-
• They are highly creative. mism, wishful thinking, and narcissism.
• They have a good sense of humour.
• They tend to be problem centred rather than Anal stage
self-centred.
• They are able to tolerate uncertainty. • Age 1–3 years.
• They exhibit spontaneous thought. • The anus and defecation are sources of sensual
• They exhibit spontaneous behaviour. pleasure.
• Even though they do not make an effort to be • Failure to negotiate leads to anal personality
unconventional, nevertheless they are resistant traits: obsessive–compulsive personality, tidi-
to enculturation. ness, parsimony, rigidity, and thoroughness.
• They have the capacity to consider life objectively.
• They form deep and satisfying relationships
Phallic stage
with relatively few others.
Behaviours that Maslow (1967) considered that may lead • Age 3–5 years.
to self-actualization include • Genital interest relates to own sexuality. Oedipus/
Electra complex.
• Being honest • Failure to negotiate leads to hysterical person-
• Assuming responsibility ality traits: competitiveness and ambitiousness.
Latency stage 3.6.8 Inventories
• Age 5–12 years. Personality inventories are questionnaires in which the

same questions are put to each person.
Genital stage
3.6.8.1 16PF
• Age 12–20 years. As mentioned earlier, Cattell et al. (1970) developed the
• Gratification from normal relations with people. 16PF that measures 16 primary factors along 16 dimensions.
• Able to relate to a partner. It was based on the use of factor analysis to identify these 16
basic personality traits, which are listed earlier, from an ini-
3.6.5.2 Erikson’s Stages of Development tial list of over 3000 personality trait names of Allport and
Odbert (1936). Over 100 questions (with yes/no answers)
Age (Years) Sense of were then selected to allow these traits to be measured. For
0 –1 Trust/security example, the following question helps to assess trait E (asser-
1– 4 Autonomy tive/dominant vs. humble/cooperative):
4 –5 Initiative
5–11 Duty/accomplishment Do you tend to keep in the background on social
11–15 Identity occasions?
15–adult Intimacy
Adulthood Generativity An affirmative reply would give the subject a point on the
Maturity Integrity humble/cooperative end of the trait E scale, while a nega-
tive reply would give a point on the assertive/domain end.
The 16PF gives scores on various personality charac-
Epigenesis is the process of development of the ego teristics such as
through these stages.
• Dominance
• Emotional stability
3.6.6 Situationist Approach • Self-control
The external situation is considered the most powerful
determinant of behaviour. Situationists maintain that 3.6.8.2 MMPI
traits result from differences in learning experiences. The opinions of experts (usually working in psychiatry)
Behaviour changes according to the situation an individ- were garnered in generating the categories for subjects on
ual finds themselves in. Proponents dismiss the trait the- whom the Minnesota Multiphasic Personality Inventory
ory. Mischel (1983) argues against the existence of any or MMPI was developed. The final version of the MMPI
stable personality dimension because of poor correlation contains over 550 (567 in one recent version) statements
between behaviour or attitudes in one situation compared (or questions), relating to
with another.
• Attitudes
3.6.7 Interactionist Approach • Emotional reactions
• Physical symptoms
Interactionism holds that behaviour depends upon both • Psychological symptoms
the situation and the person (or personality traits) as well
as their mutual interaction. Endler (1983) was a promi- The person being tested is asked to answer true, false, or
nent advocate of the interactionist approach, arguing that cannot say to each statement.
behaviour is
An example of such a statement is as follows:
a function of a continuous multidirectional process of
person-by-situation interactions; cognitive, motivational At times, my thoughts have raced ahead faster that I
and emotional factors have important determining roles could speak them.
on behaviour, regarding the person side; and the percep-
tion or psychological meaning that the situation has for An affirmative to this statement would yield a higher
the person is an essential determining factor of behaviour. score on the hypomania (Ma) scale. Scores are obtained
Basic Psychology 49
for several scales from the MMPI as follows (with their g. I find it hard to make talk when I meet new
abbreviations): people.
h. I frequently find myself worrying about
• Lie/social desirability (L) something.
• Frequency/distress (F)
Tyrer and Ferguson (2000) have made the following
• Correction/defensiveness (K)
comment:
• Hypochondriasis (Hs)
• Depression (D) …the individual scales … show a considerable degree
• Hysteria (Hy) of intercorrelation. The scales themselves have unfortu-
• Psychopathic deviancy (Pd) nately been labelled using standard psychiatric nosology
• Paranoia (Pa) (e.g. paranoia, schizophrenia and hypomania) which can
• Psychasthenia (Pt) lead to confusion with Axis I diagnosis. They should
• Schizophrenia (Sc) more properly be regarded as indicative of the presence
• Hypomania (Ma) of specific personality attributes. Although the MMPI
is currently used in candidate-selection procedures, its
• Social introversion–extraversion (Si)
principal value would appear to be in the study of clini-
• Masculinity–femininity (Mf) cally abnormal personalities where interpretation by an
experienced psychologist is required.
The first three of these scales are used for validity pur-
poses. They include the following statements: In addition to the problem of the intercorrelation of many
scales, another problem with the MMPI is that responses
may change over time. (This is a problem relating to reli-
1. L scale ability.) The same person taking the MMPI at baseline
a. Once in a while, I think of things too bad to and then a few days later may score differently overall
talk about. and on different scales.
b. At times, I feel like swearing.
c. I do not always tell the truth. 3.6.8.3 CPI
d. Once in a while, I put off until tomorrow
The California Psychological Inventory or CPI employs
what I ought to do today.
some of the same statements as the MMPI. In the devel-
e. I would rather win than lose in a game.
opment of the CPI, the opinions of nonexperts, such as
f. I do not like everyone I know.
the peers of the test subjects, were used. The CPI is con-
2. F scale
structed to measure less ‘abnormal’ personality traits
a. Evil spirits possess me at times.
than the MMPI (in ‘normal’ people), such as
b. When I am with people, I am bothered by
hearing very queer things. • Dominance
c. My soul sometimes leaves my body. • Independence
d. Someone has been trying to poison me. • Responsibility
e. Someone has been trying to rob me. • Self-acceptance
f. Everything tastes the same. • Socialization
g. My neck spots with red often. • Flexibility
h. Someone has been trying to influence my • Masculinity/femininity
mind.
3. K scale In total, the CPI has over 450 (480 in one recent version)
a. Often, I can’t understand why I have been so true/false items, of which many (178 in the same recent
cross and grouchy. version) are from the MMPI, and yields 15 scales that
b. At times, my thoughts have raced ahead measure personality and three scales that are used to
faster than I could speak them. eliminate response bias. Overall, the CPI yields the fol-
c. Criticism or scolding hurts me terribly. lowing three broad vector scales:
d. I certainly feel useless at times.
e. I have never felt better in my life than I do • Internality/externality
now. • Norm favouring/norm questioning
f. What others think of me does not bother me. • Self-fulfilled/dispirited
The CPI was given to 13,000 individuals, and separate • The inventories only rarely allow an assessment
scores were obtained for males and females. The mean of the underlying reasons for the responses to
scores for each scale were obtained. The scores of sub- questions.
jects now taking the CPI can be compared with the mean • The responses depend on an accurate knowl-
scores for these original 13,000 individuals. edge, on the part of the subject, of their beliefs,
behaviour, abilities, and feelings.
3.6.8.4 Other Inventories • The responses depend on a willingness, on the
Other personality inventories include part of the subject, to make known their beliefs,
behaviour, abilities, and feelings.
• Children’s Personality Questionnaire • Questionnaires are susceptible to contamination
• Differential Personality Inventory by reliability minor changes in the mental state
• Edwards Personality Inventory of the subject.
• Eysenck Personality Inventory (EPI) • The dimensions chosen by psychologists in cre-
• Eysenck Personality Questionnaire (EPQ) ating questionnaires may be difficult to relate
• Maudsley Personality Inventory (MPI) to personality disorder categories used by
• NEO Personality Inventory psychiatrists.
• Omnibus Personality Inventory
3.6.9 Rating Scales
The MPI was superseded by the EPI, which in turn was
superseded by the EPQ that measures psychoticism and There are several rating scales that may be used for the
contains a lie scale. assessment of personality disorder. The following are all
structured interview schedules.
3.6.8.5 Limitations
There are several limitations on the use of personality 3.6.9.1 SAP
inventories. These include the following: The Standardized Assessment of Personality or SAP is
carried out by a trained clinical interviewer. A person-
• There are limitations imposed by the cultural ality profile is obtained from an informant. An ICD-10
origins of the questionnaires. For example, in diagnosis is obtained.
assessing the answers to the MMPI and the
CPI, it needs to be borne in mind that these 3.6.9.2 SCID II
questionnaires were created for American The Structured Clinical Interview for DSM-III-R
subjects. One of the statements on the F scale Personality Disorders or SCID II is carried out by a clini-
of the MMPI is that ‘Evil spirits possess me at cian and yields DSM diagnoses.
times’; in some cultures, it is accepted as per-
fectly normal that ‘evil spirits’ should ‘pos- 3.6.9.3 SIDP
sess’ a person, while in other cultures, such The Structured Interview for DSM-III Personality
terminology might be normal but not to be Disorders or SIDP is carried out by a psychologist or psy-
taken literally. chiatrist and yields DSM-III-R diagnoses.
• Deliberate faking. Subjects may deliberately try
to come across as possessing (or not possessing) 3.6.9.4 PAS
a particular personality trait. Lie scales are often The Personality Assessment Schedule or PAS yields five
included to try to detect for this. diagnostic categories:
• Questionnaires are susceptible to response
sets—subjects may exhibit a systematic ten- • Sociopathic
dency to respond to test questions. • Schizoid
• The inventories tend to have a low validity, par- • Passive dependent
ticularly in respect of predictive validity. • Anankastic
• A social desirability bias may occur, in which • Normal
subjects may have an unconscious tendency
to give socially desirable responses that make It assesses 24 dimensions of personality and should be
them look good. carried out by a trained clinical interviewer.
Basic Psychology 51
3.6.9.5 PDE was described by sorting this deck into piles correspond-
The Personality Disorder Examination or PDE yields ing to how closely the card descriptions were deemed to
DSM diagnoses. apply to the subject. The Q-sort schedule is designed to
apply across different individuals and over time, over
3.6.9.6 IPDE different ages.
The International Personality Disorder Examination
for DSM-IV and ICD-10 personality disorders or IPDE 3.7 FACTORS AFFECTING MOTIVATION
is carried out by trained interviewers and covers DSM-
IV(-TR) and ICD-10 operational criteria. 3.7.1 Extrinsic Theories and Homeostasis
Theories based on instincts were replaced by a drive
3.6.10 Repertory Grid reduction theory in which the motivation of behaviour
is to reduce the level of arousal associated with a basic
George Kelly devised the repertory grid or role con- drive (biological drive, e.g. hunger and thirst) in order
struct repertory (REP) test. This grid assesses per- to maintain homeostatic control of the internal somatic
sonality based on an individual’s personal constructs. environment.
A typical grid might consist of 10 rows (excluding Hull developed a theory in which primary biological
rows containing headings), which need to be filled in drives are activated by needs that arise from homeostatic
by the subject. The subject begins by naming specific imbalance acting via brain receptors.
people who fit into given categories, such as a happy Mowrer developed the notion of secondary drives
person and a successful person. These form columns (e.g. anxiety), which result from generalization and
that cross the rows. Other columns correspond to conditioning.
other people, such as the subject’s father and mother,
the subject himself or herself, their children, and their
spouse or partner. There is now a grid of, say, 10 rows 3.7.2 Hypothalamic Systems and Satiety
and around 10 columns. On each row, three cells are An example of a primary biological drive is provided by
circled; no two rows contain the same three circles. hypothalamic systems and satiety. In rat experiments,
These correspond to three different individuals. Row the hypothalamic ventromedial nucleus acts as a satiety
by row, the subject must now decide for the three indi- centre, with hyperphagia occurring if it is ablated, while
viduals concerned what description shows how two of the lateral hypothalamus contains a hunger centre, with
these three individuals are similar and how they dif- aphagia occurring if it is ablated.
fer from the third individual. The former description
is placed in a column (column 1) on the left-hand side
of the grid, while the latter description is similarly 3.7.3 Intrinsic Theories
placed in a column (column 2) on the right-hand side Whereas extrinsic theories require reduction of drive
of the grid. A code is used to fill in the circles (e.g. externally, intrinsic theories propose that the activity
1 for similarity, as in the column 1 description; 2 for engaged in has its own intrinsic reward.
difference, as in column 2; and 0 if neither column
1 nor column 2 applies). Then the rest of the grid is 3.7.3.1 Optimal Arousal
filled in. There are many scoring systems available, An example is offered by optimal arousal, in which the
although the grid itself overall gives an indication of subject attains an optimal level of arousal to achieve opti-
how the subject views others. mal performance. In general, a moderate level of arousal
leads to an optimum degree of alertness and interest and
therefore to a comparatively high efficiency of perfor-
3.6.11 Q-Sort Schedule
mance. High and low arousals lead to reduced perfor-
This is an ipsative method, that is, one which compares mance and are described in the inverted U shape of the
alternatives within an individual, in which the rater (or Yerkes–Dodson curve.
coder) sorts statements into a standard distribution. Jack
Block (1961, 1971) used it in his research on childhood 3.7.3.2 Cognitive Dissonance
development. A deck of cards was produced in which According to this theory, first formulated by Festinger,
each card contained a word or phrase. An individual discomfort occurs when two or more cognitions are held
but are inconsistent with each other. The individual is 3.8 FACTORS AFFECTING EMOTION
motivated to achieve cognitive consistency and may
change one or more of the cognitions. 3.8.1 Types of Emotion
An emotion is a mental feeling or affection having cogni-
3.7.3.3 Attitude-Discrepant Behaviour tive, physiological, and social concomitants. Plutchik has
When attitude and behaviour are inconsistent (attitude- classified them into eight primary emotions:
discrepant behaviour), alteration of attitude helps bring
about cognitive consistency. • Disgust
• Anger
3.7.3.4 Need for Achievement • Anticipation
McClelland formulated a need for achievement (nAch) to • Joy
explain pleasure resulting from mastery. • Acceptance
• Fear
• Surprise
3.7.4 Curiosity Drive • Sadness
Whereas the homeostatic model predicts that once physi- Any two adjacent emotions can give rise to a secondary
ological needs such as thirst and hunger have been satis- emotion. For example, the secondary emotion of love is
fied, or aversive stimuli such as pain have successfully derived from the primary emotions of joy and accep-
been avoided, and the body returned to its normal state, tance. Similarly, submission results from acceptance and
the organism should no longer be motivated and should fear, disappointment from surprise and sadness, con-
be quiescent; in practice, this is not the case. Humans and tempt from disgust and anger, and so on.
other mammals, for example, have been noted actively
to seek stimulation. A curiosity drive has been proposed
to help explain this phenomenon, in which the organism 3.8.2 Components of Emotional Response
has drives to The main components of emotional response are
• Explore new environments • Subjective awareness

• Investigate objects • Physiological changes
• Manipulate objects (if appropriate) • Behaviour
• Seek changing sensory stimulation (and avoid
sensory deprivation)
• Seek sensation 3.8.3 James–Lange Theory
According to this theory, the experience of emotion is sec-
ondary to the somatic responses (e.g. sweating, increased
3.7.5 Maslow’s Hierarchy of Needs
cardiac rate, increased arousal) to the perception of given
This unified theory, relating to self-actualization, emotionally important events. For example, if an arachno-
integrates both extrinsic and intrinsic theories of phobe becomes aroused, experiences increased activity of
motivation. A hierarchy of needs is described in the sympathetic nervous system, and runs away after seeing
which those with survival importance take prece- a spider, the feelings of anxiety and fear are the result of the
dence over others: increased sympathetic activity and running away and not
primarily because of the emotion-evoking stimulus.
• Self-actualization needs (highest) Cannon criticized this theory. It was argued that simi-
• Aesthetic needs lar physiological changes can accompany different emo-
• Cognitive needs tions. Also, pharmacologically induced simulation of
• Self-esteem needs such physiological changes is usually not accompanied
• Love and belonging needs by these emotions. The experience of emotions can be
• Safety needs shown to be independent of somatic responses, some-
• Physical/physiological needs (lowest) times occurring before the somatic responses.
Basic Psychology 53
3.8.4 Cannon–Bard Theory 3.9.2.1 Life Events

This holds that following the perception of an emotion- These are changes in a person’s life that require read-
ally important event, both the somatic responses and the justment. They are ranked in order from most to least
experience of emotion occur together. In neurophysi- stressful. The most stressful include death of spouse,
ological terms, the perceived stimulus undergoes tha- divorce, marital separation, jail term, death of close fam-
lamic processing, and signals are then relayed to both the ily member, personal illness, and marriage. The scale has
cerebral cortex, leading to the experience of emotion, and been found to be universally applicable to people in both
other parts of the body, such as the autonomic nervous underdeveloped and Western countries. Many conditions,
system, leading to somatic responses. both physical and mental, show an excess of life events in
This theory can be criticized on the basis of the obser- the months preceding onset.
vation that there are stimuli, for example, sudden danger,
which can lead to increased sympathetic activity before 3.9.3 Vulnerability and Invulnerability
the emotion is experienced. Conversely, the experience of
emotions sometimes occurs before the somatic response. Type A behaviour is related to increased proneness to heart
disease. Such behaviour includes competitiveness, striving
for achievement, time urgency, difficulty relaxing, impa-
3.8.5 Schachter’s Cognitive Labelling tience, and anger. It is possible to modify such behaviour.
Theory and Cognitive Appraisal Type B individuals do not exhibit the earlier charac-
teristics; for example, they can relax more easily and are
According to this theory, the conscious experience of an slow to anger.
emotion is a function of the stimulus, of somatic or physi- Stress-resistant people are those who view change as
ological responses, and of cognitive factors such as the cog- a challenge and feel they have more control over events.
nitive appraisal of the situation and input from long-term
memory. The influence of cognitive factors on the conscious
experience of emotion was demonstrated in an experiment 3.9.4 Coping Mechanisms
by Schachter and Singer (1962) in which subjects were Although the following mechanisms, used to cope with
injected with adrenaline. Their cognitive appraisal of the stress, are conscious, they relate to unconscious defence
current situation, based on observation of others, influenced mechanisms too (given in parentheses):
the conscious experience of emotion. Thus, cognitive cues
were important in their interpretation of arousal. • Concentration only on the current task (denial)
• Empathy (projection)
3.9 STRESS • Logical analysis (rationalization)
• Objectivity (isolation)
Stress results when demand exceeds resources. An indi- • Playfulness (regression)
vidual’s response to a stressful situation is affected by • Substitution of other thoughts for disturbing
biological susceptibility and personality characteristics. ones (reaction formation)
• Suppression of inappropriate feelings (repression)
3.9.1 Physiological and Psychological Aspects
Physiological effects of stress include physical disor- 3.9.5 Learned Helplessness
ders (ulcers, cardiac disease, and hypertension) and Seligman found that dogs given unavoidable electric
immune response changes. Other physical disorders have shocks suffered a number of phenomena, which he con-
also been attributed to emotional stress, for example, sidered were similar to depression, such as reduced appe-
migraine, eczema, asthma, and allergies. tite, disturbed sleep, and reduced sex drive. He called this
learned helplessness.
The cognitive theory of depression is based largely
3.9.2 Situational Factors
on this concept. Further work has found that indi-
These include life events, daily hassles/uplifts, conflict, viduals who believe that they have no personal con-
and trauma (see Chapter 28). trol over events much more likely to develop learned
helplessness, whereas those believing that nobody Block J. 1971: Lives Through Time. Berkeley, CA: Bancroft
could have controlled the outcome are unlikely to do so. Books.
Thus, a person’s attribution of what is occurring influ- Boran M and Viswanathan R. 2000: Separating subculture from
psychopathology. Psychiatric Services 51:678
ences the likelihood of developing major depression in
Bower GH. 1972: Mental imagery and associative learning.
cognitive terms. In Gregg LW (ed.) Cognition in Learning and Memory.
New York: Wiley.
Bower GH, Clark M, Winzenz D, and Lesgold A. 1969:
3.9.6 Locus of Control Hierarchical retrieval schemes in recall of categori-
Rotter differentiated those who see their lives as being cal word lists. Journal of Verbal Learning and Verbal
under their own control (internal locus of control) from Behavior 8:323–343.
Bower GH and Springston F. 1970: Pauses as recoding points in let-
those who see their lives as being controlled externally
ter series. Journal of Experimental Psychology 83:421–430.
(external locus of control). Braine MDS, Reiser BJ, and Rumain B. 1984: Some empirical
justification for a theory of natural propositional logic.
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4 Social Psychology
Note that intergroup behaviour, including stigma, is con- administered. A disadvantage is that different response
sidered in Chapter 8. patterns may result in the same mean score.
4.1 ATTITUDES AND HOW 4.1.3.3 Semantic Differential Scale

THEY ARE AFFECTED This is a bipolar visual analogue scale.
Its advantages include
4.1.1 Definition
The definition of an attitude has been given variously as • Ease of use
‘a mental and neural state of readiness, organized through • Good test–retest reliability
experience, exerting a directive or dynamic influence
upon the individual’s response to all objects and situa- Its disadvantages include the following:
tions with which it is related’ (Katz, 1979), and ‘an endur-
ing organization of motivational, emotional, perceptual, • Positional response bias may occur
and cognitive processes with respect to some aspect of • No consistent meaning is attributed to a mid-
the individual’s world’ (Krech et al., 1962). They are point mark
mutually consistent and internally consistent.
4.1.4 Attitude Change
4.1.2 Components
A change in one of the three components of attitude leads
Attitudes are based on beliefs, a tendency to behave in an to changes in the other two.
observable way, and also have affective components that The origin of attitudes can be by means of the pro-
are the most resistant to change. A change in one of these cesses of learning: classical conditioning, operant con-
three components leads to changes in the other two. ditioning, and observational learning. Superimposed on
When predicting behaviour, situational variables must these are cognitive processes such as appraisal and modi-
be taken into account. Otherwise, measured attitudes are fication in the light of new information.
poor predictors of behaviour. Attitudes can be modified either by central pathways,
entailing the consideration of new information, or by
4.1.3 Measurement peripheral pathways involving the presentation of cues.
Advertising uses both pathways.
4.1.3.1 Thurstone Scale The balance theory of Heider (1946) holds that each
This is a dichotomous scale indicating agreement/dis- individual attempts to organize his or her attitudes, per-
agreement with presented and previously ranked state- ceptions, and beliefs so that they are in harmony or bal-
ments. Disadvantages of this scale include the following: ance with each other.
• Different response patterns may result in the

4.1.5 Persuasive Communication
same mean score.
• The set-up is unwieldy. The factors to consider are those concerned with the commu-
• The ranking may be biased. nicator, the recipient, and the message being communicated.
4.1.3.2 Likert Scale 4.1.5.1 Communicator

This is a five-point scale indicating level of agreement Characteristics of persuasive communicators include
with presented statements. Its advantages include the
fact that it has increased sensitivity compared with the • Attractiveness
dichotomous Thurstone scale and that it is more easily • Audience identification with the communicator
57
• Credibility 4.2.1.1 Self-Esteem

• Expertise This is one’s own evaluation of self-worth and feeling
• Genuine motivation accepted by others. Those lacking in self-esteem have
• Being an opinion leader feelings of worthlessness, alienation, and lack of accep-
• Nonverbal communication tance by others, whereas those with high self-esteem are
• Views of reference groups more socially active, less prejudiced, more risk-taking,
and warmer in social relationships. It is learned and so
4.1.5.2 Recipient may change with experience.
High self-esteem and intelligence of the recipient Self-esteem may be raised by identification with a group.
increase the likelihood that complex communications For example, deaf individuals who identify with other deaf
will be persuasive. people have a higher self-esteem, on average, than those
who do not. In turn, the raised self-esteem can help to com-
4.1.5.3 Message pensate for problems relating to personal identity.
Key aspects relating to the message and attitude change
include the following:
4.2.1.2 Self-Image
• Message repetition can be a persuasive influence Self-image is a set of beliefs held about oneself, based on
leading to attitude change. achievements and social interactions, which influences
• Explicit messages are more persuasive for personal meaning and behaviour.
the less intelligent and implicit messages for the
more intelligent recipient.
• Interactive personal discussions are more per- 4.2.2 Self-Perception Theory
suasive than mass media communication. An individual infers what his or her attitude must be by
• One-sided communications are more persuasive observation of his or her own behaviour, in a similar way
for those who are less intelligent and/or already to how other people infer his or her behaviour.
favourably disposed to the message. Self-perception theory provides a better explanation
• Two-sided presentations are more effective with than cognitive dissonance theory for behaviour that lies
intelligent and neutral recipients. within the general range of behaviours acceptable to the
• A low anxiety recipient is more influenced by a individual.
high fear message, and vice versa.
4.1.6 Cognitive Consistency and Dissonance 4.3 INTERPERSONAL ISSUES

When cognitive dissonance occurs, the individual feels 4.3.1 Interpersonal Attraction
uncomfortable, may experience increased arousal, and
is motivated to achieve cognitive consistency. This may In general, humans seek the company of others, to whom
occur by changing one or more of the cognitions involved they are attracted. In difficult situations, this may allow
in the dissonant relationship, changing the behaviour that assessment by social comparisons, taking note of the
is inconsistent with the cognition(s), or adding new cogni- opinions of others (social comparison theory [Festinger,
tions that are consonant with preexisting ones. Cognitive 1954]). An alternative theory is that seeking the company
consistency can also be achieved, when attitude and of others leads to arousal reduction (Eppley et al., 1989).
behaviour are inconsistent (attitude discrepant behaviour), Theories of interpersonal attraction include the
by altering attitude. following:
• Reinforcement theory—reciprocal reinforcement

4.2 SELF-PSYCHOLOGY of the attractions occurs with rewards in both direc-
tions (Newcomb). Conversely, punishments dimin-
4.2.1 Self-Concept
ish the probability of interpersonal attraction.
This is a set of attitudes that the individual holds about • Social exchange theory—people prefer rela-
himself or herself. It does not necessarily correspond to tionships that appear to offer an optimum cost-
reality. Self-theory was developed by Rogers (1951). benefit ratio (Homans, 1958).
Social Psychology 59
• Equity theory—the preferred relationships are A ‘hot’ theory of mind entails constructing the
those in which each feels that the cost-benefit meaningful intentions and evaluative attitudes (such as
ratio of the relationship for each person is fear, surprise, and pleasure) of others. The latter can be
approximately equal (Hatfield et al., 1978). inferred from facial expressions.
• Proxemics—relates to interpersonal space/body
buffer zone.
4.4 LEADERSHIP, SOCIAL INFLUENCE,
Factors predisposing to interpersonal attraction include POWER, AND OBEDIENCE
proximity, familiarity, similarity of interests and values,
4.4.1 Leadership
exposure, perceived competence, reciprocal liking, and
self-disclosure and physical attractiveness. Similarity is Lewin et al. distinguished between the following leader-
more important than complementarity although the latter ship styles:
increases in importance with time.
According to the matching hypothesis, pairing occurs • Autocratic—abandon task in leader’s absence;
such that individuals seek others who have a similar level good for situations of urgency
of physical attractiveness. • Democratic—yields greater productivity unless
a highly original product is required
• Laissez-faire—appropriate for creative, open-
4.3.2 Attribution Theory (Heider) ended, person-oriented tasks
This deals with the rules people use to infer the causes of
observed behaviour.
4.4.2 Social Facilitation
4.3.2.1 Internal or Dispositional Attribution This refers to the way in which tasks and responses are
This is the inference that the person is primarily respon- facilitated when carried out in the presence of others
sible for their behaviour. (Allport; Harlow). To occur, the others do not necessarily
have to be engaging in the same task. Facilitation also
4.3.2.2 External or Situational Attribution occurs if the others are simply observing; this has been
This is the inference that the cause of a behaviour is called the audience effect (Dashiell, 1930).
external to the person.
4.3.2.3 Primary (Fundamental) Attribution Error 4.4.3 Social Power

When inferring the cause of other people’s behaviour, French and Raven described the following five types of
there is a bias towards dispositional rather than situ- social power:
ational attribution.
• Authority—power derived from role
• Reward—power derived from ability to allocate
4.3.3 Theory of Mind
resources
In primate research, theory of mind refers to the abil- • Coercive—power to punish
ity of primates to mentalize their fellows. In humans, the • Referent—charismatic and liked by others
(‘cold’) theory of mind refers to the ability of most nor- • Expert—power derived from skill, knowledge,
mal people to comprehend the thought processes (such as and experience
their attention, feelings, beliefs, false beliefs, and knowl-
edge) of others.
4.4.4 Conformity
Research into children would tend to suggest that at the
age of 3 years, normal human children do not acknowl- Two types of conformity to the actions and opinions of
edge false belief as they have difficulty in differentiating others have been identified (Deutsch and Gerard, 1955):
belief from world. Formulating a theory of mind appears
not to be inevitable, but relies on cognitive changes that • Informational social influence—an individual
occur at around the age of 4. It has been suggested that conforms to the consensual opinion and behav-
a failure to acquire a theory of mind is associated with iour of the group both publicly and in his or her
disorders such as autism. own thoughts (evident with ambiguous stimuli).
• Normative social influence—situations in 4.5.1.4 Ethology

which an individual publicly conforms to the Some ethologists believe that humans and animals are
consensual opinion and behaviour of the group innately aggressive. Animal studies show that certain
but has a different view in his or her own mind. behaviours inhibit aggression:
The individual conforms to the group under
social pressure to avoid social rejection. • Maintaining a distance
• Evoking a social response incompatible with
Self-reliance, intelligent, expressive, socially effective aggression
individuals are least vulnerable to group pressure. • Familiarity
4.5.1.5 Frustration–Aggression Hypothesis

4.4.5 Obedience to Authority This proposes that preventing a person reaching their
Milgram found that most subjects would obey an experi- goal induces an aggressive drive resulting in behav-
menter’s orders to administer what they believed to be iour intended to harm the one causing the frustration.
increasingly powerful electrical shocks to others, right up Expressing this aggression reduces the aggressive drive.
to the maximum voltage available. Factors that increased
4.5.1.6 Arousal
the rate of obedience included
Emotional arousal can increase aggression.
• The presence of the experimenter
• The belief that the prior agreement was binding 4.5.2 Influence of Television
on the subject It is known that children imitate observed aggression.
• Increasing distance from the apparently suffer- Some studies suggest a relationship between exposure to
ing person violence on television and aggressive behaviour in boys,
but not in girls. It may be that this is because aggressive
behaviour in boys, but not in girls, is socially reinforced.
4.5 PHENOMENON OF AGGRESSION Ways in which filmed violence may increase aggres-
Aggression is behaviour intended to harm others. We sive behaviour include
may distinguish between the following:
• Teaching aggressive styles of conduct
• Hostile aggression—the sole intent is to inflict • Increasing arousal
injury. • Desensitizing people to violence
• Instrumental aggression—the intention is to • Reducing restraint on aggressive behaviour
obtain reward or inflict suffering. • Distorting views about conflict resolution
4.5.1 Explanations 4.6 CONCEPT OF ALTRUISM

The concept of the type of interpersonal cooperation
4.5.1.1 Psychoanalytic
known as altruism refers to an act (or acts) that is moti-
Aggression is viewed as a basic instinct. vated by the desire to benefit another person (or persons)
rather than oneself.
4.5.1.2 Social Learning Theory Altruism may be considered to be a higher defence
Aggression is viewed as a learned response. It is mechanism in which the individual deals with emotional
learned through observation, imitation, and operant conflict or internal or external stressors by dedication to
conditioning. meeting the needs of others. Unlike self-sacrifice, some-
times characteristic of reaction formation, the individual
4.5.1.3 Operant Conditioning receives gratification either vicariously or from the response
Positive reinforcers can include victim suffering and of others (APA, 1994).
material gains. The consequences of aggression play an Altruism can also be explained on the basis of social
important role in shaping future behaviour. exchange theory (see Section 4.3.1).
Social Psychology 61
It has been suggested that failure to exclude an ulterior Hatfield E, Traupmann J, and Walster GW. 1978: Equity and
motive means that, strictly speaking, altruism cannot be extramarital sexuality. Archives of Sexual Behavior,
said to have occurred under these circumstances. Indeed, 7:127–141.
Heider F. 1946: Attitudes and cognitive organization. The
there may be personal rewards of a private nature that
Journal of Psychology 21:107–112.
occur as a result of acting in this way; for instance, a per- Homans GC. 1958: Social behavior as exchange. American
son may feel virtuous. Journal of Sociology, 63:597–606.
Katz D. 1979: Floyd H. Allport (1890-1978). American
BIBLIOGRAPHY Psychologist 34:351–353.
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Bandura A and Walters RH. 1963: Social Learning and Person- to Psychology, 15th edn. Hampshire, U.K.: Cengage
ality Development. New York: Holt, Rinehart & Winston. Learning EMEA.
Dashiell JF. 1930: An experimental analysis of some group Persaud R. 2010: Social psychology. In Puri BK and Treasaden IH
effects. Abnormal Social Psychology, 25:190–199. (eds.) Psychiatry: An Evidence-Based Text, pp. 285–296.
Deutsch M, Gerard HB. 1955: A study of normative and infor- London, U.K.: Hodder Arnold.
mational social influences upon individual judgment. The Rogers C. 1951: Client-Centered Therapy: Its Current Practice,
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Human Relations 7(2):117–140. Perspectives on Behaviour. New York: John Wiley.
5 Human Growth and Development
5.1 CONCEPTUALIZING DEVELOPMENT positive emotional ties. Monotropic attachment is when

the attachment is to one individual, usually the mother.
5.1.1 Basic Concepts Polytropic attachment is less common. Attachment usu-
Human development involves an interaction between ally takes place from infant to mother. In contrast, neona-
nature and nurture. tal–maternal bonding takes place in the opposite direction.
Stage theories propose that development occurs in a Both processes can start immediately after birth.
progressive sequence reflecting maturation. Examples Some behaviourists consider attachment to result from
include Piaget’s cognitive stages, Freud’s psychosexual the mother acting as a conditioned reinforcer.
stages, and Kohlberg’s stage theory. Maturation refers to This theory was challenged by Harlow who, using
the orderly changes in behaviour that result from biolog- cuddly and wire artificial surrogate mothers and infant
ical development and whose timing and form are rela- rhesus monkeys, found that attachment is a function of
tively independent of external experience. Maturational the requirement to be in contact with a soft object (con-
tasks are influenced by biological growth, the drive for tact comfort), which provides security. Other studies have
independence, and other people’s general expectations. found that warm or rocking artificial surrogate mothers
are preferred to colder or still surrogates, respectively.
5.1.2 Gene–Environment Interactions Lorenz considered attachment to result from imprint-
ing whereby geese, during a critical period soon after
These interactions determine all psychological character- hatching, persistently follow the first nearby moving
istics, such as intelligence. Genetic factors determine the object encountered. There is no evidence that imprinting
inherited potential, while environmental factors deter- occurs in primates.
mine the degree to which this potential is fulfilled. Bowlby (1969) considered infant attachment to take
With respect to intelligence, while it is generally agreed place in the context of a warm, intimate, and continu-
that there is a genetic component to intelligence, there is ous relationship with the caregiver in which there is
disagreement about the degree of environmental influence reciprocal satisfaction. The attachment process takes
on it. The correlation coefficient for IQ between MZ twins an average of 6 months to become fully established.
is 0.86 compared with 0.60 for DZ twins. Using factor anal- Bonding is stronger if there is tactile contact as soon as
ysis, Spearman identified a general factor, g, and a specific possible after birth. The mother’s attachment behaviour
factor, s, of intelligence; it was proposed that the level of g is reinforced by infant smiling, movement, and crying.
was associated with how intelligent the individual was. Attachment behaviours are the signs of distress shown
by the child when separated from their attachment fig-
5.1.3 Historical Models ure and include
The historical developmental models of Freud and
Erikson are described in Chapter 29. Social-learning • Crying when the caregiver (usually mother)
models lay emphasis on the way in which environmental leaves the room
influences affect subsequent behaviour. The most influ- • Attempting to follow her
ential theory of cognitive development is that of Piaget • Clinging hard when distressed
(see the succeeding text). • Hugging her
• Being more playful and talkative in her company
5.2 ATTACHMENT AND BONDING • Using her as a secure base from which explora-
tion can take place
5.2.1 Attachment Theory
This comes from the work of Bowlby (1969). Attachment These start to occur at about the age of 6 months and
refers to the tendency of infants to remain close to certain decrease visibly by 3 years. Prior to this, age separation
people (attachment figures) with whom they share strong is tolerated without distress.
63
5.2.2 Attachment Abnormalities 5.2.5 Stranger Anxiety

5.2.2.1 Insecure Attachment This refers to a fear of strangers shown by infants usu-
There is chronic clinginess and ambivalence towards the ally between the ages of 8 months and 1 year. It is not
mother. Clinically, this may be relevant, as it may be a necessarily part of attachment behaviour and may occur
precursor to independently of separation anxiety.
• Childhood emotional disorders (including 5.2.6 Maternal Deprivation

school refusal) Following a failure to form adequate attachments, for exam-
• Disorders (such as agoraphobia) starting in ado- ple, because of prolonged maternal separation or rejecting
lescence and adulthood parents, the effects of maternal deprivation may include
5.2.2.2 Avoidant Attachment • Developmental language delay

• Indiscriminate affection seeking
A distance is kept from the mother, who may sometimes
• Shallow relationships
be ignored. Clinically, avoidant attachment caused by
• Enuresis
rejection by the mother may be relevant as it may be a
• Aggression
precursor to
• Lack of empathy
• Social disinhibition
• Poor social functioning in later life (including • Attention seeking and overactivity in school
aggression) • Poor growth—deprivation dwarfism
5.3 FAMILY RELATIONSHIPS
5.2.3 Separation Anxiety
AND PARENTING PRACTISE
This is the fear an infant shows of being separated
from his or her caregiver. Holding a comfort object or 5.3.1 Child-Rearing Practise
transitional object (Winnicott, 1965) may help with Table 5.1 (after Baumrind, 1967) shows how the parents
separation. of three groups of children have been found to score on
The rate of disappearance of separation anxiety varies the four dimensions of
with the child’s
• Control—by the parents of the child’s activities
• Experiences of previous separations (real or and behaviour
threatened) • Maturity demands—of the child to act at his or
• Handling by mother her ability level
• Perception of whether mother will die or depart • Communication—clarity of parent–child
• Temperament communication
• Nurturance—parental nurturance towards the
child
5.2.4 Acute Separation Reaction
TABLE 5.1
After starting to form attachments, around 6 months to 2
years of age, separation from mother leads to the follow- Way in Which Parents of Three Groups of Children
ing reaction: Score on the Dimensions of Control, Maturity
Demands, Communication, and Nurturance
• First, protest—including crying and searching Maturity
behaviour Control Demands Communication Nurturance
• Second, despair—apathy and misery with an Group I ↑↑ ↑↑ ↑↑ ↑↑
apparent belief that mother may not return Group II ↑ → ↓ ↓↓
• Finally, detachment—emotionally distant from Group III ↓↓ ↓↓ ↓↓ ↑
(and indifferent to) mother
Human Growth and Development 65
The three groups of children were • Communication difficulties—for example, ambig-

uous or incongruous communications.
• Group I—the most mature and competent • Myths—created within the families.
• Group II—moderately self-controlled and self-
reliant but somewhat withdrawn and distrustful Marital conflicts may cause the parents to need to have a
• Group III—the most immature and dependent child with a problem who can act as a scapegoat (until he
or she leaves home).
5.3.2 Family Structure
In the United Kingdom and the United States, around 5.3.5 Impact of Bereavement
25% of children are not living with both biological
parents by the age of 16 years. If orthodox families The death of a parent leads to initial bereavement reac-
are defined as those nuclear families in which there tions, which may include prolonged sadness, crying and
are two parents with a small number of children, then irritability during childhood, and
nonorthodox family structures may or may not be rel-
evant so far as healthy psychosocial development of • Young children—↑ functional enuresis
the child is concerned. ↑ Temper tantrums
• Older children (especially girls)—↑ sleep
Single parents
disturbance
↑ Behavioural and emotional problems (particularly if
↑ Clear-cut depressive reactions
no other support)
• School performance—impaired (may be only
Extended family temporary)
Not harmful
Two lesbian parents
Not harmful 5.3.6 Impact of Parental Divorce
Large family size Parental divorce is associated with an increased rate of
↑ Behavioural and educational problems disturbance in children (greater than following parental
↓ Intelligence bereavement). Protective factors include
• Amicable arrangements for access following the

5.3.3 Ordinal Position in Family divorce
The oldest child has a slight advantage in intellectual • Good parental relationship with the child
development. This also applies to only children. Twins • Good relationships of the child with other siblings
show delayed language development. • The child’s temperament
5.3.4 Distorted Family Function

5.3.7 Impact of Intrafamilial Abuse
Dysfunctional families may manifest the following:
5.3.7.1 Sexual Abuse
• Discord. Child sexual abuse is ‘the involvement of dependent, devel-
• Overprotection of the child(ren) by the parents. opmentally immature children and adolescents in sexual
• Rejection of the child(ren). activities that they do not fully comprehend, are unable to
• Enmeshment—parents may be overinvolved in give informed consent to, and that violate the social taboos
their children’s feelings and lives. of family roles’ (Schechter and Roberge, 1976).
• Disengagement—parents may be underinvolved The findings of a study by Cosentino et al. (1995)
in their children’s feelings and lives. suggest that sexual abuse in preadolescent girls is asso-
• Triangulation—exclusive alliances are formed ciated with sexual behaviour problems. This study com-
within the family, for example, father/daughter pared a group of sexually abused girls, aged 6–12 years,
alliance (although this may, e.g. be helpful in with two demographically comparable control groups,
preventing father from leaving home). girls from a child psychiatry outpatient department and
girls from a general paediatric clinic. Compared to both Recognized sequelae of physical abuse (which overlap
control groups, sexually abused girls manifested more with those of sexual abuse) include
sexual behaviour problems: masturbating openly and
excessively, exposing their genitals, indiscriminately • Anxiety states and anxiety-related symptoms
hugging and kissing strange adults and children, and (e.g. sleep disturbance, nightmares, psychoso-
attempting to insert objects into their genitals. Abuse by matic complaints, and hypervigilance), reenact-
fathers or stepfathers involving intercourse was associ- ments of the victimization, and post-traumatic
ated with particularly marked sexual behaviour distur- stress disorder (Green, 1978; Goodwin, 1988)
bances. There was a subgroup of sexually abused girls • Depression (Gaensbauer and Sands, 1979; Sgroi,
who tended to force sexual activities on siblings and 1982)
peers. All of these girls had experienced prolonged sex- • Dissociation (Kluft, 1985; Putnam, 1985)
ual abuse (>2 years) involving physical force that was • Paranoid reactions and mistrust (Green, 1978;
perpetrated by a parent. Herman, 1981)
Recognized sequelae of sexual abuse include • Excessive reliance on primitive defence mecha-
nisms (e.g. denial, projection, dissociation, and
• Anxiety states and anxiety-related symptoms splitting) (Green, 1978)
(e.g. sleep disturbance, nightmares, psychoso- • Borderline personality disorder (especially in
matic complaints, and hypervigilance), reenact- females) (Herman et al., 1989)
ments of the victimization, and post-traumatic • Aggressive and destructive behaviour at home
stress disorder (Green, 1978; Goodwin, 1988) and school (Green, 1978; George and Main,
• Depression (Gaensbauer and Sands, 1979; Sgroi, 1979)
1982) • Cognitive and developmental impairment
• Dissociation (Kluft, 1985; Putnam, 1985) (Elmer and Gregg, 1967; Oates, 1986)
• Paranoid reactions and mistrust (Green, 1978; • Delayed language development (Martin, 1972)
Herman, 1981) • Neurological impairment (Green et al., 1981)
• Excessive reliance on primitive defence mecha- • Abusive behaviour with their own children (the
nisms (e.g. denial, projection, dissociation, and cycle of abuse may continue) (Steele, 1983)
splitting) (Green, 1978)
• Borderline personality disorder (especially in
females) (Herman et al., 1989) 5.4 TEMPERAMENT
• Inability to control sexual impulses (precocious Temperament can be defined as early appearing,
sexual play with high sexual arousal) (Yates, biologically rooted, basic personality dimensions
1982; Friedrich and Reams, 1987; Cosentino (Zuckerman, 1991).
et al., 1995)
• Weakened gender identity (a tendency to reject
5.4.1 Individual Temperamental Differences
their maleness or femaleness) (Aiosa-Karpas
et al., 1991) In the New York Longitudinal Study, Thomas and Chess
• ↑ Incidence of homosexuality (Finkelhor, 1984) (1977) (Chess and Thomas, 1984) identified the following
• ↑ Incidence of molesting children (the cycle of nine categories of temperament describing how children
abuse may continue—there is a high incidence behave in daily life situations:
of sexual abuse in the backgrounds of male and
female child molesters) (Mccarty, 1986; Seghorn 1. Activity level
et al., 1987) 2. Rhythmicity (regularity of biological functions)
• Drug and alcohol abuse (Herman, 1981) 3. Approach or withdrawal to new situations
• Eating disorders (Oppenheimer et al., 1985) 4. Adaptability in new or altered situations
5. Sensory threshold of responsiveness to stimuli
5.3.7.2 Physical Abuse/Nonaccidental Injury 6. Intensity of reaction
Nonaccidental injury can be defined as occurring ‘when 7. Quality of mood
an adult inflicts a physical injury on a child more severe 8. Distractibility
than that which is culturally acceptable’ (Graham, 1991). 9. Attention span/persistence
In terms of the impact of individual temperamental dif- from the brain systems supporting emotion,
ferences on parent–child relationships, the previously attention, and activity:
mentioned nine categories have been found to cluster 1. Limbic structures
as follows: 2. Association cortex
3. Motor cortical areas
• Easy child pattern—characterized by regular- • Environmental influences affect how the bio-
ity, positive approach responses to new stimuli, logical bases of temperament are expressed. For
high adaptability to change, and expressions of example, Gunnar (1992) showed how sensitive,
mood that are mild/moderate in intensity and responsive caregivers could enhance otherwise
predominantly positive highly inhibited preschoolers’ likelihood of
• Difficult child pattern—characterized by approaching novel stimuli.
irregularity in biological functions, negative • Concepts of temperament can be useful in help-
withdrawal responses to new situations, non- ing people solve problems. When the processes
adaptability or slow adaptability to change, of linkage between temperament and the evo-
and intense, frequently negative expressions lution of character and personality are under-
of mood stood better, this should assist prevention and
• Slow-to-warm-up child—characterized by treatment.
a combination of negative responses of mild
intensity to new situations with slow adaptabil- The stability of temperament and its relationship to
ity after repeated contact the evolution of character and personality have been
demonstrated in a number of studies. Characteristics
of temperament in infants and preschool-age children
5.4.2 Origins, Typologies, and Stability predict adjustment in middle childhood and adoles-
cence. For example, Caspi and Silva (1995) showed
of Temperament
how temperamental qualities at the age of 3 years
Medieval personality theorists relied on a tempera- predict personality traits in young adulthood. In an
ment typology based on the balance of the humours, unselected sample of over 800 subjects, the following
but twentieth and twenty-first century theorists have five temperament groups were identified when the chil-
put the strongest emphasis on environmental causa- dren were aged 3 years:
tion models. Acceptance of the concept of biologi-
cally rooted personality dimensions is a fairly recent • Undercontrolled
stage in the history of scientific psychology and psy- • Inhibited
chiatry (Bates et al., 1995); important points to note • Confident
are as follows: • Reserved
• Well adjusted
• Temperament is a theoretical construct—it
is more useful to think of specific dimensions of These groups were reassessed at the age of 18 years. The
temperament, for example, activity level, socia- findings in the young adults were as follows:
bility, negative emotionality, or distractibility.
Temperament concepts can be defined at the fol- • Undercontrolled children scored high on mea-
lowing three levels (Bates, 1989): sures of impulsivity, danger seeking, aggres-
1. As patterns of surface behaviour sion, and interpersonal alienation (as young
2. As a pattern of nervous system responses adults).
3. As having inborn genetic roots • Inhibited children scored low on measures of
• There is an increased understanding of the impulsivity, danger seeking, aggression, and
biological processes involved in temperament. social potency.
Since concepts of temperament typically focus • Confident children scored high on impulsivity.
on individual differences in emotion, attention, • Reserved children scored low on social potency.
and activity (Bates, 1989), the neural basis of • Well-adjusted children continued to exhibit nor-
temperament can be thought of as emerging mative behaviours.
5.5 PIAGET’S MODEL OF COGNITIVE 5.5.2 Preoperational Stage

DEVELOPMENT This is the second stage and occurs from age 2 to 7 years.
Piaget believed that infantile and childhood intellectual During this stage, the child learns to use the symbols of
development involves interactions with the outside world language.
(e.g. through play). These lead to the following: Thought processes exhibited during this stage include
the following:
1. New cognitive structures (schemes) are con-
structed incorporating new information. • Animism—life, thoughts, and feelings are attrib-
2. In the presence of suitable existing schemes uted to all objects, including inanimate ones.
a. Assimilation: New information is incorpo- • Artificialism—natural events are attributed to
rated into appropriate existing schemes. the action of people.
b. Accommodation: Modification of existing • Authoritarian morality—it is believed that
scheme(s). wrongdoing, including breaking the rules of
a game, should be punished according to the
Piaget identified the following four stages of cognitive degree of the damage caused, whether acciden-
development: tal or not, rather than according to motive; nega-
tive events are perceived as punishments.
• Sensorimotor • Creationism—a teleological approach is taken
• Preoperational in which, for example, the stars and the moon
• Concrete operational exist in order to provide light at night.
• Formal operational • Egocentrism—as in the sensorimotor stage.
• Finalism—all things have a purpose.
5.5.1 Sensorimotor Stage • Precausal reasoning—based on internal
schemes rather than the results of observation
This is the first stage and occurs from birth to 2 years so that, for example, the same volume of liquid
of age. poured from one container to another with a dif-
Circular reactions are repeated voluntary motor activ- ferent height and diameter may be considered to
ities, for example, shaking a toy, occurring from around have changed volume.
2 months. They are classified as follows: • Syncretism—everything is believed to be con-
nected with everything else.
• Primary circular reactions—from 2 to 5 months
(approximately), when they have no apparent
purpose. 5.5.3 Concrete Operational Stage
• Secondary circular reactions—from 5 to This is the third stage and occurs from age 7 to around
9 months (approximately), experimenta- 12–14 years of age. During this stage, the child demon-
tion and purposeful behaviour are gradually strates logical thought processes and more subjective
manifested. moral judgements.
• Tertiary circular reactions—from 1 year to 18 An understanding of the laws of conservation of, ini-
months (approximately), include the creation of tially, number and volume, and then weight, is normally
original behaviour patterns and the purposeful achieved. Reversibility and some aspects of classification
quest for novel experiences. are mastered.
During this stage, the infant comes to distinguish him-

5.5.4 Formal Operational Stage
self or herself from the environment. Thought processes
exhibit egocentrism, in which the infant believes that This is the final stage and occurs from the age of around
everything happens in relation to him or her. Until around 12–14 years of age onward.
6 months, the infant believes that an object hidden from It is characterized by the achievement of being able to
view no longer exists. Object permanence is fully devel- think in the abstract, including the ability systematically
oped after around the age of 18 months. to test hypotheses.
5.6 LANGUAGE DEVELOPMENT Stimulation

Although the capacity for language and grammar may
Language can be defined as the sum of the skills required be built-in, speech and language are not achieved in the
to communicate verbally (Graham, 1991). usual manner if children are deaf or are not spoken to.
Twins
5.6.1 Normal Childhood Development Being a twin is associated with slower speech
development.
In the first hours postnatally, the baby learns to distin-
guish his or her mother’s voice:
5.7 MORAL DEVELOPMENT
By 3–4 months, babbling occurs. 5.7.1 Kohlberg’s Stage Theory
By 8 months, repetitive babbling occurs.
By 1 year, the baby has usually acquired the equiv- Kohlberg presented a set of stories, each containing a
alent designations ‘Mama’, ‘Dada’ (no matter moral dilemma, to various individuals of various ages
what language the parent speaks), and one addi- and backgrounds. Questions were posed concerning the
tional word. moral dilemmas. On the basis of the reasons given for the
By 18 months, a 20–50-word vocabulary is expressed answers, Kohlberg formulated a theory of moral devel-
in single-word utterances. opment consisting of six developmental stages of moral
By 2 years, two- or three-word utterances can be judgement categorized into three levels (I–III).
strung together with some understanding of
5.7.1.1 Preconventional Morality (Level I)
grammar. These are telegraphic utterances
omitting grammatical morphemes (e.g. small This is the level at which the moral judgements of chil-
units of meaning signifying the plural). dren up to the age of 7 years mainly lie:
At an average age of 3 years, the child can usually
• Stage 1: Punishment orientation—rules are
understand a request containing three parts.
obeyed in order to avoid punishment.
• Stage 2: Reward orientation—rules are con-
formed to in order to be rewarded.
5.6.2 Environmental Influences and
Communicative Competence 5.7.1.2 Conventional Morality (Level II)
Bilingual home This is the level at which most moral judgements of
Being brought up in a home in which two languages children lie by the age of 13 years:
are spoken is not a disadvantage unless there is another
• Stage 3: Good-boy/good-girl orientation—
cause of slowed language development.
rules are conformed to in order to avoid the dis-
Family size approval of others.
Larger family size is associated with slower speech • Stage 4: Authority orientation—laws and social
development. rules are upheld in order to avoid the censure of
authorities and because of guilt about not doing
Pregnancy
one’s duty.
Intrauterine growth retardation is associated with
slower language development. 5.7.1.3 Postconventional Morality (Level III)
Prolonged second stage labour is associated with This level, which may never be reached even in adult-
slower language development. hood, requires individuals to have achieved the later
Sex stages of Piaget’s formal operational stage:
Early language development in girls is slightly greater
• Stage 5: Social contract orientation—actions
than in boys.
are guided by principles generally agreed to be
Social class essential for public welfare. These principles are
Being middle class is associated with relatively faster upheld in order to maintain the respect of peers
language development. and self-respect.
• Stage 6: Ethical principle orientation—actions • 6–8 Months: Fear of heights begins and becomes
are guided by principles chosen by oneself, usu- worse when walking starts.
ally emphasizing dignity, equality, and justice. • 3–5 Years: Common fears are those of animals,
These principles are upheld in order to avoid the dark, and ‘monsters’.
self-condemnation. • 6–11 Years: Fear of shameful social situations
(such as ridicule) begins.
• Adolescence: Fear of death, failure, social gath-
5.7.2 Relationship to the Development erings (such as parties), and thermonuclear war
of Social Perspective Taking may be particularly evident.
Social perspective taking is the ability to take the per-
spective of others. It is a skill that may be seen at the
following levels: 5.8.3 Possible Etiological and Maintenance
Mechanisms
• Perceptual role taking—the ability to take into 5.8.3.1 Unconscious Conflict
account how a perceptual array appears to
Sigmund Freud (1926/1959) suggested that psychologi-
another person when their perspective differs
cal anxiety is a signal phenomenon and that neurotic
from that of oneself
anxiety starts as the remembrance of realistic anxiety/
• Cognitive role taking—the ability to take into
fear related to a real danger. Each stage of life was con-
account the thoughts of another person when
sidered to have age-appropriate determinants of anxiety/
they differ from those of oneself
fear, including, with increasing age
• Affective role taking—the ability to take into
account the feelings of another person when
they differ from those of oneself • Fear of birth
• Fear of separation from the mother
In addition to being necessary to being able to empathize • Fear of castration
with others, social perspective taking was considered by • Fear of the superego—fear of its anger or
Kohlberg as being necessary to develop higher stages of punishment
moral reasoning. • Fear of the superego—fear of its loss of love
• Fear of the superego—fear of death
5.8 DEVELOPMENT OF FEARS IN 5.8.3.2 Learned Response

CHILDHOOD AND ADOLESCENCE Fear/anxiety may become associated with particular situ-
ations by means of learning.
5.8.1 Definition
Fear is an unpleasant emotional state (a feeling of
5.8.3.3 Lack of Control
apprehension, tension, or uneasiness) caused by a real-
istic current or impending danger that is recognized Fear/anxiety may occur when an individual feels helpless
at a conscious level. It differs from anxiety in that in in a situation beyond his or her control.
the latter the cause is vague or not as understandable.
However, fear and anxiety are terms that are often used
interchangeably. 5.9 SEXUAL DEVELOPMENT
5.9.1 Sex Determination
5.8.2 Development with Age
Sex determination is primarily as a result of the sex chro-
The types of fear that develop in childhood and adoles- mosomes (XX female and XY male). Gonad formation is
cence differ with age (Marks, 1987): first indicated in the embryo by the appearance of an area
of thickened epithelium on the medial aspect of the meso-
• 6 Months: Fear of novel stimuli begins nephric ridge during week 5. Factors affecting subsequent
(such as fear of strangers), reaching a peak at differentiation of the genital organs into male ones (epi-
18 months–2 years. didymis, ductus [vas] deferens, ejaculatory ducts, penis,
and scrotum) or female ones (fallopian tubes, uterus, cli- 5.9.2.2 Onset in Girls
toris, and vagina) during ontogeny include the following: In 95%, onset occurs between 9 and 13 years. The first sign is
• Y chromosome—in mammals, testis determi- • Breast formation—in 80%

nation is under the control of the testis-deter- • Pubic hair growth—in 20%
mining factor borne by the Y chromosome.
SRY, a gene cloned from the sex-determining In Western countries, menarche occurs at a mean age of
region of the human Y chromosome, has been 13.5 years.
equated with the testis-determining factor in
humans. 5.9.2.3 Onset in Boys
• Degree of ripeness of the ovum at fertiliza- In 95%, onset occurs between 9.5 and 13.5 years. The
tion—overripeness of the ovum at fertilization first sign is usually testicular and scrotal enlargement,
is associated with a reduced number of primor- followed by growth of the penis and pubic hair. On aver-
dial germ cells. This in turn leads to a masculin- age, the first ejaculation occurs at around 13 years.
izing effect on genetic females.
• Endocrine actions—androgens and oestrogens 5.9.2.4 Physiological Changes
can modify the process of sexual differentia- A raising of the threshold for gonadohypothalamic nega-
tion, while in twin pregnancy with fetuses of tive feedback precedes the onset of puberty. An increase
opposite sex and anastomosed placental circu- in suprarenal androgen release (adrenarche) usually
lations, the genetically male fetus may have a begins between the ages of 6 and 8 years; these hormones
masculinizing effect on the genetically female lead to the growth of sexual hair and skeletal maturation.
fetus. A genetically female fetus may also be
masculinized (and be born with either ambigu-
ous or male genitalia) by fetal androgen from 5.9.3 Gender Identity
another source (e.g. in congenital adrenal This is an individual’s perception and self-awareness with
[suprarenal] hyperplasia). Similarly, a geneti- respect to gender. It is usually established by the age of 3 or
cally male fetus with a Y chromosome and tes- 4 years and usually remains firmly established thereafter.
tes may develop female genitalia in the absence
of fetal androgen (e.g. in enzyme deficiency) or
if androgen receptors are defective (e.g. in tes-
5.9.4 Gender/Sex Typing
ticular feminization). This is the process by which individuals acquire a sense
of gender and gender-related cultural traits appropriate to
the society and age into which they are born. It usually
5.9.2 Changes at Puberty begins at an early age with male and female infants being
treated differently, for example, with respect to the choice
Puberty consists of a series of physical and physiological
of their clothing.
changes that convert a child into an adult who is capable
of sexual reproduction.
5.9.5 Gender Role
5.9.2.1 Physical Changes This is the type of behaviour that an individual engages
These include in that identifies him or her as being male or female, for
example, with respect to the type of clothes worn and
• Growth spurt the use of cosmetics.
• Change in body proportion
• Development of sexual organs 5.9.6 Sexual Behaviour
• Development of secondary sexual characteristics
5.9.6.1 Sexual Drive
Tanner described a standardized system for recording This is the need to achieve sexual pleasure through geni-
breast, pubic hair, and genital maturation. An example tal stimulation. It exists from birth to middle childhood
of a Tanner growth chart for height for boys is shown in and increases again during adolescence as a result of
Figure 5.1. increased androgen secretion.
cm
190 97
90
180 75
50
25
170
Longitudinal 97 10
50 3
standards 3
160
150 Limits for 97

single occasions
(cross-sectional) 3
140
130
Boys (height)
120
110
100
90
80 5+
Penis 4+
stage 3+
2+
70 97 90 75 50 25 10 3
5+
Pubic hair 4+
stage 3+
2+
60 97 90 75 50 25 10 3
Testes 12 mL
vol. 4 mL
97 90 75 50 25 10 3
50
1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19
Age (years)
FIGURE 5.1 Example of Tanner growth chart for height. A series of charts of longitudinal growth standards for physical
development (including parameters for height, weight, skin folds) were developed for children according to age, sex, and sexual
maturity. (From Tanner, J.M. and Whitehouse, R.H., Arch. Dis. Child., 51, 170, 1976.)
5.9.6.2 Childhood Sexuality 5.9.7 Sexual Orientation

This may manifest itself in normal children as This is the erotic attraction that an individual feels. Its
shaping is a developmental process associated with
• Sex play in infancy certain patterns of childhood experience and activ-
• Erections in boys ity. Superimposed on this, there are arguments for and
• Vaginal lubrication in girls against the theory that human sexual orientation is bio-
• Masturbation—which may involve orgasm logically determined.
• Exploratory encounters with other children
5.9.6.3 Masturbation 5.9.7.1 Homosexuality

This is the predominant mode of sexual expression for most This term is associated with the following behavioural
adolescent males and probably fewer adolescent females. dimensions:
• Sexual fantasy homosexual men. No differences were found

• Sexual activity between the groups in the volumes of INAH 1,
• Sense of identity 2, or 4. As had been previously reported, INAH
• Social role 3 was found to be more than twice as large in
the heterosexual men as in the women. It was
The first of these is the most important dimension in also, however, more than twice as large in the
assessing homosexual orientation. If present, it does not heterosexual men as in the homosexual men.
necessarily imply sexual activity with others, as in indi- This finding indicates that INAH is dimorphic
viduals who are homosexual in orientation and celibate. with sexual orientation, at least in men. A sec-
It should be noted that there is no nonhuman mam- ond neuroanatomical difference was reported
malian species in which predominant or exclusive homo- by Allen and Gorski (1992): On the basis of the
sexuality occurs in the way it does in humans. examination of 90 postmortem brains, it was
found that the midsagittal plane of the anterior
commissure in homosexual men was 18% larger
5.9.7.2 Modern Arguments in Favour than in heterosexual women and 34% larger
of Biological Determinism than in heterosexual men. This finding of a dif-
• Endocrine. On the basis of rat and human experi- ference in a structure not known to be related
ments, Dorner (1986, 1989) has hypothesized that to reproductive functions supports the hypoth-
21-hydroxylase deficiency represents a genetic pre- esis that factors operating early in development
disposition to female homosexuality in heterozy- differentiate sexually dimorphic structures and
gous forms (homozygous forms lead to congenital functions of the brain in a global fashion.
adrenal hyperplasia), while in males 21-hydroxy- • Genetic. Bailey and Pillard (1991) found evi-
lase deficiency and/or prenatal stress leads to an dence of heritability of homosexuality in a
overall inhibition in the effects of androgen on study of monozygotic and dizygotic twins.
brain differentiation and to male homosexuality. Homosexual male probands with monozygotic
Among their experiments on humans, Dorner et co-twins, dizygotic co-twins, or adoptive broth-
al. studied the effects of oestrogen infusion on LH ers were recruited. Of the relatives whose sex-
secretion and reported that in contrast to hetero- ual orientation could be rated, 52% (29/56) of
sexual men, homosexual men manifest a positive monozygotic co-twins, 22% (12/54) of dizygotic
oestrogen feedback effect on LH secretion, which co-twins, and 11% (6/57) of adoptive brothers
was said to provide evidence that homosexual were homosexual. Childhood gender nonconfor-
men have a predominantly female-differentiated mity did not appear to be an indicator of genetic
brain. Furthermore, as a result of ACTH provo- loading for homosexuality. In a second genetic
cation tests on the suprarenal (adrenal) glands, study, Hamer et al. (1993) reported a linkage
Dorner reported that female homosexuals display between DNA markers on the X chromosome
significantly increased ratios of 17a-hydroxypro- and male sexual orientation. Pedigree and link-
gesterone/cortisol and androstenedione/cortisol age analyses on 114 families of homosexual men
after ACTH stimulation compared with female were carried out. Increased rates of homosexual
heterosexual control subjects. orientation were found in the maternal uncles
• Neuroanatomical. LeVay (1991) reported histo- and male cousins of these subjects but not in
logical differences in the interstitial nuclei of the their fathers or paternal relatives, suggesting
anterior hypothalamus (INAH) between homo- the possibility of sex-linked transmission in a
sexual and heterosexual men, suggesting that portion of the population. DNA linkage analy-
sexual orientation may be mediated by the cen- sis of a selected group of 40 families in which
tral nervous system. The anterior hypothalamus there were two gay brothers and no indication of
of the brain is known to participate in the regu- nonmaternal transmission revealed a correlation
lation of male-typical sexual behaviour. The vol- between homosexual orientation and the inheri-
umes of four cell groups in this region (INAH tance of polymorphic markers on the X chro-
1, 2, 3, and 4) were measured in postmortem mosome in approximately 64% of the sib-pairs
tissue from three subject groups: women, men tested. The linkage to markers on Xq28 had a
who were presumed to be heterosexual, and multipoint lod score of 4.0.
5.9.7.3 Arguments against Biological Determinism 5.10.1 Conflict with Parents and Authority
• Endocrine. Gooren et al. (1990) have argued Theories of why conflict between adolescents and par-
that oestrogen feedback cannot be used to assess ents and other authority figures often occurs include
the status of brain differentiation in primates in
the same way as it can in the rat. For example, • Cognitive developmental models
sexual differentiation of the control of LH secre- • Erikson’s stages of psychosocial development
tion occurs in the mouse, hamster, and guinea • Ethological and sociobiological models
pig but not in primates. Among their experi- • Social-learning theory
ments on humans, Gooren et al. studied directly • Equity theory
the control of LH secretion in homosexuals • Separation–individuation
and transsexuals compared with heterosexuals.
Following oestrogen exposure, the response of 5.10.1.1 Cognitive Developmental Models
LH to LHRH was not positive in male homo- The adolescent has newly acquired powers of hypotheti-
sexuals, transsexuals, and heterosexuals; it was cal reasoning that enable him or her to consider and artic-
positive in female homosexuals, transsexuals ulate alternatives to the status quo.
(prior to treatment), and heterosexuals; more-
over, a positive LH response to oestrogen infu- 5.10.1.2 Erikson’s Stages of Psychosocial
sion in homosexual men was not found. Development
• Neuroanatomical. LeVay (1991) pointed out that
In his fifth psychosocial developmental stage (identity vs.
his sample contained no homosexual women and
role confusion), Erikson considered adolescence to be a
that AIDS patients may constitute an unrepre-
time of identity formation during which the individual
sentative sample of homosexual men. Moreover,
pursues personal autonomy. This pursuit is associated
some presumed heterosexual men had relatively
with the potential for conflict with parents and other
small INAH 3 nuclei (within the homosexual
authority figures.
range), and some presumed homosexual men had
relatively large INAH 3 nuclei (within the het-
5.10.1.3 Ethological and Sociobiological Models
erosexual range). The effect might have resulted
from AIDS (although there was no effect of Conflict at the time of pubertal changes is considered to
AIDS on the volume of the three other INAH be adaptive, prompting the individual to spend more time
nuclei examined and the size difference in INAH with his or her peers. It forms part of the status realign-
3 was present when the homosexual men were ments of entry into adulthood.
compared with heterosexual AIDS patients).
5.10.1.4 Social-Learning Theory
• Genetic. King (1993) has pointed out that the
result of Hamer et al. (1993) is preliminary. Adolescents may be considered to have experienced
Their evidence is based on a small, highly vicarious exposure to problem-solving occurring via con-
selected group of homosexual men. The result is flict. Witnessing their parents giving in to their children’s
purely statistical. The gene is hypothetical and conflicting demands may be considered to provide inter-
has not been cloned, and the linkage has been mittent reinforcement to the children.
observed in only one series of families.
5.10.1.5 Equity Theory
According to equity theory, the preferred relationships,
5.10 ADOLESCENCE
particularly those of an intimate nature, between any
Adolescence is a time of transitions, representing a devel- two given people are those in which each feels that
opmental phase between middle childhood/latency and the cost–benefit ratio of the relationship for each per-
adulthood, but its boundaries are difficult to demarcate son is approximately equal. It has been argued that
clearly. In his model of cognitive development, Piaget the amount of emotional investment of both the ado-
viewed adolescence as the final, formal operational stage lescent and the parent(s) in their relationship means
of development; the adolescent has a greater capacity to they both want to preserve it. As the adolescent pur-
focus on himself or herself. sues autonomy, this can lead to occasional conflicts,
The pubertal changes of adolescence have been con- but these are usually not fervent enough to destroy the
sidered earlier. relationship.
5.10.1.6 Separation–Individuation 5.10.3 Normal and Abnormal

It has been argued that adolescence can be considered Adolescent Development
to represent a second separation–individuation phase,
in which continued biological, motor, and social devel- 5.10.3.1 Offer and Offer
opments now allow the adolescent to move away from Offer and Offer (1975) identified the following three
a dependent relationship with the parent(s) to take his adolescent developmental routes (the percentages given
or her own place in society. However, social and psy- are those of the sample of adolescents they studied; the
chological pulls towards dependency mean that the remaining 21% could not be classified easily but were
separation–individuation may entail ambivalence and closer to the first two categories than to the third one):
conflict.
• Continuous growth (23%). Eriksonian intimacy
was achieved, and shame and guilt could be
displayed. Major separation, death, and severe
5.10.2 Affective Stability and ‘Turmoil’
illness were less frequent. Their parents encour-
Successive developments in the psychological understand- aged independence.
ing of affective stability and ‘turmoil’ in adolescence have • Surgent growth (35%). The adolescents in this
been provided by Anna Freud, Erikson, and Offer and group were ‘late bloomers’. They were more likely
Offer. than the first group to have frequent depressive
and anxious moments. Although often success-
ful, they were less introspective and not as action
5.10.2.1 Anna Freud oriented as the first group. There were more areas
A rapid oscillation between excess and asceticism during of disagreement with their parents.
adolescence was described by Anna Freud (1936/1946). • Tumultuous growth (21%). Recurrent self-doubt
Affective instability and behaviour swings were consid- and conflict with their families occurred in this
ered to be caused by group. Their backgrounds were less stable than
in the first two groups. The arts, humanities, and
• The drives stimulated by sexual maturity social sciences were preferred to professional
• Pubertal endocrine changes and business careers.
• Instability of the newly stressed defences of the
5.10.3.2 Block and Haan
ego against these drives
Block and Haan (1971) used factor analysis to isolate the
following groups among a cohort of 84 male adolescents
5.10.2.2 Erikson studied longitudinally to adulthood:
Erikson (1959) characterized adolescence as manifesting
• Ego-resilient adolescents
‘adolescent turmoil’ and a maladaptive, temporary state
• Belated adjustors—similar to the surgent group
of ‘identity diffusion’, which he implied all adolescents
of Offer and Offer
passed through.
• Vulnerable overcontrollers
• Anomic extroverts—less inner life and rela-
5.10.2.3 Offer and Offer tively uncertain values
• Unsettled undercontrollers—given to impulsivity
Offer and Offer (1975) showed that, in general, adoles-
cence is a time of less turmoil and upheaval than previ- A similar cohort of 86 females was divided into
ously thought. They studied a cohort of American males
who had been aged 14 years in 1962. Sixty-one of these • Female prototype
adolescents were studied intensively and followed up • Cognitive type—individuals tend to be intellec-
into adulthood. They came mainly from intact families, tualized in the way problems are negotiated
and there were no serious drug problems or major delin- • Hyperfeminine repressors—similar to hysteri-
quent activity. Seventy-four per cent went to college dur- cal personality disorder
ing the 1 year after high school graduation. They showed • Dominating narcissists
no significant difference in basic values from that of • Vulnerable undercontrollers
their parents. • Lonely independents
5.11 ADAPTATIONS IN ADULT LIFE Christian, and Islamic communities) and very low in oth-
ers (such as Australia, New Zealand, North America,
5.11.1 Pairing South America, and Scandinavia—excluding their tradi-
Even in Western countries, it appears that there are a num- tional observant religious groups) (Buss et al., 1990).
ber of constraints that govern the choice of mate in much
5.11.1.7 Cross-Cultural Constancies
the same way as elders or parents do in arranged marriages.
Across cultures, men prefer mates who are physically
5.11.1.1 Homogamous Mate Selection attractive, while women prefer mates who show ambi-
tion, industriousness, and other signs of earning power
Pairing tends to occur within the same socioeconomic,
potential (Buss et al., 1990).
religious, and cultural group (Eshelman, 1985).
5.11.1.2 Reinforcement Theory 5.11.2 Parenting

People are attracted to those who reinforce the attrac- Parenting is a complex, dyadic process that is influenced
tion with rewards. This process is a reciprocal one with by a range of factors, including
rewards also passing in the opposite direction and further
reinforcing the interpersonal attraction (Newcomb, 1956). • Cultural beliefs of the parent about child rearing
(Maccoby and Martin, 1983)
5.11.1.3 Social Exchange Theory • Genetic-temperamental characteristics of the
People have a preference for relationships that appear to parent (i.e. genetic factors influencing the provi-
offer an optimum cost–benefit ratio—maximum benefits sion of parenting) (Perusse et al., 1994)
such as love with minimum costs such as time spent with • Genetic-temperamental characteristics of the
each other (Homans, 1961). child (i.e. genetic factors influencing the elicita-
tion of parenting) (Bell, 1968)
5.11.1.4 Equity Theory
As mentioned earlier, this is a modification of the social Furthermore, reporting bias is likely, with parents stress-
exchange theory in which the preferred relationships, ing the similarity with which they treat their children and
particularly of an intimate nature, between two people children emphasizing the differences in parental treat-
are those in which each feels that the cost–benefit ratio ment that they perceive (Plomin et al., 1994).
of the relationship for each person is approximately equal Abusive parenting is a strong predictor of later psy-
(Hatfield et al., 1978). chopathology. On the other hand, parental warmth and
support buffers children against externalizing and anti-
5.11.1.5 Matching Hypothesis social behaviour (Hetherington and Clingempeel, 1992)
According to this hypothesis, heterosexual pairing tends and is positively associated with a child’s self-esteem
to occur in such a way that, although ideally a person (Bell and Bell, 1983).
would prefer to pair with the most attractive people
(Huston, 1973), in practice individuals seek to pair with 5.11.3 Grief, Mourning, and Bereavement
others who have a similar level of physical attractiveness
rather than the most attractive (Berscheid and Walster, 5.11.3.1 Definitions
1974). This is felt by the individual to lead to a greater • Grief—those psychological and emotional pro-
probability of acceptance by the other person, a lower cesses, expressed both internally and externally,
probability of rejection, and a lower probability of losing that accompany bereavement.
the partner to another person in the future. • Mourning—those culture-bound social and cog-
nitive processes through which one must pass in
5.11.1.6 Cultural Differences order that grief is resolved, allowing one to return
People in Asian and African countries tend to value home- to more normal functioning; it is often used, less
keeping potential and a desire for home and children in strictly, as being synonymous with grief.
mate selection, while people in Western countries tend to • Bereavement—a term that can apply to any loss
value love, character, and emotional maturity. Chastity event, from the loss of a relative by death to
is rated very highly in some countries (such as India and unemployment, divorce, or loss of a pet; it refers
China) and cultures (such as orthodox/traditional Jewish, to being in the state of mourning.
5.11.3.2 Normal Grief c. A recognized medical disease

The symptomatology of normal grief may include the d. Alteration in relationship to friends and
following: relatives
e. Furious hostility against specific persons
• Initial shock and disbelief—‘a feeling of f. Loss of affectivity
numbness’. g. A lasting loss of patterns of social interaction
• Increasing awareness of the loss is associated h. Activities attain a colouring detrimental to
with painful emotions of sadness and anger. social and economic existence
• Anger may be denied. i. Agitated depression
• Irritability.
• Somatic distress—may include sleep disturbance, 5.11.3.5 Differentiating between Bereavement
early morning waking, tearfulness, loss of appe- and a Depressive Episode
tite, weight loss, loss of libido, and anhedonia.
The diagnosis of major depressive disorder in DSM-
• Identification phenomena—the mannerisms and
IV-TR is generally not given unless the symptoms are
characteristics of the deceased may be taken on.
still present 2 months after the loss. However, the pres-
In 1944, Lindemann read to the centenary meeting of the ence of certain symptoms that are not characteristic of
American Psychiatric Association the results of his study a normal grief reaction may be helpful in differentiating
of 101 bereaved individuals, many of whom had lost bereavement from a major depressive episode:
loved ones in the tragic Cocoanut Grove nightclub fire
in Boston, MA. He identified the following five points as • Guilt about things other than actions taken
being pathognomonic of acute grief: or not taken by the survivor at the time of the
death
• Somatic distress • Thoughts of death other than the survivor feel-
• Preoccupation with the image of the deceased ing that he or she would be better off dead or
• Guilt should have died with the deceased person
• Hostile reactions • Morbid preoccupation with worthlessness
• Loss of patterns of conduct • Marked psychomotor retardation
• Prolonged and marked functional impairment
Note that grief is not seen in babies if a parent/caregiver • Hallucinatory experiences other than thinking
dies prior to the development of attachment behaviour. that he or she hears the voice of, or transiently
sees the image of, the deceased person
5.11.3.3 Bereavement
Parkes described the following five stages of Freud (1917/1957) differentiated between normal grief and
bereavement: the depressive response by the presence of shame and guilt
in the latter. Yearning for the lost object was considered
• Alarm to be part of the normal response to loss. It was overcome
• Numbness gradually as the mental representation was decathected.
• Pining for the deceased—illusions or hallucina-
tions of the deceased may occur
• Depression 5.12 NORMAL AGEING
• Recovery and reorganization 5.12.1 Physical Aspects
5.11.3.4 Morbid Grief Reactions 5.12.1.1 Health
Lindemann described the following morbid grief reactions: In general, most elderly people in Western countries
enjoy good health, in spite of the changes that occur in
1. Delay of reaction body systems with increasing age.
2. Distorted reactions—subclassified into
a. Overactivity without a sense of loss 5.12.1.2 Cerebral Changes
b. The acquisition of symptoms belonging to Blessed et al. (1968) found no histological evidence of
the last illness of the deceased dementia in the brains of 28 nondemented individuals.
Evidence of cerebral atrophy was absent or slight in the The presumed universal decline in adult intelligence
majority, and brain mass and ventricular size did not dif- is at best a methodological artifact and at worst a
fer significantly from those of younger adults (Tomlinson popular misunderstanding of the relation between
et al., 1968). Terry and Hanson (1988) found that the individual development and sociocultural change…
the major finding…in the area of intellectual function-
neuronal loss per unit volume of the normal brain in the
ing is the demolishing of [the belief in] serious intel-
elderly was much less than that previously reported. lectual decrement in the aged.
5.12.2 Social Aspects Although the elderly do not generally perform as well

as younger subjects on cognitive tasks dependent on
5.12.2.1 Stereotyping processing speed, old age is not necessarily associated
Old age is generally a stigmatized period. For instance, with a large decline in intellectual ability (Durkin, 1995).
people are complimented for looking younger than their Reasons for this include the following:
chronological age.
• Different abilities contribute to intellectual behav-
5.12.2.2 Empty Nest Syndrome iour, so that a reduction in one (e.g. processing
Prior to the onset of old age, parents usually witness their speed) may be compensated for by an increase in
children leaving home, particularly in Western coun- another (such as experience-based judgement).
tries. The difficulties some parents encounter on being • Cross-sectional comparisons of different age
left on their own have been described as the empty nest groups may confound age differences with
syndrome. cohort effects.
• Changes in performance with age may be offset
by practice.
5.12.3 Ego Integrity versus Despair • Crystallized intelligence (the ability to store
This is Erikson’s eighth and final stage of psychosocial and manipulate learned information) increases
development, occurring in old age. through adulthood and often remains high into
old age.
5.12.3.1 Ego Integrity
Successful resolution of the psychosocial crisis of this
age leads to an integrated view of one’s life, its meaning, 5.13 DEATH AND DYING
its achievements (both for the self and others, including
5.13.1 Definitions
future generations), and the ways in which difficulties
were coped with. There is an acceptance of one’s mortal- 5.13.1.1 Timely Death
ity, a feeling that one’s life has been lived in a satisfactory This refers to the situation in which the expected life
way, and a readiness to face death. expectancy is approximately equal to the actual length
of time lived.
5.12.3.2 Despair
The alternative is despair, both on reflection of how life 5.13.1.2 Untimely Death
has been lived and the way in which others have been
This refers to the situation in which the actual length
treated and also on looking to the future and the sense
of time lived is significantly less than the expected life
of transience that is felt on facing the end of life. Rather
expectancy, as a result of one of the following:
than having a sense of contentment and completion, there
is despair at the prospect of death.
• Premature death at a young age
• Sudden unexpected death
5.12.4 Cognitive Aspects • Violent/accidental death
Prior to the late 1960s, it was generally believed that the
normal ageing brain degenerates and that this is accom- 5.13.1.3 Unintended Death
panied by intellectual deterioration. By the 1970s, this This refers to the situation in which death is unintended,
view had been challenged on the basis of new research. usually occurring as a result of pathological processes or
Thus, Schaie (1974) wrote: trauma.
5.13.1.4 Intended Death Bell DC and Bell LG. 1983: Parental validation and support in
the development of adolescent daughters. In Grotevant
This refers to the situation in which death is intended by
HD (ed.) Adolescent Development in the Family,
the deceased, who played a part in his or her suicide. pp. 27–41. San Francisco, CA: Jossey Bass.
Berscheid E and Walster E. 1974: Physical attractiveness. In
5.13.1.5 Subintended Death Berkowitz L (ed.) Advances in Experimental Social
This refers to the situation in which the deceased may Psychology, pp. 285–290. New York: Academic Press.
have manifested an unconscious desire to bring about Blessed G, Tomlinson BE, and Roth M. 1968: The association
his or her death, for example, by facilitating the onset of between quantitative measures of dementia and of senile
death through psychoactive substance abuse. change in the cerebral grey matter of elderly subjects.
British Journal of Psychiatry 114:797–811.
Block J and Haan N. 1971: Lives Through Time. Berkeley, CA:
5.13.2 Impending Death Bancroft Books.
Bowlby J. 1969: Attachment and Loss, Vol. 1: Attachment. New
If it is believed that one’s death is near, an individual York: Basic Books.
may pass through the following five stages that are simi- Buss DM et al. 1990: International preferences in selecting
lar to those recognized as occurring in the terminally ill mates: A study of 37 cultures. Journal of Cross-Cultural
(Kübler-Ross, 1969): Psychology 21:5–47.
Caspi A and Silva PA. 1995: Temperamental qualities at
• Shock and denial—the diagnosis may be dis- age three predict personality traits in young adult-
believed and another opinion sought; this first hood: Longitudinal evidence from a birth cohort. Child
stage may never be passed. Development 66:486–498.
Chess S and Thomas A. 1984: Origins and Evolution of
• Anger—the person may be angry and wonder
Behavior Disorders: From Infancy to Early Adult Life.
why this has happened to him or her. New York: Brunner/Mazel.
• Bargaining—the person may, for example, try Cosentino CE, Meyer-Bahlburg HFI, Nat DR et al. 1995: Sexual
to negotiate with God. behavior problems and psychopathology symptoms in
• Depression—the symptomatology of a depres- sexually abused girls. Journal of the American Academy of
sive episode is manifested. Child and Adolescent Psychiatry 34:1033–1042.
• Acceptance—the person may finally come to Dorner G. 1986: Hormone-dependent brain development and
preventative medicine. Monographs in Neural Sciences
terms with his or her mortality and understand
12:17–27.
the inevitability of death. Dorner G. 1989: Hormone-dependent brain development and
neuroendocrine prophylaxis. Experimental and Clinical
Endocrinology 94:4–22.
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6 Description and Measurement
6.1 DESCRIPTION program, a scientific calculator with a (pseudo)

random number generator, or a table of random
6.1.1 Types of Data numbers, can be used to choose every nth mem-
6.1.1.1 Qualitative ber of the population.
• Stratified random sampling—a given popula-
Qualitative variables refer to attributes that can be
tion is stratified before random samples are cho-
categorized such that the categories do not have a numer-
sen from each stratum. This can be useful when
ical relationship with each other, for example, eye colour.
studying a disease that varies with respect to sex
6.1.1.2 Quantitative and age, for example.
Quantitative variables refer to numerically represented
data. These can be of the following types: 6.1.4 Frequency Distributions
• Discrete quantitative variables—can only take 6.1.4.1 Frequency Distribution

on known fixed values, for example, the number This is a systematic way of arranging data, with frequen-
of new patients seen each week in a psychiatric cies being given for categories of a qualitative or quanti-
outpatient department tative variable. For continuous quantitative variables, the
• Continuous quantitative variables—can only categories should be contiguous and mutually exclusive
take on any value in a defined range, for exam- and are known as class intervals.
ple, the height of psychiatric inpatients
6.1.4.2 Frequency Table
This is a frequency distribution arranged in the form of
6.1.2 Scales of Measurement a table, with the first column giving contiguous mutually
Table 6.1 summarizes the properties of different types of exclusive values (which may be class intervals) of a vari-
measurement scale. able and the adjoining column giving the corresponding
frequencies.
6.1.3 Sampling Methods 6.1.4.3 Relative Frequency

6.1.3.1 Simple Random Sampling The relative frequency of a category/class interval/vari-
able is the proportion of the total frequency correspond-
A simple random sample is one chosen from a given pop-
ing to that category/class interval/variable:
ulation such that every possible sample of the same size
has the same probability of being chosen.
Frequency of category
Relative frequency =
6.1.3.2 Systematic Sampling Total frequency
This type of sampling saves time and effort. Common
examples include the following: 6.1.4.4 Cumulative Frequency
The cumulative frequency of a given value of a variable is
• Periodic sampling—very nth member of the the total frequency up to that value.
population is chosen. This may not always lead
to a random choice because of an unforeseen 6.1.4.5 Cumulative Frequency Table
underlying pattern. This is a cumulative frequency distribution arranged in
• Using random numbers—using random num- the form of a table, with the first column giving contigu-
bers can be a better method than periodic sam- ous mutually exclusive values (which may be class inter-
pling for ensuring random choice. Random vals) of a variable and the adjoining column giving the
numbers, obtained, for example, from a computer corresponding cumulative frequencies.
83
TABLE 6.1
Types of Measurement Scale
Property Nominal Ordinal Interval Ratio
Categories mutually exclusive ✓ ✓ ✓ ✓
Categories logically ordered ✓ ✓ ✓
Equal distance between adjacent categories ✓ ✓
True zero point ✓
Source: Reproduced from Puri, B.K., Statistics for the Health Sciences, WB Saunders,
London, U.K., 1996. With permission.
6.1.4.6 Cumulative Relative Frequency 6.1.5.4 Poisson Distribution

The cumulative relative frequency of a given value of a The Poisson distribution, Poisson (μ), is the probability
variable is the total relative frequency up to that value. distribution for a discrete infinite variable (range = 0, 1,
2, …), where μ = np:
6.1.4.7 Cumulative Relative Frequency Table
Mean = µ
This is a cumulative relative frequency distribution
arranged in the form of a table, with the first column Variance = µ
giving contiguous mutually exclusive values (which
may be class intervals) of a variable and the adjoining The Poisson distribution can be used in situations in
column giving the corresponding cumulative relative which the following criteria are fulfilled:
frequencies.
• Events occur randomly in time or space (length,
area, or volume).
6.1.5 Discrete Probability Distributions • The events are independent (i.e. the outcome of
any given event does not affect the outcome of
6.1.5.1 Bernoulli Trial any other).
This is a trial or experiment having two and only two • Two or more events cannot take place
alternative outcomes. simultaneously.
• The mean number of events per given unit of
6.1.5.2 Bernoulli Distribution time or space is constant.
This is the probability distribution for a discrete binary
variable (range = 0, 1), which is a special case of the 6.1.6 Continuous Probability Distributions
binomial distribution B(1, p), where p is the probability
of ‘success’: 6.1.6.1 Normal Distribution
The normal (or Gaussian) distribution, N (μ, σ2), is the prob-
Mean = p ability distribution for a continuous variable (range = ∞):
Variance = p (1 − p) Mean = µ
Variance = σ2
6.1.5.3 Binomial Distribution
The binomial distribution, B(n, p), is the probability distri- Properties of the normal distribution probability density
bution for a discrete finite variable (range = 0, 1, 2, …, n): function curve include the following:
Mean = np • It is unimodal.
• It is continuous.
Variance = np (1 − p) • It is symmetrical about its mean.
Description and Measurement 85
–1.96σ +1.96σ
95% of values
–2.58σ +2.58σ
99% of values
Standard deviation
–4σ –3σ –2σ –1σ 0 +1σ +2σ +3σ +4σ
from mean
Cumulative % 0.1% 2.3% 15.9% 50% 84.1% 97.7% 99.9%
z-scores –4.0 –3.0 –2.0 –1.0 0 +1.0 +2.0 +3.0 +4.0
t-scores 20 30 40 50 60 70 80
FIGURE 6.1 Normal or Gaussian distribution. (From Stahl, D. and Leese, M., Research methods and statistics, in Puri, B.K. and
Treasaden, I.H. (eds.), Psychiatry: An Evidence-Based Text, Hodder Arnold, London, U.K., 2010, pp. 34–71.)
• Its mean, median, and mode are all equal. For N (μ, σ2), the two-tailed 5% points are given by
• The area under the curve is one.
• The curve tends to zero as the variable moves in µ −1.96σ
either direction from the mean (Figure 6.1).
µ +1.96σ
The interval one standard deviation either side of the
mean of the probability density function of a normal dis-
tribution encloses 68.27% of the total area under the curve. 6.1.6.2 t Distribution
The interval two standard deviations either side of the When n < 30, the t distribution, t(ν) or tν, is used in mak-
mean of the probability density function of a normal dis- ing inferences about the mean of a normal population
tribution encloses 95.45% of the total area under the curve. when its variance is unknown. The t distribution is sym-
The interval three standard deviations either side of the metrical about the mean but has longer tails than the nor-
mean of the probability density function of a normal dis- mal distribution.
tribution encloses 99.73% of the total area under the curve. ν is the number of degrees of freedom and is given by
If X ∼ N (μ, σ2), then the standard normal variate Z is
given by ν = n −1
( X − µ) For n ≥ 30, t(ν) ≈ N (0, 1).

Z=
σ
For Z ∼ N (0, 1) 6.1.6.3 χ2 Distribution

The chi-squared distribution with ν degrees of freedom,
Mean = 0 χ2(ν), is obtained from the sum of the squares of ν inde-
pendent variables, Z1 to Z ν, where each Z ∼ N (0, 1):
Variance = 1 If W = ∑ Z i2 , where i = 1 to ν, and Zi ∼ N (0, 1),
The cumulative distribution function, P(Z < z), is given then W ∼ χ2(ν)
by Φ(z). The chi-squared distribution is asymmetrical.
6.1.6.4 F Distribution • The 9 deciles split the distribution into 10 equal

The F distribution is related to the χ2 distribution and is parts.
asymmetrical. A given F distribution is described in terms • The 99 percentiles split the distribution into
of ν1 and ν2, each of which gives a number of degrees of 100 equal parts.
freedom. This is usually abbreviated to F(ν1, ν2).
The kth quantile of n observations ranked in increasing
order from the first to the nth is calculated by interpolating
6.1.7 Summary Statistics: Measures of Location between the two observations adjacent to the qth, where q
is given by
6.1.7.1 Measures of Central Tendency
k (n + 1)
The (arithmetic) mean (or average) of a sample with n q=
items (x1, x2, x3,… xn), x, is given by Q
Σx
x= where Q is the number of groups into which the quantiles
n divide the distribution.
The population mean, μ, of a population of size N is given 6.1.8 Summary Statistics: Measures of Dispersion
by
6.1.8.1 Range
Σx The range is the difference between the smallest and
µ=
N largest values in a distribution:
The arithmetic mean is suitable for use with data mea- Range = (Largest value) − (Smallest value)
sured on at least an interval scale. A major disadvantage
is that it can be unduly influenced by an extreme value. It can be used with data that are measured on at least an
The median is the middle value of a set of observations interval scale.
ranked in order. If the number of observations is odd,
Median = Middle value 6.1.8.2 Measures Relating to Quantiles
The most commonly used measures relating to quantiles
If the number of observations is even,
include
Median = Arithmetic mean of the two middle values
• The interquartile range = the difference between
The median is suitable for use with data measured on at the third and first quartiles
least an ordinal scale. It gives a better measure of cen- • The semiquartile range = half the interquartile
tral tendency than the mean for skewed (asymmetrical) range
distributions. • The 10–90 percentile range = the difference
The mode of a distribution is the value of the obser- between the 90th and 10th (per)centiles, or
vation occurring most frequently. The category/interval equivalently, between the ninth and first deciles
occurring most frequently is the modal category. It can • The interdecile range = the difference between
be used with all measurement scales. the 90th and 10th (per)centiles, or equivalently,
between the ninth and first deciles
6.1.7.2 Quantiles
Quantiles are cutoff points that split a continuous distri- The median and interquartile or 10–90 percentile range
bution into equal groups. They include the following: can be more useful summary statistics than the mean and
standard deviation for skewed distributions.
• The median splits a distribution into 2 equal
parts.
• The 3 quartiles split the distribution into 4 equal 6.1.8.3 Standard Deviation
parts. The standard deviation of a distribution is based on devi-
• The 4 quintiles split the distribution into 5 equal ations from the mean and has the same units as the origi-
parts. nal observations.
For a population of size N and mean μ, the population 3. A clear heading/caption or reference in the
standard deviation, σ, is given by accompanying text.
4. The units for both axes are clearly stated.
∑ ( x − µ) 2 5. The scales for both axes are given; these may,

Population standard deviation, σ = for example, be
N a. Linear
b. Logarithmic
For a sample of size n and mean x, the sample standard c. Broken (which can be represented by a
deviation, s, is given by break in the axis)
6.1.9.3 Linear Relationship

Sample standard deviation, s =
∑(x − x ) 2
If the graph of variable y against variable x is a straight
n −1 line, these variables are related by the equation
y = mx + c
The standard deviation can be used for data measured on
at least an interval scale.
in which m and c are constants:
6.1.8.4 Variance
• m is the gradient of the line.
The variance is the square of the standard deviation and • c is the intercept of the line on the vertical axis
has units that are the square of those of the observations. (y-axis).
For a population of size N and mean μ, the population
variance, σ2, is given by
6.1.9.4 Power Law Relationship
If the graph of y against x is a straight line, where
Population variance, σ 2
=
∑ ( x − µ) 2
N y = logY
For a sample of size n and mean x, the sample variance, x = logX

s2, is given by
(the logarithm is to any base, so long as it is the same one in
Sample variance, s 2 =
∑(x − x ) 2 both cases), then variables X and Y are related by the equation
n −1 Y = CX m
The variance can be used for data measured on at least in which m and C are constants such that
an interval scale. • m is the gradient of the line
• log C is the intercept of the line on the vertical
6.1.9 Graphs axis (y-axis)
6.1.9.1 Definition 6.1.9.5 Exponential Relationship

The graph of a function f is the set of points (x, f(x)). If the graph of y against x is a straight line, where
6.1.9.2 Drawing Graphs y = lnY

A properly drawn graph should have the following
x=X
properties:
(lnY is the logarithm of Y to base e, i.e. loge Y),
1. Clearly labelled axes. then variables X and Y are related by the equation
2. The independent variable is usually represented
on the horizontal axis. Y = Ce mx
in which m and C are constants such that 6.1.11 Stem-and-Leaf Plots

• m is the gradient of the line Stem-and-leaf plots can be used to represent a continu-
• lnC is the intercept of the line on the vertical ous variable. Their advantage over histograms is that
axis (y-axis) they allow the representation of all the individual data.
The stems consist of a vertical column of numbers on
This exponential relationship also holds if the left-hand side of the plot. The leaves are numbers to
the right of the stems, which may, for example, represent
• e is replaced by 10 tenths. All the individual data can then be derived by
• lnY is replaced by log10 Y combining the individual leaves with their correspond-
• lnC is replaced by log10 C ing stems, while the shape of the overall plot indicates
the shape of the distribution. They are particularly easy
6.1.9.6 Other Relationships Involving Expressions to represent in computer printouts. For instance, the dis-
If the graph of y against x is a straight line, where tribution 13.5, 13.7, 14.5, 14.6, 14.6, 14.7, 15.2, 15.9, and
16.4 (arbitrary units) may be represented as the following
y = g (Y ) stem-and-leaf plot:
x = f (X)
13 57
14 5667
(f(X) is an expression involving X and g(Y) is an expres-
15 29
sion involving Y), then variables X and Y are related by
16 4
the equation
g (Y ) = mf ( X ) + c 6.1.12 Boxplots (Box-and-Whisker Plots)

in which m and c are constants: Boxplots (box-and-whisker plots) can be used to rep-
resent a continuous variable. A boxplot consists of
• m is the gradient of the line. a box whose longer sides are placed vertically, with
• c is the intercept of the line on the vertical axis vertical lines (whiskers) extending vertically. Boxplots
(y-axis). for two differently distributed samples are shown in
Figure 6.2.
The boxplot has the following features:
6.1.10 Outliers
Outliers are extreme values. • The upper boundary of the box is the upper
(third) quartile.
6.1.10.1 Measures of Central Tendency • The lower boundary of the box is the lower
Outliers can exert an extreme effect on the arithmetic (first) quartile.
mean, particularly when the total number of values is • The length of the box is the interquartile range.
small. The median is less affected in such a case and may • A thick horizontal line inside the box is the
therefore be preferred. median (second quartile).
• The lower whisker extends to the smallest obser-
6.1.10.2 Measures of Dispersion vation, excluding outliers.
Outliers exert an extreme effect on the range. Measures • The upper whisker extends to the largest obser-
relating to quantiles are less affected in such a case and may vation, excluding outliers.
therefore be preferred. Since it takes into account all the • Outliers are indicated by the symbol O.
values in a distribution, the standard deviation (or variance)
may be affected by outliers, although less so than the range. The earlier arrangement is sometimes represented hor-
izontally (the whole plot being rotated through −π/2)
6.1.10.3 Correlation and Linear Regression if more convenient. Boxplots can be useful for com-
Outliers may exert an extreme effect on the results of cor- paring two or more sets of observations diagrammati-
relation and linear regression. In such cases, it may be nec- cally, before or in addition to more formal statistical
essary to consider excluding outliers from the calculations. analyses.
120
120 10
110
110
Frequency
IQ score
100
IQ score
5
100
90
90
0 80
80 90 100 110 120 80 90 100 110 120
80 IQ score Inverse normal
800
800 20
600
Duration (days)
15
600
Frequency
400
Duration (days)
10
400 200
5 0
200
–200
0
0 200 400 600 800 –200 0 200 400
0
Duration (days) Inverse normal
FIGURE 6.2 Boxplots for two differently distributed samples. (From Stahl, D. and Leese, M., Research methods and statistics, in Puri,
B.K. and Treasaden, I.H. (eds.), Psychiatry: An Evidence-Based Text, Hodder Arnold, London, U.K., 2010, pp. 34–71.)
6.1.13 Scatter Plot (Scattergrams, Scatter is plotted. The two variables can then be compared
Diagrams, or Dot Graphs) diagrammatically, before or in addition to more formal
statistical analyses. Figure 6.3 shows a scatter plot for
Scatter plots can be used to represent two continuous a dataset, with a superimposed linear regression line of
variables. Two orthogonal axes divide 2D space into a best fit.
coordinate system, in which each pair of observations
25
Residual
20
15
Equation of line: y = –20 + 0.5x
10
10 12 14 16 18 20
Knowledge before training
Knowledge after training Fitted values
FIGURE 6.3 Scatter plot showing linear regression line. (From Stahl, D. and Leese, M., Research methods and statistics, in
Puri, B.K. and Treasaden, I.H. (eds.), Psychiatry: An Evidence-Based Text, Hodder Arnold, London, U.K., 2010, pp. 34–71.)
6.2 PRINCIPLES OF MEASUREMENT 6.2.6 Norm Referencing

6.2.1 Interviews A norm is an average, common, or standard performance
under specified conditions. A test may be standardized
Sources of error include the following: to this norm.
• Response set—the tendency always to agree or
to disagree with the questions asked. 6.2.7 Criterion Referencing
• Bias towards the centre—the tendency always to A criterion is a set of scores against which the success of
avoid extreme responses. As a result, there is an a predictive test can be compared.
excess choice of middle responses.
• Extreme responding—the opposite tendency of
selecting extreme responses. 6.3 INTELLIGENCE
• Social desirability—the choice of responses that 6.3.1 Aptitude
the subject believes the interviewer desires. May
be reduced through the inclusion of lie scales or This is the raw or potential ability of an individual.
the forced-choice technique.
• Defensiveness—the subject avoids giving too 6.3.2 Attainment
much self-related information.
• Halo effect—the observer allows his or her pre- This is the result of learning.
conception to influence the responses.
• Hawthorne effect—interviewer alters the situa- 6.3.3 Components of Intelligence
tion by their presence.
Charles Spearman, who discovered factor analysis, put
forward the notion that all individuals possess, to varying
6.2.2 Self-Predictions extents, general abilities; this general intelligence factor
A direct method of measuring behaviour in which the is known as g. The main determinant of intelligence test
subject is asked to give their own prediction concerning scores was held to be g by Spearman (1904).
the behaviour under question. It can be combined with A separate component of intelligence comprised spe-
self-recording. cific abilities, known as s. Different intelligence subtests
were held to index different s factors.
Overall, a person would be considered bright (high
6.2.3 Psychophysiological Techniques g factor) or not-so-bright (low g factor), but their actual
overall intelligence would be comprised as follows:
These involve the direct use of physiological measure-
ments in assessing behaviour.
Intelligence = g + (Sum of the magnitudes
of the various s factors)
6.2.4 Naturalistic Observations
These involve the assessment of behaviour as it occurs For example, arithmetic performance would be a func-
with minimum interference by the observer. In time-sam- tion of g plus the individual’s aptitude for arithmetic
pling techniques, the subject is observed during given (specific s).
time intervals at given times of the day or night. Louis Thurstone (1938) criticized Spearman’s g and
Naturalistic observations are used in the functional instead suggested that intelligence consisted of several
analysis of problem behaviours. This method is some- primary abilities. On the basis of the factor analysis of
times referred as ABC (for antecedents, behaviours, and a large database of intelligence test scores, he found
consequences). the following seven primary abilities (Thurstone and
Thurstone, 1963):
6.2.5 Scaling
• Verbal comprehension
This refers to the conversion of raw data into types of • Word fluency
scores more readily understood, for example, ranks, (per) • Number
centiles, and standardized scores. • Space
• Memory • Information (particularly related to that derived

• Perceptual speed from culture, such as being able to name the
• Reasoning Prime Minister of the United Kingdom or the
President of the United States of America)
6.3.4 Mental Age Scale • Comprehension (including questions evaluating
the subject’s ability to explain the meaning of
The concept of the mental age (MA) was devised by conventions and proverbs)
Binet as the average intellectual ability, as measured by
the level of problem-solving and reasoning. The scale The PRI is derived from the following five tests:
was devised such that the average range of scores cor-
responds to the chronological age (CA). • Block design
For children with a higher than average level of intel- • Matrix reasoning (solving nonverbal abstract
ligence, MA > CA. In contrast, for children with a lower problems)
than average level of intelligence, MA < CA. • Visual puzzles
The Stanford–Binet test can be applied to each year, • Picture completion
up to the age of 15 years. Its reliability and validity are • Figure weights
acceptable.
The WMI is derived from the following three tests:
6.3.5 Intelligence Quotient
• Digit span
This is the ratio of the MA to the CA, expressed as a • Arithmetic
percentage: • Letter–number sequencing
 MA  The PSI is derived from the following three tests:

IQ =   × 100
 CA 
• Symbol search
By convention, intelligence has a normal distribution • Coding (tests visuomotor coordination)
with a mean of 100 and a standard deviation of 15. • Cancellation
There is a natural decline in intellectual ability with
age. Performance IQ falls off with age more quickly The general ability index (GAI) is derived from the VCI and
than verbal IQ—the verbal–performance discrepancy. PRI. The full scale IQ (FSIQ) is derived from the VCI, PRI,
This decline is taken into account when raw scores are WMI, and PSI. The FSIQ follows a normal (Gaussian) dis-
converted into IQ equivalents. Thus, although raw abili- tribution with a mean of 100 and a standard deviation of 15.
ties decline with age, measured IQ remains constant.
6.3.7 Wechsler Intelligence Scale
6.3.6 Wechsler Adult Intelligence Scale for Children: Revised
The Wechsler Adult Intelligence Scale (WAIS)-IV was This is a modified version of the WAIS for children
released in 2008 and allows the following four index between the ages of 5 and 15 years.
scores to be derived:
6.3.8 Wechsler Preschool and Primary
• Verbal comprehension index (VCI) Scale of Intelligence
• Perceptual reasoning index (PRI) This is a modified version of the WAIS for children
• Working memory index (WMI) between the ages of 4 and 6 years and 6 months.
• Processing speed index (PSI)
6.3.9 Group Ability Tests
The VCI is derived from the following four tests:
Unlike the aforementioned, these can be used by one
• Similarities (assesses abstract verbal reasoning) examiner to assess the intellectual ability and aptitude
• Vocabulary (the subject is asked to give the of a group of people, for example, the Armed Services
meaning of words) Vocational Aptitude Battery (ASVAB).
6.3.10 Nature–Nurture • Lateral Dominance Examination—a laterality

examination.
Potential intelligence (aptitude) is inherited, but envi- • (Seashore) Rhythm Test—assesses the ability to
ronmental factors influence the fulfillment of potential discriminate nonverbal auditory stimuli.
(attainment). • Speech-Sounds Perception Test (SSPT)—the
subject is asked to match a spoken sound
6.3.11 Cultural Influences (from a recording) to the correct choice
among similar printed sounds; tests for
Tests of attainment can give rise to discrepant results when focused attention.
applied to people from different cultures. It is thought that • Tactile Form Recognition Test—tests tactile
tests measuring aptitude are less prone to such influences. perception and therefore parietal lobe function-
ing; the total time required to perform this test is
a good screen for brain impairment.
6.4 TECHNIQUES USED IN
• Tactile Performance Test (TPT)—involves tac-
NEUROPSYCHOLOGICAL ASSESSMENT tile form discrimination, kinesthesis, upper limb
6.4.1 Comprehensive Test Batteries movement coordination, manual dexterity, an
appreciation of spatial configuration, and tactile
6.4.1.1 Halstead–Reitan Battery memory.
This comprehensive test battery can detect damage to the • Trail Making Test—see succeeding text.
brain and whether such damage is
Data from the HRB, particularly from the Finger-Tapping
• Lateralized—and, if so, to which hemisphere it Test and TPT, can help differentiate frontal from non-
is lateralized frontal involvement.
• Associated with an acute or chronic disorder
• Focal or diffuse
6.4.1.2 Luria–Nebraska
The Halstead–Reitan Battery (HRB) is available in the Neuropsychological Battery
following three age-related versions, for This test battery is designed for use in individuals aged
15 years and older. It may typically take between 1½ h and
• Adults (aged 15 years and older) 2½ h to administer, depending on the subject’s condition.
• Older children (aged between 9 and 14 years) The administration does not have to be in one sitting; it
• Young children (aged between 5 and 8 years) can be broken down into a series of short administrations.
It is suitable for bedside use.
The core test procedures of the Halstead–Reitan The Luria–Nebraska neuropsychological battery
Neuropsychological Test Battery include the following: (LNNB) assesses a wide range of functions on
• Aphasia Test—naming common objects; • Clinical scales

spelling simple words; identifying individual • Localization scales
numbers and letters; reading, writing, enun- • Optional scales
ciating, and understanding spoken language; • Summary scales
identifying body parts; calculating simple
arithmetic problems; differentiating between The clinical scales assess
right and left; and copying simple geometric
shapes. • Motor functions
• Category Test—testing for learning, cogni- • Rhythm
tive flexibility, and the ability to form abstract • Tactile functions
concepts. • Visual functions
• Finger-Tapping Test—the subject taps as many • Receptive speech
times as possible over 10 trial intervals. • Expressive speech
• Fingertip Number-Writing Perception Test—a • Writing
tactile perception test. • Reading
• Arithmetic • List recognition

• Memory • Story recall
• Intellectual processes • Figure recall
• Intermediate memory (in the second of two
forms of the LNNB) These scores can be used to calculate a variety of
indices.
The localization scales assess
6.4.2 Language Tests
• Left frontal functioning
• Left sensorimotor functioning 6.4.2.1 Boston Diagnostic Aphasia
• Left parieto-occipital functioning Examination, 3rd Edition
• Left temporal functioning The Boston Diagnostic Aphasia Examination, 3rd Edition
• Right frontal functioning (BDAE-3) is a test battery for the assessment of aphasic
• Right sensorimotor functioning syndromes in adults (Goodglass et al., 2000). The short
• Right parieto-occipital functioning form takes around 35–45 min to administer. The long
• Right temporal functioning version contains 34 subtests and may take up to 4 h to
administer. The BDAE-3 tests the following domains:
The optional scales assess
1. Auditory comprehension
• Spelling a. Word discrimination
• Motor writing b. Body-part identification
c. Complex ideational material
The summary scales are 2. Oral expression
a. Verbal and nonverbal agility
• Pathognomonic—containing items best dis- b. Automatized sequences
criminating those with brain impairment from c. Recitation
those without d. Repetition
• Left hemisphere e. Word reading
• Right hemisphere f. Responsive naming
• Profile elevation g. Animal naming
• Impairment h. Visual confrontation naming
i. Oral sentence reading
Furthermore, 28 factor analysis-derived scales may 3. Written language comprehension
reflect more specific cognitive and sensory functions. a. Symbolic and word discrimination
b. Phonetic association
6.4.1.3 Repeatable Battery for the Assessment
c. Word–picture matching
of Neuropsychological Status d. Reading sentences and paragraphs
The repeatable battery for the assessment of neuropsy- 4. Writing
chological status (RBANS) can be used to test the neuro- a. Writing mechanics
psychological status of adults aged from 20 to 89 years. b. Written symbol recall
It takes approximately half an hour to administer. It gives c. Written word finding
scores on the following subtests: d. Written formulation
• List learning
• Story memory 6.4.2.2 Boston Naming Test
• Figure copy In the second edition of this language test, the subject is
• Line orientation asked to name 60 line drawings (Goodglass and Kaplan,
• Picture naming 2001). Adults are supposed to start at item number and
• Semantic fluency progress towards item 60 unless a mistake is made in
• Digit span the first 8 items (from 30 to 37) in which case the test
• Coding is proceeded with in the reverse order until the subject
• List recall correctly responds to 8 consecutive items.
6.4.2.3 Graded Naming Test The last four of these tests are concerned with spatial
In this language test, the subject is asked to name 30 line perception.
drawings (McKenna and Warrington, 1983).
6.4.3.3 Behavioural Inattention Test
6.4.2.4 Token Test This battery tests for unilateral visual neglect (Wilson
A number of tokens, such as differently coloured rectangles et al., 1987). The first six tests deal with visual neglect in
and circular discs, are used in this test. The subject is asked the usual way:
to carry out progressively more complicated verbal instruc-
tions using these tokens (De Renzi and Vignolo, 1962). • Line crossing
The Token Test is sensitive to minor impairment in lan- • Letter cancellation
guage comprehension, and performance tends to be more • Star cancellation
impaired in aphasia than in patients who are nonaphasic. • Figure copying and shape copying
• Line bisection
• Free drawing (clock, person, butterfly)
6.4.2.5 Speed and Capacity of
Language Processing Test
These are followed by nine behavioural tests:
The Speed and Capacity of Language Processing Test
(Baddeley et al., 1992) consists of two parts. The first • Picture scanning
part is the Speed of Comprehension Test, in which the • Telephone dialling
subject is asked to decide, as quickly as possible, whether • Menu reading
each of a series of statements is true/sensible or false/ • Article reading
not sensible (silly). The second part is the Spot-the-Word • Clock face—telling the time and setting the time
Test, in which 60 pairings of words with nonwords are • Coin sorting
presented and the subject must decide which of each pair, • Address copying and sentence copying
in turn, is a real word. The Spot-the-Word Test controls • Map navigation
for poor verbal skills and has been found to give a robust • Card sorting
estimate of verbal intelligence and therefore premorbid
intelligence. (In this respect, it is rather like the NART.) These nine behavioural tests include tasks that are activi-
ties of daily living and so help in rehabilitation assessments.
6.4.3 Perception Tests
6.4.3.1 Bender–Gestalt Test/Bender 6.4.4 Memory Tests
Visual Motor Gestalt Test 6.4.4.1 Benton Visual Retention Test
The subject is asked to copy nine designs in this test In the fifth edition of this visual recall test, the subject is
(Bender, 1938, 1946). serially presented with 10 designs, which he or she has
to reproduce from memory (Sivan, 1992). It may be used
6.4.3.2 Visual Object and Space in subjects aged 8 years and over. Fifteen–twenty min
Perception Battery may typically be required for administration, followed by
This battery tests visual perception (Warrington and another 5 min for scoring. It may be used to test for brain
James, 1991) and consists of the following nine tests: damage and early cognitive decline.
6.4.4.2 Graham–Kendall Memory for Designs Test

• Screening test for visual impairment
• Incomplete letters This is another visual recall test in which the subject is
• Silhouettes asked to draw from immediate recall designs that are pre-
• Object decision sented for 5 s each (Graham and Kendall, 1960).
• Progressive silhouettes
• Dot counting 6.4.4.3 Rey–Osterrieth Test
• Position discrimination In this visual memory test, the subject is presented with a
• Number location complex design. The subject is asked to copy this design,
• Cube analysis and then, 40 min later, without previous notification that this
will occur, the subject is asked to draw the same design again 6.4.4.9 Wechsler Memory Scale-IV
from memory (Rey, 1941; Osterrieth, 1944). Nondominant The fourth edition of the Wechsler Memory Scale,
temporal lobe damage can lead to impaired performance on WMS-IV, was released in 2009. It is a memory test bat-
this test, whereas domain temporal lobe damage tends not to tery that contains the following subtests:
(but is associated with verbal memory difficulties).
• Spatial addition
6.4.4.4 Paired Associate Learning Tests • Symbol span
In these tests, the subject is given paired associates to • Design memory
learn and then must respond appropriately (e.g. by stat- • General cognitive screener
ing the paired word) when the first, stimulus, words are • Temporal orientation
given. Different forms of these tests, of varying difficulty, • Mental control
have been produced (e.g. Inglis, 1959; Isaacs and Walkey, • Clock drawing
1964). These tests may be used to assess memory disor- • Memory
der in old age, independently of verbal intelligence. • Inhibitory control
• Verbal productivity
6.4.4.5 Synonym Learning Test • Logical memory
This is a modified version of the Walton–Black Modified • Verbal paired associates
Word Learning Test, specifically for use in the differential • Visual reproduction
diagnosis of dementia from depression in the elderly (par-
6.4.4.10 Rivermead Behavioural Memory Test
ticularly if combined with the Digit Copying Test). In the
Synonym Learning Test, 10 words with which the subject This is another memory test battery (Wilson, 1987;
is not familiar are first identified and then the subject is Wilson et al., 1991). It lays emphasis on tests that are
asked to learn their meanings (Kendrick et al., 1965). related to skills required in daily living. The subtests of
the Rivermead Behavioural Memory Test include
6.4.4.6 Object Learning Test
• Orientation—for time, date, and place
This test has similar aims to those of the Synonym Learning • Name recall—of a forename and surname asso-
Test but is less stressful to take for elderly patients. As ciated with a given photograph
with the Synonym Learning Test, the results of the Object • Picture recognition
Learning Test combined with those of the Digit Copying • Face recognition
Test can aid in the differential diagnosis of dementia from • Story recall—immediate recall and recall after
depression in the elderly. In the Object Learning Test, the a quarter of an hour
subject is exposed to drawings of familiar items on sections • Route memory
of cards and asked to recall them (Kendrick et al., 1979). • Prospective memory
6.4.4.7 Rey Auditory Verbal Learning Test 6.4.4.11 Adult Memory and Information
This is a word list learning test involving 5 presentations Processing Battery
of a list containing 15 words, which the subject is asked This is also a memory test battery (Coughlan and Hollows,
to recall. The same then occurs with a second list of 15 1985). It contains the following four memory subtests:
words. Finally, the subject is asked to recall words from
the first list, both immediately after completing the sec- • Short story recall
ond recall task (involving the second list) and some time • Figure copy and recall
later (say, after 30 min). Information is obtained about • List learning
immediate recall, learning curve, primacy and recency • Design learning
effects, and learning strategies used.
The Adult Memory and Information Processing Battery also
6.4.4.8 California Verbal Learning Test
contains the following two information-processing tests:
This is a word list learning test involving 16 words from
4 known categories. As with the Rey Auditory Verbal • Number cancellation
Learning Test, the California Verbal Learning Test gives • Digit cancellation
information about immediate recall, learning curve, and
learning strategies used. The norms used in this battery are age stratified.
6.4.5 Intelligence Tests answer is ‘green’.) Again, the score is the total number
of words correctly named in the 2 min period. Finally, a
6.4.5.1 WAIS and Similar Tests card constructed in a similar way to that used for the sec-
The intelligence tests based on the WAIS are considered ond part of the test is again presented to the subject, and
earlier in Section 6.3.3. this time they are asked to name the colour in which each
word is printed and to ignore the actual colour names
6.4.5.2 National Adult Reading Test printed. This is the Stroop interference test. For instance,
The National Adult Reading Test or NART (Nelson and if green is printed in blue the first time it occurs and then
McKenna, 1975; Nelson, 1982) is a reading test consisting in red the second time, then the correct answers for these
of phonetically irregular words that have to be read aloud two occasions would be ‘blue’ and ‘red’ and not ‘green’
by the subject. If a patient suffers deterioration in intel- and ‘green’.
lectual abilities, their premorbid vocabulary may remain This tests the (Stroop) interference that may occur
less affected (or unaffected). The NART can therefore be between reading words and naming colours (Stroop,
used to estimate the premorbid IQ. 1935; Trenerry et al., 1989; Lezak, 1995). Left (domi-
nant) frontal lobe lesions are associated with poor perfor-
6.4.5.3 Raven’s Progressive Matrices mance on the Stroop test. The anterior cingulate cortex
This test of nonverbal intelligence consists of a series is particularly involved in carrying out this test (Pardo
of printed designs from each of which a part is missing et al., 1990). However, activation of the anterior cingulate
(Raven, 1958, 1982). The subject is required correctly to cortex does not invariably accompany the interference
choose the missing part for each design from the alterna- task. Another region of the brain that appears to be asso-
tives offered. The test requires the perception of relations ciated with this task is the left inferior precentral sulcus
between abstract items. (at the border between the inferior frontal gyrus, the pars
opercularis, and the ventral premotor area); this region
6.4.6 Executive Function (Frontal Lobe) Tests appears to be involved with the mediation of competing
articulatory demands during the interference condition of
6.4.6.1 Stroop the Stroop test (Mead et al., 2002).
There exist several types of Stroop test. A typical Stroop
test involves asking a subject is given a card containing 6.4.6.2 Verbal Fluency
columns of colour names, printed in black on white, and A typical verbal fluency test involves asking the subject to
asked to read aloud as many of the words as possible in articulate as many words as possible, during 2 min inter-
2 min. The words might be in columns, as follows: vals, starting with the letters F, A, and S, in turn. Proper
nouns (such as the name Forsythe) and derivatives such
Red Green Blue Green as plurals and different verb endings are not allowed to
Blue Tan Red Green count together with the root words. For instance, one can-
… … … … not count both ‘font’ and ‘fonts’ or ‘float’ and ‘floated’
and ‘floating’. The score is the total number of allowable
The correct answer to this part of the test, with the subject words achieved. Verbal fluency is impaired in left (domi-
reading across rows, would be ‘red, green, blue, green, nant) frontal lobe lesions.
blue, tan, red, green, …’. The score is the total number of
words correctly named in the 2 min period. This part of 6.4.6.3 Tower of London Test
the test checks that the patient is capable of following the The Tower of London Test (Shallice, 1982) is based on
directions and of reading such words (in the given print the Tower of Hanoi game and test planning. The subject
size) out aloud. In the second part of the test, a similar is asked to move coloured discs of varying sizes between
card of columns of words is presented to the subject and three columns, either using a model or via a computer
the same instructions of reading out what the words say program (preferably with a touch screen), in order to
are given. This time, however, the words are not in black achieve a given result. Left frontal lobe lesions are asso-
but instead are printed in different colours. These colours ciated with poor performance on this test.
are those described by some of the words but such that
no given word is printed in its own colour. For example, 6.4.6.4 Wisconsin Card Sort Test
green may be printed in blue the first time it occurs and The Wisconsin Card Sort Test consists of a number of cards
then in red the second time. (In each case, the correct (64 in the original and 24 in the Modified Wisconsin Card
Sort Test) that contain different shapes (circles, crosses, On the paper are a number (say, 25) of circles, each
stars, and triangles). Other variables include the num- labelled with a different number (from 1 to 25, say). The
ber of shapes on a card and the colour of the shapes on a subject is asked to draw a trail, as quickly as possible,
given card (there are four possible colours for each card). that passes through all the circles, starting with the low-
Following the presentation of index cards, the subject has to est numbered one (say, 1) and ending with the highest
sort the remaining cards corresponding to the index cards. number (25, say). In the second part of the test (Trail B),
They are not given the variable(s) by means of which this both numbers and letters are contained in the circles, and
sorting should occur but are told if they are right or wrong this time the subject is asked to draw a trail, as quickly as
each time. For instance, the first indexing variable might possible, that passes through all the circles, starting with
be colour. After a certain number of consecutive correct the lowest numbered one (say, one) and then passing to
responses, the rule suddenly changes, without the subject the circle with the lowest letter (A, say) and continuing to
being warned in advance. These days, this test is more con- alternate between number and letter in increasing order,
veniently administered via a computer program, preferably ending with the highest number and highest letter. So the
using a touch screen. The Wisconsin Card Sort Test picks up two trails should be between circles labelled as follows:
perseverative errors (such as continuing for too long to sort
Trail A: 1 → 2 → 3 → 4 → …
cards by number, well after the indexing rule has changed
Trail B: 1 → A → 2 → B → 3 → C → …
to colour) and nonperseverative errors. Poor performance
on this task is particularly associated with dysfunction of The Trail Making Test tests the following abilities:
the left dorsolateral (pre-) frontal cortex.
• Sequencing
6.4.6.5 Cognitive Estimates Test • Cognitive flexibility
In the absence of a reduction of intelligence quotient • Visual scanning
(IQ), some frontal lobe-damaged patients may give out- • Spatial analysis
rageously incorrect cognitive estimates of commonly • Motor control
known phenomena. For instance, asked to estimate the • Alertness
length of an adult elephant, such a patient might venture • Concentration
a reply of 100 yards. This abnormality is exploited in the Difficulties with cognitive flexibility or with complex
Cognitive Estimates Test, in which the subject is asked conceptual tracking may manifest as much longer times
to give a series of cognitive estimates, such as estimating being required for Trail B than would be expected from
the height of the average man. the Trail A time score.
6.4.6.6 Six Elements Test
This is a strategy application test that attempts to uncover 6.4.7 Personality Tests
evidence of the organizational difficulty that may occur Personality inventories have been considered in Chapter 3.
as a result of frontal lobe damage. The subject is asked to Here, psychometric methods of assessing personality are
carry out six different tasks (in two groups of three) dur- summarized.
ing a quarter of an hour. In order to maximize their score,
the subject needs adequately to plan and schedule these 6.4.7.1 Objective Tests
tasks while also monitoring the time that has elapsed. The items presented have limited responses. Objective
tests include the following:
6.4.6.7 Multiple Errands Task
This is another strategy application test that attempts to • 16PF (Sixteen Personality Factor Questionnaire)
uncover evidence of the organizational difficulty that —see Chapter 3.
may occur as a result of frontal lobe damage. It is rather • MMPI (Minnesota Multiphasic Personality
more difficult than the Six Elements Test. The subject is Inventory)—see Chapter 3.
asked to carry out multiple errands, usually in a shopping • CPI (California Psychological Inventory)—see
centre that is not known to them. Chapter 3.
• EPQ (Eysenck Personality Questionnaire)—this
6.4.6.8 Trail Making Test contains 90 items in true/false format. Subjects
There are two parts to this test (Trail A and Trail B). In are rated on the following dimensions: extraver-
the first part, a piece of paper is presented to the subject. sion, introversion, and neuroticism
• HDHQ (Hostility and Direction of Hostility 6.4.8.2 Cambridge Neuropsychological

Questionnaire)—this is used to measure relation- Test Automated Battery
ships that could be affected by personality status. The Cambridge Neuropsychological Test Automated
Battery or CANTAB is an automated computerized bat-
In general, because of evidence that mental state markedly tery that offers sensitive and specific cognitive assessment,
affects scoring of questionnaires, they have been replaced preferably using a touch screen. The standard CANTAB
by interview schedules and other observer ratings. consists of the following 13 computerized tasks:
6.4.7.2 Projective Tests
• Motor screening—this screening task is admin-
The presented items have no one correct answer, instead istered before the other tasks and introduces the
taking the form of ambiguous stimuli, upon which the subject to the touch screen and checks that the
subject projects their personality. Their reliability and subject can touch this properly and that he or
validity have not been established. Examples include the she can hear, comprehend, and follow instruc-
tions appropriately.
• Rorschach Inkblot Test • Big/little circle—this tests that a subject can fol-
• Thematic Apperception Test (TAT) low an explicit instructional rule and that he or
• Sentence Completion Test (SCT) she can then reverse this rule.
• Delayed matching to sample.
6.4.8 Dementia Tests and Related Tests • ID/ED shift—this tests the ability to attend to
specific attributes of compound stimuli and then
6.4.8.1 Mini-Mental State Examination
to shift that attention as required.
The Mini-Mental State Examination or MMSE (Folstein • Matching to sample visual search—this is a
et al., 1975) is a brief test that can be routinely used rap- speed/accuracy trade-off visual search task.
idly to detect possible dementia, to estimate the severity of • Paired associates learning—this delayed response
cognitive impairment, and to follow the course of cognitive procedure tests list memory and then list learning
changes over time. It can be used to differentiate between (or visuospatial conditional learning).
delirium and dementia (Anthony et al., 1982). The combi- • Pattern recognition memory.
nation of cognitive testing and an informant questionnaire • Rapid visual information processing—this tests
has not been found to result in any advantage over the use vigilance (sustained attention) and working
of the MMSE alone in screening for dementia (Knafelc memory.
et al., 2003). The MMSE includes the following assessments: • Reaction time.
• Spatial recognition memory.
• Orientation • Spatial span—this tests spatial memory span.
• Attention—serial subtraction or spelling a word • Spatial working memory—this tests both spatial
(such as ‘world’ backward) working memory and strategy performance.
• Immediate recall • Stockings of Cambridge—this has replaced
• Short-term memory the Tower of London test in earlier versions of
• Naming common objects CANTAB and is somewhat similar to the Tower
• Following simple verbal commands of London test described earlier.
• Following simple written commands
• Writing a sentence spontaneously
• Copying a figure 6.4.8.3 Gresham Ward Questionnaire
In the Gresham Ward Questionnaire (Post, 1965), ques-
The total score that may be achieved is 30. Age and tions are asked that cover the following abilities:
MMSE scores appear to be inversely related, from
a median of 29 for Americans aged between 18 and • Orientation in time
24 years to a median of 25 in those aged over 80 years. • Orientation in place
A total MMSE score of less than 24 tends to be consid- • Memory for past personal events
ered as indicating cognitive impairment, in the absence • Memory for recent personal events
of any other cause for such a low score (such as no more • General information
than 4 years of schooling or learning disability). • Topographical orientation
6.4.8.4 Blessed’s Dementia Scale The assessment also includes a brief physical and neu-
This questionnaire (Blessed et al., 1968) is adminis- rological examination and recording the results of
tered to a relative or friend of the subject who is asked to investigations.
answer the questions on the basis of performance over the
previous 6 months. There are three sets of questions. The 6.4.8.8 Crichton Geriatric Behaviour Rating Scale
first set deals with activities of daily living such as This is a retrospective nursing-rated assessment.
• Ability to cope with small sums of money 6.4.8.9 Clifton Assessment Schedule
• Ability to remember a short list of items such as This is also a nursing-rated assessment.
a shopping list
• Ability to find their way indoors 6.4.8.10 Stockton Geriatric Rating Scale
• Ability to find their way around familiar streets This is also a nursing-rated assessment.
• Ability to grasp situations or explanations
• Ability to recall recent events 6.4.8.11 Present Behavioural Examination
• Tendency to dwell in the past The Present Behavioural Examination or PBE involves
The second set of questions deals with further activities interviewing carers and rates psychopathological and
of daily living including behavioural changes in dementia.
• Ability to feed oneself 6.4.8.12 Manchester and Oxford Universities

• Ability to dress oneself Scale for the Psychopathological
• Level of incontinence, if any Assessment of Dementia
The third set of questions is concerned with changes in The Manchester and Oxford Universities Scale for
the Psychopathological Assessment of Dementia or
• Personality MOUSEPAD also involves interviewing carers and rates
• Interest psychopathological and behavioural changes in dementia.
• Drive
6.4.8.13 Sandoz Clinical Assessment
6.4.8.5 Information–Memory–Concentration Test
The Sandoz Clinical Assessment—Geriatric or SCAG
This is a relatively straightforward set of questions that consists of 18 symptom areas and an overall global
may be tried even by those with medium to severe levels assessment, each being rated on a seven-point scale (from
of dementia. zero, not present, to seven, severe) (Shader et al., 1974):
6.4.8.6 Geriatric Mental State Schedule
• Mood depression
The Geriatric Mental State Schedule or GMS is a semi-
• Confusion
structured interview that assesses the subject’s mental state.
• Mental alertness
6.4.8.7 Cambridge Examination for • Motivation initiative
Mental Disorders • Irritability
• Hostility
The Cambridge Examination for Mental Disorders of the
• Bothersome
Elderly or CAMDEX is an interview schedule consisting
• Indifference to surroundings
of three sections (Roth et al., 1986, 1988):
• Unsociability
• A structured clinical interview with the patient • Uncooperativeness
to obtain systematic information about the • Emotional liability
present state, past history, and family history. • Fatigue
• A range of objective cognitive tests that constitute • Self-care
a mini-neuropsychological battery, known as the • Appetite
CAMCOG (Cambridge Cognitive Examination). • Dizziness
• A structured interview with a relative or other • Anxiety
informant to obtain independent information • Impairment of recent memory
about the respondent’s present state, past his- • Disorientation
tory, and family history. • Overall impression of the patient
6.4.8.14 Vineland Social Maturity Scale Isaacs B and Walkey FA. 1964: A simplified paired-associate
test for elderly hospital patients. British Journal of
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7 Cognitive Assessment and
Neuropsychological Processes
7.1 MEMORY 7.2 AMNESIA

7.1.1 Sensory Memory Amnesia is defined as the inability to recall past experi-
ence or the loss of memory (Table 7.1).
The anatomical correlate of iconic memory is probably
visual association cortex, while that of echoic memory is
probably auditory association cortex. 7.3 LANGUAGE
7.1.1.1 Short-Term Memory 7.3.1 Cerebral Dominance

The anatomical correlate of auditory verbal short-term Cerebral dominance for language is as follows:
memory is the left (dominant) parietal lobe, while that of
visual verbal short-term memory is possibly the left tem- • In 99% of right-handers, the left cerebral hemi-
poro-occipital area. That of nonverbal short-term mem- sphere is dominant.
ory is possibly the right (nondominant) temporal lobe. • In 60% of left-handers, the left cerebral hemi-
sphere is dominant.
7.1.1.2 Explicit Memory
This requires a deliberate act of recollection and can be In early life, there is plasticity for cerebral dominance for
reported verbally. It includes declarative memory and language before the functions are established.
episodic memory, which are probably stored separately,
since it is possible to lose one type of memory while 7.3.1.1 Speech and Language Areas
retaining the other. Declarative memory involves knowl- 7.3.1.1.1 Broca’s Area
edge of facts, whereas episodic memory involves mem- This is the motor speech area, occupying the opercular
ory of autobiographical events. Explicit memory involves and triangular zones of the inferior frontal gyrus (BA
the medial temporal lobes, particularly the hippocampus, 44 and 45). It is involved in coordinating the organs
entorhinal cortex, subiculum, and parahippocampal cor- of speech to produce coherent sounds. In lesions con-
tex. Damage to these structures results in an inability to fined to this area in the dominant hemisphere, speech
store new memory; they have been termed bottleneck comprehension is intact and muscles involved in speech
structures. Memory probably passes from medial tempo- production work normally, but production of speech is
ral lobe structures after a few weeks/months to longer- affected.
term storage in the cortex.
The amygdala may be involved in the emotional charg- 7.3.1.1.2 Wernicke’s Area
ing of information. It may also be a bottleneck structure. This is the sensory speech and language area, occupy-
ing the posterior part of the auditory association cortex
7.1.1.3 Implicit Memory (BA 42 and 22) of the superior temporal gyrus. It is usu-
This is recalled automatically without effort and is learned ally larger in the left hemisphere. It is involved in making
slowly through repetition. It is not readily amenable to sense of speech and language.
verbal reporting. It comprises procedural knowledge, that
is, knowing how. Its storage requires functioning of the 7.3.1.1.3 Angular Gyrus
cerebellum, amygdala, and specific sensory and motor This part of the brain (BA 39) has abundant connec-
systems used in the learned task. For example, the basal tions with the somatosensory, visual, and auditory
ganglia are involved in learning motor skills. Classical association cortices. Lesions here produce inability to
and operant learnings involve implicit memory. read or write.
103
TABLE 7.1
Summary of Various Types of Amnesia
Anterograde amnesia Anterograde amnesia refers to inability to form new memories, either because of failure to consolidate what is
perceived into permanent memory storage or because of inability to retrieve memory from the storage
Retrograde amnesia Retrograde amnesia refers to loss of memory for events that occurred prior to an event or condition (e.g. intoxication
or head injury). Such event is presumed to have caused the memory disturbance in the first place. Retrograde memory
related to public events is more likely to be subjected to a greater memory loss than personal events
In head injury, retrograde amnesia is sometimes referred as pre-traumatic amnesia, which is composed of events
the person remembers up to the immediate time of an accident. The pre-traumatic amnesia usually lasts less than
1 week. Retrograde amnesia tends to improve with more distant events in the past
Depressed patients with preexisting cognitive impairment are more likely to develop post-ECT retrograde amnesia.
Post-traumatic amnesia Post-traumatic amnesia is defined as the memory loss from the time of accident to the time that the patient can give
a clear account of the recent events. In general, the retrograde amnesia is shorter than post-traumatic amnesia.
Post-traumatic amnesia, once present, tends to remain unchanged. Post-traumatic amnesia is confounded by
sedatives given after admission and prolonged sleep. Post-traumatic amnesia does not necessarily correlate with
the duration of consciousness loss
Psychogenic amnesia Psychogenic amnesia is part of the dissociative disorder consisting of a sudden inability to recall important personal
data. The amnesia may be localized (for several hours) or generalized (for entire life is lost). The amnesia may be
selective (involving certain memories) or continuous (loss of all memories subsequent to a specific time). The
clinical presentation is usually atypical and cannot be explained by ordinary forgetfulness (e.g. loss of biographical
memory in dissociative fugue). Psychogenic amnesia is associated with ‘la belle indifference’ (lack of concerns)
and has a highly unpredictable course
Differential diagnosis includes situational amnesia, PTSD, Ganser’s syndrome (vorbeireden or approximate
answers), dissociative fugue, pseudodementia (associated with sudden onset and depressive disorder), and multiple
personality disorder
False memory False memory involves confabulation, report of false events (e.g. childhood sexual abuse), and false confessions
The false-memory syndrome is a condition in which a person’s identity and interpersonal relationships are centred
around a memory of a traumatic experience, which is objectively false, but the person strongly believes that such
experience did take place. False confessions may not have a psychiatric cause because the person falsely confesses
to enhance publicity and to conceal evidence in criminal offence
Differential diagnosis includes organic amnesias and frontal lobe syndrome
Transient global amnesia The person presents with abrupt onset of disorientation, loss of ability to encode recent memories, and retrograde
amnesia for variable durations. The patient has a remarkable degree of alertness and responsiveness. This episode
usually lasts for a few hours and is never repeated. The pathophysiology is a result of transient ischaemia of the
hippocampus–fornix–hypothalamic system. Functional neuroimaging may show transient reduction in metabolic
and functional activities in the mesial temporal lobes
For example, a 59-year-old man came to the emergency department at 9 pm and complains of memory loss for a
few hours. He claims that he cannot remember what he did in the afternoon
Amnestic syndrome Amnestic syndrome is closely related to Wernicke–Korsakoff syndrome. The person has impairment of short-term
memory (i.e. unable to recall items 30 min after presentation), but immediate memory (immediate three items
recall) is intact. Hence, anterograde amnesia is more prominent because memories cannot be consolidated and
stored. Confabulation may occur
Amnesia involving Episodic memory is time and context specific. In contrast, semantic memory that involves vocabulary and facts is not time
episodic memory or context specific. The neuroanatomical areas involved in episodic memory and semantic memory are the limbic system
and temporal neocortex, respectively. Semantic memory is assessed by the National Adult Reading Test
Acute causes of episodic memory impairment include transient global amnesia, temporal lobe epilepsy, closed head
injury, drugs (benzodiazepine and alcohol), and psychogenic fugues
Causes of chronic episodic memory impairment include hippocampal and diencephalic damages. Hippocampal
damage is caused by herpes simplex virus (HSV ) encephalitis, anoxia, surgical removal of temporal lobes, bilateral
posterior cerebral artery occlusion, closed head injury, and early Alzheimer’s disease. The causes of diencephalic
damage include Korsakoff’s syndrome, third ventricle tumours and cysts, bilateral thalamic infarction, and
post-subarachnoid haemorrhage
Cognitive Assessment and Neuropsychological Processes 105
7.3.1.2 Pathways 7.3.2.3 Conduction Dysphasia

• Understanding spoken language (hearing): Damage to the arcuate fasciculus results in a conduction
spoken word → auditory cortex → auditory dysphasia in which the person cannot repeat what is said
association cortex → Wernicke’s area → hear by another. Comprehension and verbal fluency remain
and comprehend speech intact.
• Understanding written language (reading): writ-
ten word → visual cortex → visual association 7.3.2.4 Global Dysphasia
cortex → angular gyrus → Wernicke’s area → This results from global left hemispheric dysfunction
read and comprehend and shows a combination of all the aforementioned
• Speaking: thought/cognition → Wernicke’s area → (Table 1.2).
Broca’s area → motor speech areas → speech
• Writing: thought/cognition → Wernicke’s area → 7.3.3 Mutism
angular gyrus → motor areas → write
Mutism refers to a statue of silence or voicelessness.
7.3.2 Dysphasias Aetiology: MCA infarct/haemorrhage, Broca’s aphasia,

bulbar palsy (lower motor neuron lesions), pseudobulbar
Dysphasia, paraphasia, or aphasia refers to any disturbance
palsy (upper motor neuron lesions), catatonic schizophre-
in the comprehension and expression of speech as a result
nia, severe depression, and elective mutism
of brain lesions. For example, a person says, ‘murder of
two companies’ instead of ‘merger of two companies’.
Aetiology: middle cerebral artery (MCA) infarct/haemor- 7.4 PERCEPTION
rhage, tumour, abscess, other space occupying lesions, Perception relates to the means by which the brain makes
Alzheimer’s disease, and Pick’s disease. representations of the external environment.
Pathophysiology: Damage to brain areas involved with Agnosia is the inability to interpret and recognize the
speech and language results in dysphasia; the type of dys- significance of sensory information, which does not result
phasia is determined by the areas of the brain involved. from impairment of the sensory pathways, mental dete-
rioration, disorders of consciousness and attention, or, in
the case of an object, a lack of familiarity with the object.
7.3.2.1 Receptive Dysphasia
Damage to Wernicke’s area disrupts the ability to com-
prehend language, either written or spoken. In addition
7.4.1 Visual Perception
to loss of comprehension, the person also is unaware that • Shape, colour, and spatial orientation are recog-
his or her dysphasic speech is difficult for others to fol- nized in the occipital lobes. A lesion at this level
low. Speech is normal in rhythm and intonation (because results in pseudoagnosia.
Broca’s area is intact), but the content is abnormal. Words • Visuospatial elements are drawn together into
used have lost their meaning; empty words (e.g. ‘thing’, complete percepts (objects seen as a whole)
‘it’) and paraphrasias are used liberally. Thus, damage to in the right parietal lobe. Meaning is not yet
Wernicke’s area results in a fluent receptive dysphasia. attributed to the objects. A lesion at this level
results in apperceptive agnosia. A person with
7.3.2.2 Expressive Dysphasia apperceptive agnosia is unable to copy shapes
Damage to Broca’s area results in loss of rhythm, intona- or discriminate two versions of the same object.
tion, and grammatical aspects of speech. Comprehension The person cannot name the object when he or
is normal (because Wernicke’s area is intact) and the per- she sees it but is able to name it when he or she
son is aware that his or her speech is difficult for oth- touches it. The person has preserved elementary
ers to follow, resulting in distress and frustration. Speech visual abilities (e.g. acuity or brightness dis-
is slow and hesitant, often lacking connecting words. crimination). The lesion is found in the bilateral
Speech sounds agrammatical and articulation may be posterior occipitoparietal regions. Apperceptive
crude, probably because of the close proximity of Broca’s agnosia is caused by carbon monoxide or mer-
area to motor areas. Thus, damage to Broca’s area results cury poisoning, bilateral posterior watershed
in dysfluent expressive dysphasia. strokes, and penetrating head injury (Figure 7.1).
FIGURE 7.2 Associative visual agnosia.
FIGURE 7.1 Apperceptive visual agnosia.

between colours but are impaired on tasks requir-
ing the retrieval of colour information (e.g. ‘What
• The meaning of objects is then accessed from the colour is an apple?’). Colour anomia (e.g. show-
left parietal lobe (which itself accesses meaning ing the red colour but unable to name the colour)
from semantic memory) and processed in parieto- is associated with alexia and right hemianopia as
occipital areas. A lesion at this level results in asso- a result of disconnection between the left hemi-
ciative agnosia. A person with associative agnosia sphere language centre and visual information.
is unable to recognize visually presented objects. • In simultanagnosia, the person is unable to
In contrast to apperceptive agnosia, the person has recognize the overall meaning of a picture,
a high level of perceptual processing. Preservation whereas its individual details are understood.
of the high-level perceptual processing is demon- Simultanagnosia is associated with lesion in the
strated by the normal copying of objects that the anterior part of occipital lobe or children suffer-
person cannot recognize (e.g. fountain pen in this ing from generalized brain dysfunction.
case). The person has preserved ability to match • Agraphognosia or agraphesthesia is tested by
pairs of similar stimuli. Furthermore, patients asking the person to identify, with closed eyes,
with apperceptive agnosia are unable to identify numbers or letters traced on his or her palm;
objects by any modality (e.g. touching). Aetiology this disorder is present if the person is unable to
includes moderate Alzheimer’s disease, Pick’s identify such writing.
disease, and HSV encephalitis (Figure 7.2). • In anosognosia, there is a lack of awareness of
disease, particularly of hemiplegia (most often
7.4.1.1 Other Agnosias following a right parietal lesion).
• Prosopagnosia is an inability to recognize faces. • Autotopagnosia is the inability to name, recog-
In advanced Alzheimer’s disease, a person may nize, or point on command to parts of the body.
misidentify his or her own mirrored reflec- • In astereognosia, objects cannot be recognized
tion—the mirror sign (autoprosopagnosia). by palpation.
Prosopagnosia is associated with bilateral infe- • In finger agnosia, the person is unable to recog-
rior occipitotemporal lesions. nize individual fingers.
• Achromatopsia is an acquired disorder character- • Topographical disorientation can be tested
ized by a loss of ability to discriminate between using a locomotor map-reading task in which
colours. On the other hand, people with colour the person is asked to trace out a given route
agnosia are able to perceive and distinguish by foot.
• In hemisomatognosis or hemidepersonaliza- 2. Peripheral dyslexia: Oral and written spelling is

tion, the person feels that a limb (which in fact is preserved:
present) is missing. a. Alexia without agraphia.
b. Neglect dyslexia: Errors in reading the ini-
7.4.1.1.1 Anomia (Nominal Aphasia) tial part of words. It is caused by a right
Anomia is a type of aphasia characterized by problems parietal lobe lesion affecting the left half of
recalling words or names. The person may use circumlo- words. Left hemisphere lesions affecting the
cutions (speaking in a roundabout way, e.g. the thing that right half of words are rare.
tells time) in order to express a certain word for which
they cannot remember the name (e.g. clock in this case).
Sometimes, the person can recall the name when clues 7.5.2 Dysgraphia
are given. Anomia may lead to frustration. Dysgraphia refers to impaired writing ability.
Aetiology: Anomia is caused by damage to the pari- Types of dysgraphia are as follows:
etal lobe or the temporal lobe.
1. Central dysgraphia: Written and oral spelling is
7.4.1.1.2 Dysnomia affected:
Dysnomia refers to the marked difficulty in remember- a. Lexical dysgraphia is caused by lesions in
ing names or recalling a word needed for oral or written the left temporoparietal region. The person
language. It is often a ‘tip-of-the-tongue’ phenomenon. breaks down the word’s spelling and has
difficulty in writing irregular words.
7.4.1.1.3 Dysnomic Dysphasia b. Deep dysgraphia is caused by extensive left
Dysnomic dysphasia refers to the profound word finding hemisphere lesions and a breakdown of the
difficulties. sound-based route for spelling. The person
cannot spell nonexistent words.
7.5 DYSLEXIA AND DYSGRAPHIA 2. Neglect dysgraphia is caused by right hemi-
spheric lesions and leads to misspelling of the
7.5.1 Dyslexia initial part of words.
3. Dyspraxic dysgraphia is caused by dominant
Dyslexia refers to pure word blindness. In developmental
frontal or parietal lobe lesions. This leads to
dyslexia, a young child initially manifests difficulty in
defective copying although the person can spell
learning to read. Later, the child exhibits erratic spell-
correctly (Table 7.2).
ing and lack of capacity to manipulate written language.
People with developmental dyslexia have symmetrical
planum temporale (leftward asymmetry in people with-
out dyslexia). Verbal language skills seem to be intact. In 7.6 ALEXIA AND AGRAPHIA
general, the affected persons have problems with percep- Alexia refers to reading disorder that affects learning and
tion of the shapes of words. 50% of people with dyslexia academic skills. Agraphia refers to writing impairment.
also have achromatopsia (colour blindness).
Types of dyslexia are as follows:
7.6.1 Alexia without Agraphia
1. Central dyslexia: Linguistically based and spelling 1. Clinical example: A 58-year-old man suffered
is affected: from acute stroke. At first, he developed acute
a. Surface dyslexia is caused by lesions in impairment in comprehending written materi-
left temporoparietal region. The person als including his own works although he could
breaks down the whole word (lexical read- write. When the words were spelt out loud by
ing) and has difficulty to deal with irregu- his wife, he recognized the word immediately.
larly spelt words. After 3 months, he develops a new technique
b. Deep dyslexia is caused by extensive left to help himself recognize words. He reads let-
hemisphere lesions. There is a loss of sound- ter by letter and spells the word out loud. Then
based (phonological) reading. The person he recognizes the word after hearing himself
has difficulty to deal with abstract words. spell it out.
TABLE 7.2
Examples of Dysphasia, Dyslexia, and Dysgraphia
Examples Diagnosis
Orange is named as apple. Semantic paraphasia occurs when there is an error in using the target word because of
deficits in semantic memory. It is associated with left temporal lobe tumours
Big is read as dig. Surface dyslexia occurs when reliance is placed on sub-word correspondence between
letters and sounds but not the normal way, which is spelling to sound
Bicycle is read as cycle. Neglect dyslexia occurs when the left half of the word is being ignored as a result of the
right parietal lobe lesion
Sister is read as auntie. Deep dyslexia occurs when the person produces verbal response based on the meaning
of the word but not based on sound-based reading
‘A’ is written as ‘∀’. Dyspraxic dysgraphia has the following manifestations: disturbance in writing the
smooth part of a letter, letter may be inverted or reversed, abnormal letter, and illegible
handwriting. Oral spelling is preserved
‘Cough’ is written as ‘coff’. Lexical dysgraphia: The person has difficulty to write irregular words ‘cough’ in this
case and produces an error that is phonologically similar
2. Neuroanatomical areas involved: The occlu- 7.6.2 Alexia with Agraphia

sion of left posterior cerebral artery leads
to infarction of the medial aspect of the left 1. Clinical features: The person cannot read, write,
occipital lobe and the splenium of the corpus or connect letters.
callosum. 2. Neuroanatomical area involved: Lesions of the
angular or supramarginal gyrus.
3. Pathophysiology: The explanation for the clini-
cal presentation is as follows: After the stroke,
the patient starts off with right hemianopia 7.7 APRAXIAS
and he cannot read in the right visual field. Apraxia is an inability to perform purposive voli-
Then, the words have to be seen on the left tional acts, which does not result from paresis, inco-
side, which are projected onto the right hemi- ordination, sensory loss, or involuntary movements
sphere. There is a lesion in the splenium that (Table 7.3).
prevents the transfer of visual information Dressing apraxia: A person is unable to wear clothes
from the right to the left side. The primary properly, for example, putting on a jacket upside down.
language area is disconnected from incoming Dressing apraxia is associated with nondominant parietal
visual information. As a result, he cannot com- lobe lesions (Figure 7.3).
prehend any written material although he can
write. As time goes by, he develops a strategy
7.7.1 Acalculia and Anarithmetria
of identifying the individual letters in the right
hemisphere. Saying each letter aloud enables Acalculia refers to a disturbance in the ability to compre-
him to access the pronunciation of word in the hend or write numbers properly. This condition is seen in
left hemisphere. people with aphasia. Lesion is found in the angular gyrus
4. Comorbidity: Defects in colour naming of the left hemisphere.
(although with intact colour vision) or actual Anarithmetria refers to the inability to perform num-
impairment of colour perception (achromatop- ber manipulation. This disorder is common in people
sia) may occur. with dementia of Alzheimer type.
TABLE 7.3
Summary of Various Types of Apraxia
Type Definition Lesion Example
Ideational apraxia The patient has an inability to carry Corpus callosum, extensive left A person cannot work in a café
out a complex sequence, but the hemisphere lesion, and advanced because he or she cannot make tea
individual components of the Alzheimer’s disease and serve the others. If you ask him
sequence can be successfully or her to put a tea bag into the cup,
performed he or she is able to do so
Ideomotor apraxia The patient has difficulty with Left parietal or frontal lobe. A person does not know how to use a
selection, sequencing, and spatial There is damage in the motor hammer
orientation. There are problems in programmes (e.g. cortically stored
gestures (e.g. waving) and in movement patterns) or
demonstrating the use of imagined disconnection in the flow of
household items (e.g. toothbrush) information necessary for initiating
complex motor acts
Orobuccal apraxia The patient has difficulty in Left inferior frontal lobe and insula When a person is asked to pretend to
performing learned, skilled blow out a match or suck a straw, he
movements of the face, lips, or she makes incorrect movements
tongue, cheek, larynx, and pharynx
on command
Construction apraxia The patient has difficulty in Nondominant parietal lobe Failure to draw interconnected
reproducing simple geometric double pentagon
patterns and an inability to connect
the separate parts
7.8 FRONTAL LOBE FUNCTIONS

7.8.1 Prefrontal Cortex
This is probably involved in the following functions:
• Problem-solving
• Perceptual judgement
• Memory
• Programming and planning of sequences of
behaviour
• Verbal regulation
• Level of response emission
• Adaptability of response pattern
• Tertiary level of motor control
7.8.2 Frontal Eye Fields

FIGURE 7.3 Dressing apraxia. These are involved in voluntary eye movements.
7.8.3 Motor and Premotor Cortex lobe d amage may lead to disinhibition and
antisocial behaviour (Table 7.4; Figures 7.4
These are probably involved in the following functions: through 7.6).
• Primary and secondary levels of motor control
• Design fluency
CASC STATION: ASSESS FRONTAL
LOBE FUNCTIONS (TABLE 7.6)
7.8.4 Broca’s Area
A 23-year-old man was involved in a fight in the
This is involved in expressive speech. pub and suffered head injuries. He was taken to the
hospital and treated for subdural hematoma. His
mother has noticed a change in his personality after
7.8.5 Orbital Cortex the injury.
This is probably involved in the following functions: Task: Assess his frontal lobe functions.
• Personality
• Social behaviour
Candidates are advised to familiarise with assessment of
Orbital cortex damage may lead to abnormal sexual
parietal and temporal lobe functions in the CASC exam
behaviour.
(Table 7.6).
7.8.6 Frontal Lobe Lesions 7.8.7 Assessment of Temporal Lobe Functions

These may cause the following: 1. Language function: Repeat ‘No ifs, and, or,
buts’.
• Personality change—disinhibition, reduced 2. Visual recognition: Show a pen or a watch to the
social and ethical control, sexual indiscretions, person and ask the person to name it.
poor judgement, elevated mood, lack of concern 3. Semantic memory: Test the person knowledge on
for the feelings of other people, and irritability. landmarks (e.g. Great Wall, Eiffel Tower) or the
• Perseveration. names of famous people (current Prime Minister
• Utilization behaviour. of United Kingdom, current president of the
• Palilalia. United States) and knowledge of famous people
• Impairment of attention, concentration, and (e.g. John Lennon, Tony Blair).
initiative. 4. Registration and recall after few minutes: Tell
• Aspontaneity, slowed psychomotor activity. the person three objects, ask them what the
• Motor Jacksonian fits. three objects are immediately, and recall after a
• Urinary incontinence. few minutes.
• Contralateral spastic paresis. 5. Assessment of visual field: Look for upper qua-
• Aphasia. dratic field defect.
• Primary motor aphasia.
• Motor agraphia.
• Anosmia.
7.9 LEFT AND RIGHT CEREBRAL HEMISPHERES
• Ipsilateral optic atrophy. If a person suffers damages in the left hemisphere, the
• The left frontal lobe is involved in control- intact right hemisphere can take over the task of attending
ling language-related movement (Broca’s to the right side (Tables 7.6 and 7.7). On the other hand,
area) and the right frontal lobe is involved if a person suffers damages in the right hemisphere, it
in nonverbal abilities. Left frontal lobe dam- will cause right-sided neglect because the left hemisphere
age leads to nonfluent speech (expressive cannot compensate. In this case, the person neglected the
dysphasia) and depression. Right frontal right side of the flower in the drawing (see Figure 7.7).
TABLE 7.4
Neuropsychological Assessments of Frontal Lobe Functions
Neurological Tests Methodology and Interpretation
Wisconsin card sorting task (WCST) Methodology: Patients are given a pack of cards with symbols on them, which differ in form, colour,
and numbers. Four stimulus cards are available and the patient has to place each response card in
front of one of the four stimulus cards. The psychologist then tells the person if he or she is right or
wrong. The person has to use the feedback from the psychologist to place the next card in front of the
next stimulus card. The sorting is done arbitrarily into colour, form, or number. The person is required
to shift the set from one type of stimulus response to another as indicated by the psychologist
Interpretation: People with frontal lobe lesions cannot overcome previously established responses and
show a high frequency of preservative errors
Tower of London task Methodology: The person needs to rearrange the beads on vertical rods to match a template, using as
few moves as possible. This task assesses the person’s planning skills
Interpretation: People with frontal lobe impairment have difficulty with planning and organization.
They take many more moves compared to people without frontal lobe impairment
Stroop task Methodology: The Stroop task assesses the person’s attention and ability to inhibit inappropriate
response. People have the ability to read words more quickly and automatically than naming colour.
For example, if the word ‘red’ is printed or displayed in ‘black’ ink, people will say the word ‘red’
more readily than naming the colour, ‘black’ in which it is displayed. The Stroop test involves words
in different colours, and there are three levels:
Level 1: Choose the word that matches the stated colour
Level 2: Choose the word that matches the stated word
Level 3: Choose the colour that matches the colour of a stated word
Interpretation: People with frontal lobe impairment have difficulty in dividing their attention and fail
to suppress the tendency to name the words rather than the printed colour. As a result, they will
make more mistakes in the tasks compared to people without frontal lobe impairment
Hayling and Brixton tests Methodology of the Hayling test: The first part measures the speed of response initiation.
The assessor reads each sentence and the subject has to simply complete the sentences
The second part measures response suppression. The subject completes a sentence with a nonsense
ending word and suppresses the sensible ending word
Interpretation: People with frontal lobe impairment have poor response initiation and suppression.
Methodology of the Brixton test: The Brixton test is a visuospatial sequencing test with changes in
rule in between. It is useful to assess people with speech difficulties, with rule change
Interpretation: People with frontal lobe impairment have poor visuospatial sequencing
FIGURE 7.4 Luria’s hand test (hand position test).
FIGURE 7.5 Alternating sequence test.

(a) (b)
(c)
(d) Doctor Patient
FIGURE 7.6 (a) Palmomental reflex: The psychiatrist uses an orange stick to scratch the palm. If there are wrinkles or folds
appear on the ipsilateral chin, palmomental reflex is present. (b) Visual rooting reflex: The psychiatrist uses a tendon hammer
to approach the patient. If she turns to the tendon hammer with her mouth open, the visual rooting reflex is present. (c) Snout
reflex: A tendon hammer is tapped lightly on the patient’s lip. If she forms small folds and wrinkles on the lip and around the
mouth, the pout reflex is present. This resembles the sucking reflex. (d) Grasp reflex: The psychiatrist places two fingers in the
open palm of each of the patient’s hands. If the patient grasps the psychiatrist’s fingers and resists the attempts of removal,
grasp reflex is present.
TABLE 7.5
CASC Grid
Findings in People without Frontal Lobe Findings in People with Frontal Lobe
Tasks and Instructions to Patient Impairment Impairment
Word fluency
Instruction: ‘Name as many English words as Expected response: Able to say 12–15 words The person can only mention a few words.
possible starting with letter “F”,“A”, and “S” ’. in 1 min Very often, they repeat those words that
Category fluency is for non-English speaking Some people may develop strategies to help have already been mentioned. Finally, the
patients: them to find words. A person may think of person stops and cannot provide more words
Instruction: ‘Name as many animals as a category of items starting with ‘F’ and or items
possible in 1 min’ then move to other categories. For
example, a medical student will think of
diseases started with ‘F’ and then move
onto household items started with ‘F’
Abstract thinking
Instruction: ‘Can you interpret the following Expected response: ‘People who are always Response: ‘Stone is stone. Moss is moss’.
proverb, a rolling stone gathers no moss?’ moving with no roots in one place. They The patient cannot appreciate the deeper
avoid responsibilities and cares. They meanings but just focuses on the words
cannot achieve much’ superficially
For non-English speaking patients, the Expected response: ‘Both apples and Response: ‘Apple is red. Orange is orange’. It
examiner may ask similarity between an oranges are fruits. They have skin. People is not uncommon to find a patient talking
apple and an orange and a table and a chair. can make juice from them. They have seeds about the differences as it seems to be easier
and contain nutrients’ than talking about the similarities
Cognitive estimation
Instruction: ‘How tall is an average British Expected response: ‘An average British Response: ‘10 feet tall’
woman?’ woman is 1.6–1.8 m tall’
Instruction: ‘How many elephants are there in Expected response: ‘I guess 5–10 elephants’ Response: ‘900 elephants’
Sheffield or Hong Kong?’ Candidates may not know the exact number
of elephants in Sheffield or Hong Kong, but
the answer given by the patient is obviously
beyond the normal estimates
Judgement
Instruction: ‘If you find a letter on the floor Expected response: ‘I will put in the mail Response: ‘I will bring it home and hide it’
and there is a stamp attached to it, what will box and post it’ The patient may give various responses but not
you do?’ conform with the logical actions proposed by
This task assesses the orbitofrontal lobe function. people without frontal lobe impairment
Luria’s hand test
The candidate needs to demonstrate the Luria’s Expected response: A subject without frontal Patients with frontal lobe impairment may not
hand test to the subject being examined. After the lobe impairment can appreciate the three appreciate that there are three different hand
subject has mastered the technique, he or she has different hand positions positions and cannot alternate from one to
to do it with one hand for at least five times. Then another as a result of motor preservation
the subject has to repeat with the other hand.
(See Figure 7.4.)
Alternative sequence test
The candidate draws the alternating shapes and Expected response: People without frontal Patients with frontal lobe impairment will
asks the person being examined to continue lobe impairment will recognize and continue with the last shape (a triangle in this
without telling them that there is a pattern. continue the three alternating shapes case)
The failure to appreciate the alternative
pattern is a result of preservation
(See Figure 7.5.)
Elicit primitive reflexes
(See Figure 7.6.) Expected response: no primitive reflex Patients with frontal lobe impairment show
emergence of primitive reflexes
TABLE 7.6
Assessment of Parietal Lobe Functions
Assessment of Dominant Parietal Lobe Assessment of Nondominant Parietal Lobe
1. (Gerstmann’s syndrome) 1. Asomatognosia: lack of awareness of the
a. Finger agnosia: inability to recognize the name of the finger condition of all or parts of the body
b. Left and right orientation: inability to recognize left and right 2. Constructional dyspraxia: inability to copy double
c. Acalculia: inability to recognize number and calculation interlocking pentagons
d. Dysgraphia
2. Astereoagnosia: inability to recognize the size, shape, and texture of an object
by palpation
3. Dysgraphesthesia: inability to recognize letters or numbers written on the hand
4. Ideomotor apraxia
5. Wernicke’s or Broca’s aphasia
6. Impairment in two-point discrimination (e.g. a patient cannot recognize the
presence of two sharp stimuli by placing a divider on the finger pulp)
TABLE 7.7
Summary of the Neuropsychological Impairments of the Left and Right Cerebral Hemispheres
Lesions in the Left Cerebral Hemisphere (Dominant) Lesions in the Right Cerebral Hemisphere (Nondominant)
1. Gerstmann’s syndrome: finger agnosia, left and right 1. Neglect phenomena (one side of body, sensation, reading, writing)
orientation, acalculia, and dysgraphia (lexical and deep) 2. Apraxia: depressing and constructional
2. Astereoagnosia 3. Agnosia: apperceptive
3. Dysgraphesthesia
4. Ideomotor apraxia
5. Dyslexia: surface or deep
6. Apraxia: ideation, ideomotor, and orobuccal
Brown J and Hillam J. 2004: Dementia: Your Questions

Answered. Edinburgh, U.K.: Churchill Livingstone.
Burgess P and Shallice T. 1997: The Hayling and Brixton Tests.
Test Manual. Bury St. Edmunds, U.K.: Thames Valley
Test Company.
Campanella F, Mondani M, Skrap M, and Shallice T. 2009:
Semantic access dysphasia resulting from left temporal
lobe tumours. Brain 132(1):87–102.
Campbell RJ. 1996: Psychiatric Dictionary. New York: Oxford
University Press.
Hodges J. 2002: Cognitive Assessment for Clinicians. Oxford,
U.K.: Oxford University Press.
Smith EE, Nolen-Hoeksema S, Fredrickson BL et al. (eds.)
2003: Atkinson and Hilgard’s Introduction to Psychology
(with Lecture Notes and InfoTrac), 14th edn. Florence,
KT: Wadsworth.
FIGURE 7.7 Unilateral neglect in a person with damage in
Trimble M. 2004: Somatoform Disorders—A Medico-
the right hemisphere.
Legal Guide. Cambridge, U.K.: Cambridge University
Press.
BIBLIOGRAPHY Yudofsky SC and Hales RE. 2007: The American Psychiatric
Publishing Textbook of Neuropsychiatry and Behavioural
Brandon S, Boakes J, Glaser D, and Green R. 1998: Recovered Neuroscience, 5th edn. Washington, DC: American
memories of childhood sexual abuse. Implications for clin- Psychiatric Press Inc.
ical practice. British Journal of Psychiatry 172:296–307.
8 Social Sciences and Stigma
8.1 DESCRIPTIVE TERMS 8.1.3 Relevance to Psychiatric Disorder

and Health-Care Delivery
8.1.1 Social Class
8.1.3.1 Psychiatric Disorder
A social class is a segment of the population sharing a
broadly similar type and level of resources, with a broadly The incidence and prevalence of many psychiatric dis-
similar style of living and some shared perception of its orders have been found to vary with social class. In
common condition. particular, the following disorders are more likely to be
diagnosed in the lower social classes:
8.1.1.1 Determinants • Schizophrenia
The determinants of social class include • Alcohol dependence
• Organic psychosis
• Education • Depressive episodes in women
• Financial status • Parasuicide/deliberate self-harm
• Occupation • Personality disorder
• Type of residence
• Geographic area of residence The following disorders are more likely to be diagnosed
• Leisure activities in the upper social classes:
8.1.1.2 Occupational Classification • Anorexia nervosa in females

In British psychiatry, the following occupationally based • Bulimia nervosa in females
classification given by the Office of Population Censuses • Bipolar mood disorder
and Surveys has traditionally been used:
8.1.3.2 Relationship between Social Class
• Social class I—professional, higher managerial, and Psychiatric Disorder
landowners The existence of a relationship between social class and
• Social class II—intermediate a given psychiatric disorder does not necessarily imply
• Social class III—skilled, manual, clerical causation, from social class to the disorder. In general,
• Social class IV—semiskilled the possible explanations of such a relationship may
• Social class V—unskilled include the following:
• Social class 0—unemployed, students
• Downward social drift—for example, the
Members of the same household are assigned to the social increased representation of schizophrenia in lower
class of the head of the household. social classes may be partly a result of social drift.
• Environmental stress—lower social class is
associated with adverse life situations, material
8.1.2 Socioeconomic Status
deprivation, and the lower self-esteem that man-
The socioeconomic status of an individual is his or her ual jobs entail; women in lower social classes
position in the social hierarchy. It is related to social are more likely to experience severe life events
class and may increase, for example, through educational and vulnerability factors.
achievement, or decrease, for example, through unem- • Differential labelling—for example, it may be
ployment or mental illness. that some people in Britain of Afro-Caribbean
115
origin are more likely to be detained under men- 8.1.4 Black Report on Socioeconomic
tal health legislation and diagnosed as suffering Inequalities in Health
from schizophrenia (although this may in fact
reflect genuine differences in prevalence and According to the Black Report of 1980 exploring the dif-
incidence rates). ference in health and mortality in Britain between the
• Differential treatment—for example, there is a social classes, compared with those in social class I, indi-
difference in the type of psychiatric treatment viduals in social class V
likely to be received by those from different
social classes (see the succeeding text). • Have twice the neonatal mortality
• Are twice as likely to die before retirement
• Have an increased rate of almost all diseases
8.1.3.3 Health-Care Delivery
Those with a psychiatric disorder who are from lower
social classes are more likely to 8.1.4.1 Explanations
The following explanations for the relationship between
• Be admitted to hospital as psychiatric inpatients social class and illness found in the Black Report on socio-
• Remain as psychiatric inpatients for longer economic inequalities in health have been suggested:
• Receive physical treatments, for example, elec-
troconvulsive therapy • Artefactual—the health inequalities found are
artificial.
Those with a psychiatric disorder who are from upper • Natural and social selection—good health is
social classes are more likely to associated with an improvement in social class,
while poor health is associated with social drift
• Spend a shorter period of time as psychiatric downward.
inpatients • Materialist/structural—poor health is primarily
• Be treated as psychiatric outpatients without a function of material deprivation; inequalities
inpatient admission in wealth and income distribution are associated
• Receive psychological treatments, for example, with inequalities in health.
individual psychotherapy • Cultural/behavioural—certain unhealthy behav-
iour patterns are more common in lower social
classes (e.g. smoking, unhealthy diets), leading to
8.1.3.4 Pathways to Psychiatric Care
health inequalities.
Goldberg and Huxley (1980) described the existence of
filters to psychiatric care, each of which depends on
8.1.4.2 Changes after 10 Years
• Social factors—such as age, sex, ethnic back- A decade after the publication of the Black Report, Smith
ground, socioeconomic status et al. (1990) found
• Service organization and provision—for exam-
ple, time and location of clinics, length of wait- • Social class differences in mortality had
ing list widened.
• Aspects of the disorder itself—for example, its • Better measures of socioeconomic position
severity and chronicity showed greater inequalities in mortality.
• Inequalities in health had been found in all
These filters include countries that collect relevant data.
• Measurement artefacts and social selection did
• The decision to consult the general practitioner not account for mortality differences.
• Recognition of the disorder by the general • Social class differences existed for health dur-
practitioner ing life as well as for the length of life.
• The decision by the general practitioner as to • Trends in income distribution suggested a fur-
whether or not to refer the patient to a specialist ther likely widening of mortality differences.
Social Sciences and Stigma 117
8.2 HISTORICAL SOCIOLOGICAL THEORIES 8.2.2.1 Communism

After he and his wife (newlywed) moved to Paris in 1843,
8.2.1 Weber Marx became a communist, authoring Economic and
Max Weber was born in Erfurt, Prussia, in 1864 and died Philosophic Manuscripts of 1844 (which was not pub-
in Munich, Germany, in 1920. lished for about a century; Marx et al., 2011). In collabo-
ration with Engels, he coauthored The German Ideology
8.2.1.1 Bureaucracy in 1845–1846 (published in 1932), in which it was argued
Weber studied bureaucracy, starting with his 1908 studies on that historically nation states and societies generally had
Economies of Antiquity (Love, 1991). He started by outlining developed in such a way that the interests of the economi-
the development of modern forms of administration and put cally dominant class were favoured (Marx et al., 1987).
forward the notion that states in which the political machinery (Such arguments might account for the difficulty that
was centred around officialdom formed the basis of modern Marx and Engels encountered in trying to find a publisher
bureaucratic structures. (He considered that ancient societies for this work.) Some of the unpublished ideas contained
were not bureaucratic in the same way.) He suggested that in this work were summarized by Marx and Engels in
there existed the following types of bureaucracy: their 1848 pamphlet The Communist Manifesto (Marx
and Engels, 2004). Here, they also argued that all history
• Religious communities had fundamentally been a history of class struggle.
• States
• Economies 8.2.2.2 Crime
• The judiciary Marx argued that powerful entities, such as corporations,
• The modern agency could influence the definition of crime. Thus, while white
• The military collar crime was deemed punishable, acts by more privi-
leged members of society, such as fraud and tax evasion,
8.2.1.2 Rationalization might go unpunished. Furthermore, corporate crimes
Rationalization was the term used to denote the way in which might be carried out in order to increase company profits,
nature, society, and the actions of individuals were oriented even if they involved engaging in activities that may harm
towards planning, technical procedures, and rational actions. people (for instance, not paying heed to laws on health
and safety or disposing of toxic waste inappropriately).
8.2.1.3 Religion
8.2.2.3 Religion
According to Weber et al. (2002), social change can be
caused by religious belief. He suggested that change can Arguing that religion was ‘an opiate of the masses’, Marx
both cause and be caused by ideas. His thesis of The held that religion came from the oppressed but benefited
Protestant Ethic and the Spirit of Capitalism related cap- those at the top in society. He thought that organized religion
italism to Protestantism. He had noted that, in his native
• Helped to anaesthetize the pain caused by
Germany, that there was a positive association between
oppression
success in capitalist ventures and being of the Protestant
• Promised a reward in heaven or the afterlife for
faith or background. This association was caused, accord-
those who endured oppression in their current lives
ing to Weber, by the consequences of Puritan theology
• Provided justification for the current social
(as a reaction to the severity of Calvinism). For example,
order, including the position in this that a
the combination of the work ethic (based on the Fourth
believer found themselves in
Commandment), the belief that gain of wealth was a sign
• Promised that good behaviour would be rewarded
of being blessed, and an ascetic unwillingness of Puritans
• Suggested to the population that the current
to enjoy the fruits of such labour themselves would lead
problems on the planet would be solved through
overall to yet further accumulation of capital.
divine intervention
8.2.2 Marx 8.2.3 Durkheim
Karl Heinrich Marx was born in Trier, Prussia, in 1818 Emile Durkheim was born in Epinal, France, in 1858 and
and died in London, England, in 1883. died in Paris, France, in 1917.
8.2.3.1 Anomie 8.2.4 Foucault

Durkheim introduced the term anomie to refer to social Michel Foucault was born in Poitiers, France, in 1926 and
disconnectedness or a lack of social norms, which may died in Paris, France, in 1984.
be caused by a change in an individual’s relationship with
their social group, in which norms for conduct are absent, 8.2.4.1 Principles of Exclusion
weak, or conflicting. Two types of anomie may be distin- In books such as his 1975 work Discipline and Punish:
guished (Boulton, 1998): The Birth of the Prison, Foucault put forward his thesis
that society uses institutions to carry out social exclusion
1. Acute anomie—this is caused by a sudden
(Foucault and Sheridan, 1991). Such institutions included,
change or crisis that leaves the individual in an
he argued, the following:
unfamiliar situation.
2. Chronic anomie—this refers to circumstances • Asylums
in which the rules of a social group have become • Hospitals
unclear to the individual or do not provide the • Prisons
means of meeting his or her aspirations.
In respect to mental illness, Foucault argued that one
Causes of acute anomie include of the principles of exclusion that society uses to define
• Migration itself is the distinction between sanity and insanity.
• Bereavement
8.2.4.2 Sexuality
• Redundancy
Foucault made a study of the history of sexuality from
Causes of chronic anomie include ancient times. This was published in his 1976–1984
three-volume work History of Sexuality (Foucault and
• Homelessness Hurley, 1998).
• Long-term unemployment
8.2.5 Parsons
Widespread anomie may lead to a breakdown in social
order; Durkheim considered that science (in particular, Talcott Parsons was born in Colorado Springs, the United
social science), educational reform, and religion were States of America, in 1902 and died in Munich, West
ways of avoiding this. Germany, in 1979. Aspects of his contribution to socio-
logical theories are given in Section 8.2.7.
8.2.3.2 Suicide
In his 1897 work Suicide, Durkheim suggested that there 8.2.6 Goffman
appeared to be an inverse relationship between, on the
one hand, how integrated individuals were in their soci- Erving Goffman was born in Canada in 1922 and died
ety and culture and, on the other hand, the rate of suicide in Philadelphia, the United States of America, in 1982.
(Durkheim, 1966). A major cause of suicide, then, could Aspects of his contribution to sociological theories are
be seen in terms of social forces. According to Durkheim, given in Section 8.2.6.
there were, in fact, three types of suicide:
8.2.7 Habermas
1. Altruistic suicide—this results from social inte-
gration in a culture that accepts suicide as way Jürgen Habermas was born in 1929 in Düsseldorf, Germany.
of expiating shame or blame. In his two-volume magnum opus, The Theory of
2. Egoistic suicide—this results in the context of Communicative Action (Habermas and McCarthy, 1989),
the individual being socially further distanced Habermas built on the sociological theories of Max
from social norms and restraints, such that Weber, George Herbert Mead, Emile Durkheim, and
meaning is questioned. Talcott Parsons to suggest reasoning capacities, besides
3. Anomic suicide—this also results in the con- traditional cognitive–instrumental reasoning, which
text of the individual being socially further carry out subjective and intersubjective functions within
distanced from social norms and restraints, in the framework of societal interactions. He has gone on to
which anomie exists. defend modern society and civil society.
8.3 SOCIAL ROLES OF DOCTORS 8.3.4 Illness Behaviour

AND ILLNESS Illness behaviour is a set of stages describing the
8.3.1 Social Role behaviour adopted by sick individuals (Mechanic,
1978). It describes the way in which individuals
The social role of an individual in social is the pat- respond to somatic symptoms and signs and the con-
tern of behaviour in given social situations expected ditions under which they come to view them as abnor-
of him or her in relation to his or her social status. It mal. Illness behaviour therefore involves the manner
consists of in which individuals
• Obligations—behaviours towards others expected • Monitor their bodies

of the individual • Define and interpret their symptoms and signs
• Rights—behaviours from others expected in • Take remedial action
return for obligations • Utilize sources of help
8.3.2 Social Role of Doctors 8.3.4.1 Stages

In the model proposed by Parsons (1951), the role of the Illness behaviour includes the following stages:
doctor includes
• Initially well.
• Defining illness • Symptoms of the illness begin to be experienced.
• Legitimizing illness • The opinion of immediate social contacts is
• Imposing an illness diagnosis if necessary sought.
• Offering appropriate help • Contact is made with a doctor (or doctors).
• The illness is legitimized by the doctor(s).
Doctors therefore control access to the sick role and they • The individual adopts the sick role.
and patients have reciprocal obligations and rights. • On recovery (or death), the dependent stage of
the sick role is given up.
• A rehabilitation stage is entered if the individual
8.3.3 Sick Role
recovers.
The sick role was defined by Parsons (1951) as the role
given by society to a sick individual and was considered
to carry rights or privileges and obligations. 8.3.4.2 Determinants
The determinants of illness behaviour, according to
Mechanic (1978), are
8.3.3.1 Rights (Privileges)
According to Parsons (1951), the sick role carries the fol-
lowing two rights for the sick individual: • The visibility, recognizability, or perceptual
salience of deviant signs and symptoms
• The extent to which symptoms are seen as being
• Exemption from blame for the illness
serious
• Exemption from normal responsibilities while
• The extent to which symptoms disrupt the fam-
sick, such as the need to go to work
ily, work, and other social activities
• The frequency of appearance of deviant signs or
8.3.3.2 Obligations symptoms, their persistence, and the frequency
The sick individual has the following obligations: of recurrence
• The tolerance threshold of exposed deviant
• The wish to recover as soon as possible, signs and symptoms
including seeking appropriate help from the • Available information, knowledge, and cultural
doctor understanding of exposed deviant signs and
• Cooperation with medical investigations and symptoms
acceptance of medical advice and treatment • Basic needs leading to denial
• The competition between needs and illness These theories are now out of favour, but there is evi-
responses dence for the more recent theory relating to the
• Competing interpretations assigned to recog- effects of expressed emotion with respect to relapse in
nized symptoms schizophrenia.
• The availability and physical proximity of treat-
ment resources and the costs in terms of time,
8.4.2.1 Schizophrenogenic Mother
money, effort, and stigma
This concept was put forward by Fromm-Reichmann in
1948 (Hoff, 1982). Schizophrenia was said to be a conse-
quence of an inadequate relationship between the future
8.4 FAMILY LIFE IN RELATION TO MAJOR sufferer from schizophrenia, as a child, and his or her
MENTAL ILLNESS mother. Characteristics of the schizophrenogenic mother
Family life is guided by the explicit and implicit rela- were said to include her being
tionship rules that prescribe and limit the behaviour of
members of the family and provide expectations within • Rejecting
the family with respect to the roles, actions, and conse- • Aloof
quences of individuals. • Overly protective
• Overtly hostile
8.4.1 Elements of Family Functioning 8.4.2.2 Double Bind

Elements of family functioning of importance in relation This concept was put forward by Bateson et al. (1956).
to major mental illness (after Dare, 1985) include The parents communicated with the child (the future suf-
ferer from schizophrenia) in abnormal ways leading to
• Interactional patterns—family members and feelings of ambivalence and ambiguity, with messages
relationships, communication patterns, hierar- that were typically
chical structure, control/authority systems, rela-
tionship with the outside world • Vague
• Sociocultural context of the family—socioeco- • Ambiguous
nomic status, social mobility, migration status • Confusing
• Location of the family in the life cycle—number
of transitions, adaptation requirements Schizophrenia developed as a result of exposure to such
• Intergenerational structure—experiences of double-bind situations.
parents as children, influences of grandparents
and extended family
8.4.2.3 Marital Skew and Marital Schism
• Significance of symptoms of mental illness for
the family This concept was put forward by Lidz et al. (1957):
• Family problem-solving skills—family style,
previous experience • Marital skew—dominant and eccentric mother;
passive and dependent father
• Marital schism—parental conflict, argument,
8.4.2 Schizophrenia and hostility leading to divided loyalties to
mother and father on the part of the child (the
Historically, the following types of family dysfunction were future sufferer from schizophrenia)
at various times believed to be a cause of schizophrenia:
• Schizophrenogenic mother 8.4.2.4 Abnormal Family Communication

• Double bind This concept was put forward by Wynne and colleagues
• Marital skew and marital schism in 1958 and suggested that disordered communication
• Abnormal family communication took place between the parents of schizophrenics.
8.4.2.5 Expressed Emotion 8.4.3.2 Vulnerability Factors

In an outcome study of 200 patients, mainly with schizo- Two of the four vulnerability factors found by Brown
phrenia, Brown et al. (1958) found that those discharged and Harris (1986) to make women more susceptible to
to their families had a poor outcome, with the highest suffer from depression following life events (see the
relapse rate occurring in those families having close and following) were
frequent contact with the patients.
Subsequent follow-up studies have confirmed the asso-
• A lack of a confiding relationship
ciation of high expressed emotion in families, character-
• Having three or more children under the age of
ized by the frequent, intense expression of emotion and
15 years at home
a pushy and critical attitude by relatives to the patient,
with an increased relapse rate in family members with
schizophrenia.
In assessing expressed emotion, the five relevant scales 8.4.4 Problem Drinking and Alcohol
of the Camberwell Family Interview (CFI) are Dependence
Family life often suffers as a result of excessive alco-
• Critical comments—indicating unambiguous hol consumption, with the breakdown of relationships,
dislike or disapproval marriages, and families being common. This may result
• Hostility—expressed towards the person rather from the following consequences of excessive alcohol
than his or her behaviour consumption:
• Emotional overinvolvement—exaggerated self-
sacrificing or overprotective concern
• Warmth—based on sympathy, affection, and • Mood changes
empathy • Personality deterioration
• Positive remarks—expressing praise or approval • Verbal abuse
of the patient • Physical violence
• Psychosexual disorders
The first three of these are associated with high expressed • Pathological jealousy
emotion and predict relapse (Vaughn and Leff, 1976): • Associated gambling
• Associated abuse of other psychoactive
substances
Relapse Rate in
9 Months Following
Discharge (%)
Antipsychotic medication, low expressed 12 8.4.5 Learning Disability/Mental Retardation
emotion family Psychological processes that may occur in families with
Antipsychotic medication, high expressed 42 an impaired or disabled member (after Bicknell, 1983)
emotion family, <35 h/week face-to-face
include
contact
No antipsychotic medication, high 92
expressed emotion family, >35 h/week • Shock → panic → denial
face-to-face contact • Denial → shopping around
• Denial → overprotection/rejection
• Grief → projection of grief
• Guilt
8.4.3 Mood Disorders
• Anger
8.4.3.1 Expressed Emotion • Bargaining → late rejection
As with schizophrenia, high expressed emotion at • Acceptance → infantilization
home is associated with an increased risk of relapse of • Ego-centred work → ‘other’-centred work
depression. • Overidentification
8.5 LIFE EVENTS • The relationship between life events and the
psychiatric disorder should be found to occur in
8.5.1 Definition different populations and at different times.
Life events are sudden changes, which may be positive or
negative, in an individual’s social life, which disrupt its
normal course.
8.5.4 Difficulties in the Evaluation of Life Events
Methodological problems in the evaluation of life events
8.5.2 Life-Change Scale
The following table gives some life-change values for 1. Assessments tend to be retrospective, which can
life events in the Holmes and Rahe Social Readjustment lead to difficulties such as
Rating Scale (after Holmes and Rahe, 1967): a. Biased recall
b. Falloff in recall with time
Life-Change c. Retrospective contamination
Life Event Value d. Effort after meaning
Death of spouse 100 2. Causation and association need to be separated
Divorce 73 3. Contextual evaluation
Marital separation 65 4. Subjective evaluation
Gaol term 63
Death of close family member 63 A widely used instrument for current research into life
Personal injury or illness 53 events and psychiatric disorder is the Life Events and
Marriage 50 Difficulties Schedule (LEDS) of Brown and Harris (1978,
Being sacked from job 47 1989), which has the following features:
Retirement 45
Marital reconciliation 45 • Semistructured interview schedule
Pregnancy 40 • 38 areas probed
Birth of child 39 • Detailed narratives collected about events,
Death of close friend 37 including their circumstances
Child leaving home for good 29
• High reliability
Problems with in-laws 29
• High validity
Problems with boss 23
Change in sleeping habits 16
Change in eating habits 15
8.5.5 Clinical Significance
Minor legal violation 11
8.5.5.1 Depression
The full Holmes and Rahe Social Readjustment Rating Many studies have found a relationship between life
Scale, which was introduced in 1967, consists of a self- events and the onset of depression. In 6–12 months prior
report questionnaire containing 43 classes of life event. to the onset, compared with normal controls, patients have
a three to five times greater chance of having suffered at
least one life event with major negative long-term implica-
8.5.3 Aetiology of Psychiatric Disorders
tions (involving threat or loss). However, most people who
In order to demonstrate that life events have an aetiologi- experience adverse life events do not develop depression;
cal role in a given psychiatric disorder, the following cri- as mentioned earlier, Brown and Harris (1978) identified
teria should be fulfilled: four vulnerability factors that make women more suscep-
tible to suffer from depression following life events:
• The occurrence of life events should correlate
with onset of the disorder. • Loss of mother before the age of 11 years
• The life events should precede the onset of the • Not working outside the home
disorder and not the other way round. • A lack of a confiding relationship
• A hypothetical construct should exist with con- • Having three or more children under the age of
founded variables excluded. 15 years at home
8.5.5.2 Schizophrenia 8.6.2 Total Institutions

The evidence tends to suggest that independent life events
8.6.2.1 Definition
are more likely to occur prior to relapse rather than prior
to first onset of schizophrenia (Brown and Birley, 1968; A total institution is an organization in which a large
Tennant, 1985). number of like-situated individuals, cut off from the
wider social for an appreciable period of time, together
8.5.5.3 Anxiety lead an enclosed formally administered round of life
(Goffman, 1961).
There is some evidence that life events are more likely
to occur prior to anxiety (Finlay-Jones and Brown, 1981;
8.6.2.2 Examples
Miller and Ingham, 1985). From their study of life events
occurring in the year before the onset of three types of Examples of total institutions include
cases of psychiatric disorder of recent onset (depression,
anxiety, and mixed depression/anxiety) in young women • Older large psychiatric hospitals
and normal controls, Finlay-Jones and Brown (1981) • Prisons
argued that life events involving severe loss were a causal • Monasteries
agent in the onset of depression and life events involving • Large ships
severe danger were a causal agent in the onset of anxi-
ety states. Cases of mixed depression/anxiety were more 8.6.3 Goffman
likely to report both a severe loss and a severe danger
before onset. From his study of the large St. Elizabeth’s Hospital, in
Washington, DC, Goffman (1961) was one of the first to
8.5.5.4 Mania suggest that institutions may be harmful. Concepts intro-
In general, the results of life event studies of mania are duced by Goffman include the following:
conflicting.
• Total institution.
8.5.5.5 Parasuicide/Deliberate Self-Harm • Binary management—the daily lives of patients
There is strong evidence that threatening life events were highly regulated by staff who appeared to
are more common prior to self-poisoning attempts (e.g. live in a different world to the patients.
Morgan et al., 1975; Farmer and Creed, 1989). • Binary living.
• Batch living—whereas normally life consists of
8.5.5.6 Functional Disorders a balance between work, home life, and leisure
time, these three distinct entities did not exist in
Threatening life events have been found to be more likely
the total institution studied.
to precede functional disorders presenting physically such
• Institutional perspective—the existence of an
as abdominal pain without an organic cause (Creed, 1981;
institutional perspective leads to the assumption
Craig and Brown, 1984) and menorrhagia (Harris, 1989).
that there exists an overall rational plan.
• Mortification process—the process whereby
an individual becomes an inhabitant of a total
8.6 RESIDENTIAL INSTITUTIONS
institution.
8.6.1 Social Institutions • Betrayal funnel—the start of the mortifica-
tion process through which relatives, via doc-
8.6.1.1 Definition tors, send the individual into a psychiatric
A social institution is an established and sanctioned form hospital.
of relationship between social beings. • Role stripping—the patient is processed
through the admissions procedure, which
8.6.1.2 Examples would also usually include being physically
Examples of social institutions include stripped naked for the purposes of a physical
examination.
• The family • Patient/inmate role—patients or inmates could
• Political parties be considered to be metaphorically baptized
• Religious groups into this role through the admissions procedure,
which would usually include bathing before Hospital, Essex; and Mapperley Hospital, Nottingham).
being given institutional clothing. These hospitals were chosen because they had differ-
• Moral career—gradual changes in perception ent social conditions but otherwise were similar in that
of patients about themselves and others, occur- they had patients with schizophrenia who suffered ill-
ring as a result of institutionalization. nesses of similar severity and similar catchment area
populations, and all such patients were accepted for
8.6.3.1 Reactions to the Mortification Process admission. Thus, it was hoped to test the hypothesis
According to Goffman, patients were said to show various that social environment could influence schizophrenic
possible reactions to the mortification process, including symptoms and behaviour. A strong association was
found between poverty of the social environment and
• Withdrawal severity of clinical poverty; clinical poverty consists of
• Open rebellion
• Colonization—the patient pretends to show • Blunted affect
acceptance • Poverty of speech
• Conversion • Social withdrawal
• Institutionalization—actual acceptance both
outwardly and inwardly
8.7 ETHNIC MINORITIES, ADAPTATION,
8.6.4 Institutional Neurosis AND MENTAL HEALTH
Barton (1959) used the term institutional neurosis to 8.7.1 Prevalence of Schizophrenia
describe a syndrome he considered to be caused by insti-
tutions in which the individual shows In Britain, there is a higher rate of diagnosis of schizo-
phrenia in Afro-Caribbean and Irish populations, com-
• Apathy pared with the indigenous population, and a lower rate in
• Inability to plan for the future those of South Asian origin.
• Submissiveness
• Withdrawal 8.7.2 Causes of Different Prevalence Rates
• Low self-esteem
Explanations of the different prevalence rates of schizo-
phrenia in ethnic minorities in Britain include the following:
8.6.5 Secondary Handicap
Wing (1967, 1978) used the term secondary handi- • Those who migrate from their countries of ori-
cap to include both institutional neurosis and similar gin have a greater likelihood of having schizo-
features occurring in individuals living outside total phrenia or a predisposition for schizophrenia
institutions. (social selection)—however, there is a reduced
rate in Asians and an increased rate in second-
8.6.5.1 Primary Handicap generation Afro-Caribbeans.
This may be psychiatric illness, somatic illness, or social • Migration is associated with increased stress
difficulties that the individual has to contend with. leading to an increased precipitation of schizo-
phrenia in those with an underlying predisposi-
8.6.5.2 Secondary Handicap tion—however, there is a reduced rate in Asians
This results from the unfortunate way in which other and an increased rate in second-generation
people may react to the primary handicap, both inside Afro-Caribbeans.
and outside total institutions. • Discrimination and deprivation lead to an
increased rate of schizophrenia or an increased
precipitation of schizophrenia in those with an
8.6.6 Three Mental Hospitals Study
underlying predisposition (social causation)—
Wing and Brown (1961, 1970) carried out an important however, there is a reduced rate in Asians.
comparative study in the 1960s of three British mental • Schizophrenia is overdiagnosed in Afro-
hospitals (Netherne Hospital, South London; Severalls Caribbeans.
8.7.3 Depression and Anxiety professional groups involved in patient care may decrease
their ‘professionalization’ over time, for instance, by going
Those from ethnic minorities may not tell their doctor on strike even if this adversely affects patient care.
they feel depressed or anxious. For example,
• Afro-Caribbean men when depressed may 8.9 INTERGROUP BEHAVIOUR AND STIGMA
instead complain of erectile dysfunction or
reduced libido 8.9.1 Stereotypes
• South Asians may somatize depression
A stereotype is an overgeneralized inference about a per-
• South Asians may somatize anxiety
son or group of people in which they are all assumed to
possess particular traits or characteristics.
8.8 PROFESSIONS The use of schemata (working stereotypes) is inevi-
table until further experience either refines or discred-
8.8.1 Characteristics of Professions its them. Many stereotypes are benign but may be
The characteristics of professional status include resistant to change. However, stereotypes can become
self-perpetuating and self-fulfilling.
• The possession of practical skills based on theo-
retical knowledge 8.9.2 Stigma
• Requiring an extended period formal training
and education 8.9.2.1 Definition
• Assessments of competence carried out by the Sigma is an attribute of an individual that marks him
profession or her as being unacceptable, inferior, or dangerous and
• Belonging to an organization ‘spoils’ identity.
• Recognition by the state of the professional
organization 8.9.2.2 Example
• Adherence to a code of conduct
Psychiatric disorders are highly stigmatized in societies
• Providing altruistic service
that value rationality.
• The possession of a monopoly of practice in
their field
8.9.2.3 Enacted Stigma
This is the experience of discrimination of an individual
8.8.2 Professional Groups Involved who bears a stigma.
in Patient Care
8.9.2.4 Felt Stigma
Long-established professions in health-care services
include This is the fear of discrimination of an individual who
bears a stigma.
• Doctors
8.9.2.5 Development
• Pharmacists
• Dentists Stigma first appears during the psychoanalytic stage of
latency, approximately corresponding with Erikson’s
Newer ‘semiprofessions’ or ‘subprofessions’ include stage of industry versus inferiority, during which chil-
dren develop a strong awareness of the ways in which
• Psychiatric nurses they are similar to and differ from others.
• Clinical psychologists
• Nonmedically trained psychotherapists 8.9.3 Prejudice
• Occupational therapists
8.9.3.1 Definition
‘Semiprofessions’ or ‘subprofessions’ may increase their Prejudice is a preconceived set of beliefs held about oth-
‘professionalization’ over time, for instance, by increasing ers who are ‘prejudged’ on this basis; the negative mean-
the length of training and training requirements. Conversely, ing of the term is the one usually used. It is not amenable
to discussion and is resistant to change. Prejudiced indi- Brown GW, Carstairs GM, and Topping GC. 1958: The post-
viduals may behave in ways that create stereotyped hospital adjustment of chronic mental patients. Lancet
behaviour that sustains their prejudice. 2:658–659.
Brown GW and Harris T. 1986: Stressor, vulnerability and
depression: A question of replication. Psychological
8.9.3.2 Example Medicine 16(4):739–744.
Racism or racial prejudice is the dogmatic belief that one Brown GW and Harris TO. (eds.) 1978: Social Origins of
‘race’ is superior to another one and that there exist iden- Depression: A Study of Psychiatric Disorder in Women.
tifiable ‘racial characteristics’ that influence cognition, London, U.K.: Tavistock.
Brown GW and Harris TO. (eds.) 1989: Life Events and Illness.
achievement, behaviour, etc. New York: Guilford Press.
Craig TKJ and Brown GW. 1984: Goal frustration and life
8.9.3.3 Discrimination events in the etiology of painful gastrointestinal disorder.
This is the enactment of prejudice. (In the case of racism, Journal of Psychosomatic Research 28:411–421.
Creed F. 1981: Life events and appendectomy. Lancet
the enactment is also termed racialism.)
1:1381–1385.
Creed F. 1992: Life-events. In Weller M and Eysenck M (eds.)
8.9.3.4 Causes The Scientific Basis of Psychiatry, 2nd edn. London,
Causes of prejudice may include the following: U.K.: W.B. Saunders.
Dare C. 1985: Family therapy. In Rutter M and Hersov L (eds.)
Child and Adolescent Psychiatry: Modern Approaches.
• The person holding the prejudice is rigid Oxford, U.K.: Blackwell Scientific.
in his or her beliefs and does not toler- Durkheim E. 1966: Suicide. New York, NY: Free Press.
ate weaknesses in others; this is sometimes Farmer R and Creed F. 1989: Life events and hostility in self-
referred to by sociologists as an authoritarian poisoning. British Journal of Psychiatry 154:390–395.
personality. Finlay-Jones R and Brown GW. 1981: Types of stressful life
• Scapegoating of the victims of the prejudice. event and the onset of anxiety and depressive disorders.
• Stereotyping of the victims of the prejudice. Psychological Medicine 11:803–815.
Foucault M and Hurley R. 1998: The History of Sexuality: The
Will to Knowledge, Vol. 1. London, U.K.: Penguin.
8.9.3.5 Reducing Prejudice Foucault M and Sheridan A. 1991: Discipline and Punish: The
Cook showed that the following conditions need to be Birth of the Prison. London, U.K.: Penguin.
satisfied in order to reduce prejudice: Goffman E. 1961: Asylums: Essays on the Social Situation
of Mental Patients and Other Inmates. New York:
Doubleday.
• Equal status Goldberg D and Huxley P. 1980: Mental Illness in the
• The potential for personal acquaintance Community: The Pathways to Psychiatric Care. London,
• Exposure to nonstereotypic individuals U.K.: Tavistock Publications.
• Social environment favours equality Habermas J and McCarthy R. 1989: The Theory of
• Cooperative effort Communicative Action. Cambridge, MA: Polity Press.
Harris TO. 1989: Disorders of menstruation. In Brown GW
and Harris TO (eds.) Life Events and Illness. New York:
Guildford Press.
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9 Dynamic Psychopathology and
Psychoanalytic Theories
9.1 BASIC PRINCIPLES OF DYNAMIC treated by Breuer for hysterical symptomatology,

PSYCHOTHERAPY including limb paralysis, associated with her father’s
illness. The development of hysteria in general was
Malan (2001) has summarized the basic principles of considered to take the following course:
dynamic psychotherapy as follows:
• The cause consisted of real experiences, which
Within an atmosphere of unconditional acceptance, the were usually traumatic.
therapist establishes a relationship with the patient, the aim
• The (traumatic) event(s) gave rise to painful/
of which—usually unspoken—is to enable the patient to
understand his true feelings and to bring them to the sur- unpleasant memories and represented ideas
face and experience them. For this purpose, the therapist incompatible with conscious belief structures.
uses theoretical knowledge, guided wherever possible by • These memories and ideas were then repressed.
his own self-knowledge, to identify himself with the patient • However, the powerful affects associated with
and puts his understanding to the patient in the form of them gave rise to somatic hysterical manifesta-
interpretations, which constitute his main therapeutic tool. tions, sometimes including reenactments of the
(traumatic) event(s).
9.2 SIGMUND FREUD (1856–1939) • In consciousness, there remain mnemonic sym-
bolic representations of the event(s).
9.2.1 Early Influences • Bringing the event(s) to consciousness leads to
a discharge or release of the associated affects
Those who had an important early influence on Freud,
(‘psychic pus’) and resolution of the hysterical
and his pre-psychoanalytic theories, included
symptomatology (abreaction).
• Helmholtz and Brücke—the physicochemical
basis of brain function, concepts of energy and 9.2.2.2 Technical Development
conservation, the Helmholtz School of Medicine The techniques employed by Freud progressed gradually
• Meynert—neuroanatomy and behaviour through the following major phases:
• Charcot—hysteria and hypnosis
• The use of hypnosis.
Freud also gained important ideas from the writings of • The concentration method—the patient, lying
on a couch with closed eyes, was asked leading
• Darwin—the theory of evolution by natural questions, and Freud would press his hands on
selection the patient’s forehead.
• Hughlings Jackson—the relationship of brain • Free association—the patient, with open eyes
structure and function but lying on a couch, was encouraged to articu-
late, without censorship, all thoughts that came
to mind.
9.2.2 Protopsychoanalytic Phase
(1887 to c.1897)
9.2.2.3 Project for a Scientific Psychology
9.2.2.1 Studies on Hysteria This was mostly written by Freud in 1895 and published
In 1895, Josef Breuer and Sigmund Freud published after his death in 1950 (Freud, 1950). It consists essen-
Studies on Hysteria (Freud, 1962). This included the tially of an attempt to link psychological processes
case of Anna O. (Bertha Pappenheim) who had been with neurophysiology.
129
9.2.3 Topographical Model of the Mind 9.2.3.3 Conscious

This was set out in Freud’s The Interpretation of Dreams This can be considered to be an attention sensory organ.
(1900) and developed during the following two decades Characteristic features include
until its eventual replacement by the structural model
(Freud, 2010). In this model, the mind is considered to 1. Within awareness
consist of the following three parts: 2. Operating system—secondary process thinking
3. Motivating principle—the reality principle
• The unconscious 4. Access—easy
• The preconscious 5. System position:
• The conscious a. Bound by time
b. Word oriented
c. Declarative
9.2.3.1 Unconscious d. Linear
This contains memories, ideas, and affects that are
repressed. Characteristic features include 9.2.3.4 Censorship
Freud described the censorship process in the following way
1. Outside awareness (Galison, 2012):
2. Operating system—primary process thinking
3. Motivating principle—the pleasure principle Let us compare the system of the unconscious to
4. Access—access to its repressed contents is dif- a large entrance hall, in which the mental impulses
jostle one another like separate individuals. Adjoining
ficult, occurring when the censor gives way, for
this entrance hall there is a second narrow room, a
instance, by becoming: kind of drawing room, in which consciousness also
a. Relaxed, for example, in dreaming resides but on the threshold between these two rooms
b. Fooled, for example, in jokes a watchman performs his function; he examines the
c. Overpowered, for example, in neurotic different mental impulses, acts as a censor, and will
symptomatology not admit them into the drawing room if they dis-
5. System position: please him. It does not make much difference if the
a. No negation watchman turns away from a particular impulse at
b. Timelessness (reference to time is bound up the threshold itself or if he pushes it back across the
threshold after it has entered the drawing room. If they
in unconsciousness)
have already pushed their way forward to the thresh-
c. Image oriented old and have been turned back by the watchman then
d. Connotative they are inadmissible to the consciousness; we speak
e. Symbolic of them as repressed but even the impulses which the
f. Nonlinear watchman has allowed to cross the threshold are not
on that account necessarily conscious as well; they
can only become so if they succeed in catching the eye
9.2.3.2 Preconscious of consciousness. They are therefore justified in call-
This part of the mind develops during childhood and serves ing the second room the system of the preconscious.
to maintain repression and censorship. Characteristic fea-
tures include 9.2.3.5 Primary Process
This is the operating system of the unconscious. Its attri-
1. Outside awareness butes include the following:
2. Operating system—secondary process thinking
3. Motivating principle—the reality principle • Displacement—an apparently insignificant idea is
4. Access—access can occur through focused invested with all the psychical depth of meaning
attention and intensity originally attributed to another idea.
5. System position: • Condensation—all the meanings and several
a. Bound by time chains of association converge onto a single idea
b. Word oriented standing at their point of intersection.
c. Denotative • Symbolization—symbols are used rather than
d. Linear words.
Dynamic Psychopathology and Psychoanalytic Theories 131
Characteristics of primary process thinking include the • Nocturnal stimuli—external stimuli, for exam-
following (Sklar, 1989): ple, noise, moisture, touch, and internal stimuli,
for example, pain and urinary bladder distension
• Timelessness—the concept of time only devel- • Unconscious wishes
ops after a period in the mind of a child in • Latent dream—the day residue, nocturnal stim-
connection to conscious reality, for example, uli, and unconscious wishes
periodicity or chaos of feeding.
• Disregard of reality of the conscious world.
9.2.4.2 Dream Work
• Psychical reality—memories of a real event and
of imagined experience are not distinguished; This refers to the process whereby the latent dream is
abstract symbols are treated concretely. converted into the manifest dream. Operations that con-
• Absence of contradiction—opposites have a tribute to dream work can include
psychic equivalence.
• Absence of negation. • Displacement
• Condensation
9.2.3.6 Secondary Process • Symbolization
This is the operating system of the preconscious and the • Secondary elaboration (secondary revision)—
conscious. Characteristics of secondary process thinking the process of revising and/or elaborating the
include the following: dream after awakening in order to make it more
consistent with the rules of secondary process
• Time flows forward linearly.
• Reality is regarded—the content and logical 9.2.5 Structural Model of the Mind
basis of ideas is important.
• Verbal word—presentations are used. This was set out in Freud’s The Ego and the Id (1923)
• Contradictions are recognized and should not and replaced the topographical model. In this model, the
exist. mind is considered to consist of the following three parts:
9.2.3.7 Pleasure Principle • The id

This is the motivating principle of primary process. It is • The ego
mainly inborn. Pain/‘unpleasure’ is avoided and pleasure • The superego
is sought through tension discharge. This leads to
9.2.5.1 Id
• Wish fulfillment Most of the id is unconscious. It contains primordial
• The discharge of instinctual drives energy reserves derived from instinctual drives. Its aim is
to maximize pleasure by fulfilling these drives.
9.2.3.8 Reality Principle
This is the motivating principle of secondary process. It 9.2.5.2 Ego
is the result of external reality. It leads to
According to Freud (1984), the principal characteristics
of the ego are as follows:
• Delayed gratification
In consequence of the preestablished connection
9.2.4 Dreaming between sense and perception and muscular action, the
ego has voluntary movement at its command. It has the
In his The Interpretation of Dreams (1900), Freud referred
task of self-preservation. As regards external events,
to dreams as ‘the Royal Road to the Unconscious’. it performs that task by becoming aware of stimuli by
storing up experiences about them (in the memory),
9.2.4.1 Dream Composition by avoiding excessively strong stimuli (through adap-
Dreams were considered to be composed of tation), and finally by learning to bring about expedi-
ent changes in the external world to its own advantage
• The day residue—memories of the waking hours (through activity). As regards internal events in relation
before the dream that are particularly emotion- to the id, it performs that task by gaining control over the
ally charged demands of the instinct, by deciding whether they are to
be allowed satisfaction, by postponing that satisfaction 9.2.7 Transference

to times and circumstances favourable in the external
world, or by suppressing their excitations entirely. It is Sklar (1989) described the important features of the
guided in its activity by consideration of the tension pro- transference:
duced by stimuli, whether these tensions are present in it
or introduced into it. The transference is an unconscious process in which
the patient transfers to the therapist feelings, emotions
Although much of the ego is conscious, most of its activ- and attitudes that were experienced and/or desired in
ity occurs without consciousness. Owing to its direct the patient’s childhood, usually in relation to parents
access to perception, reality testing takes place in the ego. and siblings. It can be a passionate demand for love
and hate in past relationships between the child and the
However, the ego can be said to serve the following ‘three
adult. This is a complex field that includes the uncon-
harsh masters’: scious splitting of the therapist into masculine and
feminine and locating unconscious affect and think-
• The superego ing of the ‘child’ part of the patient in relation to the
• Reality maternal and paternal aspects of the therapist (i.e. oedi-
• The id pal transference). Furthermore, the direction of such a
transference can be both positive and negative. Thus,
9.2.5.3 Superego Freud encountered transference in many variations
The superego is concerned with issues of morality. It devel- and certainly also in its hidden form, transformed by
resistance. The therapist’s transference represents on
ops initially as a result of the imposition of parental restraint.
the one hand the most powerful ally but, on the other,
Although more of the superego is conscious than is the case in terms of transference’s resistance, a therapeutic
for the id, most of its activity occurs without consciousness. difficulty.
9.2.5.4 Relationship between the Id, Ego, 9.2.8 Countertransference

and Superego
Sklar (1989) described the important features of the
Freud (1984) described this relationship in the following
countertransference:
way:
The countertransference is the therapist’s own feel-
We were justified… in dividing the ego from the id…
ings, emotions and attitudes to his patient. In the treat-
[But] the ego is identical with the id, and is merely
ment mode, the therapist needs to screen out those that
a specially differentiated part of it.… if a real split
are mediated only by the therapist, and take note of
has occurred between the two, the weakness of the
those generated in the therapist from emotional con-
ego becomes apparent. But if the ego remains bound
tact with the patient. The latter can be an interesting
up with the id and indistinguishable from it, then it
aspect of the patient, e.g. the therapist may have the
displays its strength. The same is true of the relation
feelings of the patient as child in relation to the patient
between the ego and the super-ego. In many situations
enacting the parent. Thus, in the reverse transference,
the two are merged; and as a rule we can only dis-
an aspect of the patient is located in the therapist as a
tinguish one from the other when there is a tension
communication.
or conflict between them. In repression the decisive
fact is that the ego is an organization and the id is not.
The ego is, indeed, the organized portion of the id. We 9.2.9 Instinctual Drives
should be quite wrong if we pictured the ego and the id
as two opposing camps.… Freud used the German word trieb to refer to an
instinctual drive. Unfortunately, this has often been
translated into the word ‘instinct’, a concept different
9.2.6 Resistance
from a ‘drive’. Important instinctual drives identified
This is everything, in words and actions of the analysand, by Freud were
that obstructs him or her gaining access to their uncon-
scious. It can be used in psychoanalysis as a means to • Libido—sexual ‘instinct’ and energy of the eros
reach the repressed; indeed, the forces at work in resis- • Eros—life preservation ‘instinct’
tance and repression are the same. • Thanatos—death ‘instinct’
9.2.10 Psychosexual Development 9.3.2 Differences between Jungian

and Freudian Theory
The stages of psychosexual development identified by
Freud were the Jung came to different conclusions to Freud on a number
of issues, including the following.
• Oral phase
• Anal phase
9.3.2.1 Libido Theory
• Phallic phase
• Latency phase Jung did not believe that libido was confined to being sex-
• Genital phase ual, but considered the libido as being the unitary force of
every manifestation of psychic energy.
9.2.10.1 Oral Phase
From birth to around 15–18 months of age. Erotogenic 9.3.2.2 Nature of the Unconscious
pleasure is derived from sucking. In addition to the moth- Jung believed in the collective unconscious, later referred
er’s breast, the infant has a desire to place other objects to as the objective psyche, which he considered contained
in his or her mouth. latent memories of our cultural, racial, and phylogenetic
past. In Jungian theory, the objective psyche gives rise to
9.2.10.2 Anal Phase consciousness.
From around 15–18 months to 30–36 months of age.
Erotogenic pleasure is derived from stimulation of the
9.3.2.3 Causality
anal mucosa, initially through faecal excretion and later
also through faecal retention. Rather than explaining present events in terms of
Freudian psychic determinism, Jungian theory employs
9.2.10.3 Phallic Phase
From around 3 years of age to around the end of the • Causality—offers an explanation in terms of
fifth year. Boys pass through the Oedipal complex. the past
Girls develop penis envy and pass through the Electra • Teleology—offers an explanation in terms of the
complex. future potential
• Synchronicity—offers an explanation in terms
9.2.10.4 Latency Stage of causation at the boundary of the physical
From around 5–6 years to the onset of puberty. The sex- world with the psychical (‘mystic’) world
ual drive remains relatively latent during this period.
9.3.2.4 Dreaming
9.2.10.5 Genital Stage Jungian theory views the contents of dreams within a
From the onset of puberty to young adulthood a strong phylogenetic framework in which archetypes may be pro-
resurgence in the sexual drive takes place. Successful jected onto others.
resolution of conflicts from this and previous psycho-
sexual stages leads to a mature well-integrated adult
identity. 9.3.3 Archetypes
The archetypes of the objective psyche are energy-field
configurations manifesting themselves as representa-
9.3 CARL JUNG (1875–1961) tional images having universal symbolic meaning and
Jung founded the psychoanalytic school of analytic typical emotional and behavioural patterns. Five impor-
psychology. tant types of archetype are identified in Jungian theory.
9.3.3.1 Anima
9.3.1 Early Influences The feminine prototype within each person.
Jung was originally an important member of Sigmund
Freud’s inner circle and indeed at one time his designated 9.3.3.2 Animus
successor. The masculine prototype within each person.
9.3.3.3 Persona 9.3.6 Extroversion and Introversion

The outward mask covering the individual’s personality
9.3.6.1 Extroversion
and allowing social demands to be balanced with internal
needs. Both a public and a private persona may be pos- The individual’s concerns and mental operations are
sessed by a person. The persona may be represented in directed to the objective reality in the external world.
terms of clothing in dreams.
9.3.6.2 Introversion
The individual’s concerns and mental operations are
9.3.3.4 Shadow directed to the subjective reality of the inner world.
This represents repressed animal instincts arising from
phylogenetic development and in dreams manifests itself
as another person of the same sex. 9.3.7 Individuation
This is the process of personality growth leading to the
9.3.3.5 Self development of a unique realization of what one intrin-
A central archetype holding together conscious and sically is.
unconscious aspects, including future potential, arche-
types, and complexes.
9.4 MELANIE KLEIN (1882–1960)
9.3.4 Complexes 9.4.1 Background
Complexes surround archetypes and can be defined as Klein, who lacked any formal higher education and never
feeling-toned ideas. They develop from an interaction of developed a full theory of development, was a contro-
personal experiences and archetypal models. versial figure in the British Psychoanalytical Society.
When she began developing her theories, Sigmund Freud
viewed her as potentially challenging the work in child
9.3.5 Mental Operations analysis of his daughter Anna Freud.
Jungian theory postulates four operations of the mind: It is now known that Klein analysed her three children
and wrote them up as disguised clinical cases. She pro-
• Feeling posed that the aim of child psychoanalysis was to ‘cure’
• Intuition all children of their ‘psychoses’.
• Sensation
• Thinking 9.4.2 Differences between Kleinian
and Freudian Theory
9.3.5.1 Feeling
This allows feelings: Among the important differences between the theories of
Klein and Freud were the following.
• Anger and joy
• Love and loss 9.4.2.1 Object Relations
• Pleasure and pain Klein believed that the infant was capable of object
relations.
Judgements regarding good and evil also use this operation.
9.3.5.2 Intuition 9.4.2.2 Paranoid-Schizoid Position

This is perception through unconscious processes. Rejecting the critical importance of autoeroticism
for the infant, Klein believed instead that the para-
9.3.5.3 Sensation noid position, later, under the influence of Fairburn,
This allows the acquisition of factual data. renamed the paranoid-schizoid position, developed
as a result of frustration during the first year of life
9.3.5.4 Thinking with pleasurable contact with objects such as the good
This is composed of logic and reasoning. It is verbal and breast. The paranoid-schizoid position, characterized
ideational. by isolation and persecutory fears, developed as a result
of the infant viewing the world as part objects, using 9.5 DONALD WINNICOTT (1897–1971)
the following defence mechanisms:
9.5.1 Background
• Introjection (internalization) Winnicott was a British paediatrician who became a psy-
• Projective identification choanalyst. He was a contemporary of Anna Freud and
• Splitting Melanie Klein, between whom he at one time tried to
mediate. He made important contributions to object rela-
Objects viewed by the infant as good are believed to tions theory and his reputation has grown steadily since
be introjected, while those viewed as bad are split or his death.
projected.
9.5.2 Mother–Baby Dyad
9.4.2.3 Aggression
A strong emphasis was placed on aggression, occurring Winnicott believed it was wrong to consider the baby in
particularly during the paranoid-schizoid position. isolation, noting that there was
no such thing as an infant (apart from the maternal

9.4.2.4 Depressive Position provision).
This is said to develop by the age of 6 months when
the child no longer views the world in terms of part
objects but realizes that objects are whole and the 9.5.3 Countertransference
world is not perfect. 9.5.3.1 Objective Countertransference
Winnicott broadened the understanding of the counter-
9.4.2.5 Development of the Ego and Superego transference from that of Freud, speaking of the objective
The ego and a primitive superego are present, according countertransference. The objectivity derived from his
to Klein, during the first year of life. belief that the countertransference was an understandable
and normal reaction to the personality and behaviour of
the analysand.
9.4.3 Early Development
The stages of development during the first year were con- 9.5.3.2 Countertransference Hate
sidered to include, in chronological order, Winnicott normalized the existence of countertransfer-
ence hate. He gave reasons why a mother hates her infant
• Oral frustration (male or female) even from the start of their relationship.
• Oral envy (of parental ‘oral’ sex) and oral He then drew an analogy from this mother–infant dyad
sadism, leading to Oedipal impulses to the therapist–patient relationship. Winnicott suggested
• A longing for the oral incorporation of father’s that the countertransference hate should be articulated
penis, by aggressive desires to bring about the to the analysand at the end of therapy, but most analysts
destruction of mother’s body (which contains would tend not to go this far.
father’s penis)
• Castration anxiety in boys and fear of destruc-
tion of her own body in girls 9.5.4 Motherhood
• Emergence of the primitive superego 9.5.4.1 Good-Enough Mother
• Introjection of pain-causing objects
The good-enough mother is a mother who responds to her
• Development of a cruel superego
baby’s communications and meets his or her needs within
• Ejection of the superego
an optimal zone of frustration and gratification.
9.4.4 Analytic Play Technique 9.5.4.2 Pathological Mother

The analysis of children’s play was considered to be the This is a mother who imposes her own needs over those
homologue, for children, of the free association tech- of her baby, causing her baby to create a false self in order
nique and dream interpretation for adults. to protect his or her true self.
9.5.4.3 Capacity to Be Alone unconscious. When successful, no trace remains in con-

Good parenting by the mother, allowing her child to sciousness but some affective excitation does remain.
become increasingly autonomous while at the same time
being dependent on her, results in the child being able to
9.6.2 Reaction Formation
be himself or herself in the presence of his or her mother,
and vice versa. This was termed the capacity to be alone Psychological attitude diametrically opposed to an
in the presence of another. oppressed wish and constituting a reaction against
it. Often seen in patients with obsessive–compulsive
disorder.
9.5.5 Transitional Object
This is an object, which is neither oneself nor another
person (including mother), that is selected by an infant 9.6.3 Isolation
between 4 and 18 months of age for self-soothing and Thoughts/affects/behaviours are isolated so that their
anxiety reduction. Examples include a blanket or toy links with other thoughts or memories are broken. Often
that helps the infant go to sleep. It helps during the pro- seen in patients with obsessive–compulsive disorder.
cess of separation–individuation. In adults, transitional
phenomena that may allow us to cope with loneliness
and separation can include music, religion, and scien- 9.6.4 Undoing (What Has Been Done)
tific creativity. An attempt is made to negate or atone for forbidden
thoughts, affects, or memories. This defence mecha-
9.5.6 Other Concepts nism is seen, for example, in the compulsion of magic in
patients with obsessive–compulsive disorder.
Other important concepts associated with Winnicott
include
9.6.5 Projection
• The holding environment—a therapeutic ambi- Unacceptable qualities, feelings, thoughts, or wishes are
ance or setting allowing the patient to experi- projected onto another person or thing. Often seen in
ence safety, and so facilitating psychotherapy paranoid patients.
• The potential space—an area of experiencing
identified as existing between the baby and the
object; it subsequently underlies all play, imagi- 9.6.6 Projective Identification
nation, dreams, and the interdependence of The subject not only sees the other as possessing aspects
transference and countertransference of the self that have been repressed but constrains the
• The squiggle game—a play therapy technique other to take on those aspects. It is a primitive form of
• At-one-ment projection.
• Primary maternal preoccupation
• Regression to dependence
• Going on being 9.6.7 Identification
• Impingement
Attributes of others are taken into oneself.
• Object usage
9.6 PSYCHODYNAMIC THEORY 9.6.8 Introjection

OF DEFENCE MECHANISMS In fantasy, the subject transposes objects and their quali-
ties from external world into themselves.
9.6.1 Repression
The basic defence mechanism, repression is the push-
9.6.9 Incorporation
ing away (verdrängung) of unacceptable ideas, affects,
emotions, memories, and drives, relegating them to the Another’s characteristics are taken on.
9.6.10 Turning against the Self 9.6.19 Acting Out

An impulse meant to be expressed to another is turned Expressing unconscious emotional conflicts or feelings
against oneself. directly in actions without being consciously aware of
their meaning.
9.6.11 Reversal into the Opposite
9.6.20 Displacement
The polarity of an impulse is reversed in the transition
from activity to passivity. Emotions, ideas, or wishes are transferred from their
original object to a more acceptable substitute.
9.6.12 Rationalization
9.6.21 Intellectualization
An attempt to explain in a logically consistent or ethically
acceptable way, ideas, thoughts, and feelings whose true Excessive abstract thinking occurs in order to avoid con-
motive is not perceived. It operates in everyday life and in flicts or disturbing feelings.
delusional symptoms.
BIBLIOGRAPHY
9.6.13 Sublimation Freud A. 1936: The Ego and the Mechanisms of Defence.
London, U.K.: Hogarth Press.
A process that utilizes the force of a sexual instinct Freud S. 1950: Project for a scientific psychology (1950 [1895]).
in drives, affects, and memories in order to motivate The Standard Edition of the Complete Psychological Works
creative activities having no apparent connection with of Sigmund Freud, Vol. I (1886–1899), pp. 281–391. Pre-
sexuality. Psycho-Analytic Publications and Unpublished Drafts.
Freud S. 1953–1966: The Standard Edition of the Complete
Psychological Works of Sigmund Freud, Vols. 1–24.
9.6.14 Idealization London, U.K.: Hogarth Press.
Freud S. 1962: The Standard Edition of the Complete
The object’s qualities are elevated to the point of perfection. Psychological Works of Sigmund Freud: Vol. III
(1893–1899), pp. 11–23. London, U.K.: Hogarth Press.
Freud S. 1984: On Metapsychology - The Theory of
9.6.15 Regression Psychoanalysis: ‘Beyond the Pleasure Principle’, ‘The
Ego and the Id’ and Other Works. London, U.K.: Penguin
Transition, at times of stress and threat, to moods of
Books.
expression and functioning that are on a lower level of Freud S. 2010: The Interpretation of Dreams the Illustrated
complexity, so that one returns to an earlier level of matu- Edition. London, U.K.: Sterling Press.
rational functioning. Galison P. 2012: Blacked-out spaces: Freud, censorship and
the re-territorialization of mind. British Journal for the
History of Science 45 (165):235–266.
9.6.16 Denial Hall CS. 1956: A Primer of Freudian Psychology. London,
U.K.: George Allen & Unwin.
Denying the external reality of an unwanted or unpleas- Jung CG. 1961: Memories, Dreams, Reflections. New York:
ant piece of information. Random House.
Jung CG. 1964: Man and His Symbols. New York: Doubleday.
9.6.17 Splitting Klein M. 1948: Contributions to Psycho-Analysis, 1921–1945.
London, U.K.: Hogarth Press.
Dividing ‘good’ objects, affects, and memories from Klein M. 1949: The Psycho-Analysis of Children, 3rd edn.
‘bad’ ones. Often seen in patients with borderline per- London, U.K.: Hogarth Press.
sonality disorder. Malan DH. 2001: Individual Psychotherapy and the Science of
Psychodynamics, 2nd edn. London, U.K.: Arnold.
Ogden TH. 1992: The dialectically constituted/decentred subject of
9.6.18 Distortion psychoanalysis, II: The contributions of Klein and Winnicott.
International Journal of Psycho-Analysis 73:613–626.
Reshaping external reality to suit inner needs. Segal H. 1980: Melanie Klein. New York: Viking Press.
Sklar J. 1989: Dynamic psychopathology. In Puri BK and Sklar J Winnicott DW. 1958: Collected Papers: Through Paediatrics to
(eds.) Examination Notes for the MRCPsych Part I. Psycho-Analysis. New York: Basic Books.
London, U.K.: Butterworth/Heinemann. Winnicott DW. 1965: The Maturational Processes and the
Storr A. 1990: The Art of Psychotherapy, 2nd edn. London, Facilitating Environment. New York: International
U.K.: Hodder Education. Universities Press.
Winnicott DW. 1949: Hate in the counter-transference. Intern Winnicott DW. 1971: Playing and Reality. New York: Intern
ational Journal of Psycho-Analysis 30:69–74. ational Universities Press.
10 History of Psychiatry
10.1 BEFORE COMMON ERA (BCE) Moral treatment of insanity was promoted after the
Retreat in York.
Mental illnesses were perceived as originated from God in In 1811, Wilhelm Griesinger established the modern
the ancient world. There were references to mental disorders model of the department of psychiatry in Germany. He
in Egyptian papyri in 1500 BCE and in the Old Testament. thought psychiatric illness was a brain disease. He was
In 400 BCE, Plato thought that the brain is the seat of the first psychiatrist to establish the model of general hos-
mental disorders. Hippocrates considered mental disor- pital psychiatry.
ders to be bodily conditions requiring medical treatment. In 1812, Benjamin Rush and Samuel Merritt published
Hippocrates was the first person to describe mental dis- the first textbook in psychiatry, Medical inquiries and
turbances as mania and melancholia. observations upon the diseases of the mind (Rush and
Merritt, 1812).
10.2 COMMON ERA Based on Pinel’s work, Esquirol set up a series of lec-
tures in psychological medicine to teach medical students
Melancholia was described by a Roman physician, in Edinburgh in 1823.
Celsus, as depression caused by black bile. In 1827, Johann Heinroth was appointed as the first
professor in psychological therapy in Leipzig.
10.3 MIDDLE AGES Paul Briquet coined the term hysteria or Briquet syn-
drome, which refers to multiple somatization disorder.
Mental disorders were considered to be spiritual issues
rather than medical illnesses. This concept was promi-
nent throughout the Middle Ages. 10.7 1830–1914
During the first wave of biological treatments, the fol-
10.4 1247–1320 lowing drugs were discovered: chloral hydrate (a hyp-
notic) in 1832 and barbiturates in 1903.
In 1247, the Bethlem hospital was the first mental hos-
pital in Great Britain to offer care for people who were
insane. The first lunacy (insanity) legislation was passed 10.8 1830s
in England in 1320. In 1835, Phineas Gage was the first patient to be reported
to suffer from frontal lobe syndrome in the medical lit-
10.5 1700s erature. He suffered from an injury after an iron rod went
through his frontal lobe. He was noted to have a person-
King George III suffered from recurrent mental disorder ality change but no changes in memory and intelligence.
(possible porphyria) in Great Britain. As a result of the Through his case, the neuroscientists started to have a
King’s mental illness, a committee was appointed by the better understanding of the frontal lobe functions.
House of Lords. The committee considered the mental
illness of the King and mental illnesses in general. The
10.9 1840s
King was looked after by Francis Willis who ordered
physical restraints on the King. In 1847, Wilhelm Griesinger (1817–1868) defined mental
disorder as a disease of the brain by using the general
paralysis of the insane as an example.
10.6 1790–1830
The Association of Medical Officers of Asylums and
Popularization of psychiatric treatment included the pro- Hospitals for the Insane was formed in Great Britain. It
posal of removing physical restraints. In 1793, Philippe evolved into the Medico Psychological Association that
Pinel advised the removal of chain from people who were was the former organization before the establishment of
considered to be mad in Great Britain. the Royal College of Psychiatrists.
139
10.10 1850s In 1882, Karl Kahlbaum, a German psychiatrist,

coined the term cyclothymia.
Jean-Martin Charcot (1825–1893) is the founder of mod- In 1885, Georges Gilles de la Tourette (1857–1904)
ern neurology. He coined at least 15 medical eponyms diagnosed a patient with multiple motor tics, coprolalia
including Charcot–Marie–Tooth disease and amyo- and echolalia, to suffer from Tourette’s syndrome.
trophic lateral sclerosis (Lou Gehrig’s disease). In 1897, Alois Alzheimer gave a report of neurofibril-
In 1854, Jules Falret, a French psychiatrist, described lary tangles and plaques in a 51-year-old woman with
alternating mood and depression as folie circulaire. cognitive impairment.
In 1899, Emil Kraepelin coined two terms, demen-
10.11 1860s
tia praecox (schizophrenia in modern psychiatry) and
Down syndrome was first described by Langdon Down manic–depressive psychosis (bipolar disorder in mod-
in 1866. ern psychiatry, absence of a dementia, and deteriorating
Benedict Morel proposed the degeneration theory that course).
stated that mental illness affecting one generation could Magnan coined the term bouffee delirante, which is
be passed on to the next in ever-worsening degrees. an acute delusional psychosis precipitated by stress such
Jacob Mendes Da Costa coined the term Da Costa’s as exhaustion. The person may exhibit cyclical mood dis-
syndrome or ‘soldier’s heart’ during the American Civil turbance. This phenomenon is related to acute and tran-
War. This condition is a functional heart disease and the sient psychosis in modern psychiatry.
soldiers presented with left-sided chest pain, palpitation,
breathlessness, sweating, and fatigue during exertion.
10.14 1900s
10.12 1870s Sigmund Freud was initially studying cases of hysteria
using hypnosis. Then he began to develop the technique
The following terminologies were coined in schizophre-
of psychoanalysis, which was later used to explain the
nia during this period: hebephrenia by Ewald Hecker and
psychological causes of symptoms. He helped psychia-
catatonia by Karl Ludwig Kahlbaum.
trists to establish themselves as an office-based specialty
Paul Broca (1824–1888) coined Broca’s aphasia,
and to wrest psychotherapy from the neurologists.
which involves a lesion in the ventroposterior region of
Carl Jung (1916), Alfred Adler (1912), and Pierre Janet
the frontal lobe. This leads to Broca’s aphasia that affects
(1903) gave emphasis to the unconscious mind and to
speech production but not comprehension.
underlying sexual motives. They formed the International
Carl Wernicke (1848–1905) coined Wernicke’s apha-
Psychoanalytic Association.
sia. Lesion in the left posterior and superior temporal
Henry Maudsley (1835–1918) was the first person
gyrus leads to impairment in language comprehension.
to propose the abolishment of physical restraints in
Sir William Gull (1816–1890) published his work
England. He went on to become one of the best-known
Anorexia Nervosa (Apepsia Hysterica, Anorexia Hysterica)
psychiatrists during the Victorian era. He believed psy-
in 1873 by describing three women presenting with extreme
chiatric illness to be a physical disorder of the body,
emaciation and amenorrhoea (Silverman, 1997).
similar to other medical illnesses. To him, malforma-
tion on the face is a visible sign of underlying cerebral
10.13 1880s AND 1890s
disorganization. He was the editor of the Journal of
Psychiatrists at that time were pessimistic about the pos- Mental Science that later became the British Journal
sibilities of cure. of Psychiatry. He founded the Maudsley Hospital with
There were developments in neuroanatomy during this London County Council.
period. Theodor Meynert was involved in the pioneering The concept of degeneration emerged. In modern
work on the microscopic structure of the brain and spinal genetics, degeneration is related to the trinucleotide repeat
cord. Paul Flechsig studied the basic functional aspects mutations. The mutation causes an illness to descend in
of the cerebral cortex. Wernicke tried to establish specific the family, and the subsequent generations will have ear-
symptom complex and its association with specific areas lier an onset or manifest a more severe form of the illness.
of the brain. Unfortunately, the idea of degeneration was misused and
Joseph Breuer and Sigmund Freud published two supported social policies such as sterilization, euthana-
books, Studies on Hysteria (Freud and Breuer, 1955) and sia, and the persecution of the Jews on the assumption
Interpretation of Dreams (Marinelli and Mayer, 2003). that they were degenerated people.
History of Psychiatry 141
In 1901, Ivan Petrovich Pavlov (1849–1936) proposed In 1918, Jean Piaget (1896–1980) received a doctorate
classical conditioning by demonstrating that the repeated in biology at the age of 22. He proposed cognitive devel-
pairing of a conditioned (neutral) stimulus (e.g. food) with opment stages.
an unconditioned stimulus (e.g. bell) will allow the pres- The Maudsley Hospital was opened in 1919 by Sir
ence of unconditioned stimulus alone to produce the same Aubrey Lewis (1900–1975). The first academic depart-
response (e.g. drooling of saliva) as conditioned stimulus. ment of psychiatry in the United Kingdom was opened
In 1908, Eugen Bleuler (1857–1939) proposed the in Edinburgh.
term ‘schizophrenia’.
In 1909, Emil Kraepelin (1856–1926) coined the term
10.16 1920s
late paraphrenia, which has a later onset than dementia
praecox. This condition is more common in women with In 1921, the Serbsky Institute was founded in Moscow.
sensory impairment. This institute was used to house political prisoners dur-
Pierre Janet (1859–1947) coined the term psychasthe- ing the Soviet era, and they were diagnosed to suffer
nia that is composed of anxiety, phobias, obsessions, and from progressively sluggish schizophrenia based on their
neurotic depression. struggle for truth and justice.
In the early 1900s, children suffering from enceph- Neurasthenia and related conditions were accepted
alitis often developed impulsivity, disinhibition, and as disorders for which military pensions could be
hyperactivity. This neuropsychiatric sequela is known as drawn. In 1924, Mayer-Gross coined the term oneiro-
hyperactive syndrome. phrenia, which is an acute form of illness characterized
by a dreamlike state.
In 1927, Wilhelm Reich (1897–1951) was a pioneer of
10.15 1910s
body psychotherapy and several emotion-based psycho-
Adolph Meyer (1866–1950) emphasized the need for an therapies. He also laid the foundation for Gestalt therapy
eclectic approach combining physical, social, and psycho- and primal therapy.
logical aspects when treating people with mental illnesses. Otto Rank (1884–1939) coined the term ‘primal anxi-
The Mental Deficiency Act was passed in Great Britain. ety’. Rank was an important figure to move psychother-
William H. R. Rivers (1864–1922) coined the term apy away from psychoanalysis. He developed a more
‘shell shock’. During the First World War (1914–1917), active and egalitarian psychotherapy focused on the
shell shock reached a peak incidence following the Battle here-and-now and conscious mind rather than past his-
of the Somme in 1916. The patient may develop traumatic tory, transference, and unconscious.
neurosis as a result of external source or transference Development in psychology during this period
neurosis as a result of internal source. As cowardice and included the following: The Little Albert experiment by
desertion were capital offences in the British Army at that John Watson and Rosalie Rayner, Rorschach inkblot
time, the military authorities tried to distinguish inten- test, systematic desensitization, the theory of emotions
tional from non-intentional symptoms. There was debate by Cannon–Bard, psychodrama by Jacob Levy Moreno
whether shell shock was an organic disease or a form of (1889–1974), and Gestalt psychology and psychotherapy
malingering. Mott considered that there was a pathologi- by Frederick Salomon Perls (1893–1970).
cal basis for shell shock, consisting of haemorrhages in The Medico Psychological Association received its
the brain. Shell shock finally led to an acceptance among Royal Charter.
the general public that overwhelming stress could lead to
illness even among soldiers of previously proven bravery.
10.17 1930s
The ‘malarial fever cure for neurosyphilis’ was discov-
ered by Julius Wagner-Jauregg and became the first suc- There were developments of new physical therapies dur-
cessful physical therapy in psychiatry. Wagner-Jauregg was ing this period:
awarded the Nobel Prize. During that time, there was a
deliberate denial of treatment for African Americans with • Hydrotherapy was one of the common methods
syphilis. used to treat agitated patients. The actual spa
In 1916, Alfred Binet (1857–1911) and Lewis Terman therapy of psychoses and neuroses was con-
from Stanford University proposed the Stanford–Binet ducted in the hydros.
Intelligence Scale that forms the basis of modern intel- • Manfred Sakel (1900–1957) introduced insulin
ligence quotient (IQ) test. coma therapy that was initially used to treat
drug addiction, but, later, it was widely used a toxic product. Lithium was used to dissolve the uric
to treat schizophrenia. Patients were permitted acid prior to injection. Guinea pigs injected with lithium
to spend no more than 20 min in coma before became very placid. In 1949, Cade decided to inject manic
being brought back to consciousness with a patients with lithium.
sugar solution. Paul Hoch and Philip Polatin described pseudo-
• Electroconvulsive treatment (ECT) was neurotic schizophrenia (pan-anxiety, pan-neurosis, and
introduced by Ugo Cerletti (1877–1963) who pansexuality) that later developed into the concept of
induced convulsions electronically rather than borderline personality disorder.
pharmacologically. Lucio Bini (1908–1964) In 1943, Leo Kanner coined the term infantile autism
was the first person to perform ECT using in his classic paper, ‘Autistic Disturbances of Affective
bilateral placement of electrodes. ECT was Contract’ (Kanner, 1968).
initially used to treat schizophrenia but more In 1944, Hans Asperger described a syndrome applied
widely used for severe depressive illness in to persons with normal intelligence who exhibits a quali-
the later development. tative impairment in reciprocal social interaction and
• In 1935, psychosurgery was introduced by Egas behavioural oddities without delays in language develop-
Moniz (1874–1955). Moniz got the idea for psy- ment. He named his syndrome ‘autistic psychopathy’ that
chosurgery from the observation that emotional later became Asperger’s syndrome.
changes occur in a chimpanzee following the The ICD-1 was published by the World Health
ablation of its frontal lobes. Organization (WHO, 1990).
Jacob Kasanin introduced the concept of schizoaffec- 10.18.1 Development of Psychotherapies

tive illness. in the 1940s
During the Second World War (1933–1945), the Nazi
Germany launched the operation T4 that killed around Maxwell Jones developed therapeutic community.
70,000 people suffering from incurable illness (e.g. men- The idea came from the Mill Hill Emergency Hospital
tal illnesses and learning disability). (London, United Kingdom) that specialized in the treat-
In 1935, Alcoholics Anonymous (AA) was first estab- ment of military and civilian shell-shock cases. Doctors
lished by Bill Wilson and Robert Smith in the United would bring patients together in a group to explain to
States with the aim to provide a meeting place and offer them tactfully about their conditions. Unexpectedly, the
support to people with alcohol misuse. discussion group began to affect the social structure of
William Herbert Sheldon (1899–1977) studied body the ward.
types and characters. He classified people as ectomorph, Viktor Frankl (1905–1997) developed existential
mesomorph, and endomorph somatotypes. therapy. Frankl was a Holocaust survivor. His best-
John Bowlby (1907–1990), a British psychoanalyst, selling book, Man’s Search for Meaning, described his
studied infant attachment and separation. He proposed experiences when he was a concentration camp inmate
the attachment theory. and the psychotherapeutic method of finding meaning
in all forms of existence and the reasons to continue
living (Frankl, 2006).
Carl Rogers (1902–1987) developed client-centred
10.18 1940s
psychotherapy. This was a unique approach to understand
The National Health Service (NHS) was formed in the personality and human relationships. It had wide appli-
United Kingdom in 1948 and the Institute of Psychiatry cation in psychotherapy and counselling (client-centred
(IOP) was also established at the Maudsley. The NHS therapy), education (student-centred learning), organiza-
provided a comprehensive system of general practice tions, and group settings.
allowing early treatment and permitting many milder Joseph Wolpe (1915–1997) enlisted himself in the
cases of psychiatric disorders to be treated by general South African army as a medical officer and he had to
practitioners (GPs). Furthermore, the NHS enabled large treat war neurosis among soldiers. The lack of success-
epidemiology studies to be conducted. ful treatment outcomes made him search for an effective
John Cade (1912–1980) injected guinea pigs with urine treatment. This ultimately led to the concept of system-
from patients with mania to see if mania was caused by atic desensitization.
History of Psychiatry 143
10.19 1950s 10.21 1970s

The second wave of biological treatment included the fol- The Royal College of Psychiatrists was established in
lowing developments: 1971 and the MRCPsych examination was introduced.
In the United Kingdom, Gottesman and Shields per-
• Donald Ewen Cameron (1901–1967) conducted formed twin studies in schizophrenia. Sir Michael Rutter
the ‘depatterning’ experiments with sleep therapy (1934–) published the Isle of Wight study that reported
and high-dose ECT on people with mild mental the epidemiology of psychiatric disorders among chil-
illnesses. Unfortunately, Cameron’s experiments dren (Rutter et al., 1976).
caused damage to his patients. Abraham Maslow (1908–1970) developed humanistic
• Charpentier synthesized chlorpromazine. Delay psychology, self-actualization, and the theory of hierar-
and Deniker applied chlorpromazine on patients. chy of needs.
• Monoamine oxidase inhibitors (MAOI) was In 1979, Gerald Russell (1928–) established the term
introduced in 1957. bulimia nervosa and named the Russell’s sign that refers
• Imipramine was introduced in 1958 by Roland to the calluses on the knuckles or dorsal part of the hand
Kuhn (1912–2005). as a result of chronic self-induced vomiting.
• Haloperidol and diazepam were synthesized. Clozapine was withdrawn as a result of agranulocytosis.
In 1950, Erik Erikson (1902–1994) published a book,

Childhood and Society (1965). In this book, he presented 10.22 1980s
the psychosocial theory of development. In 1983, the Mental Health Act in the United Kingdom
In 1951, Richard Asher coined the term ‘Munchausen introduced consent and approved social workers and a
syndrome’ in the Lancet, referring to a syndrome that Mental Health Act Commission.
patients fabricate symptoms in order to gain admission to In schizophrenia, Andreasen developed the Positive and
the hospital (Asher, 1951). The term ‘Munchausen’ refers Negative Syndrome Scale (PANSS), and Liddle described
to Baron Münchhausen (1720–1797), a German noble- the three-symptom cluster of schizophrenia (reality distor-
man who served in the Russian army and fabricated a tion, disorganization, and psychomotor poverty).
number of outrageous stories that were not experienced Julian Leff and Christine Vaughn performed family
by him but modified from preexisting folktales. studies on expressed emotion among relatives of schizo-
Kurt Schneider (1887–1967) coined the term ‘first- phrenia patients.
rank symptoms’ of schizophrenia. Kane reintroduced clozapine in the treatment of treat-
The Mental Health Act (1959) was passed by the ment-resistant schizophrenia.
Parliament in England. Fluvoxamine was introduced.
10.20 1960s
10.23 1990s
The mechanisms of action of antidepressants and anti-
psychotics were better understood. The antipsychotic There were speculations that fluoxetine increased suicide
effect of clozapine was recognized in the early 1960s. risk in adults with depression but turned out to be a result
Amitriptyline was launched. of poor study design.
Aaron Beck (1921–) introduced cognitive behaviour Citalopram, moclobemide, paroxetine, sertraline,
therapy (CBT). nefazodone, mirtazapine, venlafaxine, risperidone,
Token economy was developed during this period. olanzapine, and donepezil were introduced during this
The movement of anti-psychiatry: People who are anti- period.
psychiatry believed in the sociogenesis of severe mental Marsha Linehan (1943–), an American psychologist,
illness, particularly for schizophrenia. Anti-psychiatry developed the dialectical behaviour therapy for people
gained popularity in Europe and the United States. with borderline personality disorder.
Andreas Rett (1924–1997), an Austrian neurologist, Repression of Falun Gong took place in China.
coined the Rett syndrome based on 22 girls who developed Ankangs are secure psychiatric hospitals in China where
normally for the first 6 months and followed by devastat- Falun Gong ‘dissidents’ are ‘treated’ for the qigong-
ing developmental deterioration subsequently in their life. related mental disorder.
10.24 2000s Kane J, Honigfeld G, Singer J, and Meltzer H. 1988: Clozapine

for the treatment-resistant schizophrenic. A double-blind
‘Black box warning’ was issued to all selective serotonin comparison with chlorpromazine. Archives of General
reuptake inhibitors (SSRIs) (except fluoxetine) in causing Psychiatry 45(9):789–796.
suicide in adolescents with depression. Kanner L. 1968: Autistic disturbances of affective contact. Acta
Risperidone depot injection, paliperidone, and aripip- Paedopsychiatrica 35(4):100–136.
Lieberman EJ. 1985: Acts of Will: The Life and Work of Otto
razole (D2 partial agonist) were introduced.
Rank. New York, NY: Free Press.
Thioridazine was withdrawn from the market as a Macnaughton I. (ed.) 2004: Body, Breath and Consciousness: A
result of cardiotoxicity. Somatics Anthology. Berkeley, CA: North Atlantic Books.
There were advances in anti-dementia medication. Marinelli L and Mayer AA. 2003: Dreaming by the Book:
Rivastigmine, memantine, and galantamine were introduced. Freud’s ‘The Interpretation of Dreams’ and the History of
Bateman and Fonagy developed the mentalization- the Psychoanalytic Movement, New York, NY: Other Press.
based treatment for treating people with borderline per- Rush B and Merritt S. 1812: Medical Inquiries and
sonality disorder. Observations upon the Diseases of the Mind.
Philadelphia, PA: Kimber & Richardson.
In 2007, the Revised Mental Health Act in the United Russell G. 1979: Bulimia nervosa: An ominous variant of
Kingdom introduced approved clinicians and mental anorexia nervosa. Psychological Medicine 9(3):429–448.
health professionals. Rutter M, Tizard J, Yule W, Graham P, and Whitmore K. 1976:
In 2008, there were major reforms in the MRCPsych Research report: Isle of Wight Studies, 1964–1974.
examination. Psychological Medicine 6(2):313–332.
In 2013, the DSM-5 is launched. Sadock BJ and Sadock VA. 2007: Kaplan & Sadock’s Synopsis of
Psychiatry. Behavioral Sciences/Clinical Psychiatry, 10th
edn. Philadelphia, PA: Lippincott Williams & Wilkins.
BIBLIOGRAPHY Shorter E. 1997: A History of Psychiatry. New York: John Wiley
& Sons.
Asher R. 1951: Munchausen’s syndrome. Lancet 1(6650): Silverman JA. 1997: Sir William Gull (1819–1890). Limner of
339–341. anorexia nervosa and myxoedema. An historical essay and
Erikson E. 1965: Childhood and Society. London, U.K.: encomium. Eating and Weight Disorders 2(3):111–116.
Hogarth Press. Trevor T. 2010: History of psychiatry. In Puri BK and Treasaden
Frankl V. 2006: Man’s Search for Meaning. Boston, MA: IH (eds.) Psychiatry: An Evidence-Based Text, pp. 3–15.
Beacon Press. London, U.K.: Hodder Arnold.
Freud S and Breuer J. 1955: Studies on Hysteria (English trans- Watson JB. 1913: Psychology as the behaviorist views it.
lation). London, U.K.: Hogarth Press. Psychological Review 20:158–177.
Gull WW. 1997: Anorexia nervosa (apepsia hysterica, anorexia Wolpe J and Wolpe D. 1981: Our Useless Fears. Boston, MA:
hysterica). 1868. Obesity Research 5(5):498–502. Houghton Mifflin Company.
Johnstone EC, Cunningham ODG, Lawrie SM, Sharpe M, and World Health Organization. 1990; History of the development
Freeman CPL. 2004: Companion to Psychiatric Studies, of the ICD. http://www.who.int/classifications/icd/en/
7th edn, pp. 1–7. London, U.K.: Churchill Livingstone. HistoryOfICD.pdf
11 Basic Ethics, Principles of Law,
and Philosophy of Psychiatry
11.1 ETHICAL STANDARDS AND 4. A doctor should keep the information obtained

CODES OF PRACTISE from a patient as confidential. Breach of confi-
dentiality is permitted if there is serious harm
11.1.1 Hippocratic Oath to the patient or third party. The doctor should
inform the patient the actions to be taken if
1. A doctor should apply dietetic measures for the
breach of confidentiality is required.
benefit of the sick according to his or her ability
5. Psychiatric patients are vulnerable groups of
and judgement.
patients and research should safeguard their
2. A doctor should keep his or her patients from
autonomy and mental and physical integrity.
harm and injustice.
The principal investigator should seek approval
3. A doctor should never give a deadly drug to any-
from research ethics committee before com-
one even that person requests for it.
mencement of psychiatric research.
4. When it comes to patient’s care, a doctor should
be free of intentional injustice, mischief, and sex-
ual relations with both female and male patients. 11.1.4 Royal College of Psychiatrists
11.1.2 Declaration of Geneva (1948) The member should provide the highest standard of pro-
fessional psychiatric service to patients and follow the
1. A doctor should give his or her teachers respects College Guidance on Good Psychiatric Practice. The
and treat colleagues as brothers or sisters. member is committed to the elimination of unlawful dis-
2. A doctor should always give the health of his or crimination, the promotion of equality of opportunity,
her patients the first consideration. and the promotion of good race relations.
3. A doctor should not permit considerations of
religion, nationality, race, party politics, or
social standing to intervene between his or her
11.2 CLASSICAL ETHICAL THEORIES
duty with patients.
4. A doctor should hold utmost respect for human 11.2.1 Utilitarian Theories
life from the time of conception.
The utilitarian theories emphasize on minimizing the
risks and maximizing the benefits for the greatest num-
11.1.3 Declaration of Madrid ber (not necessarily the patients). There are two types
1. A doctor should offer the best, evidence-based of utilitarian approach: act utilitarian and rule utilitar-
and the least restrictive treatment to his or her ian. For example, a patient has thoughts of harming his
patients with fair allocation of health resources. or her family. In act utilitarian, the psychiatrist may
2. A doctor should accept his or her patients as part- consider disclosing confidential information (e.g. his or
ners. The patient should be informed on the purpose her intention to harm) to his or her family or police
of assessment and the doctor should empower his or by providing good or avoiding harm to the greatest
her patients to make free and informed decisions. number who stay with him or her or near him or her.
3. If a patient does not have the capacity to make In rule utilitarian, the rule of confidentiality may act
decision, the doctor should consult his or her against the rule of protecting others. If the conflict can-
family or seek legal advice to preserve human not be resolved, it will fall back on the decision of act
dignity and legal rights. utilitarian.
145
There are four subprinciples: 11.2.3.1.3 Beneficence

Beneficence refers to the fundamental commitment of a
1. Principles of utility: A doctor must maximize doctor to provide benefits to patients and to balance ben-
the act of doing good. efits against risks when making such decisions.
2. Standard of goodness: A doctor should provide
good service to his or her patients and do not 11.2.3.1.4 Justice
vary from patients to patients. Justice refers to fair distribution of medical services or
3. Consequentialism: An action is considered to be resources.
morally right if it leads to greatest human plea-
sure, happiness, and satisfaction. 11.2.3.2 Other Ethical Theories
4. Universalism: All parties must receive equal
and impartial consideration. 11.2.3.2.1 Duty-Based Approach
The duty-based approach is mainly concerned with the
11.2.2 Deontological Theories clinicians’ obligations under a set of rules.
(aka the K antian Theories) 11.2.3.2.2 Paternalism
The deontological theories emphasize on a doctor’s motive The paternalism approach occurs when beneficence over-
to provide morally correct care to his or her patients. The rules autonomy, and it is the duty of a doctor to act in his
deontological theories focus on the rightness and wrong- or her patient’s best interests. The word ‘paternal’ refers
ness of doctor’s actions but not on the consequences of to the way that a parent would treat his or her child.
the actions. Kant also developed maxims to direct moral
action. One example is the universalization of rules. He 11.2.3.2.3 Prima Facie Duty and Actual Duty
or she did not allow any exception to wrongful practice A prima facie duty is a duty that is always to be acted
such as lying by doctors as this opposes the presupposed upon unless it conflicts on a particular occasion with an
practice of truth telling. equal or stronger duty. When there is conflict between
different ethical principles, an actual duty will be per-
formed by an examination of the respective weights of
11.2.3 Virtue Theories (Plato and Aristotle) competing prima facie duties in a particular situation.
The virtue theories emphasize on the qualities of a For example, a psychiatrist always maintains his or her
personality that make a doctor a caring, compassion- patient’s confidentiality (a prima facie duty). One day, one
ate, committed, and conscientious person. Plato and of his patients mentions that he or she has a plan to harm
Aristotle regarded the cultivation of virtuous traits such his or her neighbours. Several ethical principles (e.g. the
as conscientiousness as the central feature of moral life. duty of maintaining confidentiality, nonmaleficence, and
For example, a psychiatrist in private practice advises justice) are in operation. The psychiatrist must weigh
patient to be admitted not for the patient’s safety but in the balance of the competing ethical principles and
to earn more money. One cannot find the psychiatrist’s decide whether to breach confidentiality or not.
advice unethical, but this psychiatrist simply lacks
11.2.3.2.4 Fiduciary Duty
moral character.
The fiduciary duty refers to the duty of a doctor who
should act in the patient’s best interests.
11.2.3.1 Ethical Principles A fiduciary duty exists when a patient places special
11.2.3.1.1 Autonomy trust and confidence on a doctor and relies upon the doc-
Autonomy refers to the obligation of a doctor to respect tor or the fiduciary to exercise his or her discretion or
his or her patients’ rights to make their own choices in expertise in acting for the patient.
accordance with their beliefs and responsibilities.
11.2.3.3 Confidentiality and Privileges
Confidentiality refers to the process when a patient
11.2.3.1.2 Nonmaleficence entrusts his or her doctor in keeping information private.
Nonmaleficence refers to the obligation of a doctor to The patient can consent to or not to release his or her con-
avoid harm to his or her patients. fidential information to the third party. Confidentiality is
Basic Ethics, Principles of Law, and Philosophy of Psychiatry 147
a right owned by the patient. It is the obligation of the A psychiatrist should balance the duty to inform the court
doctor to safeguard his or her patients’ confidentiality. and the duty to provide care to a patient. If the testimony is
Confidentiality is a subset of privacy. going to cause tremendous damage to the therapeutic rela-
A patient has the privileges to control his or her clini- tionship, the patient should be evaluated by an independent
cal information and decides what happens to his or her psychiatrist. Prior to forensic assessment, the psychiatrist
clinical information. should inform the patient regarding to the purpose of assess-
It is the duty of a doctor to be aware of the local ment and to whom information will be released to.
legislation safeguarding patients’ confidentiality (e.g.
the Mental Health Act, Children and Adolescents Act, 11.2.3.5 Approaches to Breach Confidentiality
Family Act, Human Rights Act, Infectious Disease Act, 1. Advance notice: The psychiatrist should alert his
privacy legislation, transportation and criminal laws). or her patient that information is to be released
and discuss the basis for decision.
2. All limits to confidentiality should be discussed
11.2.3.4 Exceptions to Confidentiality
with the patient at the outset of treatment or
11.2.3.4.1 Duty to Warn and Protect when mental state becomes stable.
1. The duty to warn and protect follows the
Tarasoff’s ruling. The Tarasoff-I (1974) refers 11.2.3.6 Confidentiality in Minors
to the duty to warn. The Tarasoff-II (1976)
1. If an informed consent is required from a parent
refers to the duty to protect.
or guardian, a doctor should provide adequate
2. The duty to warn and protect is indicated when
information to the parent or guardian.
a. There are sufficient factual grounds for high
2. If a minor undergoes psychotherapy, it is impor-
risk of harm (such as death or substantial
tant to explain to the parent or guardian at outset
bodily harm) to a third party, and the risk is
that the information gathered from psychother-
sufficiently specified
apy is confidential and the disclosure of such
b. The risk of danger to the public is imminent
information will depend on the clinical judge-
c. The harm to a third party is not likely to be
ment made by the therapist.
prevented unless the mental health profes-
3. When parents divorce, a psychiatrist needs to
sionals make a disclosure
work with the custodial parent and obtain legal
d. The third party cannot reasonably be expected
permit when disclosure of information to non-
to foresee or comprehend high risk of harm to
custodial parents is required.
himself or herself
3. The duties to community safety override con-
fidentiality. This includes passing confidential 11.3 ETHICS AND PSYCHIATRIC RESEARCH
information to a government department if public
safety is at risk (e.g. homicide, passing commu- 11.3.1 Nuremberg Code (1947)
nicable diseases such as AIDS or tuberculosis to The Nuremberg Code was developed by war crimes tribunal
others, and dangerous driving). against Nazi German doctors, and the main objective is to
protect human subjects during experiments and research. An
11.2.3.4.2 Mandatory Reporting experiment should avoid suffering and injury. Experiments
Confidence limited by legislation requires mandatory leading to death and disability should not be conducted.
reporting when the protection of the community out- Proper preparations should be performed to protect research
weighs the duty to the patient. Indications for mandatory subjects, and the experiments should be conducted by quali-
reporting include child protection, abuse of old people, fied personals. During the experiment, the research subjects
firearm possession, unfit to drive, certain infectious dis- have the liberty to withdraw at any time, and the investigators
eases (e.g. HIV), professional–patient boundary viola- should stop the experiments if continuation results in poten-
tion, and occupational hazards (e.g. sick pilots). tial injury or death of research subjects. The design should
be based on results obtained from animal experiments and
11.2.3.4.3 Court Order natural history of disease. Seeking consent from research
The court can subpoena information and override confi- subjects is absolutely necessary. Research should yield
dentiality. This can result in ethical dilemma. meaningful results for the good of mankind.
11.3.2 Declaration of Helsinki (1964) It is the responsibility of a doctor to judge whether a

patient has the capacity to give a valid consent. The doc-
The Declaration of Helsinki states the importance of for- tor has a duty to provide information in a language under-
mulation in research protocol and informs the subjects standable by a lay person about a condition, the benefits
of the protocol details. The principal investigator should and risks of a proposed treatment, and alternatives to
balance the predictable risks and foreseeable benefits, a treatment. The High Court has held that an adult has
to respect integrity and privacy, to obtain consent with capacity to consent to a medical or surgical treatment if
liberty and free from undue influence, and to preserve he or she can
accuracy in publication of results. The principal investi-
gator should obtain consent from the legal guardian if a 1. Understand and retain the information relevant
research subject does not have capacity to give consent. to the decision in question.
2. Believe in the information.
11.3.3 Belmont Report (1979) 3. Weigh the information in balance to arrive at a
The Belmont Report (Jennifer, 2010) emphasizes on jus- choice. The person has the right to refuse treat-
tice. Individual justice requires the researcher to offer ment even though the refusal is contrary to the
beneficial research to all participants independent of views of most other people. The decision should
his or her personal preference. Social justice requires an be consistent with the individual value system.
order of preference in selection of subjects (e.g. adults
before children, less burdened class before burdened 11.4.2.1.1 Testamentary Capacity
class such as institutionalized patients). To make a will, a person must be of sound disposing
mind. This means that the person must
11.4 COMPETENCY AND CAPACITY • Understand to whom he or she is giving per-
11.4.1 Competency sonal property
• Understand and recollect the extent of that per-
Competence is a legal concept and refers to the capacity sonal property
to act and understand. Competence is determined by the • Understand the nature and extent of the claims
legal system (e.g. the competence to adopt a child). upon the person, both of those included and of
those excluded from the will
11.4.2 Capacity
Capacity is a clinical concept and refers to the mental A valid will is not invalidated by the subsequent impair-
ability to make a rational decision based on understand- ment of testamentary capacity.
ing and appreciating all relevant information (e.g. testi-
11.4.2.1.2 Advocacy
monial capacity—ability to be a witness).
An advocate enters into a relationship with the patient, to
11.4.2.1 Capacity for Informed Consent speak on his or her behalf and to represent the patient’s
A valid consent has the following properties: wishes or stand up for his or her rights. An advocate has
no legal status—the patient should have an idea of per-
1. A consent is classified as an implicit consent (e.g. sonal preferences so that the advocate truly represents the
verbal consent for blood taking) or an explicit patient’s wishes.
consent (e.g. written consent to participate in a
clinical trial). 11.4.2.1.3 Appointeeship
2. The presence of capacity in a person so that he or An appointee is someone authorized by the Department
she must be able to understand the information and of Social Security to receive and administer benefits on
appreciate the foreseeable consequence of a deci- behalf of someone else, who is not able to manage his
sion and be able to communicate such decision. or her affairs. It can be used solely to administer money
3. Informed with clear information (e.g. diagnosis, derived from social security benefits and cannot be used
purpose of proposed treatment, risks and ben- to administer any other income or assets. If benefits accu-
efits, alternatives, and associated prognosis). mulate, application may need to be made to the Public
4. Voluntary and without coercion or persuasion. Trust Office or the Court of Protection to gain access to
5. Specific to the issue involved. the accumulated capital.
11.4.2.1.4 Powers of Attorney medical conditions, use of medications known to impair

A power of attorney is a means whereby one person (the driving, and alcohol use. Basic examination should include
donor) gives legal authority to another person (the attor- mini-mental state examination, neurological examination
ney) to manage his or her affairs. The donor has sole for gait and balance, Snellen eye chart for vision, whisper
responsibility for the decision as to whether power of test for hearing, and go-and-no-go test for response control.
attorney is given, provided the donor fully understands The responsibility for making the decision about
the implications of what he or she is undertaking. whether or not a person should continue to drive is that
An ordinary power of attorney allows the attorney to of the Driver and Vehicle Licensing Authority (DVLA),
deal with the donor’s financial affairs generally, or it can with a doctor acting only as a source of information and
be limited to specific matters. An ordinary power of attor- advice. The driver has a duty to keep the DVLA informed
ney is automatically revoked by law when the donor loses of any condition that may impair the ability to drive. The
his or her mental capacity to manage personal affairs. doctor is responsible for advising the patient to inform the
An enduring power of attorney allows a person to DVLA of a condition likely to make driving dangerous.
decide who should manage his or her affairs if the person If the patient fails to take this advice, the doctor may then
becomes mentally incapable. This has been possible since contact the DVLA directly. Tables 11.1 through 11.3 sum-
1985. An enduring power of attorney continues in force marize the advice of the DVLA to British doctors with
after the donor has lost the mental capacity to manage his respect to fitness to drive in patients with psychiatric dis-
or her affairs, provided it is registered with the Public Trust orders. In this table, two types of licence are referred to:
Office. It is thus of use for people with early dementia who
can set their affairs in order early in the illness provided • Group 1 licence. A driver with a mobility
the illness has not already progressed to a point where allowance may drive from the age of 16 years.
the person is unable to manage personal affairs. Once the Licences are normally issued until age 70, unless
donor is unable to manage personal affairs, the attorney restricted to a shorter duration for medical rea-
must apply to the Public Trust Office for registration of the sons. There is no upper age limit, but after the
enduring power of attorney to allow the attorney authority age of 70, licences are renewable every 3 years.
to continue to act. • Group 2 licence. These licences can be issued at
the age of 21 years and are valid until the age of
45. They are then issued every 5 years to the age
11.4.2.1.5 Court of Protection
of 65 unless restricted to a shorter duration for
This is an office of the Supreme Court. It exists to protect medical reasons. From the age of 65, the licence
the property and affairs of persons who, through mental is issued annually.
disorder, are incapable of managing personal financial
affairs. The court’s powers are limited to dealing with
the financial and legal affairs of the person concerned. 11.5 PRINCIPLES OF LAW
Only one medical certificate is required, from a regis-
tered medical practitioner who has examined the patient. 11.5.1 Mental Capacity Act (2005)
Guidance to medical practitioners accompanies the cer- (England and Wales)
tificate of incapacity. Although each country has its own mental health leg-
The court appoints somebody to manage the patient’s islation and it is impossible to discuss here, candidates
affairs on his or her behalf. This person is called the are advised to be familiar with the Mental Capacity Act
receiver. It may be a relative, friend, solicitor, or other (2005) in England and Wales that serves as a basic frame-
persons. The receiver must keep accounts and spend the work for similar legislation. The Mental Capacity Act
patient’s money on things that will benefit the patient. (2005) provides the legal framework for acting and mak-
The court must give permission before the disposal of ing decisions on behalf of people who lack the capac-
capital assets such as property. ity to make specific decisions for themselves in relation
to personal welfare, health care, and financial matters.
11.4.2.1.6 Capacity to Drive It applies to persons aged 16 and over in England and
Assessment of capacity to drive should include the following: Wales. The relevant legislation in Scotland is called the
driving patterns, driving frequency and distances, changes Adults with Incapacity Act (2000). The Act draws on
in driving patterns in the past year, number of road traffic the common law principles that have been established
accidents, use of seat belt, presence of driving-impairing through judicial decisions in previous legal cases.
TABLE 11.1
Advice of the DVLA to Doctors with Respect to Fitness to Drive in Patients with Psychiatric Disorders
Psychiatric Disorder Group 1 Entitlement Group 2 Entitlement
Neurosis, e.g. anxiety state/depression DVLA need not be notified. Driving should cease with serious acute mental
Driving need not cease. Patients must be warned illness from whatever cause. Driving may be
about the possible effects of medication which permitted when the person is symptom free and
may affect fitness. However, serious stable for a period of 6 months. Medication must
psychoneurotic episodes affecting or likely to not cause side effects that would interfere with
affect driving should be notified to DVLA and alertness or concentration. Driving may be
the person advised not to drive permitted also if the mental illness is long
standing but maintained symptom-free on small
doses of psychotropic medication with no side
effects likely to impair driving performance.
Psychiatric reports may be required.
Psychosis Six months off the road after an acute episode Recommended refusal or revocation. At least 3
Schizoaffective requiring hospital admission. Licence restored years off driving, during which must be stable
Acute psychosis after freedom from symptoms during this and symptom-free and not on major psychotropic
Schizophrenia period, and the person demonstrates that he or or neuroleptic medication, except lithium.
she complies safely with recommended Consultant psychiatric examination required
medication and shows insight into the before restoration of licence, to confirm that
condition. A 1, 2 or 3 year licence with medical there is no residual impairment; the applicant has
review on renewal. Loss of insight or insight and would be able to recognize if he or
judgement will lead to recommendation to she became unwell. There should be no
refusal/revocation of licence. significant likelihood of recurrence. Any
psychotropic medication necessary must be of
low dosage and not interfere with alertness or
concentration or in any way impair driving
performance.
Manic–depressive psychosis Six to twelve months off the road after an acute As aforementioned for psychosis.
episode of hypomania requiring hospital
admission, depending upon the severity and
frequency of relapses. Licence restored after
freedom from symptoms during this period and
safe compliance with medication.
A 1, 2 or 3 year licence with medical review on
renewal. Loss of insight or judgement will lead to
recommendation to refusal/revocation of licence.
Dementia If early dementia, driving may be permitted if Recommended permanent refusal or revocation if
Organic brain disorders, e.g. there is no significant disorientation in time and the condition is likely to impair driving
Alzheimer’s disease space, and there is adequate retention of insight performance.
NB: There is no single marker to and judgement. Annual medical review
determine fitness to drive, but it is required. Likely to be recommended to be
likely that driving may be permitted refused or revoked if disorientated in time and
if there is retention of ability to cope space and especially if insight has been lost or
with the general day-to-day needs of judgement is impaired.
living, together with adequate levels
of insight and judgement.
Severe mental handicap Severe mental handicap is a prescribed Recommended permanent refusal or revocation if
A state of arrested or incomplete disability; licence must be refused or revoked. severe. Minor degrees of mental handicap when
development of mind, which If stable, mild, to moderate mental handicap, it the condition is stable with no medical or
includes severe impairment of may be possible to hold a licence, but he or she psychiatric complications may be able to have a
intelligence and social functioning will need to demonstrate adequate functional licence. Will need to demonstrate functional
ability at the wheel and be otherwise stable. ability at the wheel.
TABLE 11.1 (continued)

Advice of the DVLA to Doctors with Respect to Fitness to Drive in Patients with Psychiatric Disorders
Psychiatric Disorder Group 1 Entitlement Group 2 Entitlement
Personality disorder If seriously disturbed such as evidence of violent Recommended refusal or revocation if associated
Including post-head injury syndrome outbreaks or alcohol abuse and likely to be a with serious behaviour disturbance likely to be a
and psychopathic disorders source of danger at the wheel, licence would be source of danger at the wheel. If the person
refused or revoked. Licence restricted after matures and psychiatric reports confirm stability
medical reports that behaviour disturbances supportive, licence may be permitted/restored.
have been satisfactorily controlled. Consultant psychiatrist report required.
Note: A person holding entitlement to Group I (i.e. motor car/motor bike) or Group II (i.e. LGV/PCV), who has been relicenced following an acute
psychotic episode, of whatever type, should be advised as part of follow-up that if the condition recurs, driving should cease and DVLA be
notified. General guidance with respect to psychotropic/neuroleptic medication is contained under the appropriate section in the text.
Alcohol and illicit drug misuse/dependency are dealt with under his or her specific sections. Reference is made in the introductory page to
the current GMC guidance to doctors concerning disclosure in the public interest without the consent of the patient.
11.5.1.1 Principles of the Mental a. Decide whether a person has capacity to

Capacity Act (2005) make a particular decision for themselves
The five main principles are as follows: b. Make declarations, decisions, or orders
on financial or welfare matters affecting
1. A person must be assumed to have capacity unless people who lack capacity to make such
it is established that he or she lacks capacity. decisions
2. A person is not to be treated as unable to c. Appoint deputies to make decisions for peo-
make a decision unless all practicable steps ple lacking capacity to make those decisions
to help him to do so have been taken without d. Decide whether an enduring or lasting
success. power of attorney is valid
3. A person is not to be treated as unable to make e. Remove deputies or attorneys who fail to
a decision merely because he or she makes an carry out their duties
unwise decision. 3. Part 3 deals with a range of miscellaneous issues
4. An act done, or decision made, under this Act relating to the Act (Table 11.4).
for or on behalf of a person who lacks capacity
must be done, or made, in his best interests. 11.5.2 Mental Health Act (MHA, 2007)
5. Before the act is done, or the decision is made, in England and Wales
regard must be had to whether the purpose for
which it is needed can be as effectively achieved The MHA (2007) has made the following amendments to
in a way that is less restrictive of the person’s the MHA (1983):
rights and freedom of action.
1. Mental disorder is defined as any disorder or
disability of the mind. The categories of ‘mental
11.5.1.2 Three Parts of the Mental impairment’ and ‘psychopathic disorder’ were
Capacity Act (2005) removed.
1. Part 1 contains the main regulatory framework. 2. Replacement of ‘treatability’ and ‘care tests’ by
2. Part 2 mentions the establishment of a new court ‘appropriate medical treatments (to alleviate, or
to deal with matters arising from the Act (the prevent a worsening of, the disorder) must be
Court of Protection) and a new office of the available for the patients’.
Public Guardian. The Court of Protection has 3. Civil partners are given the status as nearest
the same powers, rights, privileges, and author- relatives.
ity as the High Court. The Court of Protection 4. Introduction of supervised community treatment.
has the powers to 5. Sections 2–4 under the MHA (1983) are valid.
TABLE 11.2
Advice of the DVLA to Doctors with Respect to Fitness to Drive in Patients with Alcohol Problems
Alcohol Problem Group 1 Entitlement Group 2 Entitlement
Alcohol misuse/alcohol Alcohol misuse Alcohol misuse
dependency Alcohol misuse, confirmed by medical inquiry and Alcohol misuse, confirmed by medical inquiry and
(See note) by evidence of otherwise unexplained abnormal by evidence of otherwise unexplained abnormal
blood markers, requires licence revocation or blood markers, will lead to revocation or refusal of a
refusal for a minimum 6 month period, during vocational licence for at least 1 year, during which
which time controlled drinking should be attained time controlled drinking should be attained with
with normalization of blood parameters. normalization of blood parameters.
Alcohol dependency Alcohol dependency
Including detoxification and/or alcohol-related fits. Vocational licensing will not be granted where there
Alcohol dependency, confirmed by medical inquiry, is a history of alcohol dependency within the past 3
requires a recommended 1 year period of licence years
revocation or refusal, to attain abstinence or
controlled drinking and with normalization of
blood parameters if relevant
Licence restoration Licence restoration
Will require satisfactory independent medical On reapplication, independent medical examination
examination, arranged by DVLA, with satisfactory arranged by DVLA, with satisfactory blood results
blood results and medical reports from own and medical reports from own doctors. Consultant
doctors. Patients are recommended to seek advice support/referral may be necessary. If an alcohol-
from medical or other sources during the period off related seizure or seizures have occurred, the
the road. vocational Epilepsy Regulations apply.
Alcohol-related seizure(s) A licence will be revoked or refused for a minimum Vocational Epilepsy Regulations apply (see DVLA
1 year period from the date of the event. Where guidelines)
more than one seizure occurs, consideration under
the Epilepsy Regulations may be necessary
Before licence restoration, medical inquiry will be
required to confirm appropriate period free from
alcohol misuse and/or dependency.
Alcohol-related disorders Licence recommended to be refused/revoked. Recommended to be refused/revoked.
e.g. severe hepatic cirrhosis,
Wernicke’s encephalopathy,
Korsakoff’s psychosis
Note: There is no single definition that embraces all the variables in these conditions. But as a guideline, the following is offered: ‘a state which
because of consumption of alcohol, causes disturbance of behaviour, related disease or other consequences, likely to cause the patient,
his family or society harm now or in the future and which may or may not be associated with dependency. In addition, assessment of the
alcohol consumption with respect to current national advised guidelines is necessary’.
A person who has been relicenced following alcohol misuse or dependency must be advised as part of his or her follow-up that if his or her condi-
tion recurs, he or she should cease driving and notify DVLA medical branch.
High-risk offender scheme for drivers convicted of certain drink/driving offences:
1. One disqualification for drink/driving when the level of alcohol is 2.5 or more times the legal limit.
2. One disqualification that he or she failed, without reasonable excuse, to provide a specimen for analysis.
3. Two disqualifications within 10 years for being unfit through drink.
4. Two disqualifications within 10 years when the level of alcohol exceeds the legal limit. DVLA will be notified by courts. On application for
licence, satisfactory independent medical examination with completion of structured questionnaire with satisfactory liver enzyme tests and
MCV is required. If favourable, restore for Group I and can recommend issue Group II. For a high-risk offender associated with previous his-
tory of alcohol dependency or misuse, after earlier satisfactory examination and blood tests, short-period licence only for ordinary and voca-
tional use is issued, depending on time interval between previous history and reapplication. A high-risk offender found to have current
unfavourable alcohol misuse history and/or abnormal blood test analysis would have application refused.
TABLE 11.3
Advice of the DVLA to Doctors with Respect to Fitness to Drive in Patients with
Drug Misuse and Dependency
Drug Misuse and Dependency Group 1 Entitlement Group 2 Entitlement
Cannabis, ecstasy, and other ‘recreational’ The regular use of these substances, Regular use of these substances will lead to
psychoactive substances, including LSD and confirmed by medical inquiry, will lead to refusal or revocation of a vocational licence
hallucinogens licence revocation or refusal for a 6 month for at least a 1-year period. Independent
period. Independent medical assessment medical assessment and urine screen,
and urine screen, arranged by DVLA, may arranged by DVLA, may be required
be required
Amphetamines, heroin, morphine, Regular use of, or dependency on, these Regular use of, or dependency on, these
methadonea, cocaine, benzodiazepines substances, confirmed by medical inquiry, substances will require revocation or refusal
will lead to licence refusal or revocation of a vocational licence for a minimum 3 year
for a minimum 1 year period. Independent period. Independent medical assessment and
medical assessment and urine screen, urine screen, arranged by DVLA, may be
arranged by DVLA, may be required. In required. In addition, favourable consultant
addition, favourable consultant or or specialist report will be required before
specialist report will be required on relicensing
reapplication
Seizure(s) associated with illicit drug usage A seizure or seizures associated with illicit Vocational Epilepsy Regulations apply
drug usage may require a licence to be
refused or revoked for a 1 year period.
Thereafter, licence restoration will require
independent medical assessment, with
urine analysis, together with favourable
report from own doctor, to confirm no
ongoing drug misuse. In addition, patients
may be assessed against the Epilepsy
Regulations
NB: A person who has been relicenced following illicit drug misuse or dependency must be advised as part of his or her follow-up that if his or
her condition recurs, he or she should cease driving and notify DVLA medical branch.
a Applicants or drivers on consultant-supervised oral methadone withdrawal programme may be licenced, subject to annual medical review and
favourable assessment.
6. The MHA (2007) emphasizes that primary the young person has achieved a certain level
care trusts should have the responsibil- of intelligence and consent for admission.
ity to provide ‘age-appropriate’ services for The Family Law Reform Act (1969) indicates
children. This includes guidelines for good that the earlier process does not require paren-
practice and the use of Child and Adolescent tal consent. If an at-risk young person refuses
Mental Health Services (CAMHS) in the admission, the parents, the legal guardians,
assessment process. The law on the admission or the court can override the young person’s
to hospital and treatment of mental disorders decision. If both the young person and p arents
of children (under 16) is based on parental refuse admission but the young person is at
responsibility and the Human Rights Act high psychiatric risk, the psychiatrist may
(1998). consider applying for compulsory admission
7. The admission of young people (aged 16–17) under the MHA (2007) or seeking an opinion
is influenced by the Gillick competence when from the court (Tables 11.5 through 11.9).
TABLE 11.4
Summary of the Relevant Sections of the Mental Capacity Act (2005) for Psychiatric Practice in England
and Wales
Section Number Main Principle Details
Part I Determining capacity These sections set out the legal requirement for assessing capacity. The concept
Sections 2 and 3 builds on the common law test for capacity
Part I The best interest principle This section expands on the principle that any act or decision on behalf of a person
Section 4 who lacks capacity should be made in the person’s best interests. This follows the
common law principle, but the Act is more specific about the process and the best
interest checklist must be followed
Part I Connection with care or treatment This section sets out the conditions under which a person caring for someone who
Section 5 lacks capacity will not incur liability for their actions in caring for that person
Section 6 Restraining a person who lacks This section sets out the additional conditions that must be fulfilled if a person who
capacity lacks capacity is to be restrained. This section considers the degree of harm that is
likely to be suffered by the person if he or she is not restrained
Part I Lasting powers of attorney This section creates a new power, the lasting powers of attorney, by which a person
Section 9 who has capacity can confer authority on another person (the donee) to make
decisions about his or her personal welfare, property, or affairs at a future date
when he or she no longer has the capacity to make decisions. This is a new power
in England and Wales and was not legally possible under the common law
Part I Advance decisions to refuse These sections set out the legal framework within which a person with capacity can
Sections 24–26 treatment make an advance decision to refuse treatment (including life-sustaining treatment)
that is applicable when that person no longer has the capacity to make such decision.
This clarifies and sets in statute the legal position on advance refusals of treatment
Part I Research These sections set out the legal framework within which researchers must act if
Sections 30–34 they are conducting research that involves persons who lack capacity to consent
to the research being conducted
Part I Independent Mental Capacity These sections introduce and set out the role of IMCA. This is a new service
Sections 35–41 Advocates (IMCAs) created under the Act. Its aim is to provide independent safeguards for people
who lack capacity when important decisions need to be made and there is no
other person except the designated carer to represent the person who lacks
capacity or to be consulted on his or her behalf
Part I The offence of ill treatment or This section creates an offence of ill treatment or neglect. If a carer or donee of a
Section 44 neglect lasting power of attorney is found guilty, he or she is liable to imprisonment of up
to 5 years or a fine (or both)
11.6 PHILOSOPHY OF PSYCHIATRY 11.6.2 Formal and Informal Logic

11.6.1 Philosophy and Science Consider the following example:
Philosophy is concerned with conceptual problems and 1. If I have many years of life experience, I will be
science is concerned with empirical problems. Science intelligent.
and philosophy can work productively together and com- 2. If I am an old person, I should have many years
plement each other. of experience.
There are two types of logic. Formal logic is con- 3. Therefore, if I am an old person, I should be
cerned with the form of arguments and it is context-free. intelligent.
A valid argument is independent of any specific context.
Informal logic, on the other hand, cannot remove itself The earlier arguments are valid in formal logic. Informal
from the context where the arguments take place. logic is concerned with the context of an argument,
TABLE 11.5
Relevant Sections of the MHA (1983/2007) for Psychiatric Practice in England and Wales
Section
Number Purpose Duration Grounds
2 Admission for assessment or Up to 28 days from admission 1. Mental disorder that warrants detention in hospital
assessment followed by treatment for assessment.
2. Admission is necessary in interests of the
patient’s own health, or safety, or for the
protection of others
3 Admission for treatment Up to 6 months, renewable after 1. The mental disorder is of a nature or degree, which
6 months and then annually makes it appropriate for the patient to receive
medical treatment in hospital
2. Admission is necessary for the health, or safety, of
the patient or for the protection of others
3. Medical treatment is likely to alleviate or prevent
deterioration in the patient’s condition
4 Emergency admission for Up to 72 h from admission and 1. Mental disorder that warrants detention in hospital
assessment Section 2 may apply after for assessment
admission 2. Admission is necessary in the interests of the
patient’s own health or safety or for the protection
of others
TABLE 11.6
Consent to Treatment under MHA (1983). Consent to Treatment Should Be Informed and
Voluntary (Implies Mental Illness, e.g. Dementia, Does Not Affect Judgement)
Type of Treatment Informal Detained
Urgent treatment No consent No consent
Section 57: Irreversible, hazardous, or nonestablished treatments Consent and second opinion Consent and second opinion
(e.g. psychosurgery such as leucotomy), hormone implants (for sex
offenders), surgical operations (e.g. castration)
Section 58: Psychiatric drugs, ECT Consent Consent or second opinion
Source: Reproduced from Puri, B.K. and Treasaden, I.H., Textbook of Psychiatry, 3rd edn., Churchill Livingstone, Edinburgh, U.K.,
2011. With permission.
Notes: 1. For first 3 months of treatment, a detained patient’s consent is not required for Section 58 medicines but is required for ECT.
2. Patients can withdraw voluntary consent at any time.
and this example suggests the context of an argument 11.6.3 Philosophy of Anti- and Propsychiatry
can have an important effect. Informally, we are doubt-
ful of these arguments. It is unclear that the possession 11.6.3.1 Philosophy of Antipsychiatry
of many years of life experience refers to intelligence. (Fulford et al., 2006)
Furthermore, it is not necessarily true that an old person 1. The psychological model. Mental illness is not a
having many years of life experience is correlated with disorder but learned abnormalities of behaviour.
intelligence and the old person may suffer from demen- 2. The labelling model. The clinical features of men-
tia. The fallacy of formal logic illustrates that all humans tal disorder are responses of an individual to being
are prone to faults of reasoning. labelled as deviant. This model fails to explain the
TABLE 11.7
Civil Treatment Orders under MHA (1983)
Eligibility for Appeal
Medical Maximum to Mental Health
Section Grounds Application by Recommendations Duration Review Tribunal
Section 2: Admission for Mental disorder Nearest relative Two doctors (one 28 days Within 14 days
assessment or approved approved under
social worker Section 12)
Section 3: Admission for Mental illness, Nearest relative Two doctors (one 6 months Within first 6 months.
treatment impairment, severe psychopathic or approved approved under If renewed, within
mental impairment (if disorder, mental social worker Section 12) second 6 months,
psychopathic disorder or mental disorder then every year.
impairment, treatment must be Mandatory every
likely to alleviate or prevent 3 years.
deterioration)
Section 25 Supervised discharge. Same as Section 3 CRMO Social worker, one If renewed, Within first 6 months.
Hospital managers cannot doctor 6 months Renewable for
discharge. 6 months, then every
year.
Section 4 Emergency admission Mental disorder Nearest relative Any doctor 72 h
for assessment (urgent or approved
necessity) social
worker
Section 5(2) Urgent detention of Danger to self or Doctor in charge 72 h of patient’s care
voluntary in-patient to others
Section 5(4) Nurses holding Mental disorder Registered mental None 6h
power of voluntary in-patient (danger to self, nurse or
health or others) registered nurse
for mental
handicap
Section 136 Admission by police Mental disorder Police officer Allows patient in 72 h
public place to be
removed to ‘place of
safety’
Section 135 entry to home and Mental disorder Magistrates Allows power of 72 h
removal of patient to place of
safety
Source: Reproduced from Puri, B.K. and Treasaden, I.H., Textbook of Psychiatry, 3rd edn., Churchill Livingstone, Edinburgh, U.K., 2011. With
permission.
onset of psychiatric illness but explains maintain- mental activities such as unconscious motives,
ing factors that inhibit recovery. reasons, desires, and fantasies.
3. The hidden meaning model. This model argues 5. The political control model. The boundary
that the apparently meaningless or nonunder- between mental illness and normality is debat-
standable symptoms of people with schizophrenia able and often set by authority. For example,
can be understood, once the origins and underly- the authority wants to separate people with
ing context in the patient’s past experiences are antisocial personality disorder and sexual
recognized. Psychiatric symptoms are not signs deviance from the norm even in a democratic
of illnesses but contain hidden meanings. society. In some political regimes, political
4. The unconscious mind model. Mental illness dissidence has been the basis of attributions of
is not a disorder but a product of unconscious madness.
TABLE 11.8
Forensic Treatment Orders for Mental Abnormally Offenders
Eligibility for Appeal to
Medical Maximum Mental Health Review
Section Grounds Made By Recommendations Duration Tribunal
Section 35: Remand to Mental disorder Magistrates or Any doctor 28 days
hospital for report Crown Court Renewable at 28
Maximum 12 weeks day intervals
Section 36: Remand to Mental illness, severe Crown Court Two doctors: one 28 days
hospital for treatment mental impairment approved under Renewable at 28
Maximum 12 weeks (not if charged with Section 12 day intervals
murder)
Section 37: Hospital and Mental disorder. Magistrates or Two doctors, one 6 months During second 6 months,
guardianship orders (If psychopathic Crown Court approved under Renewable for then every year.
Accused of, or disorder or mental Section 12 and further 6 Mandatory every 3 years
convicted for, an impairment must be then annually months
imprisonable offence likely to alleviate or
prevent
deterioration.)
Section 41: Restriction Added to Section 37 Crown Court Oral evidence from Usually without As Section 37
order. Effect: leave, To protect public one doctor limit of time
transfer, or discharge from serious harm
only with consent of
Home Secretary
Section 38: Interim Mental disorder For Magistrates or Two doctors: one 12 weeks None
hospital order trial of treatment Crown Court approved under Renewable at
Section 12: Maximum intervals 28 day
6 months intervals
Section 47: Transfer of Mental disorder Home Secretary Two doctors: one Until earliest Once in the first 6 months,
a sentenced prisoner to approved under date of release then once in the next 6
hospital Section 12 from sentence months. Thereafter, once
a year.
Section 48: Urgent Mental disorder Home Secretary Two doctors: one Until date of Once in the first 6 months,
transfer to hospital of approved under trial then once in the next 6
remand prisoner Section 12 months. Thereafter, once a
year.
Section 49: Restriction Added to Section 47 Home Secretary — Until end of As for Sections 47 and 48
direction. Effect: leave, or 48 Section 47 or to which applied.
transfer, or discharge 48
only with consent of
Home Secretary
Source: Reproduced from Puri, B.K. and Treasaden, I.H., Textbook of Psychiatry, 3rd edn., Churchill Livingstone, Edinburgh, U.K., 2011.
With permission.
Thomas Szasz (1920–2012), a prominent anti-psychiatrist, terms of acceptable behaviours. Hence, mental illness is
identifies mental illness as problematic and somatic ill- very d ifferent in its meaning and nature from a physical
nesses as unproblematic. In a society, bodily illness is a illness. Robert Kendell (1935–2002), a prominent pro-
genuine illness, and genuine illness is defined by devia- psychiatrist, argued that the value ladenness of mental
tion from normal anatomy and physiology of a body illness can be translated into value-free factual norms.
organ. On the other hand, Szasz believes that mental Hence, mental illness is essentially no different from
illnesses are defined by deviation from social norms in physical illness.
TABLE 11.9
Other Legislations Relevant to Mental Health Services in the United Kingdom
Legislations Details of the Legislation Influence on Psychiatric Practice
The Human Rights Act (1998) Article 8: Rights to respect for private and family life. Clinical decisions must be proportional and balance
Everyone has the rights to respect for his or her the severity of the effect of an intervention with the
private and family life, his or her home, and his or severity of the presenting clinical problem
her correspondence The Mental Health Review Tribunals should refer to
There shall be no interference by a public authority the Human Rights Act when deciding the time limit
with the exercise of these rights except in the threat of involuntary hospitalization
of national security and public safety, for the For children, their consent for treatment is viewed from
prevention of disorder or crime, for the protection the human rights perspective and should be taken into
of health or morals consideration when a decision is made between the
psychiatrist and their parents or legal guardian
The Disability Discrimination 1. Definition of disability: A disabled person suffers This law offers protections for mental health service
Act (2005) from physical or mental impairment, with substantial users against discrimination in employment and
and long-term adverse effect on a person’s ability to purchasing insurance
carry out normal day-to-day activities. Psychiatrists should inform people with mental health
2. Protection of disabled people from discrimination problems on their rights and support them in job
in employment. application
3. Protection of disabled people from discrimination
in the provision of goods, services, and facilities.
4. Protection of disabled people from discrimination
in education.
The Children Act (2004) The Children Act (2004) places a duty on health If a child is suspected to be a victim or abused or in
services to ensure that every child, whatever their danger as a result of parental psychiatric illnesses, the
background or circumstances, to social worker can apply the Children Act for
1. Be healthy. Emergency Placement order to remove the child and
2. Stay safe. place the child in a safe environment. The duration of
3. Enjoy and achieve through learning. the emergency order ranges from 7 to 14 days.
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University Press. (accessed on 20 June 2012).
12 Neurology and Neurological
Examination
12.1 CRANIAL NERVES (CNs II, III, IV, lobe below the calcarine sulcus. Lesion in the
AND VI) AND THE VISUAL SYSTEM optic rations is associated with inferior homony-
mous quadrantanopia.
12.1.1 Central Visual Pathway
and Visual Field Deficits An object produces a visual image upon the nasal hemiret-
ina of the ipsilateral eye and the temporal hemiretina of
The examination of visual field is performed by asking the contralateral eye. The upper half of the visual field
the patient to cover one eye and fixate on the exam- forms images upon the lower halves of the retinae and the
iner’s opposite eye. Then the examiner tries to map lower visual field upon the upper hemiretinae.
the visual field by bringing his or her finger from the
periphery to the boundary of the visual field. This will
repeat for the four quadrants (i.e. from upper right, 12.2 CRANIAL NERVES (CNs III, IV,
upper left, lower right, and lower left to the centre) AND VI) AND DOUBLE VISION
(Figure 12.1).
After examining the visual field, the examiner can ask
the patient (without covering the eye) to follow his or
12.1.1.1 Common Lesions in the Central her finger to the left, upper left corner, lower left cor-
Visual Pathway ner, right, upper right corner, and lower right corner of
1. The axons of retinal ganglion cells assemble the visual field. The examiner needs to observe the eye
at the optic disc and pass into the optic nerve movements and the patient is asked to report any double
(CN II). Lesion in the optic nerve at this location vision. Weakness of the extraocular muscles results in
is associated with unilateral visual field loss (i.e. double vision in the direction of movement of that muscle.
monocular blindness). Ask the patient to cover each eye in turn to identify the
2. The two optic nerves converge to form the optic eye that can see the outer image. This will indicate the
chiasma at the base of the brain. Lesion at the location of lesion. If double vision does not confirm to
optic chiasma is associated with bitemporal originate from a single cranial nerve (CN), differential
hemianopia. diagnoses such as myasthenia gravis and thyroid eye dis-
3. The optic nerves from nasal hemiretinae decus- ease should be considered.
sate and pass into the contralateral optic tract. If the double images are horizontally displaced and
The optic nerves from the temporal hemiretinae parallel, this indicates a weakness in the lateral or medial
remain ipsilateral. Lesion of the optic nerves muscles (see Figure 12.2a).
at this location is associated with incongruent If the double images are at an angle, the other mus-
homonymous hemianopia. cles such as inferior oblique/superior rectus or superior
4. Most optic tract fibres pass around the cerebral oblique/inferior rectus are affected (see Figure 12.2b).
peduncle to terminate in the lateral geniculate
body of the thalamus. Some of the optic tract
12.2.1 Oculomotor Nerve (CN III)
fibres involving in papillary light reflex termi-
nate in the pretectal area and superior colliculus. The oculomotor nerve nucleus is located in the midbrain.
Lesion in the Meyer’s loop is associated with The autonomic components involve in focusing of vision
superior homonymous quadrantanopia. and pupillary constriction.
5. The optic radiations are the projection from the Oculomotor nerve palsy is caused by tumour or aneu-
internal capsule to the primary visual cortex that rysm. Ptosis occurs with failure to elevate the eyelids.
locates on the medical surface of the occipital The pupil is dilated and remains unresponsive to light
159
Eyeball 1 1 1
Optic nerve
2
2
3
Optic chiasma 4
Optic track 3
5
Lateral geniculate body 6 4
(thalamus)
Optic radiation
5 and 6
Concentration of fibres
from radiation through 7 7
occipital and parietal lobes
Visual (calcarine) cortex
FIGURE 12.1 Optic nerve and pathways to the visual cortex: 1, pathology in the eye (e.g. glaucoma)—tunnel vision (damage to
peripheral field); 2, damage to optic nerve—unilateral blindness; 3, damage to optic chiasma (e.g. pituitary tumour)—bitemporal
hemianopia; 4, damage to lateral chiasma (e.g. aneurysms)—nasal blindness on same side; 5 and 6, tumours and trauma to unilat-
eral optic tract—blindness of opposite visual field (homonymous hemianopia); 7, cortical damage may not destroy macular vision.
(From Abrahams, P.H. et al., Illustrated Clinical Anatomy, CRC Press, Oxford, U.K., 2005, p. 328.)
Up
Inferior oblique Superior rectus
III III
Medial Lateral
rectus rectus
III VI
Superior oblique Inferior rectus

(a) IV III
Down
FIGURE 12.3 The motor functions of CNs III, IV, and VI.
and accommodation. Extraocular muscle palsies are

found in the upward, downward, and inward gaze (i.e.
failure in adduction) (Figure 12.3).
12.2.2 Trochlear Nerve (CN IV)

The trochlear nerve nucleus is found in the midbrain.
Trochlear nerve palsy is caused by tumour or aneu-
rysm and results in difficulty in moving the eye down-
ward and medially.
12.2.3 Abducens Nerve (CN VI)

(b)
The abducens nerve nucleus is found in the pons.
FIGURE 12.2 The relative position of the images in diplopia Abducens nerve palsy is caused by tumour or aneu-
and location of lesions. (a) Double images are horizontally dis- rysm and leads to extraocular muscle palsy in outward
placed and parallel. (b) Double images are at an angle. gaze (i.e. failure in abduction).
Neurology and Neurological Examination 161
= Normal response; = No response
Examination
of pupils
Large pupil Small pupil
Direct
response
Consensual
response
Other — — Ptosis, Normal Slow — Ptosis and Irregular pupils,

features abnormal accommodation, reaction to enopthalmos normal
eye impaired vision accommodation accommodation
movements
Diagnosis Anisocoria Mydriatic Oculomotor Optic nerve (CN Holmes– Senile Horner’s Argyll Robertson
(unequal drugs, (CN II) II) lesion Adie pupil meiosis syndrome pupil
size of e.g. nerve palsy
pupil, anticholinergic
caused by drugs or
cocaine and hallucinogens
MDMA)
FIGURE 12.4 Summary of the examination of the pupils.
12.2.4 Medial Longitudinal Fasciculus 3. Ask the patient to look at your finger held at 15
cm from the patient’s face. The presence of con-
Lesion in the medial longitudinal fasciculus (MLF) does striction is known as accommodation response.
not produce double vision but produces upgaze, down- If there is no response in step 2 but a normal
gaze, and lateral gaze paresis. This lesion is associated response in step 3, this is known as an afferent
with internuclear ophthalmoplegia (INO). In lateral gaze, pupillary defect, which involves the optic nerve
the ipsilateral eye can abduct but the contralateral eye (CN II) (Figure 12.4).
cannot adduct. INO is associated with ataxic nystagmus.
The combined CN III, IV, and VI palsies lead to ptosis 12.2.4.1.2 Pathologies of the Pupils and Optic Disc
and dilation of the pupil, which is unresponsive to light 12.2.4.1.2.1 Holmes–Adie Pupil
and accommodation. The combined palsies may lead to Clinical features: Unilateral (80% of cases), moder-
paralysis of all eye movement. ately dilated, poor reaction to light, and slow reaction
to accommodation. It is associated with diminished and
12.2.4.1 Examination of the Pupils absent knee jerk.
and Related Conditions
12.2.4.1.2.2 Hutchison’s Pupil
12.2.4.1.1 Three-Step Approach When
Aetiology: Caused by rapidly rising unilateral intracra-
Assessing the Pupils
nial pressure (e.g. intracerebral haemorrhage).
1. Assess the size of the two pupils: large, normal,
or small size. Clinical features: Dilated and unreactive on the side of an
2. Ask the patient to look into the distance and intracranial mass lesion as a result of compression of the
shine the torch twice in each eye in turn: oculomotor nerve (CN IIII) on the ipsilateral side.
a. The response of the eye where the torch is
12.2.4.1.2.3 Argyll Robertson Pupil
directly shone into is known as the direct
Aetiology: Neurosyphilis and diabetes mellitus.
response.
b. The response of the other eye is known as Clinical features: Constricted pupils, unreactive to light
the consensual response. but reactive to accommodation.
12.2.4.1.2.4 Horner’s Syndrome 3. Physical examination. Trigeminal nerve can

Aetiology: Brain stem stroke, Pancoast tumour at the lung be tested by asking the patient to clench their
apex, and carotid dissection. teeth and feel the masseter and temporalis
(Figure 12.5).
Pathology: Lesion to the sympathetic supply to the eye
4. The mandibular branch. This supplies the lower
at the central brain stem (e.g. medulla), cervical spine,
jaw but not the angle of the jaw.
cervical ganglion, and carotid body.
5. Sensory function. Cutaneous sensation from the
Clinical features: Meiosis (a constricted pupil), anhidro- anterior part of the head including teeth, cornea,
sis, and partial ptosis. sinuses, meninges, and mouth. In herpes zoster,
the sensory root is infected and leads shingles
12.2.4.1.2.5 Papilloedema (i.e. pain and eruption of vesicles located on a
Aetiology: Increased in intracranial pressure (tumour, dermatome).
abscess, encephalitis, hydrocephalus, benign intracra- 6. The cell bodies of afferents are located in the
nial hypertension) and retro-orbital lesion (e.g. cavernous semilunar (trigeminal) ganglion where the con-
sinus thrombosis). vergence of ophthalmic, maxillary, and mandib-
Clinical features: Swelling of the optic discs is identified ular nerves lies. The sensory information will
during the fundoscopy examination. be sent to the trigeminal sensory nucleus, which
is distributed throughout the brain stem. There
12.2.4.1.2.6 Nystagmus is a separation of affect fibres: fibres conveying
Nystagmus refers to rhythmic to-and-fro movement of the touch and pressure terminate in the principal
eyes. Different types of nystagmus are listed as follows: nucleus, while those carrying pain and tempera-
ture terminate in the spinal nucleus.
12.2.4.1.2.7 Different Types of Nystagumus 7. Then the nerves will decussate to the contralat-
Ataxic Nystagmus eral trigeminothalamic tract and terminate in
the contralateral ventral posterior nucleus of
Cause: Internuclear ophthalmoplegia (INO)
Multidirectional jerk nystagmus
Cause: Central vestibular syndrome (e.g. phenytoin toxicity) Ophthalmic

branch
Unidirectional jerk nystagmus
Semilunar
Cause: Central or peripheral vestibular syndromes ganglion
Pendular nystagmus (symmetrical in primary gaze)

Maxillary
Cause: Albinism, coal miners branch
12.2.5 Trigeminal Nerve (CN V)

1. The ophthalmic branch. This supplies from
the tip of the nose to the forehead and vertex,
including the cornea. If a cotton wool touches
the cornea, it will lead to a brisk contraction of
both orbicularis oculi. This response is known
as the corneal reflex. A lesion in this branch
leads to loss of the corneal reflex.
2. The maxillary branch. This supplies the cheek Mandibular
branch
to the angle of the jaw (including the inner
aspect of the mouth and the upper palate). FIGURE 12.5 The anatomy of the trigeminal nerve (CN V).
the thalamus. The sensory information will be c. Autonomic component: causing lacrimation
sent to the sensory cortex of parietal lobe. In and salivation from the sublingual and sub-
syringobulbia, there is a compressive destruc- mandibular glands.
tion of the decussating trigeminothalamic tract 2. The facial nerve joins the brain stem at the cer-
that leads to selective loss of pain and tempera- ebellopontine angle.
ture in the face. Cell bodies of primary afferent lie in the
8. Motor function: Mastication and movement of geniculate ganglion in the facial canal of the
the soft palate. The motor cell bodies are located petrous temporal bone. The fibres terminate
in the mesencephalic nucleus of the trigeminal, in the nucleus solitarius of the medulla and
which sends fibres to the cerebellum to facilitate project to the ventral posterior nucleus of the
movement coordination. thalamus. The information will be sent to the
parietal lobe.
3. The corticobulbar fibres from the motor cortex
12.2.6 Facial Nerve
innervate the facial motor nucleus, which sup-
1. The facial nerve has three components (Figure 12.6): plies the muscles of the bilateral upper face
a. Sensory component: to detect taste on the (frontalis, orbicularis oculi), while the lower
anterior 2/3 of the tongue. face is supplied by contralateral fibres. Hence,
b. Motor component: facial expression, eleva- upper motor and lower motor neuron lesions
tion of hyoid tension of stapes muscle, and (UMNL and LMNL) lead to different conse-
corneal reflex. Lesion affects reflex on the quences as illustrated in Figure 12.7.
ipsilateral side of the face. 4. Postganglionic fibres from the pterygopalatine
ganglion innervate the lacrimal gland and the
The facial nerve
nasal and oral mucous membrane.
splits into several
branches and
controls many of Figure 12.7a shows the facial features of the right-sided
the muscles in UMNL. The signs include sparing of the forehead mus-
the face
cles, weakness of the lower face, loss of nasolabial fold,
and drooping of the mouth.
Figure 12.7b shows that facial features of the right-
sided LMNL or Bell’s palsy. All facial muscles are
affected. Other signs include loss of eyebrow lines,
inability to close the eyes, loss of nasolabial fold, and
drooping of the mouth. Patients suffering from Bell’s
palsy also complain of pain behind the ear, altered
taste on one side of the tongue, and hyperacusis. Bell’s
palsy is associated with herpes zoster virus, which
causes vesicular rash in the external auditory canal.
This phenomenon is known as the Ramsay Hunt syn-
drome. The treatment of the Bell’s palsy includes
steroid and artificial tears.
Parotid
gland
12.2.7 Vestibulocochlear Nerve (CN VIII)
A branch of
the nerve
12.2.7.1 Weber’s Test
Facial nerve comes
carries taste 12.2.7.1.1 Instructions for Weber’s Test
sensations
out just below the ear
from the front
1. Place the tuning fork on the vertex.
and passes through the 2. Ask the patient where the sound is heard.
of the tongue
parotid salivary gland
3. Normally, the sound is heard at the centre of the
FIGURE 12.6 The anatomy of facial nerve (CN VII). head (Figure 12.8).
(a)
FIGURE 12.8 Weber’s test.
(b)
FIGURE 12.7 Upper and lower motor neuron lesions of the

facial nerve (CN VII). (a) Right-sided upper motor neuron lesion
(UMNL) and (b) right-sided lower motor neuron lesion (LMNL)
or Bell’s palsy. (a)
12.2.7.2 Rinne’s Test

12.2.7.2.1 Instruction
1. Hold a tuning fork (512 Hz) in front of the
patient’s ear.
2. Transfer the fork to the mastoid process behind
the ear.
3. Ask which sound is louder.
4. Conduction in air should be louder than that in
bone (Figure 12.9 and Table 12.1).
12.2.7.3 Anatomy of the Auditory System

The vestibulocochlear nerve (CN VIII) conveys sen-
(b)
sory impulses from the inner ear. It has two compo-
nents: (1) the vestibular nerve, which carries information FIGURE 12.9 Rinne’s test. Conduction in (a) bone and (b) air.
3. The cochlear nerve connects to the cochlear

TABLE 12.1 nuclei, which lie in the inferior cerebellar
Interpretation of the Results of Weber’s peduncle. Acoustic neuroma in the cerebello-
and Rinne’s Tests pontine angle leads to dizziness with deafness
by compression on the nerve. In severe case, it
Conditions Weber’s Test Rinne’s Test
leads to ataxia and paralysis.
Normal The sound is heard Conduction in air 4. From the cochlear nuclei, the cochlear nerve
in the centre of should be louder
decussates to the contralateral superior olivary
the head. than that in bone.
nucleus in the pons and the inferior colliculus in
Conductive hearing loss Lateralization to Bone conduction is
the affected ear better than air
the midbrain.
conduction. 5. The fibres will send from the inferior colliculus to
Sensorineural deafness Lateralization to Air conduction is the medial geniculate nucleus of the thalamus.
the good ear better than bone 6. The auditory information will finally reach the
conduction. primary auditory cortex in the Heschl’s gyri on
the superior temporal gyrus. The primary audi-
tory cortex is surrounded by Wernicke’s area
related to position and movement of the head, and (2) the where the auditory information is interpreted
cochlear nerve, which carries auditory information: and given contextual significance.
1. The vestibular nuclei contribute fibres to the MLF,
which connects with nuclei of CNs III, IV, and VI to 12.3 OTHER CRANIAL NERVES (TABLE 12.2)
coordinate head and eye movements. It is also con-
12.3.1 Spinal Cord
nected to the cerebellum to maintain equilibrium.
2. The cochlear nerve makes dendritic contact Note that diagrams of the ascending and descending
with the hair cells of the organ of Corti. white column tracts are considered in Chapter 13.
TABLE 12.2
Summary of Other Cranial Nerves (CN)
CN/Physical Examination Autonomic
Technique Motor Component Sensory Component Component Clinical Significance
Olfactory nerve (CN I) — Olfactory sensation — Olfaction
Ask the patient for the quality
of smell
Glossopharyngeal nerve Stylopharyngeus Pharynx, posterior third of Stimulates the parotid Motor: swallowing
(CN IX) muscle tongue, Eustachian tube, salivary gland via the and salivation
It is tested by gag reflex. middle ear, carotid body, parasympathetic Sensory: general
and carotid sinus fibres sensation,
chemo- and
baroreception
Vagus nerve (CN X) Soft palate, pharynx, Pharynx, larynx, Parasympathetic in Motor: swallowing
larynx, and upper oesophagus, and external thoracic and and speech
oesophagus ear abdominal viscera
Accessory nerve (CN XI) Sternocleidomastoid — — Movement of head
Ask the patient to shrug the and trapezius muscles and shoulder
shoulders.
Hypoglossal nerve (CN XII) Intrinsic and extrinsic — — Movement of the
It is tested by asking the patient muscles of the tongue tongue
to move the tongue and look LMNL: wasting and
for wasting or fasciculation weakness of the
tongue
12.3.1.1 Spinothalamic Tracts In syringomyelia, there is an enlargement in the cen-

Function: The spinothalamic tract carries information tral canal that compresses the lateral spinothalamic tract
related to pain and temperature via the lateral spinotha- at the decussation, and the ventral spinothalamic tract
lamic tracts. Information related to the nondiscriminative is not affected. This leads to dissociated sensory loss.
touch and pressure is carried by the ventral spinothalamic The loss of sensation in pain and temperature makes the
tracts of the contralateral side of the body. The spinoreticu- patient injure his or her hands without awareness. This
lothalamic tract involves in the dull pain transmission. leads to the Charcot’s joint.
Lesion of the spinothalamic tract is associated with the
loss of contralateral sensation of pain, thermosensations, 12.3.1.2 Second-Order Neurons
nondiscriminative touch, and pressure. The spinothalamic In the brain stem, the spinothalamic fibres run in proxim-
tract is selectively damaged in syringomyelia (Table 12.3). ity to the medial lemniscus and form the spinal lemniscus.
The dorsal root ganglion consists of the slow-conducting
(C and A delta) fibres. Pain has two components: the first 12.3.1.3 Third-Order Neurons
pain, a well-localized sharp sensation, is carried by small The majority of the fibres terminate in the ventral pos-
myelinated fibres and the second pain, an unlocalized burn- terior nucleus of the thalamus and then projects to the
ing sensation, is carried by unmyelinated fibres. After leaving somatosensory cortex.
the dorsal root ganglion, the spinothalamic axons decussate
to the opposite side of the cord by passing through the ventral
white commissure and then enter the contralateral spinotha- 12.3.2 Dorsal Column
lamic tract. The lateral spinothalamic tract decussates within Functions: The dorsal column carries sensory informa-
one segment of the origin, and the ventral spinothalamic tract tion concerning proprioception (movement and joint
decussates several segments after crossing. position sense) and discriminative touch.
Aetiologies: There are several conditions that affect the
dorsal columns:
TABLE 12.3
Summary of the Spinal Cord Lesions • Tabes dorsalis (tertiary syphilis) is associated
with sensory ataxia (high steppage and unsteady
Lesions Clinical Features
gait) with Romberg’s sign.
Central cord lesions 1. Early sphincter disturbance • The combined subacute degeneration of the
2. Spinothalamic loss (unilateral or cord is caused by vitamin B12 deficiency and
bilateral) leads to sensory ataxia (lesions of the dorsal col-
3. Loss of pain and temperature sensation
umn) and spasticity of the limbs (lesions in the
4. Weakness, wasting, and areflexia in the
lateral columns). This condition is associated
affected segment with spasticity below
the level of lesion
with pernicious anaemia.
Anterior cord 1. Preservation of dorsal column • Multiple sclerosis leads to the loss of propriocep-
syndrome functions (i.e. proprioception of tion in hands and fingers and causes astereognosis.
movement, joint position sense, and
discriminative touch) There are two tracts in the dorsal column:
2. Loss of all other functions
Dorsal column loss 1. Ataxia 1. The cuneate fasciculus lies in the medial tract
2. Loss of proprioception and vibration and fibres join at the upper thoracic levels or cer-
sense vical dorsal roots. Multiple sclerosis damages
Brown–Sequard 1. Ipsilateral spasticity and pyramidal this area and leads to astereognosis.
syndrome signs 2. The gracilis fasciculus lies in the lateral tract
2. Posterior column sensory loss and fibres join at sacral, lumber, and lower tho-
3. Contralateral spinothalamic loss
racic levels.
Total spinal 1. Loss of all function below the level of
transection the lesion (paraplegia or tetraplegia)
2. Urinary retention 12.3.2.1 Ascending Dorsal Columns
3. Constipation The sensation reaches the spinal cord via the fast con-
ducting myelinated axons. There is no decussation until
the fibres reach the medulla oblongata. Hence, the dorsal

column carries the ipsilateral sensory information before TABLE 12.4
it reaches the brain stem. Compare and Contrast LMNLs and UMNLs
LMNL UMNL
12.3.2.2 Decussation in the Medulla
Weakness Weakness or paralysis of Weakness or paralysis
The axons of second-order neurons decussate in the individual muscles of individual
medulla. The internal arcuate fibres ascent through the movements
brain stem as the medial lemniscus. Muscles Wasting of muscles No wasting of muscles
Reflexes Loss of deep tendon Hyperactivity of deep
12.3.2.3 Third-Order Neurons reflexes/hypotonia tendon reflexes/
hyperreflexia
The medial lemniscus terminates in the ventral posterior
Tone Hypotonia (reduced Hypertonia (increased
nucleus of the thalamus and projects to the somatosen-
resistance to passive resistance to passive
sory cortex.
stretching) stretching)
Fasciculation Fasciculation (spontaneous No fasciculation
12.3.4 Corticospinal and Corticobulbar Tracts contractions)
Functions: The corticospinal tracts are involved with vol-

untary and skilled movement of the limbs.
Lesions
TABLE 12.5
1. Lesion in the corticospinal tract causes weak- Compare and Contrast Bulbar
ness, unsteadiness, and stiffness in walking and Pseudobulbar Palsy
with spontaneous spasms of the legs. Physical
examination reveals increased tone, reflexes, Bulbar Palsy Pseudobulbar Palsy
and extensor plantar responses. Lesions Lower motor neuron Upper motor neuron
2. Lesion in the bilateral lateral corticospinal Causes MNDs, Guillain–Barré Bilateral lesions above the
tract is associated with incontinence. syndrome, polio, midpons. For example, in
3. Hereditary spastic paraparesis is an autoso- syringobulbia, brain stem the corticobulbar tracts in
mal dominant disorder that involves the degen- tumours, central pontine multiple sclerosis, MND,
myelinolysis in people and stroke. It is commoner
eration of the lateral corticospinal tracts. This
with alcohol misuse than bulbar palsy.
causes a spastic paraparesis with hyperreflexia
Tongue Flaccid and fasciculating Spastic
and extensor plantar responses but spares the
Jaw jerk Normal Increased
bladder function. Speech Quiet, hoarse, and nasal Donald Duck speech
4. Motor neuron disease (MND) is a chronic degen- Inappropriate laughter or
erative disorder seen in patients aged over 50 emotional incontinence
years. MND involves degeneration of the corti-
cobulbar tracts projecting to the nucleus ambigu-
ous and hypoglossal nucleus. MND is associated
with the following conditions (Table 12.4): Anatomy
a. Bulbar palsy is an LMNL that leads to flaccid,
fasciculating tongue with normal jaw jerk and 1. The neurons of the corticospinal tract neuron
quiet and nasal speech. It also occurs in syrin- arise from cell bodies in the precentral gyrus or
gobulbia, central pontine myelinolysis (due to primary motor cortex.
alcohol misuse), and brain stem tumours. 2. The corticospinal tract passes through the
b. Pseudobulbar palsy is a UMNLs and com- corona radiata and internal capsule and enters
moner than bulbar palsy. Clinical features the crus cerebri of the midbrain.
include a spastic tongue, increase in jaw jerk, 3. 75%–90% of the fibres decussate and enter the
Donald Duck speech, emotional incontinence, contralateral lateral corticospinal tract. The
and hollow laugher. It is caused by head injury, sphincter function is supplied by bilateral lateral
stroke, and multiple sclerosis (Table 12.5). corticospinal tracts.
4. 10%–25% of the fibres remain ipsilateral and 4. Elbow extension (Figure 12.13)
enter the ventral corticospinal tract and decus- Muscle: Triceps
sate near termination. Nerve: Radial nerve
5. Corticospinal neurons terminate at the follow- Myotomes: C6, C7, C8
ing sites: Reflex at triceps: C7, C8
a. The cervical levels: 55%
b. The thoracic levels: 20%
c. The lumbosacral levels: 25%
12.4 MYOTOMES AND NEUROLOGICAL

EXAMINATION IN THE CASC
12.4.1 Myotomes of the Upper Limb
1. Shoulder abduction and adduction (Figure 12.10)
Muscle: Deltoid
Nerve: Axillary nerve
Myotome: C5
2. Internal and external rotation (Figure 12.11)
Muscle: Supraspinatus muscle (abduction), the
infraspinatus and teres minor (external rota-
tion), and the subscapularis (internal rotation)
Nerve: Suprascapular nerve
Myotomes: C5, C6
3. Elbow flexion (Figure 12.12)
Muscle: Biceps
Nerve: Musculocutaneous nerve
Myotomes: C5, C6 FIGURE 12.11 Internal and external rotation.
Reflex at biceps: C5, C6
FIGURE 12.10 Shoulder abduction and adduction. FIGURE 12.12 Elbow flexion.
FIGURE 12.13 Elbow extension. FIGURE 12.15 Pronation.
6. Pronation (Figure 12.15)

Muscle: Pronator teres and quadratus
Nerve: Median nerve
Myotomes: C6, C7 (Tables 12.6 and 12.7)
12.4.2 Myotomes of the Lower Limb

1. Hip flexion (Figure 12.16)
Muscle: Iliopsoas
Nerve: Lumbar plexus and femoral nerve
Myotome: L1 and L2
TABLE 12.6
Summary of Other Movements of the Upper Limbs
Movements Muscles Nerves Myotomes
Wrist Extensors carpi Radial nerve C6 and C7
extension radialis and ulnaris
Wrist flexion Flexors carpi Median and C7 and C8
radialis and ulnaris ulnar nerve
Finger Extensor digitorum Radial nerve C7
extension
Finger flexion Flexors digitorum Median and C8 and T1
FIGURE 12.14 Supination.
profundus and ulnar nerves
superficialis
5. Supination (Figure 12.14) Thumb Abductor pollicis Median nerve T1
Muscle: Biceps abduction brevis
Nerve: Musculocutaneous nerve Index finger Dorsal interossei Ulnar nerve T1
Myotomes: C6, C7 abduction
Reflex at supinator: C5, C6
TABLE 12.7
Summary of the Medical Research Council (United Kingdom) Grades for Muscle Power
Grade 0 1 2 3 4 5
Clinical features No movement Flicker of Moves when gravity Moves against the gravity Some movement Full power
movement is eliminated but not resistance against resistance
FIGURE 12.16 Hip flexion.
FIGURE 12.18 Hip abduction.
FIGURE 12.17 Hip extension.

2. Hip extension (Figure 12.17)
Muscle: Gluteus maximus
Nerve: Inferior gluteal nerve
Myotomes: L5 and S1
3. Hip abduction (Figure 12.18)
Muscle: Gluteus medius
Nerve: Lumbosacral plexus
Myotomes: L5
4. Hip adduction (Figure 12.19)
Muscle: Hip adductors
Nerve: Lumbosacral plexus
Myotomes: L2–L4 FIGURE 12.19 Hip adduction.
12.5 DERMATOMES
Dermatome is the area of the skin or cutaneous dis-
tribution that is supplied by a particular spinal nerve
(Table 12.8). Dermatomes are arranged as a succession
of bands encircling the trunk in a manner that reflects the
segmentation of the spinal cord (Figures 12.22 and 12.23).
TABLE 12.8
Summary of Plexuses and Innervations
FIGURE 12.20 Knee flexion.
Plexus Nerves Functions
Cervical plexus C1–C4 Innervation of the
5. Knee flexion (Figure 12.20) diaphragm, shoulder,
and neck
Muscle: Hamstrings
Brachial plexus C5–T1 Innervation of the upper
Nerve: Sciatic nerve
limbs
Myotomes: S1 and S2
Lumbar plexus T12/L1–L4 Innervation of the thigh
6. Knee extension Sacral plexus L4–S4 Innervation of the leg
Muscle: Quadriceps femoris and foot
Nerve: Femoral nerve
Myotomes: L3 and L4
7. Knee jerk: L3, L4
8. Ankle dorsiflexion (Figure 12.21)
Muscle: Tibialis anterior
Nerve: Deep peroneal nerve
Myotomes: L4 and L5
9. Ankle plantar flexion
Muscle: Gastrocnemius and soleus
Nerve: Sciatic nerve C4 C4
Myotomes: S1 and S2
T2
10. Ankle jerk: S1, S2 C5 T4-line
T4 of nipple
T1
(in males)
T10 T10-level
C6 C8
of umbilicus
T12
L1 T12-into
S2/3 groin
L2 L2
C7
L3 L3
L4 L4
L5 L5
S1 S1
FIGURE 12.21 Ankle dorsiflexion. FIGURE 12.22 Dermatomes from the anterior view.
L1 12.7.1.1.2 Cluster Headache

S5 Involves severe headache or facial pain. Cluster headache
L2 S4 is often described by patients as red-hot poker sticking
S3
in the face. This headache occurs in cluster that appears
quickly and lasts for 1–3 h. It is associated with unilat-
S2 eral lacrimation and local erythema of skin. Treatments
L2 include NSAIDs and antimigraine medications.
12.7.1.1.3 Tension Headache

L3
This bitemporal headache is like a circumstantial band
around the head. It gives rise to pressure-like sensation.
Treatment includes relaxation therapy and β-blockers.
L5 L4
12.7.2 Pellagra
S1 Aetiology: Nicotinic acid deficiency.
Clinical triad: Diarrhoea, dermatitis, and dementia.
12.7.3 Blepharospasm
L4 L5
Definition: An adult-onset focal dystonia involving spasm
S1
of the orbicularis oculi.
Aetiology: Associated with Parkinson’s disease, demy-
FIGURE 12.23 Dermatomes from the posterior view. elinating disease, and brain stem infarction.
Epidemiology: Onset in the fifth decade; M/F = 1:2.

12.6 COMPRESSION AND ENTRAPMENT
NEUROPATHIES (TABLE 12.9) Clinical features: Bilateral forced eye closure, exacer-
bated by bright lights but improved by relaxation, yawn-
12.7 OTHER NEUROLOGICAL CONDITIONS
ing, singing, and talking.
12.7.1 Headache
Comorbidity: 75% of patients have other form of dystonia
12.7.1.1 Types of Headache (usually facial).
12.7.1.1.1 Migraine Headache Treatment: Anticholinergics or surgical treatments
Causes: Vascular causes involving the muscle involved. Botulinum toxin may give
benefits to 70% of the patients.
12.7.1.1.1.1 Clinical Features
• Throbbing unilateral or occipital pain. Prognosis: Spontaneous remission in 10%; 50% are func-
• Preceded by or associated with nausea, vomit- tionally blind.
ing, and photophobia.
• Migraine aura precedes the headache, and
patients may see teichopsia (wavy lines or forti- 12.7.4 Other Dystonia
fication spectra) or scotoma. Spasmodic torticollis: Commonest focal dystonia involv-
• Motor deficits may be present. ing sudden contraction of the neck and leads to devia-
tion of the head to one side. Treatment is similar to
12.7.1.1.1.2 Treatment
blepharospasm.
• Prophylaxis includes β-blockers and clonidine.
• Acute episode is treated by ergotamine and Writer’s cramp: Dystonia involving hand movement
methysergide. when controlling a pen.
TABLE 12.9
Summary of the Compression and Entrapment Neuropathies
Nerves Site of Compression Muscles Affected Distribution of Sensory Impairment
Radial nerve Compression in the Finger dorsiflexors
spiral groove of the Thumb dorsiflexors and
humerus abductors
Wrist dorsiflexors
Brachioradialis
Median nerve Compression at the Abductor pollicis brevis

wrist
Ulnar nerve Compression at the Small muscles of the

elbow hand except abductor
pollicis brevis
Ulnar half of flexor
Digitorum profundus
Flexor carpi ulnaris
Common Compression at the head Toe dorsiflexors

peroneal nerve of the fibula of the Foot dorsiflexors
lower limb Foot evertors
12.7.4.1 Gait Abnormalities Aetiology: Campylobacter jejuni, cytomegalovirus, and

Shuffling gait: Short paced, stooped, poor arm swing, Epstein–Barr virus infection. H1N1 vaccine
difficulty in starting and stopping, and trying to catch up Clinical course: From days to a month
(festinant gait); associated with Parkinson’s disease
Clinical features: This syndrome affects the limbs and
Marche à petit pas: Associated with hydrocephalus CNs. Clinical features range from mild weakness to
Broad-based gait: As a result of loss of proprioception complete paralysis. Ten to twenty percentage of patients
and coordination and associated with lesion in the dorsal require ventilatory support. This syndrome leads to car-
column diac arrhythmias and hypo- or hypertension.
High stepping gait: As a result of bilateral foot drop Diagnosis: Acellular CSF with raised protein
caused by peripheral neuropathy Treatment: Plasma exchange and intravenous immuno-
globulins shorten the duration of illness.
12.7.4.2 Ekbom’s Syndrome (Restless Leg Syndrome) Prognosis: Mortality rate is 5%. Twenty per cent of
Aetiology: Most cases are idiopathic; secondary causes patients suffer from motor deficits at 1 year and 3% of
include iron deficiency, uraemia, gestational diabetes, patients have recurrence of the syndrome.
polyneuropathy, and rheumatoid arthritis. Huntington’s disease, Parkinson’s disease, epilepsy,
Clinical features: Irresistible desire to move the legs and multiple sclerosis are considered in Chapter 31.
when in bed with unpleasant leg sensations.
Treatment: Dopamine agonist and benzodiazepines such
as clonazepam. ACKNOWLEDGMENTS
The authors of this book would like to acknowledge
12.7.4.3 Peripheral Neuropathies Dr. Anselm Mak M.D. (HK), FRCP (Edin) Assistant
12.7.4.3.1 Pathogenesis Professor and Consultant Physician, Department
1. Axon degeneration (as a result of toxic, meta- of Medicine, Yong Loo Lin School of Medicine,
bolic, nutritional, physical insults, genetic National University of Singapore for his contribution to
conditions). this chapter.
2. Demyelination (as a result of inflammatory and
metabolic neuropathies).
3. Vascular nerve damage. BIBLIOGRAPHY
Abrahams PH, Craven JL, Lumley JSP. 2005: Illustrated
12.7.4.3.1.1 Clinical Features Clinical Anatomy, p. 328. Oxford, U.K.: CRC Press.
1. Distal symmetrical neuropathy: the most com- Butler S. 1993: Functional neuroanatomy. In Morgan G
and Butler S (eds.) Seminars in Basic Neurosciences,
mon presentation of axonal neuropathies.
pp. 1–41. London, U.K.: Gaskell.
2. Multifocal/asymmetrical neuropathies: as a Crossman AR and Neary D. 2000: Neuroanatomy: An Illustrated
result of demyelinating or vasculitic neuropathy. Colour Text, 2nd edn. Edinburgh, U.K.: Churchill
3. Mononeuropathies: affecting an individual nerve. Livingstone.
4. Mononeuritis multiplex: affecting multiple Fuller G and Manford M. 2003: Neurology: An Illustrated
named muscles including vasculitis, diabetes, Colour Text. Edinburgh, U.K.: Churchill Livingstone.
lupus, sarcoidosis, and leprosy. Longmore M, Wilkinson I, Turmezei T, and Cheung CK. 2007:
Oxford Handbook of Clinical Medicine, 7th edn. Oxford,
5. Demyelination produces weakness but not wasting.
Logan S. 1993: Neurophysiology. In Morgan G and Butler S (eds.)
12.7.4.4 Guillain–Barré Syndrome Seminars in Basic Neurosciences, pp. 42–70. London,
Epidemiology: 2/100,000 per year U.K.: Gaskell.
13 Neuroanatomy
13.1 ORGANIZATION OF THE 13.1.2.1 Somatic Nervous System

NERVOUS SYSTEM This is concerned primarily with the innervation of vol-
untary structures.
13.1.1 Structural Organization
13.1.2.2 Autonomic Nervous System
The nervous system can be divided structurally into
This is concerned primarily with the innervation of vol-
• The central nervous system (CNS) untary structures. It is subdivided into two parts:
• The peripheral nervous system (PNS)
• The sympathetic
• The parasympathetic
13.1.1.1 Central Nervous System
The CNS consists of
13.1.3 Developmental Organization
• The brain During ontogeny, the midline neural tube differentiates
• The spinal cord into the following vesicles:
Prosencephalon, which differentiates into the telencepha-
It is well protected by the skull and vertebral column and lon, gives rise to the cerebral hemispheres and contains the
the meninges (layers of connective tissue membrane):
1. Pallium
• The dura mater—outermost layer 2. Rhinencephalon
• The arachnoid mater—middle layer 3. Corpus striatum
• The pia mater—inner layer 4. Medullary centre
Cerebrospinal fluid (CSF) in the subarachnoid space Diencephalon—consisting of the

offers further protection of the CNS.
1. Thalamus
13.1.1.2 Peripheral Nervous System 2. Subthalamus
3. Hypothalamus
The PNS consists of
4. Epithalamus, consisting of the
a. Habenular nucleus
• The cranial nerves
b. Pineal gland
• The spinal nerves
• Other neuronal processes and cell bodies lying
Mesencephalon, consisting of the tectum, consisting of
outside the CNS
the corpora quadrigemina, made up of the
It is not as well protected as the CNS.
1. Superior colliculi
2. Inferior colliculi
a. Basis pedunculi
13.1.2 Functional Organization
b. Tegmentum, containing
The nervous system can be divided functionally into i. The red nucleus
ii. Fibre tracts
• The somatic nervous system iii. Grey matter surrounding the cerebral
• The autonomic nervous system aqueduct
175
Prosencephalon
Prosencephalon
Telencephalon
Mesencephalon
Diencephalon
Rhombencephalon Mesencephalon
Rhombencephalon
Metencephalon
Myelencephalon
(a) (b)
FIGURE 13.1 Ontological development of the cerebral vesicles. (a) At an early stage. (b) At a later stage.
Rhombencephalon, which differentiates into the meten- 13.2.2 Neuroglia

cephalon, consisting of the
13.2.2.1 Relative Numbers
1. Pons Neuroglia, or interstitial cells, outnumber neurons by a
2. Oral part of the medulla oblongata factor of 5–10 times.
3. Cerebellum
13.2.2.2 Central Nervous System
Myelencephalon—the caudal part of the medulla
The main types of neuroglia in the CNS are
oblongata
The main ontological divisions are shown diagram-
• Astrocytes
matically at an early stage and a later stage of neurode-
• Oligodendrocytes
velopment in Figure 13.1.
• Microglia
• Ependyma
13.2 TYPES OF NERVOUS SYSTEM CELL
13.2.1 Neurons 13.2.2.3 Peripheral Nervous System
The main types of neuroglia in the PNS are
13.2.1.1 Classification by Morphology
On a morphological basis, neurons can be classified as • Schwann cells
follows: • Satellite cells
• Unipolar—the perikaryon has one neurite.

• Bipolar—the perikaryon has two neurites. 13.2.2.4 Astrocytes
• Multipolar—each neuron has one axon and more There are two types of astrocytes or astroglia:
than one dendrite.
• Fibrous astrocytes
• Protoplasmic astrocytes
13.2.1.2 Classification by Size
An alternative classification is on the basis of size: They are multipolar and their functions include
• Golgi type I—long axon • Structural support of neurons

• Golgi type II—short axon terminating near the • Phagocytosis
parent cell • Forming CNS neuroglial scar tissue
• Amacrine—no axon • Contributing to the blood–brain barrier
Neuroanatomy 177
13.2.2.5 Oligodendrocytes 13.3.1.1 Broca’s Area

The functions of oligodendrocytes or oligodendroglia This is the core of the frontal operculum on the domi-
include nant (usually left) side and consists of areas 44 and 45.
A lesion in this region can lead to expressive (motor)
• CNS myelin sheath formation aphasia (Broca’s nonfluent aphasia). This is shown in
• Phagocytosis Figure 13.3.
13.2.2.6 Microglia 13.3.1.2 Right Side
They are the smallest neuroglial cells and are most abun- Lesions in the nondominant frontal operculum can lead
dant in the grey matter. One of their functions is to dysprosody.
• Acting as scavenger cells at sites of CNS injury
13.3.2 Superior Mesial Region
13.2.2.7 Ependymal Cells
They line the cavities of the CNS. One of their functions is This contains
• Aiding the flow of CSF (cilial beating) • Supplementary motor area (SMA) (mesial part
of area 6)
Types of ependymal cell include • Anterior cingulate cortex (area 24)
• Choroidal epithelial cells—cover the surfaces of
the choroidal plexuses Lesions of the left or right superior mesial region can lead
• Ependymocytes—line the central canal of the to akinetic mutism.
spinal cord and ventricles
• Tanycytes—line the floor of the third ventricle 13.3.3 Inferior Mesial Region
over the hypothalamic median eminence
This consists of
13.2.2.8 Schwann Cells
In addition to being part of myelinated peripheral nerves, • Orbital cortex (including areas 11, 12, and 32)
Schwann cells encircle some unmyelinated peripheral • Basal forebrain
nerve axons. Their functions include
13.3.3.1 Orbital Cortex
• PNS myelin sheath formation Lesions of the orbital cortex (either side) can lead to a
• Neurilemma formation form of acquired sociopathy.
13.2.2.9 Satellite Cells 13.3.3.2 Basal Forebrain

Satellite cells, or capsular cells, are found in This includes the following nuclei:
• Sensory ganglia • Diagonal band of Broca

• Autonomic ganglia • Nucleus accumbens
• Septal nuclei
One of their functions is • Substantia innominata
• Neuronal support in sensory and autonomic
Lesions of the basal forebrain (either side) can lead to
ganglia
amnesia (retrograde and anterograde) and confabulation.
13.3 FRONTAL LOBES

13.3.4 Dorsolateral Prefrontal Cortex
13.3.1 Frontal Operculum
The dorsolateral prefrontal cortex (DLPFC) contains areas
This consists of Brodmann areas 44, 45, and 47 (see 8, 9, 10, and 46. Lesions in this region can lead to abnor-
Figure 13.2). malities in cognitive executive functions, impairment of
Primary somatosensory
Primary motor cortex (4) cortex (3,1,2)
Frontal eye field (8) Vestibular cortex (2)
6
Somatosensory
3,1,2 5
association
4
cortex (5,7,40)
9 7
Prefrontal cortex 40 Visual association
(9,10,11,12)
cortex (39,19,18)
10 45 39
44
22
11 19 18
21 Primary visual
38 17
Broca’s speech area of 37 cortex (17)
left hemisphere (44,45)
20
Secondary somatosensory Auditory association cortex

and gustatory cortex Primary auditory (Wernicke’s speech area of
cortex (41,42) left hemisphere) (22)
(a)
Primary somatosensory
Primary motor cortex (4) cortex (3,1,2)
Premotor cortex (6)

6
Somatosensory
4 association cortex (5,7)
Prefrontal cortex
8 3,1,2
(9,10,11,12)
9 o rtex
te c
gula 4
Cin 2 5
Limbic lobe
10 Visual association
12
19 cortex (19,18)
11 Uncus 18
Limbic lobe
28 17
Parahippocampal 18
38 gyrus 37 19
Septal area
20
Limbic lobe Primary visual cortex (17)

(b)
FIGURE 13.2 (a) Lateral and (b) medial aspects of the cerebral hemisphere, showing important Brodmann areas (numbered).
(Reproduced from Graham, D.I. et al., Adams & Graham’s Introduction to Neuropathology, 3rd edn., Hodder, London, U.K.,
2006. With permission.)
verbal (left) or nonverbal (right) intellectual functions, 13.4 TEMPORAL LOBES

memory impairments affecting recency and frequency
judgements, poor organization, poor planning, poor 13.4.1 Superior Temporal Gyrus
abstraction, and disturbances in motor programming. The posterior part of the superior temporal gyrus, area 22,
Left-sided lesions may cause impaired verbal fluency, forms Wernicke’s area in the left hemisphere (see Figure
while right lesions may cause impaired nonverbal (design) 13.2). Lesions in this region can lead to a receptive (sen-
fluency. sory) aphasia (Wernicke’s fluent aphasia; see Figure 13.3).
Neuroanatomy 179
Arcuate fasciculus
(conduction aphasia)
Motor cortex (6,4)
Angular gyrus (39)
Visual association
cortex (18,19)
Primary visual
cortex (17)
Broca’s area (44,45)
(Broca’s aphasia)
Wernicke’s area (22)
(Wernicke’s aphasia)
Gerstmann syndrome
FIGURE 13.3 Left hemisphere: language, vision, and Gerstmann syndrome. (Reproduced from Graham, D.I. et al., Adams &
Graham’s Introduction to Neuropathology, 3rd edn., Hodder, London, U.K., 2006. With permission.)
13.4.2 Posterior Inferolateral Region side can lead to an inability to name facial expressions.
Retrograde amnesia may result from bilateral lesions.
This consists of
• Posterior portion of the middle temporal gyrus 13.4.4 Mesial Temporal Region

(part of area 37) This consists of
• Posterior portion of the inferior temporal gyrus
(part of area 37) • Parahippocampal gyrus (areas 27 and 28)
• Posterior portion of the fourth temporal gyrus • Amygdala
(part of area 37) • Entorhinal cortex
• Hippocampus
Lesions in this region, and in the adjoining occipitotem-
poral junction, can lead to prosopagnosia and impaired Left-sided lesions can lead to anterograde amnesia affect-
object recognition. ing verbal information, while right-sided lesions can lead
to anterograde amnesia affecting nonverbal information.
Bilateral lesions can lead to verbal and nonverbal antero-
13.4.3 Anterior Inferolateral Region
grade amnesia.
This consists of
• Anterior portion of the middle temporal gyrus 13.5 PARIETAL LOBES

(part of area 21)
13.5.1 Temporoparietal Junction
• Anterior portion of the inferior temporal gyrus
(part of area 20) The posterior part of the inferior parietal lobule together with
• Anterior portion of the fourth temporal gyrus the posterior part of the superior temporal gyrus (Wernicke’s
(part of area 20) area) forms the greater Wernicke’s area. Left-sided lesions
• Temporal pole (area 38) can lead to a receptive (sensory) aphasia (Wernicke’s fluent
aphasia), while right-sided lesions can lead to phonagnosia
Lesions in the left side can lead to anomia and defects (impairment in the ability to recognize familiar voices) and
in accessing the reference lexicon. Lesions in the right amusia (impaired ability to recognize and process music).
13.5.2 Inferior Parietal Lobule hemiachromatopsia affecting the whole visual field,

associative visual agnosia, and prosopagnosia.
This consists of
• Angular gyrus (area 39) 13.7 BASAL GANGLIA

• Supramarginal gyrus (area 40)
13.7.1 Components
Lesions on the left can lead to conduction aphasia (see Authorities differ on the components of the basal ganglia.
Figure 13.3) and tactile agnosia. Lesions on the right According to Snell (1987), the basal ganglia consist of the
can lead to anosognosia, neglect, tactile agnosia, and
anosodiaphoria (impaired concern with respect to neu- 1. Corpus striatum
rological deficits). a. Caudate nucleus
b. Lentiform nucleus
2. Amygdala (amygdaloid nucleus or amygdaloid
13.6 OCCIPITAL LOBES body)
The occipital lobe contains 3. Claustrum
• Primary visual cortex (area 17) The lentiform nucleus consists of the
• Visual association cortices (areas 18 and 19)
1. Globus pallidus
Lesions of the dorsal region (superior to the calcarine fis- 2. Putamen
sure) and adjoining parietal region (areas 7 and 39) can
lead to partial (unilateral lesions) or a full-blown (bilat- Some of these structures are shown in the diagrammatic
eral lesions) Balint’s syndrome, consisting of sketch of Figure 13.4.
• Simultanagnosia 13.7.2 Connections of the Lentiform Nucleus

• Ocular apraxia or psychic gaze paralysis
• Optic ataxia 13.7.2.1 Afferents
Afferents to the putamen come from the
Bilateral dorsal lesions can also lead to astereopsis
and impaired visual motion perception. Lesions of the • Caudate nucleus
left ventral region (inferior to the calcarine fissure) • Cerebral cortex
can lead to contralateral (right) acquired (central)
hemiachromatopsia (impaired visual colour percep- Afferents to the globus pallidus come from the
tion) and acquired (pure) dyslexia. Lesions of the right
ventral region can lead to contralateral (left) acquired • Caudate nucleus
(central) hemiachromatopsia and apperceptive visual • Putamen
agnosia. Bilateral lesions can lead to acquired (central) • Substantia nigra
Body of caudate nucleus
Head of
Putamen
caudate nucleus
Amygdala (amygdaloid
nucleus or amygdaloid body)
Tail of caudate nucleus
FIGURE 13.4 Sketch of the basal ganglia of the left adult cerebral hemisphere.
Neuroanatomy 181
13.7.2.2 Efferents 13.8 LIMBIC SYSTEM

Efferents from the putamen pass to the
13.8.1 Limbic Lobe
• Globus pallidus This was described by Broca in 1878 as an arrange-
ment of cortical structures around the diencephalon,
Efferents from the globus pallidus pass to the
forming a border on the medial side of each cerebral
hemisphere between the neocortex and the remainder
• Hypothalamus
of the brain.
• Reticular formation
• Substantia nigra
• Subthalamus 13.8.1.1 Cortical Areas
• Ventroanterior nucleus of the thalamus Cortical areas of the limbic lobe form the limbic cortex
• Ventrolateral nucleus of the thalamus and include the
13.7.3 Frontal–Subcortical Circuits • Cingulate gyrus

• Parahippocampal gyrus
Alexander et al. (1986) have identified five parallel • Subcallosal gyrus
frontal–subcortical circuits that together form one of the
main organizational networks of the brain and are central
to brain–behaviour relationships. They connect specific 13.8.1.2 Nuclei
regions of the frontal cortex with the basal ganglia and Subcortical nuclei that are part of the limbic lobe include
the thalamus in circuits that mediate the
• Motor activity • Amygdaloid nucleus

• Eye movements • Septal nucleus
• Behaviour
The overall structure of each circuit is as follows: 13.8.2 Components

Frontal lobe cortex → caudate nucleus → globus
pallidus/substantia nigra → thalamus → frontal lobe cortex There is disagreement as to precisely which structures
form part of the modern definition of the limbic sys-
13.7.3.1 Motor Circuit tem. A good guide is provided by both Snell (1987) and
Trimble (1981).
This circuit originates in SMA and subserves motor
function.
13.8.2.1 Cortical Areas
13.7.3.2 Oculomotor Circuit Cortical areas that are generally considered to be part of
This circuit originates in the frontal eye fields and sub- the limbic system nowadays include the
serves eye movements.
1. Cingulate gyrus
13.7.3.3 Dorsolateral Prefrontal Circuit 2. Gyrus fasciolaris
This circuit originates in DLPFC and subserves executive 3. Hippocampal formation
cognitive functions. a. Dentate gyrus
b. Hippocampus
c. Parahippocampal gyrus
13.7.3.4 Lateral Orbitofrontal Circuit
4. Indusium griseum
This circuit originates in the lateral orbital cortex and 5. Olfactory tubercle
subserves personality. 6. Paraterminal gyrus (precommissural septum)
7. Prepyriform cortex
13.7.3.5 Anterior Cingulate Circuit 8. Secondary olfactory area (entorhinal area)
This circuit originates in the anterior cingulate cortex 9. Subcallosal gyrus
and subserves motivation. 10. Subiculum
13.8.2.2 Nuclei 13.9.1.2 Hippocampus

Subcortical nuclear groups that are generally considered This grey matter structure lies mainly in the floor of the infe-
to be part of the limbic system nowadays include the rior horn of the lateral ventricle. Anteriorly, it forms the pes
hippocampus. Posteriorly, it ends inferior to the splenium of
• Amygdala (amygdaloid nucleus) the corpus callosum. Axons from each alveus converge medi-
• Anterior thalamic nucleus ally to form the fimbria and crus of the fornix. Histologically,
• Dorsal tegmental nucleus the hippocampus is made up of the following three layers:
• Epithalamic nucleus
• Habenula • Molecular layer (outer)
• Hypothalamic nuclei • Pyramidal layer
• Mammillary bodies • Polymorphic layer (inner)
• Raphe nucleus
• Septal nucleus (septal area) Afferent connections of the hippocampus include fibres
• Superior central nucleus that originate from the
• Ventral tegmental area
• Cingulate gyrus
13.8.2.3 Connecting Pathways • Dentate gyrus
Connecting pathways of the limbic system include the • Hippocampus (the opposite one)
• Indusium griseum
• Anterior commissure • Parahippocampal gyrus
• Cingulum • Secondary olfactory area (entorhinal area)
• Dorsal longitudinal fasciculus • Septal nucleus (septal area)
• Fornix
• Lateral longitudinal striae 13.9.1.3 Parahippocampal Gyrus
• Mammillotegmental tract This gyrus is separated from the remaining cerebral cortex
• Mammillothalamic tract by the collateral sulcus. Anteriorly, it is continuous with the
• Medial forebrain bundle uncus. The subiculum of the parahippocampal gyrus allows
• Medial longitudinal striae the passage of nerve fibres from the secondary olfactory cor-
• Stria terminalis tex (entorhinal area) to the dentate gyrus.
• Stria medullaris thalami
13.9.2 Amygdala
13.9 INTERNAL ANATOMY OF
THE TEMPORAL LOBES The amygdala is also known as the amygdaloid nucleus,
body, or complex. It is continuous with the tail of the cau-
13.9.1 Hippocampal Formation date nucleus, lying anterior and superior to the tip of the
The hippocampal formation consists of the inferior horn of the lateral ventricle.
• Dentate gyrus 13.9.2.1 Afferent Connections

• Hippocampus Afferent connections received by the amygdala include the
• Amygdala (the opposite one, via the anterior
13.9.1.1 Dentate Gyrus commissure)
This gyrus lies between the hippocampal fimbria and the • Dopaminergic brain stem nuclei
parahippocampal gyrus. Anteriorly, it is continuous with the • Frontal association area
uncus. Posteriorly, it is continuous with the indusium griseum. • Lateral olfactory stria
Histologically, it is made up of the following three layers: • Noradrenergic brain stem nuclei
• Septal nucleus (septal area)
• Molecular layer (outer) • Serotonergic brain stem nuclei
• Granular layer • Temporal association area
• Polymorphic layer (inner) • Uncus
Neuroanatomy 183
13.9.2.2 Efferent Connections 13.10.2 Fornix

Parts of the brain to which efferent connections pass from This is the major efferent subcortical white matter
the amygdala include the tract of the hippocampus. The two crura of the fornix,
each formed from axons from the alveus of the hip-
• Hypothalamus (via the stria terminalis) pocampus, converge inferior to the corpus callosum
• Septal nucleus (septal area) (via the stria terminalis) and form the body of the fornix. The body of the for-
• Corpus striatum nix is connected anteriorly with the inferior surface of
• Frontal association area the corpus callosum via the septum pellucidum. The
• Lateral olfactory stria body of the fornix then divides into the two columns
• Temporal association area of the fornix.
• Thalamus
13.10.2.1 Destination of Fibres in the Fornix
The efferent connections of the hippocampus, via the for-
13.10 MAJOR WHITE MATTER PATHWAYS
nix, include the
13.10.1 Corpus Callosum
• Anterior hypothalamus
This is the largest set of interhemispheric connecting • Anterior nucleus of the thalamus
fibres. It lies inferior to the longitudinal fissure and supe- • Habenular nucleus
rior to the diencephalon. It connects homologous neocor- • Lateral preoptic area
tical areas. • Mammillary body (medial nucleus)
• Septal nucleus (septal area)
13.10.1.1 Divisions • Tegmentum of the mesencephalon
The main divisions of the corpus callosum (rostral first)
are the
13.10.3 Papez Circuit
• Rostrum This is the concept introduced by Papez, in 1937, of a
• Genu supposed limbic system reverberating circuit constituting
• Body the neuronal mechanism of emotion. It consisted of the
• Splenium
• Hippocampus
These are shown in the diagrammatic sketch of the cor- • Hypothalamus
pus callosum of Figure 13.5, which also shows some adja- • Anterior nucleus of the thalamus
cent structures. • Cingulate gyrus
Anterior column of Cingulate cortex (gyrus)

fornix (shaded)
Body of corpus callosum
Choroid plexus
Septum pellucidum (of third ventricle)
Genu of corpus callosum Thalamus
Rostrum of corpus callosum Interthalamic connection
Splenium of
Anterior commissure corpus callosum
Mammillary body
Cranial nerve III Fourth ventricle
Pons
FIGURE 13.5 Sketch of the corpus callosum in a midsagittal section of the adult human brain. The adjacent cingulate cortex
and septum pellucidum are also indicated. Note that the rostral direction is towards the left.
The postulated circuit was as follows: Lateral geniculate body
Hippocampus → (via the fornix)

Mammillary bodies of the hypothalamus → (via a
synaptic connection)
Anterior nucleus of the thalamus → (the neuroim- Optic radiation
pulse then radiates up) (lower field)
Cingulate gyrus → (via the cingulum)
Hippocampus
Calcarine
cortex
13.10.4 Arcuate Bundle Eye
This is a specific group of association fibres arranged in a

Optic nerve
curved shape running parallel to the cortical surface that, Optic radiation
Chiasm Optic tract (upper field)
on the dominant (usually left) side, connects the more
rostral Broca’s area with Wernicke’s area. FIGURE 13.6 Medial sagittal view of the brain, showing
the visual pathways that traverse the brain from the front to
the back. (Reproduced from Fowler, T.J. and Scadding, J.W.,
13.10.5 Anterior Commissure Clinical Neurology, 3rd edn., Hodder, London, U.K., 2003.
This small nerve fibre bundle crosses the midline in the With permission.)
lamina terminalis and connects homologous areas of the
neocortex and paleocortex. Parts of the limbic system in
Most optic tract fibres synapse in the thalamic lateral
the two cerebral hemispheres that are connected via the
geniculate body, while a minority (concerned with pap-
anterior commissure include the
illary and ocular reflexes) pass directly to the pretec-
tal nucleus and superior colliculi, bypassing the lateral
• Amygdala
geniculate body. From the lateral geniculate body, the
• Hippocampus
optic radiation passes, via the retrolenticular part of the
internal capsule, to the visual cortex (see Figure 13.6).
13.11 CRANIAL NERVES

13.11.3 Oculomotor Nerve
13.11.1 Olfactory Nerve This nerve has two motor nuclei:
This contains the central processes of the olfactory
receptors, which pass from the olfactory mucosa, through • The main oculomotor nucleus (also known as
the cribriform plate of the ethmoid, to synapse with the the somatic efferent nucleus)—supplies all the
olfactory bulb mitral cells. Axons then pass in the olfac- extrinsic ocular muscles with the exception of
tory tract to the primary olfactory cortex (also known as the superior oblique and lateral rectus
the periamygdaloid and prepyriform areas) via the lateral • The accessory parasympathetic nucleus (also
olfactory striae. known as the Edinger–Westphal nucleus)—
sends preganglionic parasympathetic fibres to
the constrictor pupillae and ciliary muscles
13.11.2 Optic Nerve
This contains retinal ganglion cell axons that pass to the
optic chiasma. At the optic chiasma,
13.11.4 Trochlear Nerve
This supplies one extrinsic ocular muscle, namely, the
• Medial retinal fibres, containing temporal visual superior oblique.
field information, pass to the contralateral optic
tract
• Lateral retinal fibres, containing nasal visual field
13.11.5 Trigeminal Nerve
information, pass to the ipsilateral optic tract This is the largest cranial nerve.
Neuroanatomy 185
13.11.5.1 Nuclei b. Buccal nerve: innervates the

The trigeminal nerve has four nuclei, the i. Skin of the cheek
ii. Mucous membrane of the cheek
c. Inferior alveolar nerve: innervates the
• Main sensory nucleus
i. Lower teeth
• Spinal nucleus
• Mesencephalic nucleus ii. Lower lip
• Motor nucleus iii. Skin of the chin
d. Lingual nerve: innervates the
13.11.5.2 Sensory Components i. Anterior two-thirds of the tongue
ii. Mucous membrane of the mouth
The main divisions and branches of the trigeminal nerve,
which together constitute the main sensory innervation of
most of the head and face, are as follows: 13.11.5.3 Motor Component
The motor component of the trigeminal nerve supplies the
1. Ophthalmic nerve or division
a. Frontal nerve: innervates, via the supraorbital • Muscles of mastication
and supratrochlear branches, the • Anterior belly of the digastric
i. Upper eyelid • Mylohyoid
ii. Scalp (anterior to the lambdoid suture) • Tensor tympani
b. Lacrimal nerve: innervates the • Tensor veli palatini
i. Lacrimal gland
ii. Lateral conjunctiva
13.11.6 Abducens Nerve
iii. Upper eyelid
c. Nasociliary nerve: innervates the This supplies one extrinsic ocular muscle, namely, the
i. Eyeball lateral rectus.
ii. Medial lower eyelid
iii. Nasal skin
iv. Nasal mucosa 13.11.7 Facial Nerve
2. Maxillary nerve or division 13.11.7.1 Nuclei
a. Infraorbital nerve: innervates the
The facial nerve has three nuclei:
i. Skin of the cheek
b. Superior alveolar nerve: innervates the
• Main motor nucleus
i. Upper teeth • Parasympathetic nuclei
c. Zygomatic nerve: innervates the • Sensory nucleus (the superior part of the tractus
i. Skin of the temple (via the zygomatico- solitarius nucleus)
temporal branch)
ii. Skin of the cheek (via the zygomaticofa- 13.11.7.2 Main Motor Nucleus
cial branch)
This supplies the
d. Branches from the sphenopalatine ganglion
include the
• Muscles of facial expression
i. Greater palatine nerve • Auricular muscles
ii. Lesser palatine nerve • Posterior belly of the digastric
iii. Long sphenopalatine nerve • Stapedius
iv. Nasal branches • Stylohyoid
v. Pharyngeal branches
vi. Short sphenopalatine nerve Corticonuclear fibres from the contralateral cerebral hemi-
3. Mandibular nerve or division sphere are received by the part of the main motor nucleus
a. Auriculotemporal nerve: innervates the supplying the lower face muscles. Corticonuclear fibres
i. Skin of the temple from both cerebral hemispheres are received by the part of
ii. Auricle division the main motor nucleus supplying the upper face muscles.
13.11.7.3 Parasympathetic Nuclei • Parasympathetic nucleus (the inferior salivary

These include the nucleus)
• Sensory nucleus (part of the tractus solitarius
• Lacrimal nucleus: supplies the nucleus)
Lacrimal gland
• Superior salivary nucleus: supplies the 13.11.9.2 Main Motor Nucleus
Nasal gland This supplies the
Palatine gland
Sublingual gland • Stylopharyngeus
Submandibular gland
Corticonuclear fibres from both cerebral hemispheres are
13.11.7.4 Sensory Nucleus received by the main motor nucleus.
This receives taste fibres, via the geniculate ganglion,
from the
13.11.9.3 Parasympathetic Nucleus
• Anterior two-thirds of the tongue This receives inputs from the
• Floor of the mouth
• Hard palate • Hypothalamus
• Soft palate • Olfactory system
• Tractus solitarius nucleus
• Trigeminal sensory nucleus
13.11.7.5 Chorda Tympani
This is a branch of the facial nerve given off before it Preganglionic fibres reach the otic ganglion via the tym-
passes through the stylomastoid foramen. The chorda panic plexus and the lesser petrosal nerve. Postganglionic
tympani joins the lingual branch of the mandibular divi- fibres supply the parotid gland by means of the auriculo-
sion of the trigeminal nerve. temporal branch of the mandibular nerve.
13.11.8 Vestibulocochlear Nerve 13.11.9.4 Sensory Nucleus

This nerve consists of the following two parts, the This receives taste information from the posterior one-
third of the tongue.
• Cochlear nerve—concerned with hearing
• Vestibular nerve—concerned with the mainte-
nance of equilibrium 13.11.10 Vagus Nerve
13.11.10.1 Nuclei
13.11.8.1 Cochlear Nerve
The vagus nerve has three nuclei, the
Its fibres are the central processes of the cochlear spiral
ganglion cells, terminating in the anterior and posterior
• Main motor nucleus
cochlear nuclei.
• Parasympathetic nucleus (the dorsal nucleus)
13.11.8.2 Vestibular Nerve • Sensory nucleus (the inferior part of the tractus
Its fibres are the central processes of vestibular ganglion solitarius nucleus)
neurons, terminating in the lateral, medial, superior, and
inferior vestibular nuclei. 13.11.10.2 Main Motor Nucleus
This supplies the
13.11.9 Glossopharyngeal Nerve
• Intrinsic muscles of the larynx
13.11.9.1 Nuclei • Constrictor muscles of the pharynx
The glossopharyngeal nerve has three nuclei
Corticonuclear fibres from both cerebral hemispheres are
• Main motor nucleus received by the main motor nucleus.
Neuroanatomy 187
13.11.10.3 Parasympathetic Nucleus 13.12 SPINAL CORD

This receives inputs from the
13.12.1 Divisions
• Hypothalamus From rostral to caudal, the spinal cord is divided into the
• Glossopharyngeal nerve following five parts:
• Heart
• Lower respiratory tract • Cervical—8 pairs of spinal nerves
• Gastrointestinal tract, as far as the transverse • Thoracic—12 pairs of spinal nerves
colon • Lumbar—5 pairs of spinal nerves
• Sacral—5 pairs of spinal nerves
It supplies the • Coccygeal—1 pair of spinal nerves
13.12.2 Ascending White Column Tracts

• Involuntary muscle of the heart
• Lower respiratory tract The anatomy of the ascending white column tract is
• Gastrointestinal tract, as far as the distal one- shown in Figure 13.7.
third of the transverse colon
Thalamus
13.11.10.4 Sensory Nucleus
Thalamus
This receives taste information from the inferior ganglion
of the vagus nerve.
13.11.11 Accessory Nerve
This nerve consists of the following two parts Midbrain
• Cranial root Ascending tract

trigeminal nerve
• Spinal root
Trigeminal
Pons
nerve
13.11.11.1 Cranial Root
Lateral
This supplies, via the vagus nerve, muscles of the spinothalamic tract
Descending root
• Larynx trigeminal nerve Upper
• Pharynx Medial medulla
• Soft palate lemniscus
Nucleus
Lower
13.11.11.2 Spinal Root gracilis
medulla
This supplies the Nucleus
Dorsal root
cuneatus
ganglion
• Sternocleidomastoid
• Trapezius Spinothalamic Posterior
pathway column route
Lateral
13.11.12 Hypoglossal Nerve spinothalamic tract
This supplies the Spinothalamic (pain, temperature)

Posterior columns (position, vibration)
• Intrinsic muscles of the tongue
• Styloglossus FIGURE 13.7 Ascending sensory pathways. (Reproduced
• Hyoglossus from Fowler, T.J. and Scadding, J.W., Clinical Neurology, 3rd
• Genioglossus edn., Hodder, London, U.K., 2003. With permission.)
13.12.2.1 Anterior • Spino-olivary tract—carries proprioceptive and

The ascending anterior white column tracts include the cutaneous sensations
• Spinotectal tract—involved with spinovisual reflexes
• Anterior spinothalamic tract—carries light touch
and pressure sensations 13.12.2.3 Posterior
The ascending posterior white column tracts include the
13.12.2.2 Lateral • Fasciculus cuneatus—carries discriminative
The ascending lateral white column tracts include the touch and proprioceptive sensations
• Fasciculus gracilis—carries vibration sensations
• Anterior and posterior spinocerebellar tracts—
carry proprioceptive, pressure, and touch
13.12.3 Descending White Column Tracts
sensations
• Lateral spinothalamic tract—carries pain and The anatomy of the descending white column tracts is
temperature sensations shown in Figure 13.8.
Anterior central
convolution
From
area
8
Tail of caudate
nucleus Thalamus
Lenticular nucleus
Internal capsule
Head of caudate nucleus
Mesencephalon
Corticomesencephalic tract
Corticonuclear tract III Corticopontine tract
Corticospinal tract IV
(pyramidal) Cerebral peduncle
V Pons
VI
VII
IX
X
Pyramid XII Medulla oblongata
XI
Pyramidal decussation
C1
Anterior corticospinal Lateral corticospinal
tract (direct) tract (crossed)
T
Motor
endplate
FIGURE 13.8 Course of the corticospinal tracts. (Reproduced from Fowler, T.J. and Scadding, J.W., Clinical Neurology,
3rd edn., Hodder, London, U.K., 2003. With permission.)
Neuroanatomy 189
13.12.3.1 Anterior • Lateral reticulospinal tract—involved with

The descending anterior white column tracts include the muscular activity
• Descending autonomic fibres—involved with
• Anterior corticospinal tract—involved with volun- visceral function control
tary movement • Olivospinal tract—?involved with muscular
• Reticulospinal fibres—involved with motor activity
function
• Vestibulospinal tract—involved with muscle tone
control 13.13 MAJOR NEUROCHEMICAL PATHWAYS
• Tectospinal tract—involved with a head-turn-
ing reflex and movement of the upper limbs in 13.13.1 Nigrostriatal Dopaminergic Pathway
response to acoustic, cutaneous, and visual stimuli
This is shown in Figure 13.9. The presynaptic compo-
13.12.3.2 Lateral nents of this pathway are formed by
The descending lateral white column tracts include the
• A8 dopaminergic neurons—located in the retic-
• Lateral corticospinal tract—involved with vol- ular formation of the mesencephalon
untary movement • A9 dopaminergic neurons—located in the pars
• Rubrospinal tract—involved with muscular activity compacta of the substantia nigra
Dopamine pathways and key brain regions
DLPFC
Striatum
Nucleus
Thalamus accumbens
a b c
Substantia
nigra e
Hypothalamus VMFC
Pituitary
Tegmentum
FIGURE 13.9 Major dopamine pathways in the brain. (a) The nigrostriatal dopamine pathway, which projects from the substantia
nigra to the corpus striatum of the basal ganglia, is part of the extrapyramidal system and controls motor function and movement.
(b) The mesolimbic dopamine pathway projects from the midbrain ventral tegmental area to the nucleus accumbens, a part of the
limbic system thought to be involved in many behaviours such as pleasurable sensations, the powerful euphoria of drugs of abuse,
and delusions and hallucinations of psychosis. (c) The mesocortical dopamine pathway is related to the mesolimbic pathway and also
projects from the ventral tegmental area but sends its axons to areas of the prefrontal cortex, where they may have a role in mediat-
ing cognitive symptomatology (DLPFC) and affective symptomatology (ventromedial prefrontal cortex) of schizophrenia. (d) The
tuberoinfundibular dopamine pathway projects from the hypothalamus to the anterior pituitary gland and controls prolactin secretion.
(e) A fifth dopamine pathway arises from multiple sites, including the periaqueductal grey, ventral mesencephalon, hypothalamic
nuclei, and lateral parabrachial nucleus, and projects to the thalamus. Its function is not currently well known. (Reproduced from Stahl,
S.M., Stahl’s Essential Psychopharmacology, 3rd edn., Cambridge University Press, Cambridge, U.K., 2008. With permission.)
Their axons pass, via the medial forebrain bundle, to ter- • Lateral septum
minate mostly in the • Cingulate cortex
• Entorhinal cortex
• Caudate nucleus • Medial prefrontal cortex
• Putamen
• Amygdala
13.13.3 Ascending Noradrenergic Pathway
This pathway is concerned with sensorimotor from the Locus Coeruleus
coordination.
This is shown in Figure 13.10. The main noradrenergic
13.13.2 Mesolimbic–Mesocortical nucleus is the locus coeruleus, located in the dorsal pons.
Dopaminergic Pathway At least five noradrenergic tracts arise from it:
The two parts of this pathway are shown in Figure 13.9.
This pathway originates in 1. Three ascend, via the medial forebrain bundle,
to supply mainly the
• A10 dopaminergic neurons—located in the ven- a. Ipsilateral cerebral cortex
tral tegmental area of the mesencephalon b. Thalamus
c. Hypothalamus
Their axons pass, via the medial forebrain bundle, to ter- d. Limbic system
minate mostly in the e. Olfactory bulb
2. The fourth, via the superior cerebellar peduncle,
• Nucleus accumbens supplies the cerebellar cortex.
• Olfactory tubercle 3. The fifth descends in the mesencephalon and
• Bed nucleus of the stria terminalis spinal cord.
S
PFC
T
NA
BF
Hy
C
A NT
SC
FIGURE 13.10 Major noradrenergic projections. Ascending noradrenergic projections originate mainly in the locus coeruleus
of the brainstem; they extend to multiple brain regions, as shown here, and regulate mood, arousal, cognition, and other functions.
Descending noradrenergic projections extend down the spinal cord and regulate pain pathways A, amygdala; BF, basal forebrain;
C, cerebellum; H, hippocampus; Hy, hypothalamus; NA, nucleus accumbens; NT, brainstem neurotransmitter centres; PFC, pre-
frontal cortex; S, striatum; SC, spinal cord; T, thalamus. (Reproduced from Stahl, S.M., Stahl’s Essential Psychopharmacology,
3rd edn., Cambridge University Press, Cambridge, U.K., 2008. With permission.)
Neuroanatomy 191
13.13.4 Basal Forebrain Cholinergic Pathway 13.13.5 Brain Stem Cholinergic Pathway

This is shown in Figure 13.11. Cholinergic neurons of this This is shown in Figure 13.12. Cholinergic neurons of
pathway originate in the basal forebrain, including this pathway originate in the brainstem, including
• Ch5 cholinergic neurons—located in the pedun-

• Ch4 cholinergic neurons—located in the nucleus
culopontine nucleus
basalis of Meynert
• Ch6 cholinergic neurons—located in the lat-
• Ch2 and Ch3 cholinergic neurons—located in
erodorsal tegmental nucleus
the diagonal band nucleus (of Broca)
• Ch1 cholinergic neurons—located in the medial
Their (Ch5 and Ch6) main innervation is to the
septal nucleus
• Thalamus
Their main innervation is as follows: • Cerebral cortex
• Basal forebrain
• Corpus striatum
• Ch4—cerebral cortex, amygdala, and corpus
• Globus pallidus
striatum
• Subthalamic nucleus
• Ch1—hippocampal formation
• Substantia nigra
• Ch2—hippocampal formation
• Ch3—olfactory bulb
Ch5 neurons are more closely interconnected with extra-
pyramidal structures, while Ch6 neurons send more
(Note that most of the cholinergic innervation of the cor- projections to nuclei of the limbic system and to medial
pus striatum is intrinsic and not from this pathway.) prefrontal cortex.
Cholinergic projections from basal forebrain
S
PFC T
NA
BF
Hy
C
NT
A
H
SC
FIGURE 13.11 Basal forebrain cholinergic pathway. Cholinergic neurons originating in the basal forebrain project to the pre-
frontal cortex, hippocampus, and amygdala; they are believed to be involved in memory A, amygdala; BF, basal forebrain; C,
cerebellum; H, hippocampus; Hy, hypothalamus; NA, nucleus accumbens; NT, brainstem neurotransmitter centres; PFC, prefron-
tal cortex; S, striatum; SC, spinal cord; T, thalamus. (Reproduced from Stahl, S.M., Stahl’s Essential Psychopharmacology, 3rd
edn., Cambridge University Press, Cambridge, U.K., 2008. With permission.)
PFC S
T
NA
BF
Hy
A NT
H
SC
FIGURE 13.12 Brainstem cholinergic pathway. Acetylcholine projections originating in the brainstem extend to many regions,
including the prefrontal cortex, basal forebrain, thalamus, hypothalamus, amygdala, and hippocampus. These projections regulate
arousal, cognition, and other functions A, amygdala; BF, basal forebrain; C, cerebellum; H, hippocampus; Hy, hypothalamus; NA,
nucleus accumbens; NT, brainstem neurotransmitter centres; PFC, prefrontal cortex; S, striatum; SC, spinal cord; T, thalamus.
(Reproduced from Stahl, S.M., Stahl’s Essential Psychopharmacology, 3rd edn., Cambridge University Press, Cambridge, U.K.,
2008. With permission.)
PFC S
T
NA
BF
Hy
C
NT
A
H
SC
FIGURE 13.13 Major serotonergic projections. Like noradrenaline, serotonin has both ascending and descending projections.
Ascending serotonergic projections originate in the brainstem and extend to many of the same regions as noradrenergic projec-
tions, with additional projections to the striatum and nucleus accumbens. These ascending projections may regulate mood, anxiety,
sleep, and other functions. Descending serotonergic projections extend down the brainstem and through the spinal cord; they may
regulate pain A, amygdala; BF, basal forebrain; C, cerebellum; H, hippocampus; Hy, hypothalamus; NA, nucleus accumbens; NT,
brainstem neurotransmitter centres; PFC, prefrontal cortex; S, striatum; SC, spinal cord; T, thalamus. (Reproduced from Stahl,
S.M., Stahl’s Essential Psychopharmacology, 3rd edn., Cambridge University Press, Cambridge, U.K., 2008. With permission.)
Neuroanatomy 193
13.13.6 Glutamate System • Median raphe nucleus

• Supralemniscal nucleus
Neurons using glutamate, an excitatory neurotransmitter,
include Ascending fibres pass from the superior raphe nuclei, via
pathways such as the dorsal raphe cortical tract (the larg-
• Cerebral cortical pyramidal cells
est pathway in primates) and the medial forebrain bundle
• Hippocampal pyramidal cells
(the largest pathway in the rat), to innervate the forebrain.
• Primary sensory afferents
Particularly important destinations include the
• Cerebellar granule cells
• Cerebellar climbing fibres
• Suprachiasmatic nucleus
The cerebral cortex contains abundant N-methyl-d- • Substantia nigra
aspartate (NMDA) receptors, which serve an integral • Limbic system
role in corticocortical and corticofugal glutamatergic • Periventricular regions
neurotransmission. • Primary sensory areas of the cerebral cortex
• Association areas of the cerebral cortex
13.13.7 Ascending Serotonin System
This is shown in Figure 13.13. During embryogenesis, BIBLIOGRAPHY
two groups of serotonergic neurons develop: Alexander GE, DeLong MR, and Strick PL. 1986: Parallel
organization of functionally segregated circuits linking
• A superior group—located at the boundary basal ganglia and cortex. Annual Review of Neuroscience
between the mesencephalon and the pons 9:357–381.
• An inferior group—located from the pons cau- Fitzgerald MJT, Gruener G, and Mtui E. 2012: Clinical
dally to the cervical spinal cord Neuroanatomy and Neuroscience, 6th edn. Edinburgh,
U.K.: Saunders Elsevier.
The superior group gives rise to the superior raphe nuclei Moore DP and Puri BK. 2012: Textbook of Clinical
and is largely responsible for the origin of ascending Neuropsychiatry and Behavioral Neuroscience, 3rd edn.
London, U.K.: Hodder Arnold.
serotonergic fibres projecting to the forebrain. The main
Puri BK and Logan BM 2010: Neuroanatomy. In Puri BK and
superior raphe nuclei are the Treasaden IH (eds.) Psychiatry: An Evidence-Based Text.
• Caudal linear nucleus (the most rostral) Snell RS. 2010: Clinical Neuroanatomy, 7th edn. Baltimore,
• Dorsal raphe nucleus MD: Lippincott, Williams & Wilkins.
14 Neuropathology
14.1 DEMENTIAS of the amyloid-β peptide Aβ, which is a 39–43-amino

acid peptide. Scattered deposits of amyloid-β protein
14.1.1 Alzheimer’s Disease in the brain in Alzheimer’s disease have been found to
The neuropathology of presenile dementia (later called localize to activated microglia.
Alzheimer’s disease by Emil Kraepelin) was first Aβ is derived from the membrane-bound β-amyloid
described in 1906 by Aloysius (or ‘Alois’) Alzheimer precursor protein (APP).
(1864–1915) (Berrios, 1991).
14.1.1.4 Neurochemical Pathology
14.1.1.1 Macroscopic Neuropathology
Neurochemical changes that have been reported in
Macroscopic changes in Alzheimer’s disease include Alzheimer’s disease include
• Global brain atrophy and low brain mass • ↓ Acetylcholinesterase
• Ventricular enlargement (particularly of the lat- • ↓ Choline acetyltransferase
eral ventricular inferior horn) • ↓ GABA
• Sulcal widening • ↓ Noradrenaline
The atrophy is usually most marked in the frontal, medial
temporal, and parietal lobes. 14.1.2 Pick’s Disease
14.1.1.2 Histopathology Pick’s disease is one histological type of frontotemporal
Histological changes in the cerebral cortex in Alzheimer’s dementia.
disease include
• Neuronal loss Macroscopic changes in Pick’s disease include
• Shrinking of dendritic branching
• Reactive astrocytosis • Selective asymmetrical atrophy of the anterior
• Neurofibrillary tangles—intracellular temporal lobes and frontal lobes
• Neuritic plaques (senile plaques)—extracellular • Knife-blade gyri
• Ventricular enlargement
There is a positive correlation between the number of neu-
rofibrillary tangles and neuritic plaques, on the one hand, 14.1.2.2 Histopathology
and, on the other, the degree of cognitive impairment. Histological changes in Pick’s disease include
Histological changes seen commonly in the hippo-
campus include • Pick’s bodies
• Neuronal loss
• Granulovacuolar degeneration • Reactive astrocytosis
• Hirano bodies
• Neurofibrillary tangles These changes may be seen in the
• Neuritic plaques (senile plaques)
• Cerebral cortex
14.1.1.3 Ultrastructural Pathology • Basal ganglia
Neuritic plaques contain a core made of amyloid. This • Locus coeruleus
consists of 8 nm extracellular filaments made up mainly • Substantia nigra
195
14.1.2.3 Ultrastructural Pathology Compared with Parkinson’s disease, in which Lewy bod-
Pick’s bodies consist of ies are also found, in dementia caused by Lewy body dis-
ease, the density of Lewy bodies is much higher in the
• Straight neurofilaments
• Paired helical filaments • Cingulate gyrus
• Endoplasmic reticulum • Parahippocampal gyrus
• Temporal cortex
14.1.3 Multi-Infarct Dementia
ICD-10 classes multi-infarct dementia under vascular 14.1.4.2 Ultrastructural Pathology
dementia. Lewy bodies contain
14.1.3.1 Macroscopic Neuropathology • Protein neurofilaments

Macroscopic changes in multi-infarct dementia include • Granular material
• Dense core vesicles
• Multiple cerebral infarcts • Microtubule assembly protein
• Local or general brain atrophy • Ubiquitin
• Ventricular enlargement • Tau protein
• Arteriosclerotic changes in major arteries
Clinically, the following relationships have been found 14.1.5 Creutzfeldt–Jakob Disease

usually to hold approximately for the total volume of the
Creutzfeldt–Jakob disease (CJD) is transmitted by
infarcts:
infection with a prion. In addition to the brain changes
mentioned in the succeeding text, CJD is also associ-
• 50 mL < volume ≤ 100 mL: cognitive impairment
ated with degeneration in spinal cord long descend-
• Volume > 100 mL: dementia
ing tracts. It has an incubation period of many years.
14.1.3.2 Histopathology Infection may be transmitted from surgical specimens,
postmortem preparations (such as corneal grafts), and
Histological changes include those of infarction and
human pituitary glands; the latter have been used to
ischaemia.
produce human somatotropin for clinical use. In 1995
in Britain, a new variant of CJD (nvCJD) was reported,
14.1.4 Lewy Body Disease which, it has been suggested, may be linked to trans-
The generic term ‘dementia with Lewy bodies’ was pro- mission, possibly via the food chain, from the neu-
posed at the first International Workshop on Lewy Body ropathologically related disorder bovine spongiform
Dementia in 1995 (McKeith, 2006). It was described in encephalopathy (BSE).
1923 by Friedrich Lewy in a large proportion of his patients
suffering from paralysis agitans, which had coincident 14.1.5.1 Macroscopic Neuropathology
plaques and neurofibrillary tangles (Holdorff, 2002). Lewy There may be little or no gross atrophy of the cerebral
body dementia includes the following types of dementia: cortex evident in rapidly developing cases. In those sur-
viving the longest, changes seen may include
• Diffuse Lewy body disease
• Senile dementia of Lewy body type • Selective cerebellar atrophy
• Lewy body variant of Alzheimer’s disease • Generalized cerebral atrophy
• Ventricular enlargement
14.1.4.1 Histopathology
Histological changes in the brain in dementia caused by 14.1.5.2 Histopathology
Lewy body disease include Histological changes in the brain in dementia caused by
CJD include
• Lewy bodies
• Neuronal loss • Status spongiosus
• Neurofibrillary tangles • Neuronal degeneration without inflammation
• Neuritis plaques (senile plaques) • Astrocytic proliferation
Neuropathology 197
14.1.6 Punch-Drunk Syndrome • Kidney

• Colon
This is also known as post-traumatic dementia, dementia • Ovary
pugilistica, or boxing encephalopathy. In addition to occur- • Prostate
ring in boxers who have received repeated punches to the • Thyroid
head, other contact sports involving repeated head injury,
such as rugby union, may also put participants at risk.
14.2.4 Meningeal Tumours
These include
Typical macroscopic changes include
• Cerebral atrophy • Meningiomas

• Ventricular enlargement • Meningeal sarcomas—very rare
• Perforation of the cavum septum pellucidum • Primary malignant melanomas derived from
• Thinning of the corpus callosum pia–arachnoid melanocytes—very rare
14.1.6.2 Histopathology
14.2.5 Pituitary Adenomas
Histological changes in the brain in punch-drunk syn-
drome include These include, in approximate order of relative frequency
(commonest first),
• Neuronal loss
• Neurofibrillary tangles • Sparsely granulated PRL (prolactin/lactotrophin/
mamotrophin) cell adenomas
14.2 CEREBRAL TUMOURS • Oncocytomas
• Null cell adenomas
14.2.1 Types • Gonadotroph cell adenomas
The main types of cerebral tumours, listed in order of • Corticotroph cell adenomas
relative frequency, are • Densely granulated GH (growth hormone/
somatotropin) cell adenomas
• Gliomas • Sparsely granulated GH cell adenomas
• Metastases • Mixed (GH cell–PRL cell) adenomas
• Meningeal tumours • Silent ‘corticotroph’ adenomas, subtype 2
• Pituitary adenomas • Unclassified adenomas
• Neurilemmomas • Acidophil stem cell adenomas
• Haemangioblastomas • Silent ‘corticotroph’ adenomas, subtype 1
• Medulloblastomas • Silent ‘corticotroph’ adenomas, subtype 3
• Mammosomatotroph cell adenomas
14.2.2 Gliomas • Thyrotroph cell adenomas
These are tumours derived from glial cells and their pre- • Densely granulated GH cell adenomas
cursors and include
• Astrocytomas—derived from astrocytes 14.2.6 Neurilemmomas
• Oligodendrocytomas—derived from These are also known as schwannomas. They are derived
oligodendrocytes from Schwann cells and include acoustic neuromas.
• Ependymomas—derived from ependymal cells
14.2.3 Metastases 14.2.7 Haemangioblastomas
Cerebral metastases derive particularly from primary These are derived from blood vessels.
neoplasia in the
14.2.8 Medulloblastomas
• Lung
• Breast These cerebellar tumours are embryonal tumours.
14.3 SCHIZOPHRENIA The ventricular enlargement particularly affects the tem-

poral horn (Crow et al., 1989), indicating temporal lobe
14.3.1 Gross Neuropathology neuropathology.
14.3.1.1 Brain Mass
14.3.1.6 Temporal Lobe
There is a slight but significant reduction in brain mass
The major of postmortem studies have found a reduc-
in schizophrenia, compared with controls, allowing for
tion in temporal lobe volume in schizophrenia. While the
differences in height, body mass, sex, and year of birth
grey matter is reduced in volume, particularly at the level
(Brown et al., 1986; Pakkenburg, 1987; Bruton et al., 1990).
of the amygdala and anterior hippocampus, the volume of
14.3.1.2 Brain Length the white matter tends not to be reduced.
Bruton et al. (1990) found a significant reduction in the
maximum anteroposterior length of formalin-fixed cere- 14.3.2 Morphometric Studies
bral hemispheres in schizophrenia, compared with age-
14.3.2.1 Temporal Lobe
and sex-matched normal controls. Both hemispheres were
shorter in schizophrenia compared with the controls. Pyramidal cell disorientation in the hippocampus has
been reported by Kovelman and Scheibel (1984) and by
14.3.1.3 Cerebral Volumes Conrad et al. (1991), although this failed to be found by
In the postmortem brains of patients with schizophre- Altshuler et al. (1987).
nia, compared with age- and sex-matched controls, Jeste and Lohr (1989) found that schizophrenic
Pakkenburg (1987) found a significant reduction in the patients had a significantly lower pyramidal cell den-
volumes of the sity than normal controls in the left CA4 hippocampal
region.
• Cerebral hemispheres Cytoarchitectural abnormalities have been reported
• Cerebral cortex in the entorhinal cortex in schizophrenia (Arnold et al.,
• Central grey matter 1991). These changes, which suggest disturbed develop-
ment, included
The volumes of the white matter did not differ
• Aberrant invaginations of the surface
significantly.
• Disruption of cortical layers
• Heterotopic displacement of neurons
14.3.1.4 Hippocampus and
• Paucity of neurons in superficial layers
Parahippocampal Gyrus
Altshuler et al. (1990) studied the area and shape of Arnold et al. (1995) found that schizophrenic postmor-
the anterior hippocampus and parahippocampal gyrus tem brains had a smaller neuron size in the hippocampal
in postmortem brains from schizophrenic, nonschizo- regions of
phrenic suicide, and nonpsychiatric controls. No signifi-
cant differences were found in hippocampal area, but the • The subiculum
parahippocampal gyrus was significantly smaller in the • CA1
schizophrenic group compared with the control group. • Layer II of the entorhinal cortex
Bogerts et al. (1990) also studied postmortem brains
of schizophrenic patients and control subjects. Compared It is of note that the subiculum, CA1, and the entorhinal
with the controls, in the schizophrenic group, the hippo- cortex are the major subfields of the hippocampal region
campal formation was significantly smaller in the right that maintain the afferent and efferent connections of
and left hemispheres. The reduction in hippocampal vol- the hippocampus with widespread cortical and subcorti-
ume in the male schizophrenics was greater than in the cal targets. It was therefore concluded that the smaller
female schizophrenics. size of neurons in these subfields may reflect the pres-
ence of structural or functional impairments that disrupt
14.3.1.5 Ventricular Volume these connections, which in turn could have behavioural
Ventricular enlargement has been found in a number of sequelae.
postmortem studies of schizophrenic brains (e.g. Brown Reduced hippocampal mossy cell fibre staining has
et al., 1986; Pakkenburg, 1987; Bruton et al., 1990). also been reported by Goldsmith and Joyce (1995).
Neuropathology 199
Akbarian et al. (1993b) found a distorted distribu- 14.3.3.2 Synaptophysin

tion of nicotinamide-adenine dinucleotide phosphate- Synaptophysin is a presynaptic vesicle protein, the distri-
diaphorase (NADPH-d) neurons in the hippocampal bution and abundance of which provide a synaptic marker
formation and in the neocortex of the lateral temporal that can be reliably measured in postmortem brain.
lobe, consistent with anomalous cortical development in Eastwood et al. (1995) found that in schizophrenic
the lateral temporal lobe. brains, compared with controls, synaptophysin mRNA
was reduced bilaterally in
14.3.2.2 Other Cortical Areas
Compared with control brains, Benes et al. (1986) found • CA4
significantly lower neuronal density in the following cor- • CA3
tical regions in schizophrenic brains: • The subiculum
• The parahippocampal gyrus
• Prefrontal cortex—layer VI
• Anterior cingulate cortex—layer V (The effect of antipsychotic medication was dis-
• Primary motor cortex—layer III counted as a separate rat study showed no effect of
haloperidol treatment on hippocampal synaptophysin
The glial density also tended to be lower throughout most mRNA.) Furthermore, Eastwood and Harrison (1995)
layers of all three aforementioned regions. However, there found decreased synaptophysin in the medial temporal
were no differences in the neuron: glia ratios or neuronal lobe in schizophrenia, compared with controls, using
size between the two groups. These results suggest the immunoautoradiography. Significant reductions were
occurrence of a dysplastic process rather than degenera- found in the
tion in schizophrenia.
Benes et al. (1987) confirmed the presence of • Dentate gyrus
greater numbers of long, vertical, associative axons in • Subiculum
the anterior cingulate cortex of schizophrenic patients • Parahippocampal gyrus
relative to control subjects. On the basis of this find-
ing, they suggested that there might be an increase of
associative inputs into the anterior cingulate cortex in 14.3.4 Gliosis
schizophrenia. Almost all recent quantitative studies investigating
Akbarian et al. (1993a) found a distorted distribution the regions of greatest structural differences in schizo-
of NADPH-d neurons in the dorsolateral prefrontal area phrenic patients have not shown significant gliosis (e.g.
of schizophrenic postmortem brains, consistent with Jellinger, 1985; Roberts et al., 1987; Bruton et al., 1990).
anomalous cortical development in this region. This negative finding is consistent with either of the fol-
Akbarian et al. (1995) have also found that the prefron- lowing possibilities:
tal cortex of schizophrenics shows reduced expression for
glutamic acid decarboxylase (GAD) in the absence of sig- • The structural change in schizophrenic brains
nificant cell loss, suggesting an activity-dependent down- results from an embryonic insult prior to the
regulation of neurotransmitter gene expression. third trimester (since the developing brain does
not show reactive gliosis until approximately the
14.3.2.3 Other Brain Regions third trimester).
The results of studies of the corpus callosum and cerebel- • A neuropathological process occurs at or after
lum have yielded inconsistent results. the third trimester but does not usually initiate
a glial reaction.
14.3.3 Synaptic Pathology
14.3.3.1 Synaptic Vesicles 14.3.5 Antipsychotic Medication
Soustek (1989) found clusters of large numbers of synap- It has been suggested that some of the neuropathological
tic vesicles in presynaptic knobs in the cerebral cortex of (and magnetic resonance imaging [MRI]) changes seen
schizophrenic postmortem brains but not in brains from in schizophrenia may be the result of pharmacotherapy
control subjects. with antipsychotic medication (Puri, 2011).
14.4 AUTISM with autism. The authors suggested that this localized
maldevelopment might serve as a temporal marker to
14.4.1 Histological Changes identify the events that damage the brain in autism, as
Bauman and Kemper (1985) studied the brain of a well as other neural structures that might be concomi-
29-year-old autistic man and found, compared with the tantly damaged. They concluded that the neocerebellar
brain of an age- and sex-matched normal control, abnor- abnormality may
malities in the
• Directly impair cognitive functions that may be
• Hippocampus attributable to the neocerebellum
• Subiculum • Indirectly affect, through its connections to the
• Entorhinal cortex brain stem, hypothalamus, and thalamus, the
• Septal nuclei development and functioning of one or more sys-
• Mammillary body tems involved in cognitive, sensory, autonomic,
• Amygdala (selected nuclei) and motor activities
• Neocerebellar cortex • Occur concomitantly with damage to other
• Roof nuclei of the cerebellum neural sites, the dysfunction of which directly
• Inferior olivary nucleus underlies the cognitive deficits in autism
Neuropathological studies suggest that the microscopic 14.5 MOVEMENT DISORDERS

neuroanatomical abnormalities in autism begin early in
gestation, probably in the second trimester (Bauman, 1991). 14.5.1 Parkinson’s Disease
Idiopathic Parkinson’s disease is characterized by a loss
14.4.2 Cerebellar Pathology of dopaminergic neurons in the substantia nigra.
Both neuropathological and structural neuroimaging 14.5.1.1 Macroscopic Neuropathology

studies have indicated that hypoplastia of the cerebel- Macroscopic changes in idiopathic Parkinson’s disease
lar vermis as well as hypoplasia of the cerebellar hemi- include
spheres occurs in some subjects with autism.
• Depigmentation of the substantia nigra—
14.4.2.1 Reduced Purkinje Cell Count particularly the zona compacta
Ritvo et al. (1986) compared the cerebellums of four autis- • Depigmentation of the locus coeruleus
tic subjects with those of three comparison subjects without
Diffuse cortical atrophy may take place.
central nervous system pathology and one with phenytoin
toxicity. Total Purkinje cell counts were found to be sig- 14.5.1.2 Histopathology
nificantly lower in the cerebellar hemisphere and vermis
Histological changes in idiopathic Parkinson’s disease
of each autistic subject than in the comparison subjects.
include
14.4.2.2 Neocerebellar Abnormality 1. Neuronal loss

In their study of subjects with autism, Courchesne et al. 2. Reactive astrocytosis
(1988) measured the size of the cerebellar vermis using 3. The presence of Lewy bodies in the
MRI and compared these with its size in controls. The a. Substantia nigra
neocerebellar vermal lobules VI and VII were found to b. Dorsal motor nucleus of the vagus
be significantly smaller in autism. This appeared to be a c. Hypothalamus
result of developmental hypoplasia rather than shrinkage d. Nucleus basalis of Meynert
or deterioration after full development had been achieved. e. Locus coeruleus
In contrast, the adjacent vermal lobules I–V, which are f. Edinger–Westphal nucleus
ontogenetically, developmentally, and anatomically dis- g. Raphe nuclei
tinct from lobules VI and VII, were found to be of nor- h. Cerebral cortex
mal size. Maldevelopment of the vermal neocerebellum i. Olfactory bulb
had occurred in both retarded and nonretarded patients 4. The presence of melanin-containing macrophages
Neuropathology 201
14.5.1.3 Neurochemical Pathology • ↑ Somatostatin

Neurochemical changes in idiopathic Parkinson’s disease • ↓ Corticotrophin-releasing factor (CRF)
include reduced inhibitory dopaminergic action of the • Dopamine hypersensitivity
nigrostriatal pathway on striatal cholinergic neurons.
Evidence has been put forward suggesting that phospho-
lipid-related signal transduction in advanced Huntington’s
14.5.2 Huntington’s Disease (Chorea) disease is impaired (Puri, 2001).
Huntington’s disease (or chorea) results from a mutation
of the protein huntingtin and is characterized by a selec- 14.5.3 Tardive Dyskinesia
tive loss of discrete neuronal populations in the brain with
progressive degeneration of efferent neurons of the neo- Tardive dyskinesia is a syndrome of potentially irre-
striatum and sparing of dopaminergic afferents, resulting versible involuntary hyperkinetic dyskinesias that may
in progressive atrophy of the neostriatum. occur during long-term treatment with antipsychotic
(neuroleptic) medication. The most important hypoth-
14.5.2.1 Macroscopic Neuropathology eses concerning the neurochemical pathology of tardive
Macroscopic changes in Huntington’s disease include dyskinesia are
• Small brain with reduced mass • Dopamine hypersensitivity

• Marked atrophy of the corpus striatum— • Free-radical-induced neurotoxicity
particularly the caudate nucleus • GABA insufficiency
• Marked atrophy of the cerebral cortex—particularly • Noradrenergic dysfunction
the frontal lobe gyri (the parietal lobe is less often
affected) 14.5.3.1 Dopamine Hypersensitivity Hypothesis
• Dilatation of the lateral and third ventricles According to this hypothesis, the following sequence of
events takes place:
14.5.2.2 Histopathology Long-term treatment with antipsychotic (neuroleptic)
Histological changes in Huntington’s disease include medication
1. Neuronal loss in the cerebral cortex—particularly → Chronic dopamine receptor blockade

the frontal cortex → Dopamine D2 receptor hypersensitivity in the
2. Neuronal loss in the corpus striatum—particularly nigrostriatal pathway
neurons using as neurotransmitters → Tardive dyskinesia
a. GABA and enkephalin
b. GABA and substance P Evidence in favour of this hypothesis includes
3. Astrocytosis in affected regions
• Studies of denervation-induced hypersensitivity
In the affected regions, there is relative sparing of the fol- in muscles
lowing neuronal populations: • Animal experiments in which, following discon-
tinuation of antipsychotic drugs, acute dopamine
• Diaphorase-positive neurons containing nitric agonist challenges → ↑ oral stereotyped behaviour
oxide synthase (NOS) • Animal experiments in which repeated antipsy-
• Large cholinesterase-positive neurons chotic treatment may → ↑ brain dopamine D2
receptors
14.5.2.3 Neurochemical Pathology
Neurochemical changes that have been reported in Problems with the hypothesis include the following:
Huntington’s disease include
• Differences in the chronology of onset of symp-
• ↓ GABA toms between humans and animal models.
• ↓ GAD • Only limited support for dopamine hypersensi-
• ↓ Acetylcholine tivity from post-antipsychotic dopamine turn-
• ↓ Substance P over experiments in monkeys.
• Postmortem human brain tissue studies have Problems with the hypothesis include
not shown significant differences in D2 recep-
tor binding between schizophrenic patients with • Vitamin E treatment of tardive dyskinesia in gen-
tardive dyskinesia and schizophrenic patients eral does not lead to major clinical improvement.
without tardive dyskinesia. 14.5.3.3 GABA Insufficiency
• Blood biochemical assays have not shown con-
According to one version of this hypothesis, the follow-
sistent significant differences between patients
ing sequence of events takes place:
with tardive dyskinesia and patients without tar-
Long-term treatment with antipsychotic (neuroleptic)
dive dyskinesia with respect to
medication
Prolactin
Somatotropin → Destruction of GABAergic neurons in the striatum
• No consistent significant differences have been → ↓ Feedback inhibition
shown between patients with tardive dyskine- → Tardive dyskinesia
sia and patients without tardive dyskinesia with
respect to According to another version, the sequence of events is
Plasma homovanillic acid Long-term treatment with antipsychotic (neuroleptic)
Urinary homovanillic acid medication
CSF homovanillic acid
→ ↓ GABAergic neuronal activity in the pars retic-
• Dopamine agonists do not strikingly exacerbate
ulata of the substantia nigra
tardive dyskinesia.
→ ↓ Inhibition of involuntary movements
• Dopamine antagonist antipsychotics may some-
→ Tardive dyskinesia
times worsen tardive dyskinesia.
Evidence in favour of these hypotheses includes the
A modification of this hypothesis includes a role for following:
dopamine D1 receptors, but many of the previously men-
tioned problems also apply again. Moreover, postmortem 1. It has been shown that striatonigral GABAergic
human brain tissue studies have not shown significant dif- neurons feed back on dopaminergic nigrostria-
ferences in D1 receptor binding between schizophrenic tal neurons to reduce their activity.
patients with tardive dyskinesia and schizophrenic patients 2. Antipsychotic-treated dyskinetic monkeys have
without tardive dyskinesia. been found to have a decrease in GAD, com-
pared with similarly treated monkeys without
14.5.3.2 Free-Radical-Induced Neurotoxicity tardive dyskinesia, in the
According to this hypothesis, the following sequence of a. Substantia nigra
events takes place: b. Globus pallidus
Long-term treatment with antipsychotic (neuroleptic) c. Subthalamic nucleus
medication 3. Patients with tardive dyskinesia have been found
on postmortem to have a significant decrease in
→ ↑ Catecholamine turnover GAD activity, compared with patients without
→ Free-radical by-products tardive dyskinesia, in the subthalamic nucleus
→ Membrane lipid peroxidation in the basal gan- 4. The following GABAergic agonists have gener-
glia (the basal ganglia have a high oxidative ally shown promise as potential therapeutic agents
metabolism) a. Benzodiazepines
→ Tardive dyskinesia b. Baclofen
c. Gamma-vinyl GABA
Evidence in favour of this hypothesis includes the following:
Problems with the hypothesis include the following:
• α-Tocopherol (vitamin E) is of benefit in rodent
models of antipsychotic-induced dyskinesia. • Rodent models of tardive dyskinesia do not
• Some studies have shown ↑ blood or CSF levels show consistent GABA function changes with
of lipid peroxidation by-products in patients antipsychotic treatment.
with tardive dyskinesia compared with those • It has not so far proved possible effectively to
without tardive dyskinesia. treat tardive dyskinesia with GABAergic drugs.
Neuropathology 203
14.5.3.4 Noradrenergic Dysfunction Bauman ML. 1991: Microscopic neuroanatomic abnormalities

in autism. Pediatrics 87:791–796.
According to this hypothesis, noradrenergic overactivity
Bauman M and Kemper TL. 1985: Histoanatomic obser-
contributes to the pathophysiology of tardive dyskine- vations of brain in early infantile autism. Neurology
sia. Evidence in favour of these hypotheses includes the 35:866–874.
following: Benes FM, Davidson J, and Bird ED. 1986: Quantitative cytoar-
chitectural studies of the cerebral cortex of schizophren-
• Patients with tardive dyskinesia have been found to ics. Archives of General Psychiatry 43:31–35.
have significantly greater dopamine β-hydroxylase Benes FM, Majocha R, Bird ED, and Marotta CA. 1987:
activity than those without tardive dyskinesia. Increased vertical axon numbers in cingulate cor-
tex of schizophrenics. Archives of General Psychiatry
• Platelet H-dihydroergocryptine-α2 adrenergic
3
44:1017–1021.
receptor binding and CSF noradrenaline have Berrios GE. 1991: Alzheimer’s disease: A conceptual history.
been found to be significantly correlated with International Journal of Geriatric Psychiatry 5:355–365.
the severity of tardive dyskinesia Bogerts B, Falkai P, Haupts M, Greve B, Ernst S, Tapernon-
Franz U, and Heinzmann U. 1990: Post-mortem volume
Problems with the hypothesis include measurements of limbic system and basal ganglia struc-
tures in chronic schizophrenics. Initial results from a new
brain collection. Schizophrenia Research 3:295–301.
• It has not so far proved possible effectively to
Brown R, Colter N, Corsellis JA, Crow TJ, Frith CD, Jagoe R,
treat tardive dyskinesia with noradrenergic drugs. Johnstone EC, and Marsh L. 1986: Postmortem evidence
of structural brain changes in schizophrenia. Differences
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15 Neuroimaging Techniques
15.1 X-RAY 15.2.3 Neuropsychiatric Applications

15.1.1 Basis Where available, CT and MRI have largely replaced skull
radiography. Its clinical uses include the detection of
Radiography utilizes x-rays.
• Shifts of intracranial structures
15.1.2 Type of Imaging • Intracranial expanding lesions
• Cerebral infarction
X-ray radiography is a form of structural imaging. • Cerebral oedema
• Cerebral atrophy and ventricular dilatation
15.1.3 Neuropsychiatric Applications • Atrophy of other structures
• Demyelination changes and other causes of
The main use nowadays of skull radiography is radiodensity change
• Assessment of trauma It is also widely used in neuropsychiatric research.
It may also be useful in the detection of intracranial
expanding lesions. 15.3 PET
PET is positron emission tomography.
15.2 CT
15.3.1 Basis
CT is x-ray computerized tomography or computed
tomography. It was previously known as computerized The basis of PET neuroimaging is as follows:
axial tomography, or CAT.
A positron-emitting radioisotope or radiolabelled
ligand is introduced into the cerebral circula-
15.2.1 Basis
tion; routes commonly used are
The basis of CT is as follows: • Intravenous administration (the radioactive
X-ray beams are passed through a given tissue plane substance is in solution)
in different directions: • By inhalation (the radioactive substance is in
gaseous form)
Scintillation counters record the emerging x-rays. Blood flow ± cerebral tissue binding in the brain.
Computer reconstruction of emerging x-ray data. Emission of positrons.
Radiodensity maps. Positron–electron interactions.
Dual γ-photon emissions.
This procedure is repeated for successive adjacent Detection of γ-photons.
planes, thereby building up an image of, for example, the Computer reconstruction of emerging γ-photon data.
whole brain. Slice images of the distribution of the radioisotopes
in the brain.
15.2.2 Type of Imaging
The positron-emitting radioisotopes used can be pro-
CT is a form of structural imaging. duced in small cyclotrons.
205
15.3.2 Type of Imaging 15.4.3 Neuropsychiatric Applications

PET is a form of functional imaging. SPECT neuroimaging can give information about
15.3.3 Neuropsychiatric Applications • rCBF

• Ligand binding
PET neuroimaging can give information about
It is also of use in conditions in which the onset of the
• Metabolic changes
symptomatology being studied (e.g. epileptic seizures,
• Regional cerebral blood flow (rCBF)
auditory hallucinations) may occur at a time when the
• Ligand binding
patient is not in or near a scanner; a suitable radioligand
Clinical applications of PET include (e.g. 99 m technetium hexamethylpropylene amine oxime
[HMPAO]) can be administered at the material time and
• Cerebrovascular disease the patient scanned afterward.
• Alzheimer’s disease Clinical applications of SPECT include
• Epilepsy, prior to neurosurgery
• Head injury • Alzheimer’s disease
Some measurements made by PET, for example, the The resolution of SPECT is generally poorer than that of
study of rCBF, are likely to be increasingly replaced by PET, and both are likely to be increasingly replaced by
functional magnetic resonance imaging (fMRI), since the fMRI. However, fMRI is not a suitable replacement for
latter does not require the use of radioactive isotopes. On SPECT for ligand studies or for the type of study mentioned
the other hand, fMRI is not a suitable replacement for earlier in which the onset of the symptomatology being
PET for ligand-binding studies. studied may occur at a time when the subject is not in or
near a scanner.
15.4 SPECT
15.5 MRI
SPECT is single-photon emission computerized tomog-
raphy. It is also known as SPET or single-photon emis- MRI is magnetic resonance imaging. It was previously
sion tomography. referred to as NMR or nuclear magnetic resonance.
In vivo NMR is now taken to include arterial spin
15.4.1 Basis labelling (ASL), diffusion kurtosis imaging (DKI),
diffusion tensor imaging (DTI), diffusion-weighted
The basis of SPECT neuroimaging is as follows: imaging (DWI), MRI, magnetic resonance angi-
ography (MRA), magnetic resonance spectroscopy
A radioisotope or radiolabelled ligand is intro- (MRS), and fMRI. In addition, it is possible to carry
duced into the cerebral circulation; routes com- out in vitro NMR studies of tissues at higher mag-
monly used are netic field strengths (say, over 11 T) than are currently
• Intravenous administration (the radioactive allowed for human subjects.
substance is in solution)
• By inhalation (the radioactive substance is in 15.5.1 Basis
gaseous form)
Blood flow ± cerebral tissue binding in the brain. The basis of MRI is as follows:
Single γ-photon emissions. The patient is placed in a strong static magnetic
Detection of γ-photons. field → alignment of proton spin axes:
Computer reconstruction of emerging γ-photon data.
Slice images of the distribution of the radioisotopes Pulses of radio-frequency waves at specified fre-
in the brain. quencies are administered.
This additional energy is absorbed.
Some protons jump to a higher quantum level.
15.4.2 Type of Imaging
Radio waves are emitted when these protons return
SPECT is a form of functional imaging. to the lower quantum level.
Neuroimaging Techniques 207
The radio-frequency (rf) wave frequencies are In some circumstances, it may be useful to admin-
measured. ister a paramagnetic contrast-enhancing agent such as
Precession in each voxel is determined and T1 (lon- gadolinium-DTPA.
gitudinal relaxation time) and T2 (transverse fMRI can use the blood oxygen level-dependent
relaxation time) calculated. (BOLD) effect, whereby whereas oxyhaemoglobin is
Proton density, T1, T2 → pixel intensities. diamagnetic, deoxyhaemoglobin is paramagnetic and
Anatomical magnetic resonance images. so may be used as an endogenous contrast agent. Images
from the first published human study of V1 activation
(The data are actually collected in the temporal domain during photic stimulation using BOLD fMRI, by Bruce
and need to be converted into the frequency domain Rosen’s group at Harvard Medical School, are shown
using Fourier transformation.) in Figure 15.1.
Baseline 30 s 50 s
OFF OFF
110 s 130 s 170 s
ON ON OFF
190 s 250 s 270 s
OFF ON ON
FIGURE 15.1 Images from the first published human study of V1 activation during photic stimulation using BOLD fMRI. The
upper left image was acquired during darkness (baseline) and this baseline image was subtracted from subsequent images. OFF, dark-
ness; ON, photic stimulation. (Reproduced from Kwong, K.K. et al., Proc. Natl. Acad. Sci. USA, 89, 5675, 1992. With permission.)
15.5.2 Type of Imaging BIBLIOGRAPHY

DKI, DTI, DWI, MRI, and MRA are forms of structural Ketonen LM and Berg MJ. 1996: Clinical Neuroradiology.
imaging. DKI and DTI are particularly useful for map- London, U.K.: Arnold.
ping white matter tracts in the brain. Kwong KK, Belliveau JW, Chesler DA et al. 1992: Dynamic
magnetic resonance imaging of human brain activ-
ASL, MRS, and fMRI are types of functional imag- ity during primary sensory stimulation. Proceedings
ing. ASL allows cerebral blood flow to be measured non- of the National Academy of Sciences of the United
invasively. MRS allows the relative concentrations in the States of America 89:5675–5679.
brain (and other organs) of certain substances to be mea- Puri BK. 2000: MRI and MRS in neuropsychiatry. In Young IR,
sured noninvasively. Grant DM, and Harris RK (eds.) Methods in Biomedical
Magnetic Resonance Imaging and Spectroscopy, pp. 1135–
1142. New York, NY: Wiley.
Puri BK. 2010: Neuroimaging. In Puri BK and Treasaden IH
15.5.3 Neuropsychiatric Applications (eds.) Psychiatry: An Evidence-Based Text, pp. 445–464.
MRI is useful in most clinical and research studies Yousem DM and Grossman RI. 2010: Neuroradiology: The
requiring high-resolution neuroanatomical imaging. Requisites, 3rd edn. Philadelphia, PA: Mosby Elsevier.
16 Neurophysiology
16.1 PHYSIOLOGY OF NEURONS, negative membrane potential. The sodium pump then

SYNAPSES, AND RECEPTORS restores the original ionic concentrations.
16.1.1 Neurons 16.1.1.5 Propagation of Action Potential

16.1.1.1 Resting Membrane Ion Permeabilities An AP is propagated by the depolarization spreading
laterally to adjacent parts of the neuron.
The comparative permeabilities to different ions of the
resting neuronal membrane are as follows:
16.1.1.6 All-or-None Phenomenon
• K (potassium ions)—relatively permeable
+ The passage of an AP along a neuron is an all-or-none
• Na+ (sodium ions)—relatively impermeable phenomenon.
• Cl− (chloride ions)—freely permeable
• Organic anions—relatively impermeable 16.1.1.7 Absolute Refractory Period
This is the period during which the active part of the neu-
16.1.1.2 Resting Membrane Potential ronal membrane has a reversed polarity so that conduction
There is a negative resting membrane potential of around or initiation of another AP is not possible in it.
−70 mV. It is maintained by the sodium pump, which
actively transports Na+ out of the cell and K+ into the cell. 16.1.1.8 Relative Refractory Period
Energy for this process is provided by ATP. This is the period of repolarization after an AP, during
which hyperpolarization occurs, making it more difficult
16.1.1.3 Changes in Membrane Ion Permeabilities for stimulation to allow the membrane potential to reach
The neuronal membrane ion permeabilities may change the critical threshold.
in response to stimulation:
16.1.1.9 Conduction in Unmyelinated Fibres
• Depolarization—the membrane potential increa The greater the diameter of the fibre, the faster is the rate
ses, that is, it becomes less negative. of transmission.
• This increases the probability of an action
potential (AP) being generated. 16.1.1.10 Conduction in Myelinated Fibres
• Hyperpolarization—the membrane potential The AP appears to jump from one node of Ranvier to
decreases, that is, it becomes more negative. the next, skipping the intervening myelinated parts.
This rapid form of conduction is known as saltatory
This decreases the probability of an action potential conduction.
being generated.
16.1.1.4 Action Potential 16.1.2 Synapses

Details of the AP are shown in Figure 16.1. 16.1.2.1 Synaptic Cleft
Neuronal stimulation leads to local depolarization. This is the gap at a synapse between the membrane of a
If (degree of depolarization) > (a critical threshold) → presynaptic fibre and that of the postsynaptic fibre.
nerve impulse or AP
During an AP, the membrane potential rapidly 16.1.2.2 Location
becomes positive, before returning to become negative. Synapses may be found between
This is caused by an increase first in Na+ permeability,
allowing the inflow of Na+, and then in K+ permeability • Two neurons
(with a rapid reduction in Na+ permeability at the same • Motor neurons and muscle cells
time), causing an outflow of K+ and thereby restoring the • Sensory neurons and sensory receptors
209
Key:
Depolarizing Repolarizing
+30 phase Resting membrane potential: Voltage-gated
phase Reversal of Na+ channels are in the resting state and
Membrane potential (mV)
polarization voltage-gated K+ channels are closed

0 Stimulus causes depolarization to threshold
Voltage-gated Na+ channel

activation gates are open Absolute
refractory
Voltage-gated K+ channels are
period
–55 Threshold open; Na+ channels are
inactivating
–70 Resting Relative
Voltage-gated K+ channels are
membrane refractory
still open; Na+ channels are in
Stimulus After-hyperpolarizing potential period
the resting state
phase
Time (ms)
FIGURE 16.1 AP or impulse. When a stimulus depolarizes the membrane to threshold −55 mV, an AP is generated. The AP
arises at the trigger zone (at the junction of the axon hillock and the initial segment) and then propagates along the axon to the axon
terminals. (Redrawn from Tortora, G.J. and Derrickson, B., Principles of Anatomy and Physiology, 11th edn., Wiley-Blackwell,
New York, 2006. With permission.)
16.1.2.3 Types 16.1.2.6 Inhibitory Postsynaptic Potentials

There are two types of synapse: Inhibitory postsynaptic potentials, or IPSPs, occur in the
postsynaptic membrane (because of hyperpolarization)
1. Chemical—the commoner type, in which a following release of an inhibitory neurotransmitter from
chemical neurotransmitter is stored in presyn- the presynaptic neuron at central inhibitory synapses.
aptic vesicles
2. Electrical—faster than chemical synapses, with 16.1.2.7 Summation
direct membrane to membrane connection via One EPSP on its own is not usually sufficient to initiate
gap junctions an AP. However, temporal and/or spatial summation may
allow the degree of depolarization to reach the critical
16.1.2.4 Synaptic Transmission threshold, as shown in Figure 16.2. IPSPs, on summating
At chemical synapses, the following events take place with EPSPs, counter the effect of the latter.
during synaptic transmission:
16.1.3 Receptors
Arrival of AP at presynaptic membrane.
Influx of Ca2+ (calcium ions). 16.1.3.1 Sensory Receptors
Presynaptic vesicles fuse to the presynaptic membrane. The main types of sensory receptor in humans are
Release of neurotransmitter into the synaptic cleft.
Passage of neurotransmitter across the synaptic • Mechanoreceptors
cleft. • Thermoreceptors
Binding of neurotransmitter to postsynaptic receptors. • Light receptors
Ion permeability changes in postsynaptic membrane. • Nociceptors
Postsynaptic depolarization or hyperpolarization • Chemoreceptors
(depending on the type of neurotransmitter).
16.1.3.2 Adaptation
16.1.2.5 Excitatory Postsynaptic Potentials In response to a continuous prolonged appropriate stimu-
Excitatory postsynaptic potentials, or EPSPs, occur in lus, most sensory receptors exhibit adaptation:
the postsynaptic membrane (because of depolariza-
tion) following release of an excitatory neurotransmit- • Phasic receptors—the receptor firing stops.
ter from the presynaptic neuron at central excitatory • Tonic receptors—the receptor firing frequency
synapses. falls to a low maintained level.
Neurophysiology 211
Recording
1 2 3 4 5
microelectrode
+30 Temporal Spatial
Membrane potential (mV)

Inhibitory
summation summation
synapse
A C
Threshold
B
–70
Excitatory
synapses
A A AA B A+B AA B B C A+C
Axon
Time
FIGURE 16.2 Interaction of excitatory postsynaptic potentials (EPSPs) and inhibitory postsynaptic potentials (IPSPs) at the
postsynaptic neuron. Presynaptic neurons (A–C) were stimulated at times indicated by the arrows, and the resulting membrane
potential was recorded in the postsynaptic cell by a recording microelectrode. (Redrawn from Widmaier, E.P. et al., Vander’s
Human Physiology, 11th edn., McGraw Hill, Berkshire, England, 2008. With permission.)
16.2 PITUITARY HORMONES a negative feedback on the secretion of FSH by the

anterior pituitary gland.)
16.2.1 Anterior Pituitary Hormones In females, FSH stimulates the development of fol-
The following table gives the anterior pituitary hormones licles. It also stimulates the activity of aromatase, which
and their corresponding hypothalamic-releasing factors in turn stimulates the conversion of ovarian androgens
(hormones) and release-inhibiting factors (hormones). into oestrogens. As in males, FSH stimulates the release
Hypothalamic-Releasing Factor (Hormone) and/or Release-

Anterior Pituitary Hormone Inhibiting Factor (Hormone)
Corticotropin (adrenocorticotropic hormone, ACTH) Corticotropin-releasing factor (hormone) (CRF or CRH)
Follicle-stimulating hormone (FSH) Gonadotropin-releasing factor (hormone) (GnRF or GnRH)
Luteinizing hormone (LH) GnRF or GnRH
Melanocyte-stimulating hormone (MSH) MSH release inhibitory factor (MIH)
Prolactin Prolactin-releasing factor (PRF)
Prolactin release inhibitory factor (PIF) (dopamine)
Somatotropin (growth hormone, GH) Growth hormone-releasing factor (hormone) (GRF or GRH; somatocrinin)
GH release inhibitory factor (somatostatin)
Thyrotropin (thyroid-stimulating hormone, TSH) Thyrotropin releasing factor (hormone) (TRF or TRH)
16.2.1.1 ACTH of inhibin (from stromal cells of the ovary), which in turn
This is a single-chain peptide that stimulates the pro- causes a negative feedback on the secretion of FSH by the
duction by the adrenal glands of the steroid hormone anterior pituitary gland.
cortisol.
16.2.1.3 LH
LH consists of two peptide chains, α and β; the α-chain of
16.2.1.2 FSH LH is the same as that of FSH. LH stimulates the gonads
FSH consists of two peptide chains, α and β. FSH stimu- (ovaries and testes).
lates the gonads (ovaries and testes). In males, LH stimulates the testicular Leydig cells to
In males, FSH stimulates seminiferous tubule produce testosterone.
Sertoli cells to promote the growth of spermatozoa and In females, LH stimulates the ovaries to produce
also stimulates the release of inhibin A (the α subunit) androgens. In menstruating females, a surge of LH mid-
and inhibin B (the β subunit). (In turn, inhibin causes cycle induces ovulation.
16.2.1.4 MSH 16.2.2.2 Oxytocin

MSH does not appear to be found in the human anterior Oxytocin is a nonapeptide that stimulates contraction of
pituitary. Its functions in relation to pigmentation appear the uterine myometrium during parturition (and perhaps
to have been taken over by ACTH and β-lipotropin. during sexual intercourse), and postpartum, it stimulates
the ejection of milk from the mammary glands during
16.2.1.5 Prolactin lactation. In rats, it has been found that centrally admin-
Prolactin is a single-chain peptide hormone that acts on istered oxytocin has a satiety action (in both males and
the mammary glands to stimulate the secretion of milk females). Oxytocin also has a natriuretic action in both
(normally during lactation). It also inhibits activity of the males and females.
testes and ovaries.
16.2.1.6 GH 16.3 INTEGRATED BEHAVIOURS

GH is a peptide hormone that stimulates the hepatic 16.3.1 Regulatory Behaviour
secretion of IGF-1 (insulin-like growth factor-1; previ-
ously termed somatomedin C). In turn, binding of IGF-1 A regulatory behaviour is one that is controlled by a
to widespread IGF-binding proteins (IGF-BP) leads to homeostatic mechanism. Examples include behaviours
the stimulation of anabolism (e.g. by stimulating the related to hunger (feeding) and thirst (drinking).
retention of calcium, phosphorus, and nitrogen, thereby In contrast, a non-regulatory behaviour is one that is
promoting growth in bones) and stimulating the wide- not controlled by a homeostatic mechanism. Examples
spread biosynthesis of protein and collagen. Another include sexual behaviour and parenting behaviour.
important action of IGF-1 is in terms of opposing the
action of insulin. 16.3.2 Pain
16.2.1.7 TSH The neural pathway for pain is as follows:

Pain detection by receptors (e.g. nociceptors in the skin)
TSH consists of two peptide chains, α and β; the α-chain
of TSH is the same as that of LH (and of FSH). TSH stim-
• Dorsal root ganglion neurons to spinal cord
ulates the synthesis by the thyroid gland of the thyroid
• Ventral spinothalamic tract
hormones T4 and T3. TSH also stimulates the release of T4
• Medial lemniscus
and T3 from the thyroid gland. (In turn, T3 exerts a nega-
• Ventrolateral thalamus
tive feedback control on the secretion of TRH and TSH.)
• Primary somatosensory cortex
16.2.2 Posterior Pituitary Hormones According to the gate theory of pain, gates in the spi-
nal cord, involving activity in spinal cord interneurons,
The hypothalamus is responsible for the neurosecretion can modify the perception of pain. These gates may also
of the two posterior pituitary hormones: exist in the brain stem and even the cerebral cortex. This
theory may explain why shifting attention away from
• Arginine vasopressin (AVP) (argipressin or the source of pain to something else may help reduce
antidiuretic hormone [ADH]) the severity of the pain that the subject is conscious of.
• Oxytocin Hormonal substances, such as endorphins, may also
influence the perception of pain. For example, during
Note that, strictly speaking, these are actually hypotha- times of war, a soldier at the front may hardly feel any
lamic hormones rather than pituitary hormones, as they pain initially following a traumatic bodily injury such as
are synthesized in the supraoptic and paraventricular the loss of part of a limb. In contrast, the same injury
nuclei of the anterior hypothalamus and then transported incurred in civilian life during peace time may cause the
to and stored in the posterior pituitary gland. same person to scream out in agony.
16.2.2.1 AVP or ADH

16.3.3 Motor Function
AVP or ADH is a nonapeptide that acts on the distal con-
voluted tubule and collecting ducts of the renal nephron At its simplest, motor activity involves the following
to exert an antidiuretic effect. pathway:
Neurophysiology 213
Activity in the motor cortex (primary motor cortex— medial preoptic area in male monkeys, in which testoster-
precentral gyrus, Brodmann area 4) one is circulating, is associated with an abolition of mating,
but masturbation in the presence of out-of-reach females
• Ipsilateral corticospinal tract has been noted.) In female adults, ovarian hormones also
• Pyramidal decussation appear to act on the amygdala to stimulate the motivation to
• Ipsilateral (mainly) ventral corticospinal tract carry out sexual activity. In infrahuman quadrupedal mam-
(moves midline muscles) and contralateral (mainly) mals, the action of ovarian hormones on the ventromedial
lateral corticospinal tract (moves limb muscles) hypothalamus (VMH) stimulates lordosis (arching of the
back, staying still with the back side elevated—a position
that is receptive for copulatory behaviour).
16.3.4 Arousal
Humans are aware of the importance of cognitive
Further details regarding sleep and arousal are given in influences on sexual behaviour. The influence of cerebral
Section 16.4. Here, we consider the changes in thalamo- cortex in the context is clearly important but complex.
cortical systems that occur in sleep and arousal. Basically, For instance, while frontal lobe patients often are associ-
the hypothalamus appears to contain neuronal circuits ated with a loss of sexual inhibition, loss of libido may
that mediate homeostatic sleep mechanisms. also occur in some cases.
One important subcortical circuit involved is as fol-
lows. Output from the ventrolateral preoptic area, supra- 16.3.6 Hunger
chiasmatic nucleus, and tuberomammillary nucleus of
the hypothalamus synchronizes the non-rapid eye move- Feeding is a regulatory behaviour that particularly
ment–rapid eye movement (NREM–REM) sleep cycle involves inputs from the following systems:
mechanisms of the pontine brain stem. The parts of the
latter that appear to be particularly involved are the • Digestive system (including insulin) and satiety
signals
• Locus coeruleus • Hypothalamus
• Raphe nuclei • Cognitive factors
• Dorsolateral tegmental nucleus
• Pedunculopontine tegmental nucleus 16.3.6.1 Insulin
The most important hormone that affects caloric
A second subcortical system of importance involves out- homeostasis is insulin. When hungry, first the smell and
put from the ventrolateral preoptic area, suprachiasmatic then the taste of a meal cause signals to be sent in the
nucleus, and tuberomammillary nucleus of the hypothal- following way:
amus to the thalamus and thence to the cerebral cortex. Smell of food ± taste of food
16.3.5 Sexual Behaviour • Aroma and taste signals

• Cerebral cortex
This is a non-regulatory form of behaviour with complex • Hypothalamus
control mechanisms. • Dorsal motor nucleus of the vagus nerve (cranial
Sex hormones have an important effect on the brain. nerve X)
In male fetuses, during development testosterone mas- • Vagal cholinergic fibres
culinizes the brain. This is the organizing effect of the • Pancreas
hormone. This effect is particularly noteworthy in the • Insulin secretion from pancreatic B cells
hypothalamic preoptic area; this area is much larger in
males following exposure to testosterone. This is known as the cephalic phase of insulin secretion.
In the adult brain, sex hormones have an activating effect. Entry of food into the stomach and duodenum leads to
In male adults, testosterone acts on the amygdala to stimu- a further secretion of insulin; this is the gastrointestinal
late the motivation to carry out sexual activity. Testosterone phase of insulin secretion.
also acts on the hypothalamus to stimulate copulatory Breakdown products from digested food enter the
behaviour. In particular, stimulation of the medial preop- bloodstream and directly act on the pancreas, further
tic area, in the presence of circulating testosterone, induces stimulating the secretion of insulin. This is known as the
copulatory behaviour in primates. (Destruction of the substrate phase of insulin secretion.
16.3.6.2 Satiety Signals This is known as the dual centre hypothesis. More recent
Gastric distension, for example, following the ingestion evidence has suggested that this simple hypothesis is, in
of food, gives rise to satiety signals along the following fact, incorrect. The true reason why bilateral ventromedial
pathway: hypothalamic damage leads to hyperphagia is related to
Food ingestion
• An increase in parasympathetic tone
• Gastric distension • An increase in vagal reflexes (and therefore an
• Stimulation of gastric wall stretch receptors increased rate of gastric emptying)
• Vagal nerve transmission • A reduction in sympathetic tone
• Nucleus of tractus solitarius and area postrema • A resetting of a hypothetical homeostatic set point
(in the brain stem) • An increase in the accumulation of stored fat
• Hypothalamus • A reduction in satiety duration following feeding
• Cerebral cortex
• Perception of gastric distension Opposite effects occur following bilateral VLH damage.
The neuropeptide Y (NPY) appears to act on the para-
There exist other systems that also provide feedback to ventricular nucleus to increase food intake.
the brain from the alimentary canal. For example, as the
ingested (and partially digested) food reaches the intes- 16.3.6.4 Ghrelin
tines, many different peptides are released. Just one of Ghrelin is a ligand for the growth hormone secretagogue
these, cholecystokinin (CCK), can stimulate vagal affer- receptor (GHSR). It is an octanoylated 28-amino-acid
ents carrying pyloric gastric stretch receptor signals to peptide produced and secreted by gastric oxyntic gland
the brain stem, thereby providing synergy with the satiety cells. It has been proposed that ghrelin acts as an enteric
signal system just mentioned earlier. Moreover, infrahu- signal that stimulates appetite.
man mammalian experiments have demonstrated the
16.3.6.5 Cognitive Factors
satiety action of CCK directly infused into the hypo-
thalamus. Another neuropeptide that may affect hunger As with sexual behaviour, cognitive factors are clearly
is oxytocin, intracerebroventricular injection of which of importance in the integrated behaviour of hunger and
decreases food intake in rats. feeding. The ability of people to fast, for example, shows
Caloric intake also has a direct satiety effect, although that cognitive activity can override satiety signalling and
the precise mechanism(s) by which this occur(s) is(are) any putative hypothalamic factors.
not clear at the time of writing. The amygdala is thought to play some role in hunger
Satiety signals are also given rise to by postgastric and feeding. It is known, for example, that damage to
actions of ingested food. One mechanism involved is the amygdala is associated with the abolition of taste-
undoubtedly related to the liver. aversion learning and also with a change in the types of
The hormone leptin (or Ob protein), biosynthesized food that are preferred.
in adipose tissue, has a circulating plasma concentration Damage to the inferior prefrontal cortex often appears
that is positively correlated with overall adiposity. Leptin to be associated with reduced food intake. This may,
has a satiety action when experimentally directly infused however, be at least partly related to the fact that this part
into cerebral ventricles, and hypothalamic leptin recep- of the cerebral cortex receives olfactory signals, so that
tors have been identified. damage to the cortex may reduce the ability to respond to
the aroma and taste of food.
16.3.6.3 Hypothalamus
16.3.7 Thirst
Rodent experiments from the 1950s onward have sug-
gested that Drinking is a regulatory behaviour. There are two types
of homeostatic mechanisms that are of relevance and that
• The ventrolateral hypothalamus (VLH) con- give rise to two different types of thirst. They are
tains a hunger centre; bilateral damage to this
area causes aphagia in rats. • Osmotic homeostasis (related to osmotic thirst)
• The VMH contains a satiety centre; damage to • Volume homeostasis (related to hypovolaemic
this area may cause hyperphagia in rats. thirst)
Neurophysiology 215
16.3.7.1 Osmotic Thirst 16.3.7.2 Hypovolaemic Thirst

Osmotic thirst occurs when the concentrations of solutes Hypovolaemic thirst occurs when the total volume of body
in body fluids such as the plasma become too high. This fluids such as the plasma becomes too low. This may occur
may occur as a result of a rise in concentration of one as a result of blood loss, for example. The hypovolaemic
or more solutes (e.g. following sodium loading after eat- homeostatic mechanism requires that fluids that contain sol-
ing a meal rich in sodium salts such as sodium chloride utes be drunk; if only pure water were drunk, then hyposmo-
and monosodium glutamate). It may also occur as a result lality would result. In experiments, hypovolaemic rats that
of water deprivation (dehydration) or the copious loss of are given a choice of pure water or concentrated sodium
dilute fluids such as sweat. Under any of these circum- chloride solution have been observed to drink enough of
stances, the osmotic homeostatic mechanism requires each in order to be imbibing isotonic levels overall.
that water be drunk.
Before the behaviour associated with osmotic thirst One mechanism involved is the following:
kicks in, the body relies on its large posterior pituitary
stores of AVP to try to rectify the osmolality of the extra- Blood loss of greater than 10% of normal blood volume
cellular and intracellular fluid compartments. The mech-
anism appears to involve the following pathway: • Detection by stretch receptors in veins that enter
Increase in solutes/water deprivation/dehydration/loss the cardiac right atrium; larger blood volume
of dilute fluid decreases are also detected by stretch receptors
in the aortic arch and carotid sinus.
• Raised extracellular fluid osmolality (and there- • Vagal nerve transmission.
fore also raised intracellular fluid osmolality via • Nucleus of tractus solitarius (in the medulla
osmosis) oblongata).
• Stimulation of osmoreceptor cells in the organ of • Supraoptic nucleus and paraventricular nucleus
the lamina terminalis, subfornical organ, median of hypothalamus (including via a noradrenergic
preoptic nucleus, and magnocellular neurons pathway from ventrolateral medulla A1 cells).
in the supraoptic nucleus and paraventricular • Secretion of AVP from the posterior pituitary.
nucleus • Stimulation of AVP V2 renal receptors.
• Projections from the organ of the lamina ter- • Increased water permeability of distal convo-
minalis to the median preoptic nucleus and to luted tubules and collecting ducts of nephrons.
the magnocellular AVP-secreting cells of the • Increased water retention, increased urinary
supraoptic nucleus and paraventricular nucleus osmolality, and reduced urinary volume.
further stimulate these other brain regions • Reverses hypovolaemia.
• Secretion of AVP from the posterior pituitary
• Stimulation of AVP V2 renal receptors Another mechanism that also operates starts with the
• Increased water permeability of distal convo- kidneys, as follows:
luted tubules and collecting ducts of nephrons
• Increased water retention, increased urinary Hypovolaemia
osmolality, and reduced urinary volume
• Restoration of extracellular fluid osmolality • Reduced renal perfusion pressure and reduced
delivery of sodium ions to the distal tubule of
At the time of writing, the neural pathways in the fore- the nephron.
brain that are related to thirst have not been clearly • Renal secretion of renin.
identified. • Catalyses the conversion of hepatic angioten-
Another mechanism involved in osmotic homeostasis sinogen into angiotensin I.
and osmotic thirst is the increased urinary excretion of • Conversion into angiotensin II (A II) (catalysed by
sodium ions as a result of the actions of atrial natriuretic angiotensin-converting enzyme from the lungs).
peptide (ANP) and oxytocin. ANP is released from the • Vasoconstriction and stimulation of adrenal
cardiac atria in response to increased atrial distension, in secretion of aldosterone.
turn caused by hyperosmolality of the extracellular fluid. • Aldosterone stimulates renal conservation of
The release of oxytocin from the posterior pituitary has sodium ions.
been mentioned in Section 16.2.2. • Reverses hypovolaemia.
A II also acts as a neurotransmitter in the brain in the • ↑ Sympathetic activity

following way: • Transient runs of conjugate ocular movements
• Maximal loss of muscle tone
A II
• ↑ Heart rate
• Binding to A II receptors in the subfornical organ • ↑ Systolic blood pressure
(which does not have a blood–brain barrier) • ↑ Respiratory rate
• Supraoptic nucleus and paraventricular nucleus • ↑ Cerebral blood flow
• Secretion of AVP from the posterior pituitary • Occasional myoclonic jerks
• Stimulation of AVP V2 renal receptors • Penile erection or ↑vaginal blood flow
• Increased water permeability of distal convo- • ↑ Protein synthesis (rat brain)
luted tubules and collecting ducts of nephrons
• Increased water retention, increased urinary 16.4.2.2 NREM Sleep
osmolality, and reduced urinary volume Features of NREM sleep include
• Reverses hypovolaemia
• ↓ Recall of dreaming if awoken during REM sleep
The central actions of A II also stimulate thirst. • ↓ Complexity of dreams
• ↑ Parasympathetic activity
• Upward ocular deviation with few or no
16.4 AROUSAL AND SLEEP
movements
16.4.1 Sleep Architecture • Abolition of tendon reflexes
• ↓ Heart rate
16.4.1.1 REM and NREM Sleep • ↓ Systolic blood pressure
Sleep is divided into the following two phases: • ↓ Respiratory rate
• ↓ Cerebral blood flow
• REM sleep—during which the eyes undergo • Penis not usually erect
rapid movements and there is a high level of
brain activity
16.4.3 Causes of the Sleeping–Waking Cycle
• NREM sleep—during which there is reduced
neuronal activity There are two main theories accounting for the sleeping–
waking cycle:
16.4.1.2 Stages of Sleep
The following stages normally occur during normal • Monoaminergic (or biochemical, two-stage,
NREM sleep: Jouvet’s) model
• Cellular (or Hobson’s) model
• Stage 0—quiet wakefulness and shut eyes; elec-
troencephalogram (EEG): alpha activity 16.4.3.1 Monoaminergic Model
• Stage 1—falling asleep; EEG: low amplitude, In this model:
↓ alpha activity, low-voltage theta activity
• Stage 2—light sleep; EEG: 2–7 Hz, occasional • NREM sleep is associated with serotonergic
sleep spindles and K complexes neuronal activity—raphe complex
• Stage 3—deep sleep; ↑ delta activity (20%–50%) • REM sleep is associated with noradrenergic
• Stage 4—deep sleep; ↑↑ delta activity (>50%) neuronal activity—locus coeruleus
Stage 3 + stage 4 = slow-wave sleep (SWS) 16.4.3.2 Cellular Model

In this model, three groups of central neurons are of
16.4.2 Physiological Correlates of Sleep importance. These groups, and their corresponding neu-
rotransmitters, are the
16.4.2.1 REM Sleep
Features of REM sleep include • Pontine gigantocellular tegmental fields (nucleus
reticularis pontis caudalis)—acetylcholine
• ↑ Recall of dreaming if awoken during REM sleep • Dorsal raphe nuclei—serotonin
• ↑ Complexity of dreams • Locus coeruleus—noradrenaline
Neurophysiology 217
16.5 EEG 16.5.2.2 Lambda Activity

Lambda activity occurs over the occipital region in sub-
16.5.1 Recording Techniques jects with their eyes open. It is related to ocular move-
16.5.1.1 Conventional ments during visual attention.
The conventional EEG recording involves placing elec-
16.5.2.3 Mu Activity
trodes on the scalp and is therefore noninvasive. The
positions of the electrodes are usually according to the Mu activity occurs over the motor cortex. It is related to
International 10–20 System, which entails measurements motor activity and is abolished by movement of the con-
from the following scalp landmarks: tralateral limb.
• The nasion 16.5.3 Spikes and Waves

• The inion
16.5.3.1 Spikes
• The right auricular depression
• The left auricular depression Spikes are transient high peaks that last less than 80 ms.
16.5.3.2 Sharp Waves

In this system, proportions of scalp distances are 10% Sharp waves are conspicuous sharply defined wave for-
or 20%, and midline electrodes are denoted by the sub- mations that rise rapidly, fall more slowly, and last more
script z. than 80 ms.
In ambulatory electroencephalography, the output is
stored on a suitable portable recorder.
16.5.4 Effect of Drugs
16.5.1.2 Specialized 16.5.4.1 Antidepressants

Specialized recording techniques include the following: In general, antidepressants cause
• ↑ Delta activity
• Nasopharyngeal leads—electrodes are posi-
tioned in the superior part of the nasopharynx; 16.5.4.2 Antipsychotics
can be used to obtain recordings from the infe- In general, antipsychotic drugs cause
rior and medial temporal lobe.
• Sphenoidal electrodes—electrodes are inserted • ↓ Beta activity
between the mandibular coronoid notch and the • ↑L ow-frequency delta activity and/or ↑ theta
zygoma; can be used to obtain recordings from activity
the inferior temporal lobe.
• Electrocorticography—electrodes are placed 16.5.4.3 Anxiolytics
directly on the surface of the brain. In general, anxiolytics, including barbiturates and benzo-
• Depth electroencephalography—electrodes are diazepines, cause
placed inside the brain.
• ↑ Beta activity
• ↓ Alpha activity (sometimes)
16.5.2 Normal EEG Rhythms
16.5.4.4 Lithium
16.5.2.1 Classification according Therapeutic levels of lithium lead to only small EEG
to Frequency Band effects that are likely to be missed on visual analysis of
Normal EEG rhythms are classified according to fre- routine recordings.
quency as follows:
BIBLIOGRAPHY
• Delta: frequency < 4 Hz Carpenter RHS. 2012: Neurophysiology: A Conceptual Approach,
• Theta: 4 Hz ≤ frequency < 8 Hz 5th edn. London, U.K.: Hodder Arnold.
• Alpha: 8 Hz ≤ frequency < 13 Hz Hall JE. 2011: Guyton and Hall Textbook of Medical Physiology,
• Beta: frequency ≥ 13 Hz 12th edn. Philadelphia, PA: Saunders, Elsevier.
Puri BK. 2010: Neurophysiology of integrated behaviour. In Tortora GJ and Derrickson B. 2006: Principles of
Puri BK and Treasaden IH (eds.) Psychiatry: An Evidence- Anatomy and Physiology, 11th edn. New York, NY:
Based Text, pp. 361–373. London, U.K.: Hodder Arnold. Wiley-Blackwell.
Stein JF and Stoodley C. 2006: Neuroscience: An Introduction. Widmaier EP, Raff H, and Strang KT. 2008: Vander’s Human
Chichester, England: Wiley-Blackwell. Physiology, 11th edn. Berkshire, England: McGraw
Strutton P. 2010: Basic concepts in neurophysiology. In Puri BK Hill.
and Treasaden IH (eds.) Psychiatry: An Evidence-Based
Text, pp. 354–360. London, U.K.: Hodder Arnold.
17 Neurochemistry
17.1 TRANSMITTER SYNTHESIS, 17.2.1 6-Transmembrane (TM) Family

STORAGE, AND RELEASE These are voltage-gated ion channels that each contain six
17.1.1 Transmitter Synthesis transmembrane segments (hence their name). Members
of this family include the following ion channels:
The synthesis of the neurotransmitters noradrenaline
(NA), serotonin (5-HT), dopamine (DA), γ-aminobutyric • Voltage-gated sodium channels
acid (GABA), and acetylcholine (ACh) is considered • Voltage-gated calcium channels
later in this chapter (Sections 17.3.3.6, 17.3.4.3, 17.3.3.3, • Voltage-gated potassium channels
17.3.5.1, and 17.3.2.3, respectively). • Calcium-activated potassium channels
• Hyperpolarization-activated cation channels
17.1.2 Transmitter Storage involved in rhythmic activities
• Cyclic nucleotide-gated cation channels involved
The transmitter at a synaptic cleft is stored in presynaptic in sensory transduction
vesicles. Each vesicle contains one quantum, usually cor- • Vanilloid receptors involved in sensory transduction
responding to several thousand molecules, of transmitter.
17.2.2 2-TM Family
17.1.3 Transmitter Release
These ion channels each have two transmembrane seg-
Transmitter release from synaptic vesicles takes place by ments in each pore-lining subunit. They include
exocytosis in a process controlled by Ca2+ influx. Because
the number of vesicles released is an integer, transmit- • Kir (inwardly rectifying potassium ion channels)
ter release is essentially quantal in nature. The Ca2+ • Amiloride-sensitive epithelial sodium ion channel
enters via voltage-dependent ion channels. Importantly, • The P2X adenosine-5′-triphosphate (ATP) receptor
Na+ influx and/or K+ efflux is not needed for transmitter • The Phe-Met-Arg-Phe-amide–activated sodium
release. Ca2+ influences or regulates ion channel
• The probability of vesicular transmitter release 17.2.3 4-TM or 8-TM Family
• Vesicular fusion
• The transport of synaptic vesicles to the presyn- These are two-pore potassium ion channels. They are
aptic active zone of exocytosis leak channels that partly help bring about the resting
• Post-tetanic potentiation membrane potential of cells.
• Tonic depolarization of the presynaptic neuron
17.2.4 Ionotropic Glutamate Receptors
17.2 ION CHANNELS These ligand-gated channels have a pore-lining domain
Ion channels are now classified into families on the basis that is similar to that of the Kir α-subunit, except that it
of genetic sequence homology and, usually, pore-lining is ‘upside down’.
α-subunit topology. The main families are as follows:
17.2.5 Nicotinic ACh and Related Receptors
• 6-Transmembrane (TM)
These receptors each contain five subunits. Members of
• 2-TM
this family include
• 4-TM or 8-TM
• Ionotropic glutamate receptors • Nicotinic ACh receptor
• Nicotinic ACh and related receptors • 5-HT3 serotonergic receptor
• Intracellular calcium ion channels • Glycine receptor
• Chloride ion channels • GABAA receptor
219
17.2.6 Intracellular Calcium Ion Channels 17.3.2.2 Second Messengers

Members of this family include Two of the most important second messenger systems are
as follows:
• IP3 (inositol triphosphate) receptors
• Receptor–neurotransmitter complex → G protein
• Ryanodine receptors
binding to receptor–neurotransmitter complex
→ adenylate cyclase activation (or inhibition) →
17.2.7 Chloride Ion Channels cyclic AMP (cAMP).
These have a widespread distribution. • Neurotransmitter binding → hydrolysis of phos-
phatidylinositol bisphosphate (a membrane
17.3 RECEPTORS phospholipid) → diacylglycerol and IP3 (inositol
triphosphate); diacylglycerol activates protein
17.3.1 Structure kinase C (PKC), while IP3 causes endoplasmic
reticulum calcium release, in turn activating
In general, the receptors to which neurotransmitters bind
calmodulin-dependent protein kinase.
are proteins located on the external surface of cell mem-
branes. Until the 1980s, receptors were classified and 17.3.2.3 Acetylcholine (ACh) (Figure 17.1)
identified pharmacologically but not according to their 1. ACh is synthesized from acetyl-coA and choline
structures. Since 1983, however, when the primary amino in the cytoplasm of the cholinergic nerve termi-
acid sequence of a receptor subunit of the nicotinic ACh nals. Choline comes from dietary sources. The
receptor was discovered, the DNA of an increasing num- availability of choline is increased by lecithin
ber of receptor proteins have been sequenced, and hence, (yellow-brownish substance found in egg yolk)
their amino acid sequences discovered. This has led to a but decreased by hemicholinium (a drug used in
further clarification of receptor classification. It has also research). Black widow spider venom produces
become evident that, as expected, for receptors of classi- a rapid release of ACh.
cal neurotransmitters, the amino acids forming the binding 2. The final step in the synthesis is catalyzed by
site are on or close to the extracellular side of the receptor. the enzyme choline acetyltransferase (ChAT). In
Alzheimer’s disease, ChAT is less active and leads
17.3.2 Function to a reduction in the synthesis of ACh. The deficit
The main function of a receptor is the molecular rec-
ognition of a signalling molecule, which in the case of
neurotransmission is a neurotransmitter, leading in turn
to signal transduction. A receptor generally responds to
neurotransmitter binding in one of two ways:
• Neurotransmitter binding → opening of trans- Acetyl CoA

membrane ion channel ACh +
• Receptor–neurotransmitter → second messenger ChAT Choline
system activation/inhibition
17.3.2.1 G Proteins
G proteins (named after their ability to bind guanosine tri-
phosphate [GTP] and guanosine diphosphate [GDP]) are
often involved in transmembrane signalling, linking recep- ACh release
tors to intracellular effector systems. For neurotransmitter
binding, the following types of G protein may be involved:
Choline
• Gs ACh
Acetylcholinesterase Acetic acid
• Gi
(AChE)
• Go
• Gq FIGURE 17.1 The synthesis and degradation of ACh.
Neurochemistry 221
in ACh results in reduced n eurotransmission and Acetylcholine

memory deficits.
3. ACh is the primary excitatory transmitter at the
neuromuscular junction and preganglionic auto-
nomic nerves. The main cholinergic neurons are
found in the basal nucleus of Meynert. Alzheimer’s
disease is associated with a reduction of choliner- PIP2
gic neurons in the subcortical areas of the brain, PLC
γ
leading to reduced availability of ACh. Local cho- PKC
β α
linergic neurons are found in the cortex and stria-
α
tum and their main function is for motor control. IP3
4. ACh is then packaged into synaptic vesicles and G-protein
transported to synapses. γ
β Ca2+
5. Cholinergic nerve transmission is terminated by
the enzyme acetylcholinesterase (AChE). AChE
is found on the postsynaptic membrane of cho- FIGURE 17.2 Muscarinic receptors (M1, M3, M5).
linergic synapses. ACh binds to AChE and is
hydrolyzed into acetic acid and choline. The hydro- Type of receptors: Muscarinic receptors are classified
lysis inactivates the ACh and the nerve impulse is as M1, M2, M3, M4, and M5. The M1 receptor is the most
stopped. Acetylcholinesterase inhibitors (AChEIs; significant receptor in the central nervous system (CNS)
e.g. rivastigmine) prevent the hydrolysis of ACh, and is highly expressed in human brain and nerves. M1,
which increases the concentration of ACh in the M3, and M5 receptor subtypes have a stimulatory effect
synaptic cleft. AChEIs are used in the treatment on the target tissues, whereas the M2 and M4 subtypes
of Alzheimer’s disease. Nerve gas or organophos- are inhibitory.
phate, a chemical weapon, inhibits the AChEI and
causes continuous muscle contraction in victims. Clinical relevance:
1. M1 agonists increase ACh transmission in the

17.3.3 Cholinergic Receptors
brain and alleviate some of the symptoms of
Cholinergic receptors transduce signals via coupling with Alzheimer’s disease.
G proteins. At the time of writing, the following types are 2. M3 agonists, such as pilocarpine, are used to
recognized: treat chronic open-angle glaucoma and acute
angle-closure glaucoma.
17.3.3.1 Muscarinic Receptors (Figure 17.2) 3. Antidepressants: paroxetine is the most anticho-
Mechanisms of actions: Binding of ACh to excitatory M1, linergic selective serotonin reuptake inhibitor
M3, and M5 receptors activates the Gq/11 family of G pro- (SSRI).
teins that in turn activates phospholipase C (PLC) and can 4. Anticholinergic drugs (e.g. benzhexol) are used to
lead to membrane phosphatidylinositol-4,5-bisphosphate block DA uptake and improve pseudoparkinson-
(PIP2) breakdown, PKC activation, and intracellular cal- ism induced by antipsychotics. These drugs are
cium mobilization. M1, M3, and M5 are PLC coupled to reported to have mood-elevating effect that may
Ca2+/Na+ channels. Activation of these ion channels leads lead to misuse and worsen amnesia in elderly.
to depolarizing currents and increased cell excitability 5. Psychotropic drugs (e.g. chlorpromazine,
thereby promoting the propagation of nerve impulses. tricyclic antidepressants [TCAs], and par-

M2 and M4 are coupled to K+ channels. It is the activa- oxetine) have high affinity at muscarinic
tion of these K+ channels that leads to hyperpolarizing receptors and lead to anticholinergic effects.
currents and reduced cell excitability thereby preventing Chlorpromazine is associated with potent anti-
propagation of nerve impulses. cholinergic actions and prevents extrapyrami-
Locations of muscarinic receptors: Parasympathetic dal side effects (EPSE).
nervous system, midbrain, medulla, pons, corpus stria- 6. Atropine is an antagonist at the muscarinic ACh
tum, cerebral cortex, hippocampus, thalamus, hypothala- receptor. Scopolamine, a muscarinic antagonist,
mus, and cerebellum. is used to treat nausea and morning sickness.
Na+ the catecholamine levels. Carbidopa increases

Na + the availability of dopa by inhibiting DOPA
Acetylcholine Na+ decarboxylase and improve parkinsonism:
Na+
• l-dopa: The administration of l-dopa can
increase the production of DA. Amphetamine
Alpha can release DA directly in the mesolim-
sub-units bic pathway. Electroconvulsive therapy
(ECT) increases the DA function. ECT also
increases oral intake and decreases psycho-
motor retardation.
3. DA: DA is stored in vesicles in the nerve
terminals and is released by depolarization.
The largest production site is the substantia
nigra. Cocaine has high affinity to the DA
FIGURE 17.3 Nicotinic acetylcholine receptors. transporter and prevents DA reuptake and
increases its availability in the synapses in the
mesolimbic pathway. Bupropion inhibits DA
17.3.3.2 Nicotinic Receptors (Figure 17.3)
reuptake.
Mechanisms of actions: The nicotinic receptor is acti- 4. Reuptake and monoamine oxidase A (MAO-A):
vated by the binding of two ACh molecules that permits The DA transporter is a high-affinity uptake
the movement of sodium ions. system that takes DA back to the nerve terminal.
Locations of the nicotinic receptors: Neuromuscular junc- DA is metabolized by MAO-A. MAO-A is more
tions, autonomic nervous system ganglia, substantia nigra, effective in degrading NA, DA, and serotonin
locus coeruleus, septum, corpus striatum, cerebral cortex, (5-HT) than monoamine oxidase B (MAO-B).
hippocampus, thalamus, hypothalamus, and cerebellum. MAO-B inhibitors slow the progression of
Types of receptors: There are two types: NN and NM. Parkinson’s diseases.
Clinical relevance: 5. Catechol-o-methyl transferase (COMT) is respon-
sible for extra-neuronal metabolism of DA (e.g. in
1. Nicotine found in tobacco is an agonist at the liver and kidney).
nicotinic receptors. Nicotine can improve cogni- 6. MAO-B is the nonneuronal MAO and the end
tive performance and reduce anxiety. Its depen- product is Homovanillic acid (HVA). HVA is an
dence potential is related to its ability to release indicator of DA turnover.
DA in the nucleus accumbens.
The prevalence of smoking in schizophrenia There are four types of DA pathways:
patients is two to three times higher than the general
population. Patients with schizophrenia may smoke 1. Nigrostriatal pathway: from the substantia nigra
heavily as a result of antipsychotic medication, to the striatum
which produces marked DA receptor blockade. 2. Mesocortical pathway: from the ventral tegmen-
A very high level of smoking is necessary to over- tal area to the cortex
come this blockade and produce the reward effects. 3. Mesolimbic pathway: from the ventral tegmen-
2. Antagonists at nicotinic receptors include tubo- tal area to the limbic system
curarine (an old anaesthesia agent). 4. Tuberoinfundibular: local network of DA in
hypothalamus
17.3.3.3 Dopamine (DA) (Figure 17.4)
1. DA is produced from tyrosine that is a dietary Functions of DA
amino acid. A small of part of tyrosine derives from
phenylalanine by hydroxylation. Phenylalanine 1. DA allows the expression of cortically initiated
hydroxylase is absent in phenylketonuria (PKU). voluntary movements through its actions in the
2. Tyrosine hydroxylase is the rate-limiting striatum.
step in the synthesis of the catecholamines. 2. The mesolimbic pathways promote drive and
Hence, increasing tyrosine does not influence reinforcement.
Neurochemistry 223
Phenylalanine
Phenylalanine
hydroxylase
Tyrosine
Tyrosine
hydroxylase
Dopa
DOPA
decarboxylase
DA-β- Mitochondria
hydroxylase
MAO MAO
DOPAC DA NA NA
aldehyde
DA NA
release release
COMT
DA NA
COMT
3-Methoxy-
4-hydroxy-
Homovanillic acid MAO 3-Methoxytyramine phenethyleneglycol
Normetanephrine
(HVA) (MHPG)
MAO
Vanillylmandelic
acid (VMA)
Sulfotransferase
Excretion MHPG sulphate
FIGURE 17.4 The synthesis and degradation of DA.
17.3.3.4 Disease Processes Involving DA lactotroph cells in the anterior pituitary and causes exces-
Schizophrenia sive release of prolactin.
↓ DA in the mesocortical pathway: Anergy and loss of Depression: The mesolimbic DA system is implicated.
drive (negative symptoms) There is low cerebrospinal fluid (CSF) HVA in depressed
↑ DA in the mesolimbic pathway patients and signify low DA turnover.
The DA hypothesis proposes that increased levels of Obsessive-compulsive disorder (OCD): ↑ DA in the
DA or DA receptors cause schizophrenia. nigrostriatal pathway (e.g. compulsive behaviour)
Galactorrhoea is seen in antipsychotic treatment Bipolar disorder: ↑ DA in the nigrostriatal pathway (↑ sen-
as a result of blockade of DA receptors located on the sory stimuli and movement), ↑ CSF HVA in manic patients
17.3.3.5 Dopamine Receptors (e.g. hallucinations and delusions) by blocking the D2

The dopaminergic receptors are coupled to G proteins, receptors in the mesolimbic and mesocortical pathways
via which they produce their physiological effects. At supports the DA hypothesis of schizophrenia.
the time of writing, the main dopaminergic receptors For example, risperidone is an antagonist that is more
and their main effectors (via G protein α-subunits) are D2 selective. Risperidone has a higher affinity for the D2
believed to be receptors than for the D3 receptors. Seventy-five per cent
of blockade of D2 receptors is useful to achieve therapeu-
tic response.
• D1 → ↑ adenylate cyclase (via Gs)
Antipsychotics may block the D2 receptors in the
• D2 → ↓ adenylate cyclase, ↑ K+, ↓ Ca2+ (via Gi/Go)
nigrostriatal pathway and cause EPSE. EPSE emerge
when 80% D2 receptors in the nigrostriatal pathway are
blocked.
• D5 → ↑ adenylate cyclase (via Gs)
The second-generation antipsychotics, which have lit-
tle or no affinity for D1 receptors, can prevent side effects
The D1-like receptors comprise D1 and D5 receptor sub- associated with D1 antagonism that are found in the older
types that are associated with stimulation of adenylate antipsychotics. DA agonists, such as apomorphine and
cyclase. D1 receptors are found in the striatum, limbic bromocriptine, have greater potency at D2 receptors.
system, thalamus, and hypothalamus. Bromocriptine is used to suppress prolactin secretion
The D2-like receptors comprise D2, D3, and D4 recep- arising from the pituitary tumours.
tor subtypes that are associated with inhibition of adenyl- Clozapine is used in treatment-resistant schizophre-
ate cyclase. D2 receptors are found in the striatum, limbic nia, and it has considerably higher affinity for other
system, thalamus, hypothalamus, and pituitary gland. receptors (e.g. 5-HT2A/2C, α1-, α2-, and D4 receptors) than
D3 and D4 receptors are found in the limbic system (see for D2 receptors. Clozapine is almost 20–25 times more
Figure 17.5). potent at the D4 receptors than the D2 receptors. Its anti-
Schizophrenia is associated with dopaminergic psychotic effects are thought to be mediated primarily by
hyperactivity. Excessive DA activates the inhibitory 5-HT2A/2c and D2 receptor antagonism.
G protein and inhibits the adenyl cyclase. There is an Parkinson’s disease is associated with dopaminergic
imbalance between D1 and D2 receptor functions in hypoactivity as a result of degeneration of cells in the
schizophrenia. pars compacta of substantia nigra. It leads to a relative
Long-term consumption of cocaine, methamphet- excess of cholinergic activity. DA agonists such as bro-
amine, heroin, and alcohol reduces the levels of striatal mocriptine are sometimes used as adjuncts to l-dopa in
D2 receptors compared to healthy controls. treatment for Parkinson’s disease.
The ability of antipsychotics (e.g. chlorpromazine, The decrease in number of D2 receptors in the stria-
haloperidol, risperidone) to reduce positive symptoms tum in old people inversely correlates with severity of
cognitive impairment.
DA 17.3.3.6 Noradrenaline (NA) (Figure 17.6)

1. NA is synthesized by the hydroxylation of DA by
DA-β-hydroxylase. It is mainly stored in the pre-
synaptic complexes with ATP and metallic ions.
It is released from the storage vesicles by Ca2+-
dependent process. Its release from the storage
is inhibited by antihypertensive agents such
as guanethidine. Alpha-methyl-paratyrosine
γ (AMPT) inhibits the tyrosine hydroxylase and
β Adenylate
α results in depressive relapse in antidepressant-
α cyclase
treated patients.
Inhibitory γ 2. NA is mainly produced by the locus coeru-
G-protein β leus. NA is involved in attention, learning, and
emotional behaviour. In the adrenal medulla,
FIGURE 17.5 DA D2 receptor. NA is methylated to adrenaline and it is involved
Neurochemistry 225
Phenylalanine
Phenylalanine
hydroxylase
Tyrosine
Tyrosine
hydroxylase
Dopa
DOPA
decarboxylase
DA-β-
Mitochondria
MAO hydroxylase
MAO
DOPAC DA NA NA
aldehyde
DA NA
release release
COMT
DA NA
COMT
3-Methoxy-
4-hydroxy-
MAO phenethyleneglycol
Homovanillic acid 3-methoxytyramine Normetanephrine
(HVA) (MHPG)
MAO
Vanillylmandelic
acid (VMA)
Sulfotransferase
Excretion
MHPG sulphate
FIGURE 17.6 Synthesis and degradation of NA.
in the fight and flight response. In peripheral tis- tetrabenazine prevent vesicular accumulation of
sues, NA plays a role in stress responses. NA and leads to depression. This supports the
3. NA metabolism: NA is metabolized by COMT NA theory of depressive disorder.
to normetanephrine and then by MAO-B to 4. NA reuptake: NA is transported back into neu-
vanillyl mandelic acid (VMA). It can also be rons by a high-affinity uptake system and it is
metabolized to 3-methoxy-4-hydroxyphenylg- energy consuming. Reuptake is more affected
lycol (MHPG) by MAO and COMT in a step- by secondary amines than tertiary amines.
wise manner. Forty per cent of plasma MHPG Cocaine also inhibits the presynaptic reuptake
is derived from the brain and it indicates of NA. TCA and serotonin–noradrenaline reup-
the NA turnover in the CNS. Reserpine and take inhibitors (SNRIs) are potent blockers for
NA reuptake. SNRIs (e.g. venlafaxine) restore time of writing, the main adrenergic receptors and their
the levels of NA in the synaptic cleft by binding main effectors (via G protein α-subunits) are believed
at the NA reuptake transporters, preventing the to be
reuptake and subsequent degradation. During
opioid and alcohol withdrawal, high concentra- • α1A → ↑ Ca2+ (via Gi/Go)
tion of NA in the synapse is a result of attenua- • α1B → ↑ IP3 (via Gq)
tion of the autoinhibitory mechanisms. • α1C → ↑ IP3 (via Gq)
5. Monoamine oxidase inhibitors (MAOIs) (irre- • α1D → ↑ IP3 (via Gq)
versible MAOIs, phenelzine and tranylcypro- • α2A (human)/a2D (probably rat homologue)
mine, or reversible MAOI, moclobemide) inhibit ↓ adenylyl cyclase, ↑ K+, ↓ Ca2+ (via Gi)
MAO and increase the brain levels of NA. This • α2B → ↓ adenylate cyclase (via Gi)
will help to treat depression. Tyramine-rich • α2C → ↓ adenylate cyclase (via Go)
foods such as cheese (except cream and cot- • β1 → ↑ adenylate cyclase (via Gs)
tage), bean curd, offal (liver), Chianti, alcohol, • β2 → ↑ adenylate cyclase (via Gs)
smoked and pickled fish, sausage, and banana
skin should be avoided as it can inhibit the 17.3.4.1 α-Adrenoceptors
peripheral metabolism of pressor amines. α1-Receptors act via stimulation of phosphoinositol. They
are located postsynaptically. Their functions include
Conversion to adrenaline: The conversion from NA arousal and causing vascular smooth muscles to con-
to adrenaline involves phenylethanolamine-N-methyl tract. Some TCAs and antipsychotics cause sedation
transferase. and postural hypotension that is a result of blocking the
α1-receptors.
17.3.3.7 NA and Psychiatric Disorders The α 2-receptors act via the activation of inhibitory
Generalized anxiety disorder and panic disorder: There G proteins. They are found both pre- and postsynap-
is increased NA transmission from both the locus coe- tically. The α 2-adrenoceptors are widely distributed
ruleus and the caudal raphe nuclei. The NA projection throughout the body and are found in adrenergic neu-
from the ventral locus coeruleus to the hypothalamus rons, blood vessels, pancreas, and smooth muscle. When
will produce autonomic symptoms such as increased stimulated, these receptors reduce the blood pressure
heart rate, dilated pupils, tremor, and sweating. The and suppress symptoms of opiate withdrawal. By cou-
NA projection from the dorsal locus coeruleus to the pling to the inhibitory G proteins, the α 2-adrenoceptors
cortex and hippocampus affects fear-related processing have an inhibitory effect on neurotransmission when
and fear responses. bound by an agonist. The α 2-receptor densities are
OCD: Increased in NA transmission from the locus found to be increased on platelets of depressed patients
coeruleus to the frontal cortex, thalamus, hypothalamus, and the brains of suicide victims. Lofexidine is an
and limbic system α 2-receptor agonist. These receptors are blocked by
Depression: Reduced NA transmission from the locus mianserin. Mirtazapine exerts α 2-autoreceptor and het-
coeruleus and the caudal raphe nuclei. SNRIs increase eroreceptor antagonism.
the NA level in frontal and prefrontal cortex. This will The presynaptic α2-receptors control NA release. The
improve mood and attention in depressed patients. NA in the synapse activates the presynaptic α2-receptors
Chronic antidepressant treatment leads to changes in NA and leads to increase in potassium conductance and hyper-
reuptake transporter gene expression. polarization of the cells. This autoinhibitory mechanism
Bipolar disorder: Increased NA transmission in the reduces NA release. When antidepressants such as TCAs
caudal nucleus and the locus coeruleus. block the NA reuptake, more NA is released in the syn-
Alzheimer’s disease, Korsakoff’s psychosis, Parkinson’s apses and enhances the autoinhibitory mechanism. This
disease, and progressive supranuclear palsy: These disor- leads to downregulation of the presynaptic α2-receptors.
ders are associated with significant loss of NA neurons. The tolerance of autoinhibitory effect takes place over a
few weeks. Hence, the antidepressant can lead to thera-
peutic effect on depressed mood by increasing the avail-
17.3.4 Adrenoceptors
ability of NA through reuptake inhibition and reduction of
The adrenergic receptors are coupled to G proteins, via autoinhibitory mechanism after a time period of several
which they produce their physiological effects. At the weeks. In clinical practice, psychiatrists often remind the
Neurochemistry 227
patients taking antidepressants for the first time to wait for

several weeks before they can see the treatment response.
The autoinhibitory process can be mimicked by
α2-adrenoceptor agonists such as clonidine that reduces
the NA release. In opioid withdrawal, there is an attenu-
ation of the autoinhibitory mechanisms that leads to
higher level of NA in the synapses. Clonidine can be used
to reduce the NA levels and it can also stop the lactate-
induced panic attacks. On the other hand, α2-adrenoceptor
antagonists such as yohimbine stop the autoinhibitory
process and increase the availability of NA. Although
yohimbine has antidepressant properties, it causes anxi-
ety and increases the frequency of panic attacks. NA
The postsynaptic α2-receptors are involved in growth β-Adrenergic receptor
hormone production. Administration of α2-agonists such
as clonidine to patients suffering from depressive or panic
disorder shows a blunted growth hormone response. This
observation resulted from the downregulation of postsyn-
aptic α2-receptors in depressed patients.
The adverse effects associated with first-generation anti-
psychotics such as tachycardia, impotence, and dizziness
are caused by the nonselective binding to α-adrenoceptors. cAMP
17.3.4.2 β-Adrenoceptors
β-Receptors act via activation of stimulatory G protein. FIGURE 17.7 The effect of acute antidepressant treatment on
β-Receptors also stimulate melatonin production in the pineal β1-receptors.
gland. There are three types of β-receptors: β1-receptors
predominate in the cortex. Stimulation of β1-receptors
also increases the rates and force of cardiac contractions.
β2-Receptors predominate in the cerebellum. Stimulation of
β2-receptors causes bronchodilation. β3-Receptors predomi-
nate in the brown fat. Chronic antidepressant treatments
affect the G protein-coupled adenylate cyclase and induce a
reduction in β1-receptor density in the brain. The β-receptor
density is increased in the brains of suicide victims and
MAOIs produce β-receptor downregulation.
Phobia: There is an excess of NA in the principal
noradrenergic pathways in the brain, and this results in
a downregulation of postsynaptic adrenergic receptors. NA
Transmissions of NA from the caudal raphe nuclei and β-Adrenergic receptor
the locus coeruleus are increased in phobia.
The effect of acute and chronic antidepressant treat-
ment on β1-receptors is summarized as follows:
There is an increase of NA and the density of post-
synaptic β1-receptors that stimulate the cAMP formation
during acute antidepressant treatment (Figure 17.7).
The long-term increase in NA leads to downregulation
cAMP
of the postsynaptic β1-receptors and reduce cAMP forma-
tion (Figure 17.8). Nevertheless, the amount of cAMP pro-
duction is still higher than those depressed patients without FIGURE 17.8 The effect of chronic antidepressant treatment
treatment. on β1-receptors.
17.3.4.3 Serotonin (5-HT) of the 5-HT levels in the platelet but increase in
5-HT is a monoamine neurotransmitter. 5-HT is the plasma 5-HT levels.
produced by dorsal and median raphe nuclei. 5-HT plays 4. Degradation of 5-HT: 5-HT is taken back into
a key role in appetite, sleep, mood, impulse control, sui- the neuron and degraded by MAO-A. SSRI
cide, and personality. 5-HT in the CNS accounts for less blocks the 5-HT reuptake. This will lead to
than 20% of the total body 5-HT. Eighty per cent of 5-HT mood improvement in depressed patients, but
are found in the intestine and platelets (Figure 17.9). nausea and impaired sexual function may arise
as possible side effects.
5. 5-Hydroxyindoleacetic acid (5-HIAA): 5-HIAA
1. 5-HT is synthesized from dietary amino
will be transferred out of the brain via CSF or
acid, l-tryptophan. Tryptophan hydroxylase
blood. The concentration of 5-HIAA in CSF cor-
does not saturate and higher level of 5-HT
relates with the concentration in brain tissue. CSF
can be achieved by taking l-tryptophan
5-HIAA is a useful index of central 5-HT turn-
alongside with antidepressants. On the other
over. Low CSF 5-HIAA is found in patients with
hand, depletion of 5-HT can be achieved by
violent behaviours and untreated depression.
inhibiting tryptophan hydroxylase, removing
l-tryptophan from the diet or adding natural
amino acid such as alanine to compete for the 17.3.4.4 Serotonin and Psychiatric Disorders
transport process with l-tryptophan. This will Anxiety and OCD: m-Chlorophenylpiperazine (mCPP)
lead to depression. is a direct 5-HT receptor agonist and it can induce
2. Release of 5-HT: The release of 5-HT is depen- anxiety and obsessional symptoms. mCPP demon-
dent on calcium ions. strates the role of 5-HT dysfunction in anxiety disor-
3. 5-HT and platelets: Most of the p eripheral 5-HTs ders and OCD.
are stored in the platelets. When depressed Depression: 5-HT transmission from the caudal raphe
patients take the SSRI, this will lead to reduction nuclei and rostral raphe nuclei is reduced in patients
L-Tryptophan L-Tryptophan
Tryptophan
5-Hydroxy-indole- hydroxylase
3-acetic acid (5-HIAA)
Aldehyde 5-Hydroxy-tryptophan
dehydrogenase
Aromatic-L amino acid

5-Hydroxy-indole decarboxylase
acetic acid
5-Hydroxy-tryptamine (5-HT)
MAO
Mitochondria
5-HT
release
5-HT
FIGURE 17.9 The synthesis and degradation of serotonin.

Neurochemistry 229
with depression. It leads to insomnia and suicide ide- 17.3.5.1 γ-Aminobutyric Acid (GABA)
ation. Presynaptic 5-HT dysfunction is a state marker in GABA is the main inhibitory neurotransmitter in the
depression. CNS. GABAergic inhibition is seen at the hypothalamus,
Mania: 5-HT transmission from the caudal raphe hippocampus, cerebral cortex, and cerebellum.
nuclei and rostral raphe nuclei is increased in patients
with mania. Biosynthesis
Schizophrenia: There is an interesting relationship GABA is derived from glutamic acid via the action of
between 5-HT and DA. The two 5-HT pathways that are glutamic acid decarboxylase (GAD) (see Figure 17.10).
affected in schizophrenia include (1) the projections from GAD is a marker of GABAergic neurons. It requires pyri-
dorsal raphe nuclei to the substantia nigra and (2) the doxal phosphate that is a vitamin B6 cofactor. Inhibitors
projections from the rostral raphe nuclei ascending into of this enzyme may cause seizure. In schizophrenia,
the cerebral cortex, limbic regions, and basal ganglia. there is a decreased expression of the messenger RNA for
5-HT2A receptor agonism inhibits DA release. When this enzyme in the prefrontal cortex.
there is excess 5-HT produced by these two pathways,
there is a reduction of the availability of DA that can give Metabolism
rise to the negative symptoms of schizophrenia. Second- The metabolic breakdown of GABA to glutamic acid
generation antipsychotics such as risperidone bind to the and succinic semialdehyde involves the action of GABA
D2, 5-HT2A, and α2-adrenergic receptors in the brain. transaminase (GABA-T). GABA-T is often the target
Risperidone competes with 5-HT and its antagonism for anticonvulsants (e.g. sodium valproate). Inhibitor
at 5-HT2A receptors causes an increase in DA to relieve of this enzyme will increase GABA levels and prevent
negative symptoms. As risperidone also blocks D2 recep- convulsion.
tors, the positive symptoms are reduced at the same time.
Alzheimer’s disease: 5-HT transmission from the
17.3.5.2 GABA and Disease Processes
rostral raphe nuclei to the temporal lobe is reduced in
patients suffering from Alzheimer’s disease. Generalized anxiety disorder: ↓ GABA activity
Cloninger’s type 2 alcoholism: This is characterized Schizophrenia: ↑ GABA activity
by young men with impulsive behaviours and low 5-HT Depression: GABAB agonists enhance monoaminer-
levels. gic neurotransmission.
17.3.5 Serotonergic Receptors 17.3.5.3 GABA Receptors

The GABA receptor superfamilies may be large, with
The main serotonergic receptors, grouped according to multiple types of GABA subunits having been cloned. In
their relative homologies, and their signalling systems, general, there are two main types of receptor, the main
believed to exist at the time of writing, are as follows effects of which are
(Table 17.1):
GABA A → ↑ Cl − (via a receptor-gated ion channel)

• 5-HT1A → ↓ adenylate cyclase
• 5-HT1B → ↓ adenylate cyclase
• 5-HT1Da → ↓ adenylate cyclase GABAA receptors gate a chloride ion channel and are
• 5-HT1Db → ↓ adenylate cyclase responsible for inhibitory activity. It has at least 16 dif-
• 5-HT1E → ↓ adenylate cyclase ferent subunits (e.g. there is a binding site for alcohol to
• 5-HT2A → ↑ IP3 increase sedation). For example, diazepam is a GABA-A
• 5-HT2B → ↑ IP3 agonist.
• 5-HT2C → ↑ IP3
• 5-HT3—ion channel GABA B → ↑ K + ± Ca 2 + effects (via G protein coupling)
• 5-HT5A—signalling system not known at the
time of writing
• 5-HT5B—signalling system not known at the GABAB receptors are positively coupled to G pro-
time of writing teins and presynaptically modulate transmitter release.
• 5-HT6 → ↑ adenylate cyclase Baclofen (a medication used to treat spasticity) only binds
• 5-HT7 → ↑ adenylate cyclase to GABAB receptors (see Figure 17.11).
TABLE 17.1
Summary of the 5-HT Receptors
Receptor Type Locations Mechanisms Clinical Relevance
5-HT1A 1. Widely expressed Coupled to a G protein that inhibits the Depression:
throughout the brain intracellular messenger adenylate cyclase ↑ 5-HT1A receptor density in the hippocampus and
2. High density in the 5-HT1A acts as an accelerator of DA medial temporal cortex
hippocampus, raphe release ↓ 5-HT1A receptor density in the cerebellum, basal
nucleus, and medial ganglia, and prefrontal cortex. Chronic
temporal cortex antidepressant treatment leads to downregulation
3. Lower density in the Buspirone exerts anxiolytic and antidepressant effects
prefrontal cortex through partial agonism at the 5-HT1A receptor
and basal ganglia Aripiprazole is a 5-HT1A agonist
5-HT1B Autoreceptors Coupled to a G protein that inhibits the Reduce 5-HT release
intracellular messenger Implicated in Cloninger’s type II alcoholism
adenylate cyclase
5-HT1D Autoreceptors Coupled to a G protein that inhibits the Blunted growth hormone response to sumatriptan in
intracellular messenger depressed patients
adenylate cyclase
5-HT2 Cortex Phosphoinositol turnover Depression: ↑ receptor density on platelets of
The secondary messenger (IP3) will depressed patents; ↓ in the 5-HT2 receptor density in
regulate substrate proteins (e.g. the frontal, temporal, parietal, and occipital cortical
receptors, ion channels, cytoskeletal regions after chronic antidepressant (TCA and
proteins, and transcription factors). This SSRI) treatment
will lead to short- and long-term Slow-wave sleep regulation
regulation of neuronal function Implicated in anxiety disorders
5-HT2A inhibits DA release upon binding ↑ in 5-HT2 receptor binding in suicide victims
of 5-HT. 5-HT2A receptor antagonism Second-generation antipsychotics: 5-HT2A
leads to anxiolytic effects. 5-HT2A antagonists
receptor agonism is associated with Hallucinogens stimulate 5-HT2A receptors in the
circadian rhythm disturbance and sexual frontal cortex and reduce activities of GABAergic
dysfunction neurons
5-HT2B causes mild anxiety and Lysergic acid diethylamide (LSD) is a partial 5-HT2
hyperphagia upon stimulation agonist
5-HT2c regulates DA and NA release Mianserin is a 5-HT2 antagonist
Fluoxetine reduces binge eating and
bulimia through 5-HT2c agonism. Weight
gain and anxiolytic effects are associated
with 5-HT2c antagonism
5-HT2C Choroid plexus Phosphoinositol turnover Implicated in feeding
Agomelatine is a 5-HT2C antagonist
5-HT3 1. Brain stem: the Ligand-gated channel and causes Controls DA release
putative vomiting depolarization Gastrointestinal side effects and nausea associated
centre and the 5-HT3 receptors regulate inhibitory with SSRIs (5-HT3 agonism)
nucleus tractus interneurons in the brain and also Mirtazapine does not have nausea side effects due to
solitarius mediate vomiting via the vagal nerve its antagonism on 5-HT3 receptors
2. Vagus nerve Anxiety disorders
3. Limbic system, Alcohol acts on 5-HT3 receptors
hippocampus, and
the cerebral cortex
Neurochemistry 231

Summary of the 5-HT Receptors
Receptor Type Locations Mechanisms Clinical Relevance
5-HT4 1. Brain stem (caudate Coupled to a G protein that stimulates the This receptor mediates cortisol secretion and
nucleus, lenticular intracellular messenger adenylate cyclase contraction of colon and bladder
nucleus, putamen and regulates neurotransmission
and globus pallidus) 5-HT4 mediates DA release
2. Substantia nigra
3. Low levels in
hippocampus and
frontal cortex
4. Heart
5-HT6 1. H
igh levels: olfactory Coupled to a G protein that stimulates the 5-HT6 receptors may regulate release of
tubercle, corpus intracellular messenger adenylate cyclase neurotrophic factors. Antagonism may enhance
striatum, nucleus and regulates neurotransmission cognition
accumbens, dentate
gyrus, and
hippocampus
2. Low levels:
cerebellum and
amygdala
5-HT7 1. Thalamus Coupled to a G protein that stimulates the 5-HT7 receptors may be involved in circadian
intracellular messenger adenylate cyclase rhythms. Antagonism may enhance cognition
and regulates neurotransmission
Succinic
Glutamate GABA semialdehyde
Glutamatic acid GABA
decarboxylase transaminase
(GABA-T)
FIGURE 17.10 Synthesis and degradation of GABA.

Alcohol
binding site Cl– Cl–
Cl–
Cl– Cl– Cl– Cl
–
Alcohol GABA
Cl– Cl– Cl– Cl– Cl–
Gamma Alpha
sub-unit sub-unit Cl–
GABA
1 2 3
Cl–
Cl–
Cl–
FIGURE 17.11 The GABAA receptor.

1. Benzodiazepine binds to the benzodiazepine 17.3.6 Glutamate Receptors

binding site that overlaps between the γ2- and
α1-subunits of GABAA receptors. If a patient The types of glutamate receptor recognized are
is oversedated after an overdose of benzodiaz- • NMDA receptors
epine, the administration of flumazenil will dis- • a-Amino-3-hydroxy-5-methyl-4-isoxazolepro-
place benzodiazepine from its binding sites and pionic acid (AMPA) receptors
reverse its sedative effect. Hence, flumazenil • Kainic acid (KA) receptors
can lead to anxiogenic effects in normal adults. • Metabotropic glutamate receptors (mGluRs)
2. After the binding of benzodiazepine to its recep- (=trans-ACPD receptors)
tor, the GABA binds to the GABA receptor that
overlaps between the α1- and β2-receptors. New The first three classes are ionotropic glutamate receptors
benzodiazepines such as zopiclone show high that are coupled directly to cation-specific ion channels.
affinity only to the α1-subunits of GABAA recep-
tors. The benzodiazepine-mediated increases in 17.3.6.1 NMDA Receptors
GABA neurotransmission may lead to a decrease The NMDA receptor is the main mediator of excitatory neu-
in the restraining influence of the cortex, result- rotransmission. At the time of writing, the NMDA receptor
ing in disinhibition observed in patients taking subtype is believed to include two families of subunits:
benzodiazepine.
3. The influx of chloride ions leads to sedative • NMDAR1 (=NR1)
effects. Alcohol opens the Cl− ions directly and • NMDAR2 (=NR2)
it has been misused as an anxiolytic agent.
In turn, the following splice variants of NMDAR1 have
been recognized:
17.3.5.4 Glutamate
Glutamate is an excitatory amino acid that is essential in • NMDAR1A (=NR1a)
learning and memory. It is also a potent neurotoxin that • NMDAR1B (=NR1b)
gives rise to excitotoxicity. The main glutamate pathways • NMDAR1C (=NR1c)
include • NMDAR1D (=NR1d)
• NMDAR1E (=NR1e)
1. The corticocortical pathways • NMDAR1F (=NR1f)
2. The pathways between the thalamus and the • NMDAR1G (=NR1g)
cortex
3. The extrapyramidal pathway (the projections Variants of NMDAR2 are modulatory subunits that form
between the cortex and striatum) heteromeric channels but not homomeric channels.
Glutamate is involved in the process of long-term poten- 17.3.6.2 AMPA Receptors

tiation that is seen as the basis of learning and memory. AMPA receptors can be formed from one or any two of
the following:
17.3.5.5 Clinical Relevance of Glutamate
• GluR1
1. In schizophrenia patients, the glutamatergic path- • GluR2
ways are hypoactive. Similarly, the N-methyl- • GluR3
d-aspartate (NMDA) antagonists produce • GluR4
broad-spectrum cognitive impairments, and pro-
nounced negative symptom. NMDA receptors 17.3.6.3 KA Receptors
will be the next targets of antipsychotic treat- KA receptors include
ments. In contrast, the glutamatergic pathways are
hyperactive in epilepsy. • GluR5
2. Lamotrigine and lithium reduce the glutamate • GluR6
transmission in depressed patients. • GluR7
3. The NMDA glutamate receptor is blocked by • KA1
phencyclidine (PCP). • KA2
Neurochemistry 233
17.3.6.4 mGluRs This block is released by AMPA receptor-

The mGluRs are coupled to G proteins, unlike the other induced depolarization. This allows NMDA
classes of glutamate receptor. At the time of writing, the receptor activation and Ca2+ influx. Prolonged
following subtypes have been cloned: Ca2+ influx leads to excitotoxicity. Chronic anti-
depressant treatment reduces the affinity of gly-
• mGluR1 cine site and reduces excitotoxicity.
• mGluR2 2. The NMDA receptor can be modulated by a
• mGluR3 number of antagonists, including competitive
• mGluR4 antagonists at the glycine and glutamate bind-
• mGluR5 ing sites or noncompetitive NMDA receptor
• mGluR6 channel blockers such as PCP and ketamine.
High concentration of alcohol antagonizes
These have been categorized into the following subgroups: the receptor function. Memantine (M) is a
low-affinity voltage-dependent uncompetitive
• Subgroup I = mGluR1 and mGluR5 antagonist at the NMDA receptors, and it can
• Subgroup II = mGluR2 and mGluR3 reduce the calcium influx and stop the excito-
• Subgroup III = mGluR4 and mGluR6 toxicity. Memantine is used to treat moderate to
severe dementia.
The effector system for subgroup I involves stimu- 3. Memantine (M) has low affinity to the NMDA
lation of PLC, while that for both subgroup II and receptors with rapid off-rate kinetics that
subgroup III involves inhibition of adenylate cyclase allows NMDA receptors to be activated by
(Figure 17.12). the relatively high concentrations of glutamate
released following depolarization of the pre-
1. NMDA receptor is a ligand-gated ion channel. synaptic neurons.
Its activation is dependent on the binding of both
glycine and glutamate (G). Glutamate produces 17.3.6.5 Neuropeptides
slow, long-lasting depolarizations by opening Neuropeptides have a higher potency and affinity for
the calcium (Ca2+) channels. NMDA receptors their receptors and they are active in lower concentrations
are usually blocked by magnesium (Mg2+) ions. than classical neurotransmitters (Table 17.2).
G G
G G G
G G G G G
G G G G G
G G
G G G G
G G
G NMDA G G G G
Ca Ca G G Ca receptor Ca Ca G Ca Ca Ca G G Ca
G Ca Ca
Ca Ca Ca G Glycine Ca G Glycine Ca G Glycine
Ca G 2+ Ca GMg2+
Mg Ca G Mg2+
M
Ca2+ Ca2+
Ca2+
FIGURE 17.12 NMDA receptors (M stands for memantine).

TABLE 17.2
Summary of Neuropeptides and Clinical Relevance
Neuropeptides Functions Clinical Relevance
Corticotropin release CRF controls the release of adrenocorticotropic 1. ↑ CRF concentration in CSF of depressed patients
factor (CRF) hormone from the anterior pituitary 2. ↓ CRF level in CSF of depressed patients after
Injections of CRH lead to depressive symptoms such as normalization with antidepressant treatment
reduced appetite and sex drives, weight loss, and 3. ↑ CRF mRNA in the postmortem brains of suicide
altered circadian rhythms victims
NA causes CRH release. Then CRH stimulates the locus 4. ↓ CRF receptors in the postmortem brains of suicide
coeruleus firing by stopping its inhibitory controls victims
5. Blunted ACTH release in response to CRF challenge
in depressed patients
6. CRH overactivity provokes excessive NA release in
panic attacks and alcohol withdrawal
Somatostatin It has inhibitory effects on growth hormone release 1. ↓ CSF concentration in unipolar and bipolar depression
2. ↓ in Alzheimer’s disease
Thyrotropin-releasing TRH is the smallest brain peptide and has the ability to 1. ↑ concentration in CSF of depressed patients
hormone (TRH) reverse sedation caused by drugs due to release of DA 2. 25%–30% of euthyroid depressives have blunted TSH
and ACh in the brain response to TRH challenge or abnormal T3/T4 levels
3. TRH may have a role in learning and memory
Cholecystokinin (CCK) CCK regulates the postprandial release of bile locally in 1. CCKA receptors seem to be involved in appetite and
the gut and control the appetite in the CNS feeding
2. CCKB is involved in emotional behaviour
Vasoactive intestinal VIP is found in the cerebral cortex, hypothalamus, 1. VIP stimulates the release of ACTH, growth hormone,
peptide (VIP) amygdala, hippocampus, autonomic ganglia, intestinal, and prolactin
and respiratory tracts 2. VIP inhibits the release of somatostatin
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18 General Principles of
Psychopharmacology
18.1 HISTORICAL OVERVIEW 18.1.3.2 Typical Antipsychotics

Important dates in the introduction of typical antipsy-
18.1.1 Antidepressants chotics in psychiatric treatment in the twentieth century
18.1.1.1 Tricyclic Antidepressants and MAOIs include the following:
Tricyclic antidepressants and monoamine oxidase inhibi-
tors (MAOIs) were introduced between 1955 and 1958: • 1950—chlorpromazine synthesized by Charpentier,
who was attempting to synthesize an antihista-
• MAOIs—this arose from the observation of ele- minergic agent for anaesthetic use; Laborit then
vated mood in patients with tuberculosis being reported that chlorpromazine could induce an
treated with the MAOI iproniazid, and less toxic artificial hibernation.
MAOIs were subsequently developed; Kline was • The efficacy of chlorpromazine in the treat-
one of the first to report the value of MAOI treatment of psychosis was reported by Paraire and
ment in depression. Sigwald in 1951 and by Delay and Deniker
• Tricyclic antidepressants—Kuhn observed the in 1952 (López-Muñoz et al., 2005).
antidepressant action of imipramine while study- • 1958—haloperidol was synthesized by Janssen.
ing chlorpromazine-like agents.
18.1.3.3 Clozapine
18.1.1.2 SSRIs
Important dates in the introduction and, after 1988, the
The selective serotonin reuptake inhibitors (SSRIs) were
reintroduction of the atypical antipsychotic clozapine
introduced in the late 1980s.
18.1.1.3 RIMA, SNRI, NARI, and NaSSA
The reversible inhibitor of monoamine oxidase-A (RIMA), • 1958—clozapine synthesized as an imipramine
serotonin–noradrenaline reuptake inhibitor (SNRI), selec- analogue; its actions appeared to be closer to
tive noradrenaline reuptake inhibitor (NARI), and norad- chlorpromazine than to imipramine.
renergic and specific serotonergic antidepressant (NaSSA) • 1961–1962—first clinical trial in schizophrenia
were introduced in the 1990s. (University Psychiatric Clinic, Bern) gave dis-
appointing results; low doses of clozapine were
used.
18.1.2 Lithium
• 1966—Gross and Langner reported good results
In 1886, Lange proposed the use of lithium for treating in chronic schizophrenia (Gross and Langner,
excited states (Schioldann, 2009). Lithium was intro- 1966).
duced by Cade in 1949. Following his finding from • 1975 and thereafter—clozapine was withdrawn
animal experiments that lithium caused lethargy, Cade from general clinical use in some countries
observed (in 1948) that it led to clinical improvement in a owing to cases of fatal agranulocytosis (includ-
patient with mania (Cade, 1949). ing eight such deaths in Finland in 1975).
• 1988—Kane and colleagues reported positive
18.1.3 Antipsychotics results from their multicentre double-blind study
of clozapine versus chlorpromazine in treatment
18.1.3.1 Reserpine resistant schizophrenia; subsequent studies
Reserpine was introduced by Sen and Bose in 1931; in 1953, showed that social functioning also improved in
Kline confirmed that it was a treatment for schizophrenia. response to clozapine (Kane et al., 1988).
237
18.1.4 Anxiolytics • Risperidone
• Amisulpride
18.1.4.1 Barbiturates • Olanzapine
The first barbiturate, barbituric acid (malonylurea), was syn- • Aripiprazole
thesized in 1864. The barbiturates were introduced in 1903. • Paliperidone
18.1.4.2 Benzodiazepines
18.2.2 Antimuscarinics (Anticholinergics)
The benzodiazepine chlordiazepoxide was synthesized
in the late 1950s by Sternbach (working for Roche) and Antimuscarinic (anticholinergic) drugs used in the treat-
introduced in 1960. ment of parkinsonism resulting from pharmacotherapy
with antipsychotics include
18.2 CLASSIFICATION • Procyclidine
The examples given in each class of drug are not meant • Orphenadrine
to be exhaustive. • Trihexyphenidyl (benzhexol)
• Biperiden
18.2.1 Antipsychotics (Neuroleptics) • Benzatropine
18.2.1.1 First-Generation (Typical) Antipsychotics

18.2.3 Prophylaxis of Bipolar Mood Disorder
• Phenothiazines—aliphatic The drugs most commonly used in the prophylaxis of
Chlorpromazine bipolar mood disorder are
Levomepromazine (methotrimeprazine)
Promazine • Lithium salts (carbonate and citrate)
• Phenothiazines—piperazines • Carbamazepine
Fluphenazine
Trifluoperazine
Perphenazine
18.2.4 Antidepressants
Prochlorperazine 18.2.4.1 Tricyclic Antidepressants
• Phenothiazines—piperidines Tricyclic antidepressants include
Pipotiazine palmitate
Pericyazine • Dibenzocycloheptanes
• Butyrophenones Amitriptyline
Haloperidol Nortriptyline
Benperidol • Iminodibenzyls
• Thioxanthenes Clomipramine
Flupentixol Imipramine
Zuclopenthixol Trimipramine
• Diphenylbutylpiperidines • Others
Pimozide • Dosulepin (dothiepin)
Fluspirilene Doxepin
• Substituted benzamides Lofepramine
• Sulpiride (some class this as an atypical
antipsychotic) 18.2.4.2 Tricyclic-Related Antidepressants
• Metoclopramide Tricyclic-related antidepressants include
18.2.1.2 Second-Generation (Atypical) • Trazodone

Antipsychotics
The atypical antipsychotics include 18.2.4.3 Tetracyclic Antidepressants
Tetracyclic antidepressants include
• Clozapine
• Quetiapine • Mianserin
General Principles of Psychopharmacology 239
18.2.4.4 MAOIs 18.2.6 Benzodiazepines

MAOIs include Long-acting benzodiazepines include
• Hydrazine compounds
• Diazepam
Phenelzine
• Chlordiazepoxide
Isocarboxazid
• Nitrazepam
• Non-hydrazine compounds
Tranylcypromine Short-acting benzodiazepines include
18.2.4.5 SSRIs • Lorazepam
SSRIs include • Temazepam
• Fluvoxamine
• Fluoxetine 18.2.7 Other Anxiolytics
• Sertraline Nonbenzodiazepine anxiolytics in clinical use include
• Paroxetine
• Citalopram • Azaspirodecanediones—buspirone
• Escitalopram • β-Adrenoceptor blocking drugs—for example,
propranolol
18.2.4.6 RIMA
There is currently one RIMA in clinical use: 18.2.8 Drugs Used in Alcohol Dependence
• Moclobemide The following drugs are used in alcohol dependence:
18.2.4.7 SNRI • Acamprosate

At the time of writing, there is one SNRI in clinical use: • Disulfiram
• Benzodiazepines
• Venlafaxine • Clomethiazole
18.2.4.8 NARI
18.2.9 Drugs Used in Opioid Dependence
The NARI in clinical use is
The following drugs are used in opioid dependence:
• Reboxetine
• Methadone
18.2.4.9 NaSSA
• Lofexidine
The NaSSA in clinical use is • Naltrexone
• Mirtazapine • Buprenorphine
18.2.4.10 Others 18.2.10 Antiandrogens

Other antidepressants include At the time of writing, there is one antiandrogen used for
• Duloxetine psychiatric reasons:
• Agomelatine
• Cyproterone acetate
18.2.5 Nonbenzodiazepine Hypnotics
18.2.11 Drugs for Alzheimer’s Disease
The following short-acting hypnotics are less likely to
cause dependency than benzodiazepines and may be These include
used for the short-term relief of insomnia:
• Donepezil
• Zaleplon—may be used for up to a fortnight • Galantamine
• Zolpidem—may be used for up to a month • Rivastigmine
• Zopiclone—may be used for up to a month • Memantine
18.3 OPTIMIZING PATIENT COMPLIANCE 18.4.3 Pill Factors

Factors that can help optimize patient compliance include The strength of the placebo effect varies with the physical
form of the medication, including the size, type, colour,
• Patient education and number of pills (Blakwell et al., 1972; Buckalew and
• Setting reasonable expectations Coffield, 1982). For example, the relative placebo effect for
• ↓ Number of tablets to be taken the following physical forms has been found to be stronger:
• ↓ Dosage frequency
• Multiple pills > single pills
• Labelling medicine containers clearly
• Larger pills > smaller pills
• Parenteral/depot administration
• Capsules > tablets
• Using alternative medication if there are trou-
blesome side effects Again, examples of the relative potency of medication
• Involving family members varying with pill colour include the following (Schapira
et al., 1970):
It is particularly important to avoid polypharmacy, if
possible, and to prescribe a simple, straightforward drug • Anxiety symptoms responded better to green
regime for elderly patients. Containers used by the elderly tablets.
should take into account the possibility that the patient • Depressive symptoms responded better to
may have arthritis and may also be designed to allow the yellow tablets.
pharmacist to place the appropriate medication for each
intake in clearly labelled boxes.
18.4.4 Controlling for the Placebo Effect
The previously mentioned factors can be taken into account
in clinical practice. In clinical trials, it is important to control
18.4 PLACEBO EFFECT for the placebo effect, and this is achieved in the randomized
double-blind placebo-controlled design (see Chapter 23).
18.4.1 Definition
A placebo refers to any therapy or component of therapy 18.5 PRESCRIBING FOR
that is deliberately used for its nonspecific, psychologi- PSYCHIATRIC PATIENTS
cal, or psychophysiological effect or its presumed specific
effect, but that is without specific activity for the condi- Prescribing for psychiatric patients includes taking into
tion being treated. consideration the following factors (Cookson et al., 2002):
• The symptoms to be targeted in the short and
long term
18.4.2 Mechanisms of the Placebo Effect
• Age
White et al. (1985) have proposed the following bio- • Physical health
psychosocial model for the mechanisms of the placebo • Circumstances
effect: • Drugs already being taken, including home
remedies
• Homeostatic mechanisms • The effectiveness, or otherwise, of previous
Central nervous system function drug treatments
Autonomic nervous system function • Personality
Peripheral nervous system function • Lifestyle
Endocrine function • Social setting
Immune function • The choice of actual drugs
• Classical conditioning Dose size
• Operant conditioning Dose schedule
• Cognitive–affective–behavioural self-control • When to review outcome and who should help
• Hypnosis report it
• The doctor’s attitude • The role of the community psychiatry nurse and
• The patient’s expectations the GP in providing medication and monitoring
• Transitional object phenomena progress
18.6 PHARMACOKINETICS 18.6.1.3.3 Factors Influencing Absorption

Factors influencing absorption of drugs from the gastro-
18.6.1 Absorption intestinal tract include
18.6.1.1 Routes of Administration
• Gastric emptying
18.6.1.1.1 Enteral Administration
• Gastric pH
Enteral administration routes employ the gastrointesti- • Intestinal motility
nal tract, from which the drug is absorbed into the cir- • Presence/absence of food—the presence of food
culation. They include administration via the following delays gastric emptying
routes: • Intestinal microflora
• Area of absorption
• Oral • Blood flow
• Buccal
• Sublingual The antimuscarinic actions of some psychotropic medi-
• Rectal cation lead to delayed gastric emptying.
18.6.1.1.2 Parenteral Administration 18.6.1.4 Rectal Administration
This includes administration via the following routes: 18.6.1.4.1 Advantages
Advantages of rectal administration over the oral route
• Intramuscular include the following:
• Intravenous
• Subcutaneous • It can be used if the patient cannot swallow—for
• Inhalational example, because of vomiting.
• Topical • Gastric factors are bypassed.
• It can be used for drugs that are irritant to the
18.6.1.2 Rate of Absorption stomach.
The rate of absorption of a drug from its site of adminis- • There is reduced first-pass metabolism.
tration depends on the following factors: • It can be useful in uncooperative patients.
• It can be used to administer diazepam during an
• The form of the drug epileptic seizure, for example, in a patient with a
• The solubility of the drug, which is influenced learning difficulty.
by factors such as
The pKa of the drug 18.6.1.4.2 Disadvantages
Particle size Disadvantages of rectal administration include the
The ambient pH following:
• The rate of blood flow through the tissue in
which the drug is sited • Embarrassment.
• Presence of a variable amount of faecal matter
18.6.1.3 Oral Administration → unpredictable rate of absorption.
18.6.1.3.1 Mechanisms of Absorption • Local inflammation may occur following the
The main mechanisms of absorption of drugs from the frequenct use of this route.
gastrointestinal tract are
18.6.1.5 Intramuscular Administration
• Passive diffusion 18.6.1.5.1 Factors Influencing Absorption
• Pore filtration The rate of absorption of drugs administered intramuscu-
• Active transport larly is increased in the following circumstances:
18.6.1.3.2 Site of Absorption • Lipid-soluble drugs

The main site of absorption of most psychotropic drugs • Drugs with a low relative molecular mass
(which tend to be lipophilic at a physiological pH) from • Increased muscle blood flow—for example, after
the gastrointestinal tract is the small intestine. physical exercise or during emotional excitement
18.6.1.5.2 Disadvantages 18.6.2 Distribution

Disadvantages of intramuscular administration include The rate and degree of distribution of psychotropic drugs
the following: between the lipid, protein, and water components of the
body are influenced by the
• Pain.
• Usually unacceptable for self-administration. • Lipid solubility of the drug
• Risk of damage to structures such as nerves. • Plasma-protein binding
• Some drugs, for example, paraldehyde, may • Volume of distribution
cause sterile abscess formation. • Blood–brain barrier
• Reduced muscle blood flow (e.g. in cardiac fail- • Placenta
ure) leading to reduced absorption.
• Tissue binding or precipitation from solution 18.6.2.1 Lipid Solubility
after intramuscular administration (e.g. for Increased lipid solubility is associated with increased
chlordiazepoxide, diazepam, phenytoin) leading volume of distribution. This is the case for most psycho-
to reduced absorption. tropic drugs at physiological pH.
• This route should not be used if the patient is
receiving anticoagulant therapy. 18.6.2.2 Plasma–Protein Binding
• Increased creatine phosphokinase occurs, which Drugs circulate around the body partly bound to plasma
may interfere with diagnostic cardiac enzyme proteins and partly free in the water phase of plasma. This
assays. plasma-protein binding, which is reversible and competitive,
acts as a reservoir for the drug. The main plasma-binding pro-
18.6.1.6 Intravenous Administration tein for acidic drugs is albumin, while basic drugs, including
many psychotropic drugs, can also bind to other plasma pro-
18.6.1.6.1 Advantages teins such as lipoprotein and α1-acid glycoprotein. The extent
Advantages of intravenous administration include the of plasma-protein binding varies with a number of factors:
following:
• Plasma drug concentration
• Rapid intravenous administration → rapid • Plasma-protein concentration—reduced in
action; useful in emergency situations. Hepatic disease
• Drug dose can be titrated against patient response. Renal disease
• Large volumes can be administered slowly. Cardiac failure
• This route can be used for drugs that cannot be Malnutrition
absorbed by other routes. Carcinoma
• First-pass metabolism is bypassed. Surgery
Burns
• Drug interactions
18.6.1.6.2 Disadvantages
Displacement
Disadvantages of intravenous administration include the Plasma-protein tertiary structure change
following: • Concentration of physiological substances—
for example, urea, bilirubin, and free fatty acid
• Adverse effects may occur rapidly. Displacement
• Dangerously high blood levels may be achieved. Plasma-protein tertiary structure change
• It is difficult to recall the drug once administered.
• Risk of sepsis. 18.6.2.3 Volume of Distribution
• Risk of thrombosis. This is a theoretical concept relating the mass of a drug in
• Risk of air embolism. the body to the blood or plasma concentration:
• Risk of injection into tissues surrounding the
vein, which may lead to necrosis. Mass of a drug in the body
• Risk of injection into an artery, which may lead Volume of at a given time
=
to spasm. distribution Concentration of the drug at that time
• Cannot be used with insoluble drugs. in the bloood or the plasma
A higher volume of distribution in general corresponds to 18.6.2.4.6 Diffusion

a shorter duration of drug action. Factors that may influ- Some small molecules diffuse readily into the brain and
ence the volume of distribution include CSF from the cerebral circulation, for example, lithium ions.
• Drug lipid solubility—increased lipid solubility 18.6.2.5 Placenta

(e.g. most psychotropic drugs) is associated with Drugs may transfer into the fetal circulation from the
an increased volume of distribution maternal circulation across the placenta by means of
• Adipose tissue—for example, some psychotro-
pic drugs → weight gain → increased adipose • Passive diffusion
tissue → an increased volume of distribution • Active transport
• Increasing age: proportion of lean tissue → • Pinocytosis
increased volume of distribution
• Sex Since drugs may cause teratogenesis during the first tri-
• Physical disease mester, they should be avoided during this time if at all
possible.
18.6.2.4 Blood–Brain Barrier and
Brain Distribution 18.6.3 Metabolism
18.6.2.4.1 Components While some highly water-soluble drugs, for example,
Components of the blood–brain barrier include lithium, are excreted unchanged by the kidneys, others,
such as most highly lipid-soluble psychotropic drugs, first
• Tight junctions between adjacent cerebral capil- undergo metabolism (biotransformation) to reduce their
lary endothelial cells lipid solubility and make them more water soluble, prior
• Cerebral capillary basement membrane to renal excretion. Metabolism sometimes results in the
• Gliovascular membrane production of pharmacologically active metabolites, for
example, amitriptyline → nortriptyline. Sites of metabo-
lism include the following:
18.6.2.4.2 Drug Lipid Solubility
A high rate of penetration of the blood–brain barrier • Liver—this is the most important site of
occurs for nonpolar highly lipid-soluble drugs, since the metabolism.
brain is a highly lipid organ. Most psychotropic drugs, • Kidney.
being highly lipid soluble, can therefore easily cross the • Adrenal (suprarenal) cortex.
blood–brain barrier. • Gastrointestinal tract.
• Lung.
18.6.2.4.3 Infection • Placenta.
Infection may alter the normal functioning of the blood– • Skin.
brain barrier. • Lymphocytes.
18.6.2.4.4 Receptors 18.6.3.1 Hepatic Phase I Metabolism

(Biotransformation)
The existence of specific brain receptors for many psy-
chotropic drugs leads to psychotropic drug protein bind- This leads to a change in the drug molecular structure by
ing in the brain, thereby forming a central nervous system the following nonsynthetic reactions:
reservoir. This does not occur in the CSF, with its very
low protein concentration. • Oxidation—the most common
• Hydrolysis
• Reduction
18.6.2.4.5 Active Transport
Active transport mechanisms are used to cross the The most important type of oxidation reaction is that car-
blood–brain barrier by some physiological substances ried out by microsomal mixed-function oxidases, involv-
and drugs, for example, levodopa. ing the cytochrome P450 isoenzymes.
18.6.3.2 Hepatic Phase II Metabolism 18.7 PHARMACODYNAMICS

(Biotransformation)
18.7.1 Antipsychotics
This is a synthetic reaction involving conjugation between
a parent drug/drug metabolite/endogenous substance and 18.7.1.1 First-Generation Antipsychotics
a polar endogenous molecule/group. Examples of the lat- Many of the actions of chlorpromazine, the archetypal
ter include antipsychotic, are believed to result from antagonist
action to the following neurotransmitters:
• Glucuronic acid
• Sulphate • Dopamine
• Acetate • Acetylcholine—muscarinic receptors
• Glutathione • Adrenaline/noradrenaline
• Glycine • Histamine
• Glutamine
Many of these actions also occur, to varying extents, with
The resulting water-soluble conjugate can be other typical antipsychotics.
excreted by the kidney if the relative molecular mass
< approximately 300. If the relative molecular mass > 18.7.1.1.1 Antidopaminergic Action
approximately 300, the conjugate can be excreted in In general, typical antipsychotics are postulated to act
the bile. clinically by causing postsynaptic blockade of dopa-
mine D2 receptors; their antagonism at these receptors is
related to their clinical antipsychotic potencies. It is the
18.6.3.3 First-Pass Effect antidopaminergic action on the mesolimbic–mesocortical
The first-pass effect (first-pass metabolism or presys- pathway that is believed to be the effect required for this
temic elimination) is the metabolism undergone by an clinical action.
orally absorbed drug during its passage from the hepatic The antidopaminergic action on the tuberoinfundibular
portal system through the liver before entering the sys- pathway causes hormonal side effects. Hyperprolactinaemia,
temic circulation. It varies between individuals and may resulting from the fact that dopamine is prolactin-inhibitory
be reduced by, for example, hepatic disease, food, or factor, causes
drugs that increase hepatic blood flow.
• Galactorrhoea
• Gynaecomastia
18.6.4 Elimination • Menstrual disturbances
• Reduced sperm count
Elimination (excretion) of drugs and drug metabolites • Reduced libido
can take place by means of the
The antidopaminergic action on the nigrostriatal pathway
• Kidney—the most important organ for such causes extrapyramidal symptoms:
elimination
• Bile and faeces • Parkinsonism
• Lung • Dystonias
• Saliva • Akathisia
• Sweat • Tardive dyskinesia
• Sebum
• Milk 18.7.1.1.2 Antimuscarinic Action
The central antimuscarinic (anticholinergic) actions may
With the exception of pulmonary excretion, in general, cause
water-soluble polar drugs and drug metabolites are elimi-
nated more readily by excretory organs than are highly • Convulsions
lipid-soluble nonpolar ones. • Pyrexia
Peripheral antimuscarinic symptoms include • ↑ Dopamine turnover in hypothalamic-tuber-

oinfundibular dopaminergic neurons
• Dry mouth • ↓ Central dopamine synthesis (dose dependent)
• Blurred vision • Normalization of low plasma and CSF levels of
• Urinary retention GABA in bipolar disorder
• Constipation • ↑ GABAergic neurotransmission
• Nasal congestion • ↓ Low-affinity GABA receptors in the corpus
striatum and hypothalamus (chronic lithium
18.7.1.1.3 Antiadrenergic Action administration)
Antiadrenergic actions may cause • ↑ Met-enkephalin and leu-enkephalin in the
basal ganglia and nucleus accumbens
• Postural hypotension • ↑ Dynorphin in the corpus striatum
• Ejaculatory failure
18.7.2.2 Tricyclic Antidepressants
18.7.1.1.4 Antihistaminic Action The most important postulated modes of action in the
Antihistaminic effects include drowsiness. brain of tricyclic antidepressants in achieving therapeutic
effects are
18.7.1.2 Second-Generation Antipsychotics
• Inhibition of reuptake of noradrenaline
The second-generation or atypical antipsychotics have a
• Inhibition of reuptake of serotonin
greater action than do first-generation or typical antipsy-
chotics on receptors other than dopamine D2 receptors. For this reason, tricyclic antidepressants are also
For example, clozapine, the archetypal atypical antipsy- known as monoamine reuptake inhibitors, or MARIs.
chotic, has a higher potency of action than do typical Peripherally, most tricyclic antidepressants also have
antipsychotics on the following receptors: an antimuscarinic action, which gives rise to peripheral
antimuscarinic side effects such as
• 5-HT2
• D4 • Dry mouth
• D1 • Blurred vision
• Muscarinic • Drowsiness
• α-Adrenergic • Urinary retention
• Constipation
18.7.2 Drugs Used in the Treatment Postural hypotension occurs as a result of the antiadren-
of Mood Disorder
ergic action.
18.7.2.1 Lithium 18.7.2.3 SSRIs

Lithium ions, Li+, are monovalent cations that cause a The most important postulated mode of action in the
number of effects, some of which may account for its brain of SSRIs in achieving therapeutic effects is
therapeutic actions, including
• Inhibition of reuptake of serotonin
• ↑ Intracellular Na +
Their relatively selective action on serotonin reuptake
• ↓ Na,K-ATPase pump activity means that SSRIs are less likely than tricyclic antide-
• ↑ Intracellular Ca2+ in erythrocytes in mania pressants to cause antimuscarinic side effects. They are,
and depression however, more likely to cause gastrointestinal side effects
• ↑ Erythrocyte choline such as nausea and vomiting.
• ↑ Erythrocyte phospholipid catabolism (via
phospholipase D) 18.7.2.4 MAOIs
• ↓ Ca2+ in platelets in bipolar disorder The most important postulated mode of action in the
• ↑ Serotonergic neurotransmission brain of MAOIs in achieving therapeutic effects is
• ↓ Central 5-HT1 and 5-HT2 receptor density
(demonstrated in the hippocampus) • Irreversible inhibition of MAO-A and MAO-B
In the central nervous system, MAO-A (monoamine oxi- 18.7.2.9 Asenapine

dase type A) acts on This recently introduced sublingually administered tet-
racyclic antipsychotic is indicated in the treatment of
• Noradrenaline mania. It has high affinity for
• Serotonin
• Dopamine • α2B-Adrenergic receptors
• Tyramine • Serotonin 5-HT2A receptors
• Serotonin 5-HT2B receptors
In the central nervous system, MAO-B (monoamine oxi-
• Serotonin 5-HT2C receptors
dase type B) acts on
• Serotonin 5-HT6 receptors
• Dopamine • Serotonin 5-HT7 receptors
• Tyramine • Dopamine D3 receptors
• Phenylethylamine
• Benzylamine Cognitive, antianxiety, and mood stabilization beneficial
actions may result from strong antagonism to 5-HT6 and
The inhibition of peripheral pressor amines, particularly 5-HT7 receptors. There is little binding of asenapine to
dietary tyramine, by MAOIs can lead to a hypertensive crisis muscarinic receptors, thereby leading to a low likelihood
when foodstuffs rich in tyramine are eaten (see Chapter 19). of antimuscarinic side effects.
18.7.2.5 RIMA
18.7.2.10 Agomelatine
The most important postulated mode of action in the
brain of the RIMA in achieving therapeutic effects is This recently introduced antidepressant has the following
actions:
• Reversible inhibition of MAO-A
• Agonist at MT1 melatonergic receptors
18.7.2.6 SNRI • Agonist at MT2 melatonergic receptors
The most important postulated modes of action in the • Antagonist at 5-HT2C receptors
brain of the SNRIs in achieving therapeutic effects are
18.7.3 Anxiolytics and Hypnotics
• Inhibition of reuptake of noradrenaline
• Inhibition of reuptake of serotonin 18.7.3.1 Benzodiazepines
The most important postulated mode of action in the
18.7.2.7 NARI brain of benzodiazepines in achieving central therapeutic
The most important postulated mode of action in the effects is
brain of the NARI in achieving therapeutic effects is
• Binding to GABAA receptors
• Selective inhibition of the reuptake of
noradrenaline 18.7.3.2 Buspirone
18.7.2.8 NaSSA The most important postulated mode of action in the
The most important postulated modes of action in the brain of the azaspirodecanedione buspirone in achieving
brain of the NaSSA in achieving therapeutic effects are central therapeutic effects is
• Increased release of noradrenaline by antago- • Partial agonism at 5-HT1A receptors

nism of inhibitory presynaptic α2-adrenoceptors
• Increased release of serotonin by enhancement 18.7.3.3 β-Adrenoceptor Blocking Drugs
of a facilitatory noradrenergic input to seroto- The most important postulated mode of action of the
nergic cell bodies β-adrenoceptor blocking drugs in achieving anxiolytic
• Increased release of serotonin by antagonism effects is
of inhibitory presynaptic α2-adrenoceptors on
serotonergic neuronal terminals • Antagonism at peripheral β-adrenoceptors
18.7.3.4 Zopiclone 18.7.5.3 Phenytoin

The cyclopyrrolone zopiclone is believed to achieve a The mechanism of anticonvulsant action of phenytoin is
central hypnotic effect by acting on the same receptors as unknown but may involve
do benzodiazepines.
• Membrane stabilization
18.7.3.5 Zolpidem Na+ channel binding
The imidazopyridine zolpidem is believed to achieve a Ca2+ channel binding
central hypnotic effect by acting on the same receptors as • Benzodiazepine receptor binding
do benzodiazepines. • GABA receptor function modulation
18.7.3.6 Zaleplon
18.7.5.4 Phenobarbitone
The pyrazolopyrimidine zaleplon is believed to achieve a
central hypnotic effect by acting on the same receptors as The actions of phenobarbitone may be similar to those
do benzodiazepines. given earlier for phenytoin.
18.7.4 Drugs for Alzheimer’s Disease 18.7.5.5 Gabapentin

Gabapentin is believed to achieve its anticonvulsant
These have the following actions:
effect by means of the following action:
• Donepezil—reversible inhibitor of
acetylcholinesterase • Binding to a unique cerebral receptor site
• Galantamine—reversible inhibitor of
acetylcholinesterase 18.7.5.6 Vigabatrin
• Rivastigmine—reversible inhibitor of Vigabatrin is believed to achieve its anticonvulsant effect
acetylcholinesterase by means of the following action:
• Memantine—NMDA antagonist
• Inhibition of GABA transaminase, leading to
18.7.5 Antiepileptic Agents increased GABA release
18.7.5.1 Carbamazepine
18.7.5.7 Lamotrigine
Carbamazepine, which has a tricyclic antidepressant-like
structure, may achieve its anticonvulsant effect on the Lamotrigine is believed to achieve its anticonvulsant
basis of the following actions: effect by means of the following action:
• Binding to and inactivation of voltage-depen- • Inhibition of glutamate release

dent Na+ channels
• Increased K+ conductance 18.7.5.8 Levetiracetam
• Partial agonism at the adenosine A1 subclass of Levetiracetam, the S-enantiomer of etiracetam, may
P1 purinoceptors achieve its anticonvulsant effect by means of the follow-
ing actions:
18.7.5.2 Sodium Valproate
Sodium valproate may achieve its anticonvulsant effect • Binding to synaptic vesicle glycoprotein 2A
on the basis of the following actions: (SV2A)
• Inhibition of presynaptic Ca2+ channels
• Increased GABA
Decreased GABA breakdown
Increased GABA release 18.7.5.9 Lacosamide
Decreased GABA turnover Lacosamide, a functionalized amino acid, may achieve
Increased GABAB receptor density its anticonvulsant effect by means of the following
Increased neuronal responsiveness to GABA action:
• Reduced Na+ influx
• Increased K+ conductance • ↑ slow inactivation of voltage-gated Na+ channels
18.7.6 Neurochemical Effects of ECT • Reduced cerebral acetylcholine concentration

• Increased cerebral acetyltransferase activity
18.7.6.1 Noradrenaline • Increased cerebral acetylcholinesterase activity
Electroconvulsive therapy (ECT) probably leads to • Increased CSF acetylcholine concentration
increased noradrenergic function. In particular, ECT
acutely causes Chronic ECS leads to
• Increased cerebral noradrenaline activity • Reduced muscarinic cholinergic receptor density

• Increased cerebral tyrosine hydroxylase activity in the cerebral cortex
• Increased plasma catecholamines, particularly • Reduced muscarinic cholinergic receptor density
adrenaline in the hippocampus
• Reduced second-messenger response in the
Chronic ECS (electroconvulsive shock) leads to hippocampus
• Reduced β-adrenergic receptor density 18.7.6.6 Endogenous Opioids

Chronic ECS leads to
The last effect may be a result of receptor downregulation.
• Increased cerebral met-enkephalin concentra-
18.7.6.2 Serotonin tion and synthesis
ECT probably leads to increased serotonergic function. • Increased cerebral β-endorphin concentration
In particular, ECT acutely causes and synthesis
• Changes in opioid ligand binding
• Increased cerebral serotonin concentration
18.7.6.7 Adenosine
Chronic ECT leads to
Chronic ECS leads to
• Increased 5-HT2 receptor density • Increased cerebral adenosine A1 purinoceptor
density
18.7.6.3 Dopamine
ECT probably leads to increased dopaminergic function.
BIBLIOGRAPHY
In particular, ECT acutely causes
Blackwell B, Bloomfield SS, and Buncher CR. 1972:
• Increased cerebral dopamine concentration Demonstration to medical students of placebo responses
• Increased cerebral concentration of dopamine and nondrug factors. Lancet 1:1279–1282.
Buckalew LW and Coffield KE. 1982: An investigation of drug
metabolites expectancy as a function of capsule color and size and prep-
• Increased behavioural responsiveness to dopa- aration form. Journal of Clinical Psychopharmacology
mine agonists 2:245–248.
Cookson J, Taylor J, and Katona C. 2002: Use of Drugs in
In rat substantia nigra, repeated ECSs lead to Psychiatry: The Evidence from Psychopharmacology, 5th
edn. London, U.K.: Gaskell.
• Increased dopamine D1 receptor density Ettinger RH. 2011: Psychopharmacology. London, U.K.: Pearson.
Gross H and Langner E. 1966: Effect profile of a chemi-
• Increased second-messenger potentiation at
cally new broad spectrum neuroleptic of the dibenzo-
dopamine D1 receptors diazepine group. Wiener Medizinische Wochenschrift
116:814–816.
18.7.6.4 GABA Healy D (ed.). 2008: Psychiatric Drugs Explained, 5th edn.
ECT may cause a functional increase in GABAergic Edinburgh, U.K.: Churchill Livingstone.
Kane J, Honigfeld G, Singer J, and Meltzer H. 1988: Clozapine
activity.
for the treatment-resistant schizophrenic: A double-blind
comparison versus chlorpromazine/benztropine. Archives
18.7.6.5 Acetylcholine of General Psychiatry 45(9):789–796.
ECT probably leads to decreased central cholinergic King DJ (ed.). 2004: Seminars in Clinical Psychopharmacology,
function. In particular, ECT acutely causes 2nd edn. London, U.K.: Gaskell.
López-Muñoz F, Alamo C, Cuenca E, Shen WW, Clervoy P, Schioldann J. 2009: History of the Introduction of Lithium into
and Rubio G. 2005: History of the discovery and clini- Medicine and Psychiatry, p. 390. Adelaide, Australia:
cal introduction of chlorpromazine. Annals of Clinical Adelaide Academic Press.
Psychiatry 17(3):113–135. Silverstone T and Turner P. 1995: Drug Treatment in Psychiatry,
Puri BK. 2013: Drugs in Psychiatry, 2nd edn. Oxford, U.K.: 5th edn. London, U.K.: Routledge.
Oxford University Press. White L, Tursky B, and Schwartz G (eds.). 1985: Proposed
Schapira K, McClelland HA, Griffiths NR et al. 1970: Study synthesis of placebo models. In Placebo: Theory,
of the effects of tablet colour in the treatment of anxiety Research, and Mechanisms, pp. 431–447. New York:
states. BMJ 2:446–449. Guildford Press.
19 Psychotropic Drugs and
Adverse Drug Reactions
19.1 DO PSYCHOTROPIC DRUGS WORK? antipsychotics (apart from clozapine). Two hundred and
twenty-seven patients with schizophrenia and related disor-
There is controversy over the issue of whether or not ders were assessed for medication review because of inade-
psychotropic drugs really do have beneficial psychotropic quate response or adverse effects and randomly prescribed
actions that are significantly greater than those of place- either first-generation antipsychotics or second-generation
bos. Based on his meta-analytic statistical reviews, Irving antipsychotics (other than clozapine), the individual medi-
Kirsch has argued that antidepressant medication is not cation choice in each arm being made by each patient’s psy-
significantly better than placebo at treating depression chiatrist (Jones et al., 2006). Key results were as follows:
(Kirsch, 2009a,b). Moncrieff (2007) has also published a
strong critique of psychotropic drugs. • Patients in the first-generation antipsychotic arm
showed a trend towards greater improvement in
19.1.1 CATIE and CUtLASS Quality of Life Scale and symptom scores.
• Overall, patients reported no clear preference for
These two large studies compared first-generation anti- either first- or second-generation antipsychotics.
psychotics with second-generation antipsychotics.
19.1.1.1 CATIE 19.2 TYPES OF ADVERSE DRUG REACTIONS

CATIE (Clinical Antipsychotic Trials of Intervention
Effectiveness), funded by the National Institute of Mental 19.2.1 Classification
Health (Bethesda, MD), compared olanzapine, quetiapine, Adverse drug reactions may be classified as
risperidone, and ziprasidone (second-generation antipsy-
chotics) and perphenazine (a first-generation antipsychotic). • Intolerance
Almost 1500 chronic schizophrenia patients were ran- • Idiosyncratic reactions
domly assigned to treatment with one of these antipsychotic • Allergic reactions
drugs in a double-blind design, with the primary outcome • Drug interactions
measure being discontinuation of treatment for any cause
(Lieberman et al., 2005). Key results were as follows:
19.2.2 Causal Relationship
• The efficacy of the first-generation antipsychotic The following criteria have been suggested as making
was similar to that of the second-generation it more likely that a causal connection exists between a
antipsychotics. drug and an alleged effect (Edwards, 1995):
• Olanzapine was the most effective in terms of
the rates of discontinuation. • There is a close temporal relationship between
• Olanzapine was associated with greater weight the effect and the taking of the drug, or toxic
gain and increases in measures of glucose and levels of the drug or its active metabolites in
lipid metabolism. body fluids have been demonstrated.
• The effect differs from manifestations of the
19.1.1.2 CUtLASS disorder being treated.
CUtLASS (Cost Utility of the Latest Antipsychotic drugs • No other substances are being taken or with-
in Schizophrenia Study), funded by the Health Technology drawn when the effect occurs.
Assessment Programme (Southampton, U.K.), compared • The reaction disappears when treatment is stopped.
first-generation antipsychotics and second-generation • The effect reappears with a rechallenge test.
251
19.2.3 Intolerance 19.2.6.1 Pharmacokinetic Interactions

In drug intolerance, the adverse reactions are consistent Pharmacokinetic interactions between drugs include
with the known pharmacological actions of the drug.
These adverse drug reactions may be dose related. • Precipitation or inactivation following the mix-
ing of drugs
19.2.4 Idiosyncratic Reactions • Chelation
• Changes in gastrointestinal tract motility
Idiosyncratic adverse drug reactions are reactions that are • Changes in gastrointestinal tract pH
not characteristic or predictable and that are associated • Drug displacement from binding sites
with an individual human difference not present in mem- • Enzyme induction
bers of the general population. • Enzyme inhibition
• Competition for renal tubular transport
19.2.5 Allergic Reactions • Changes in urinary pH → changes in drug
Allergic reactions to drugs involve the body’s immune excretion
system, with the drug interacting with a protein to form
an immunogen that causes sensitization and the induction 19.2.6.2 Pharmacodynamic Interactions
of an immune response. Criteria suggesting an allergic Pharmacodynamic interactions between drugs include
reaction include the following:
• Inhibition of drug uptake
• A different time course from that of the pharma- • Inhibition of drug transport
codynamic action, for example: • Interaction at receptors
Delayed onset of the adverse drug reaction. • Synergism
The adverse drug reaction manifests only fol- • Changes in fluid and electrolyte balance
lowing repeated drug exposure.
• There may be no dose-related effect, with sub-
therapeutically small doses leading to sensitiza- 19.3 PSYCHOTROPIC MEDICATION
tion or allergic reactions. 19.3.1 First-Generation Antipsychotics
• A hypersensitivity reaction, unrelated to the
pharmacological actions of the drug, occurs. In Chapter 18, the major categories of adverse drug
reactions are given that are believed to be caused by
Types of allergic reaction to drugs include antagonist action to the following neurotransmitters:
• Anaphylactic shock—type I hypersensitivity
• Dopamine
reaction
• Acetylcholine—muscarinic receptors
• Haematological reactions—type II, III, or IV
• Adrenaline/noradrenaline
hypersensitivity reaction; for example:
• Histamine
Haemolytic anaemia
Agranulocytosis
Other important adverse drug reactions include
Thrombocytopenia
• Allergic liver damage—type II ± III hypersen-
• Photosensitization
sitivity reaction
• Hypothermia or pyrexia
• Skin rashes—type IV hypersensitivity reaction
• Allergic (sensitivity) reactions
• Generalized autoimmune (systemic lupus ery-
• Neuroleptic malignant syndrome
thematosus-like) disease—type IV hypersensi-
tivity reaction
19.3.1.1 Photosensitization
19.2.6 Drug Interactions Photosensitization is more common with chlorpromazine
than with other typical antipsychotics.
Adverse drug reactions may result from interactions
between different drugs. These may result from 19.3.1.2 Hypothermia or Pyrexia
• Pharmacokinetic interactions Interference with temperature regulation is a dose-related
• Pharmacodynamic interactions side effect.
Psychotropic Drugs and Adverse Drug Reactions 253
19.3.1.3 Allergic (Sensitivity) Reactions 19.3.2.2 General Side Effects

Sensitivity reactions include Treatment with second-generation antipsychotics may be
associated with
• Agranulocytosis
• Leukopenia • Weight gain
• Leukocytosis • Hyperglycaemia—for example, with clozapine
• Haemolytic anaemia and olanzapine
• Type 2 diabetes mellitus—for example, with clo-
19.3.1.4 Neuroleptic Malignant Syndrome zapine and olanzapine
• Dizziness
Neuroleptic malignant syndrome is characterized by
• Postural hypotension
• Extrapyramidal symptoms and occasionally tar-
• Hyperthermia
dive dyskinesia
• Fluctuating level of consciousness
• Neuroleptic malignant syndrome (rare)
• Muscular rigidity
• Autonomic dysfunction Given the risk of hyperglycaemia, metabolic syndrome, and
Tachycardia type 2 diabetes mellitus, when treating a patient with a sec-
Labile blood pressure ond-generation antipsychotic drug, the patient’s body mass
Pallor and plasma glucose level should be monitored regularly.
Sweating
Urinary incontinence
19.3.3 Antimuscarinic Drugs
Laboratory investigations commonly, but not invariably, Antimuscarinic drugs used in parkinsonism may give
demonstrate rise to the following side effects:
• ↑ Creatinine phosphokinase • Antimuscarinic side effects (see Chapter 18)

• ↑ White blood count • Worsening of tardive dyskinesia
• Abnormal liver function tests • Gastrointestinal tract disturbances
• Hypersensitivity
Neuroleptic malignant syndrome requires urgent medical
treatment. 19.3.4 Lithium
19.3.4.1 Renal Function
19.3.1.5 Chronic Pharmacotherapy
Since lithium ions are excreted mainly by the kidneys,
Long-term high-dose pharmacotherapy may cause ocular
renal function must be checked prior to commencing
and skin changes, such as
pharmacotherapy with lithium.
• Opacity of the lens 19.3.4.2 Plasma Levels
• Opacity of the cornea
The therapeutic index of lithium is low and therefore regular
• Purplish pigmentation of the skin
plasma lithium level monitoring is required. (Therapeutic
• Purplish pigmentation of the conjunctiva
index = [toxic dose]/[therapeutic dose].) The dose is adjusted
• Purplish pigmentation of the cornea
to achieve a lithium level of 0.4–1.0 mM for prophylactic
• Purplish pigmentation of the retina
purposes, with lower levels being used in the elderly.
19.3.2 Second-Generation Antipsychotics 19.3.4.3 Side Effects

Side effects of lithium therapy include
19.3.2.1 Clozapine
Clozapine may cause neutropenia and potentially fatal • Fatigue
agranulocytosis, because of which regular haematologi- • Drowsiness
cal monitoring is required. Other side effects of clozap- • Dry mouth
ine include hypersalivation and side effects common to • A metallic taste
chlorpromazine, including extrapyramidal symptoms. • Polydipsia
• Polyuria Thyroid function tests are usually carried out routinely

• Nausea every 6 months in order to check for lithium-induced
• Vomiting disturbances.
• Weight gain
• Diarrhoea
• Fine tremor 19.3.5 Carbamazepine
• Muscle weakness Since carbamazepine may lower the white blood count,
• Oedema regular monitoring of plasma carbamazepine levels
should be carried out.
Oedema should not be treated with diuretics since thia-
zide and loop diuretics reduce lithium excretion and can
thereby cause lithium intoxication. 19.3.6 Tricyclic Antidepressants
19.3.4.4 Intoxication The psychopharmacological basis of important side
effects of tricyclic antidepressants is as follows:
Signs of lithium intoxication include
• Mild drowsiness and sluggishness → giddiness • Blockade of ACh muscarinic receptors

and ataxia • Blockade of histamine H1 receptors
• Lack of coordination • Blockade of α1-adrenoceptors
• Blurred vision • Blockade of 5-HT2/1c serotonergic receptors
• Tinnitus • Membrane stabilization
• Anorexia
• Dysarthria 19.3.6.1 Blockade of Muscarinic Receptors
• Vomiting This leads to antimuscarinic side effects (see Chapter 18).
• Diarrhoea
• Coarse tremor
• Muscle weakness 19.3.6.2 Blockade of Histamine H1 Receptors
This can lead to
19.3.4.5 Severe Overdosage
At lithium plasma levels of greater than 2 mM, the fol- • Weight gain
lowing effects can occur: • Drowsiness
• Hyperreflexia and hyperextension of the limbs

19.3.6.3 Blockade of α1-Adrenoceptors
• Toxic psychoses
• Convulsions This can lead to
• Syncope
• Oliguria • Drowsiness
• Circulatory failure • Postural hypotension
• Coma • Sexual dysfunction
• Death • Cognitive impairment
19.3.4.6 Chronic Therapy 19.3.6.4 Blockade of 5-HT2/1c Receptors

Long-term treatment with lithium may give rise to This can lead to
• Thyroid function disturbances
Goitre • Weight gain
Hypothyroidism
• Memory impairment 19.3.6.5 Membrane Stabilization
• Nephrotoxicity Membrane stabilization can lead to
• Cardiovascular changes
T-wave flattening on the ECG • Cardiotoxicity
Arrhythmias • ↓ Seizure threshold
19.3.6.6 Cardiovascular Side Effects • Restlessness

These include • Sleep disturbance
• Anxiety
• ECG changes • Delayed orgasm
• Arrhythmias
• Postural hypotension 19.3.8 MAOIs
• Tachycardia
• Syncope 19.3.8.1 Dangerous Food Interactions
As mentioned Chapter 18, the inhibition of peripheral
19.3.6.7 Allergic and Haematological Reactions pressor amines, particularly dietary tyramine, by MAOIs
These include can lead to a hypertensive crisis when foodstuffs rich
in tyramine are eaten. Foods that should therefore be
• Agranulocytosis avoided when on treatment with MAOIs include
• Leukopenia
• Eosinophilia • Cheese—except cottage cheese and cream cheese
• Thrombocytopenia • Meat extracts and yeast extracts
• Skin rash • Alcohol—particularly chianti, fortified wines,
• Photosensitization and beer
• Facial oedema • Non-fresh fish
• Allergic cholestatic jaundice • Non-fresh meat
• Non-fresh poultry
19.3.6.8 Endocrine Side Effects • Offal
These include • Avocado
• Banana skins
• Testicular enlargement • Broad-bean pods
• Gynaecomastia • Caviar
• Galactorrhoea • Herring—pickled or smoked
19.3.6.9 Others 19.3.8.2 Dangerous Drug Interactions
Other side effects include Medicines that should be avoided by patients taking
• Tremor MAOIs include
• Black tongue
• Indirectly acting sympathomimetic amines, for
• Paralytic ileus
example:
• Sweating
Amphetamine
• Hyponatraemia—particularly in the elderly
Fenfluramine
• Neuroleptic malignant syndrome—very rare
Ephedrine
with tricyclic antidepressants
Phenylpropanolamine
• Abnormal liver function tests
• Cough mixtures containing sympathomimetics
• Movement disorders
• Nasal decongestants containing sympathomimetics
• Pyrexia
• l-dopa
• (Hypo)mania
• Pethidine
• Blood glucose changes
• Tricyclic antidepressants
19.3.7 SSRIs 19.3.8.3 Other Side Effects
Important side effects that may occur with SSRIs include Other side effects of MAOIs include
• Dose-related gastrointestinal side effects • Antimuscarinic actions.

Nausea • Hepatotoxicity.
Vomiting • Appetite stimulation.
Diarrhoea • Weight gain.
• Headache • Tranylcypromine may cause dependency.
19.3.9 Benzodiazepines • Palpitations
• Tachycardia
An important side effect of benzodiazepines is • Nausea
psychomotor impairment. If benzodiazepines are taken • Vomiting
regularly for 4 weeks or more, dependence may develop,
so that sudden cessation of intake may then lead to a Ingestion of large amounts of alcohol while being treated
withdrawal syndrome whose main features include with disulfiram can lead to
• Anxiety symptoms • Air hunger
• Palpitations • Arrhythmias
• Tremor • Severe hypotension
• Panic
• Dizziness 19.3.12 Cyproterone Acetate
• Nausea
• Sweating Side effects of this antiandrogen agent in males include
• Other somatic symptoms
• Low mood • Inhibition of spermatogenesis
• Abnormal experiences • Tiredness
• Depersonalization • Gynaecomastia
• Derealization • Weight gain
• Hypersensitivity to sensations in all modalities • Improvement of existing acne vulgaris
• Distorted perception of space • ↑ Scalp hair growth
• Tinnitus • Female pattern of pubic hair growth
• Formication
• A strange taste Liver function tests should be carried out regularly owing
• Influenza-like symptoms to a theoretical risk to the liver. Dyspnea may result from
• Psychiatric/neurological symptoms high-dose treatment.
• Epileptic seizures
• Confusional states 19.4 OFFICIAL GUIDANCE
• Psychotic episodes The official guidance in Britain on the use of antipsy-
• Insomnia chotic drugs and benzodiazepines is given in this section.
• Loss of appetite The BNF is the abbreviation for the latest British National
• Weight loss Formulary, a bi-annual publication of the British Medical
Association and the Royal Pharmaceutical Society of
19.3.10 Buspirone Great Britain.
The main side effects of buspirone are
19.4.1 Antipsychotic Doses above
• Dizziness the BNF Upper Limit
• Headache The Royal College of Psychiatrists has published advice
• Excitement on the use of antipsychotic doses above the BNF upper
• Nausea limit. This advice is reproduced in the BNF:
Unless otherwise stated, doses in the BNF are licensed
19.3.11 Disulfiram doses—any higher dose is therefore unlicensed:
If alcohol is drunk while disulfiram is being taken regu- 1. Consider alternative approaches including adju-
larly, acetaldehyde accumulates. Thus, ingesting even vant therapy and newer or second-generation
small amounts of alcohol then causes unpleasant sys- antipsychotics such as clozapine.
temic reactions, including 2. Bear in mind risk factors, including obesity;
particular caution is indicated in older patients,
• Facial flushing especially those over 70.
• Headache 3. Consider potential for drug interactions.
4. Carry out ECG to exclude untoward abnormali- 2. It is very important to recognize allergy
ties such as prolonged QT interval; repeat ECG and idiosyncrasy as causes of adverse drug
periodically and reduce dose if prolonged QT reactions. Ask if the patient had previous
interval or other adverse abnormality develops. reactions.
5. Increase dose slowly and not more often than 3. Ask if the patient is already taking other drugs
once weekly. including self-medication; remember that inter-
6. Carry out regular pulse, blood pressure, and actions may occur.
temperature checks; ensure that patient main- 4. Age and hepatic or renal disease may alter
tains adequate fluid intake. the metabolism or excretion of drugs, so
7. Consider high-dose therapy to be for limited period that much smaller doses may need to be pre-
and review regularly; abandon if no improvement scribed. Pharmacogenetic factors may also be
after 3 months (return to standard dosage). responsible for variations in the rate of metab-
olism, notably of isoniazid and the tricyclic
In addition, the British National Formulary offers the antidepressants.
following advice: 5. Prescribe as few drugs as possible and give very
Important: When prescribing an antipsychotic for admin- clear instructions to the elderly or any patient
istration on an emergency basis, the intramuscular dose likely to misunderstand complicated instructions.
should be lower than the corresponding oral dose (owing 6. When possible use a familiar drug. With a new
to absence of first-pass effect), particularly if the patient drug be particularly alert for adverse reactions
is very active (increased blood flow to muscle consider- or unexpected events.
ably increases the rate of absorption). The prescription 7. If serious adverse reactions are liable to occur
should specify the dose for each route and should not warn the patient.
imply that the same dose can be given by mouth or by
intramuscular injection. The dose of antipsychotic for
emergency use should be reviewed at least daily.
19.5 REPORTING
19.4.2 Benzodiazepines 19.5.1 Britain
In Britain, the Committee on Safety of Medicines has In Britain, the CSM holds an information database for
issued the following advice with respect to the prescrip- adverse drug reactions. Doctors practicing in Britain are
tion of benzodiazepines: asked to report adverse drug reactions to the Medicines and
Healthcare products Regulatory Agency via the internet
1. Benzodiazepines are indicated for the short- on the following web site: www.mca.gov.uk/yellowcard.
term relief (2–4 weeks only) of anxiety that is
severe, disabling or subjecting the individual
19.6 ADROIT
to unacceptable distress, occurring alone or in
association with insomnia or short-term psycho- ADROIT (Adverse Drug Reactions On-line Information
somatic, organic or psychotic illness. Tracking) is an online service used in Britain to monitor
2. The use of benzodiazepines to treat short-term adverse drug reactions.
‘mild’ anxiety is inappropriate and unsuitable.
3. Benzodiazepines should be used to treat insom-
19.6.1 Newer Drugs
nia only when it is severe, disabling or subject-
ing the individual to extreme distress. In the BNF, these are indicated by the symbol ∇. The
BNF advises that doctors are asked to report all sus-
pected reactions.
19.4.3 Prevention of Adverse Drug Reactions
The BNF gives the following advice for preventing 19.6.2 Established Drugs
adverse drug reactions:
The BNF advises that doctors are asked to report all
1. Never use any drug unless there is a good indi- serious suspected reactions. These include those that are
cation. If the patient is pregnant do not use a fatal, life threatening, disabling, incapacitating, or that
drug unless the need for it is imperative. result in or prolong hospitalization.
BIBLIOGRAPHY Life of second- vs first-generation antipsychotic drugs in

schizophrenia: Cost Utility of the Latest Antipsychotic
British Medical Association and Royal Pharmaceutical Drugs in Schizophrenia Study (CUtLASS 1). Archives of
Society of Great Britain. British National Formulary. General Psychiatry 63:1079–1087.
London, U.K.: British Medical Association & Royal Kirsch I. 2009: The Emperor’s New Drugs: Exploding the
Pharmaceutical Society of Great Britain. Antidepressant Myth. London, U.K.: The Bodley Head.
Cookson J, Taylor J, and Katona C. 2002: Use of Drugs in Kirsch I. 2009: Antidepressants and the placebo response.
Psychiatry: The Evidence from Psychopharmacology, Epidemiologia e Psichiatria Sociale 18:318–322.
5th edn. London, U.K.: Gaskell. Lieberman JA, Stroup TS, McEvoy JP, Swartz MS, Rosenheck
Edwards JG. 1995: Adverse reactions to and interactions with RA, Perkins DO, Keefe RS, Davis SM, Davis CE,
psychotropic drugs: Mechanisms, methods of assess- Lebowitz BD, Severe J, Hsiao JK, and Clinical
ment, and medicolegal considerations. In King DJ (ed.) Antipsychotic Trials of Intervention Effectiveness
Seminars in Clinical Psychopharmacology, pp. 480–513. (CATIE) Investigators. 2005: Effectiveness of antipsy-
London, U.K.: Gaskell Press. chotic drugs in patients with chronic schizophrenia. New
Ettinger RH. 2011: Psychopharmacology. London, U.K.: England Journal of Medicine 353:1209–1223.
Pearson. Moncrieff J. 2007: The Myth of the Chemical Cure: A Critique
Healy D (ed.). 2008: Psychiatric Drugs Explained, 5th edn. of Psychiatric Drug Treatment. Basingstoke, Hampshire,
Edinburgh, Scotland: Churchill Livingstone. England: Palgrave Macmillan.
Jones PB, Barnes TR, Davies L, Dunn G, Lloyd H, Hayhurst Puri BK. 2013: Drugs in Psychiatry, 2nd edn. Oxford, U.K.:
KP, Murray RM, Markwick A, and Lewis SW. 2006: Oxford University Press.
Randomized controlled trial of the effect on Quality of
20 Genetics
20.1 DNA AND THE DOUBLE HELIX 20.2.3 Centromere

A pair of complementary bases, for example, C with G, This is the constricted region of each chromosome that
or A with T, is referred to as a base pair. The human is particularly evident during mitosis and meiosis. The
genome is made up of approximately 3.2 × 109 base centromere plays a major role in chromosome assortment
pairs organized into 23 pairs of chromosomes. Somatic during cell division as it attaches itself to the spindle
cells have 44 autosomes and 2 sex chromosomes apparatus (Figure 20.1).
for the diploid count of 46. Gametes such as sperms
and ova have the haploid count of 23 chromosomes.
Somatic cells are divided by mitosis where chromo- 20.2.4 Telomere
somes are duplicated during the prophase of the cell Telomere confers stability to chromosomes by protect-
cycle. Gametes are formed by meiosis. The first meiotic ing ends and allowing the chromosome ends to be copied
division involves duplication of chromosomal material, properly during replication.
while the second meiosis produces four gametes with- Each chromatid has telomere capping at the ends with
out chromosomal duplication. centromere in the centre.
Genes are made up of DNA that consists of two anti-
parallel strands held together in a double helix by hydro-
gen bonds between complementary nitrogenous bases. 20.2.5 Metacentric Chromosomes
Adenine (A) always pairs with thymine (T). Guanine (G)
These are chromosomes with a centrally or almost cen-
always pairs with cytosine (C). Approximately 30% of
trally positioned centromere.
human genes are involved in the development and func-
tion of the central nervous system (CNS).
20.2.6 Acrocentric Chromosomes
20.2 CHROMOSOMES These are chromosomes in which the centromere is very
near to one end.
20.2.1 Number
In normal humans, the genome is distributed on 46 chro- 20.2.7 Chromosomal Map
mosomes in each somatic cell nucleus:
The system agreed at the International Paris Conference
• One pair of sex chromosomes (normal females: in 1971 is as follows:
XX, normal males: XY)
• 44 autosomes = 22 pairs of chromosomes First position—a number (1–22) or letter (X or Y)
that identifies the chromosome
Second position—p (short arm of chromosome) or
20.2.2 K aryotype q (long arm of chromosome)
This is an arrangement of the chromosomal makeup of Third position (region)—a digit correspond-
somatic cells that can be produced by carrying out the ing to a stretch of the chromosome lying
following procedures in turn: arrest cell division at an between two relatively distinct morphological
appropriate stage, disperse the chromosomes, fix the landmarks
chromosomes, stain the chromosomes, photograph the Fourth position (band)—a digit corresponding to a
chromosomes, identify the chromosomes, and arrange band derived from the staining properties of the
the chromosomes. chromosome (Table 20.1)
259
Telomere—containing 20.3 AUTOSOMAL ABNORMALITIES

tandem repeats
20.3.1 Down’s Syndrome
Short The causes of Down’s syndrome are
p (petit)
arm 1. Approximately 95% of cases result from trisomy 21
(47, +21) following nondisjunction during meiosis.
2. Approximately 4% result from transloca-
Centromere—repeats
of alphoid DNA
tion involving chromosome 21; exchange of
chromosomal substance may occur between

chromosome 21 and
a. Chromosome 13
Long b. Chromosome 14
q (queue) c. Chromosome 15
arm d. Chromosome 21
e. Chromosome 22
3. The remaining cases are mosaics.
Note that almost all subjects with Down’s syndrome
who live beyond the age of 40 years show evidence of
FIGURE 20.1 Structure of chromosome. Alzheimer’s disease.
TABLE 20.1
Relationship between Chromosome Number and Psychiatric Disorders
Chromosome Gene and Psychiatric Disorder Chromosome Gene and Psychiatric Disorder
Chromosome 1 DISC-1: schizophrenia and bipolar disorder Chromosome 14 Presenilin 1: Alzheimer’s disease
DISC-2: schizophrenia
Presenilin 2: Alzheimer’s disease
Chromosome 2 2q: autistic spectrum disorder Chromosome 15 Angelman’s syndrome (maternal microdeletion)
Prader–Willi syndrome (paternal microdeletion)
Chromosome 4 Alcohol dehydrogenase gene Chromosome 17 Neurofibromatosis
Huntington’s disease (CAG trinucleotide repeat) Familial frontotemporal dementia
4p: Wolf–Hirschhorn disease Smith–Magenis syndrome
Chromosome 5 5p: cri-du-chat syndrome Chromosome 18 Edward’s syndrome (trisomy)
Chromosome 6 6p: dysbindin gene and schizophrenia Chromosome 19 APOE gene: Alzheimer’s disease
CADASIL gene: Notch 3
Chromosome 7 7q: autism Chromosome 20 PrP in inherited CJD
Williams syndrome (microdeletion)
Chromosome 8 8p: neuregulin and schizophrenia Chromosome 21 Amyloid precursor protein gene: Alzheimer’s
disease
Down’s Syndrome (trisomy)
Chromosome 11 11p: brain-derived neurotrophic factor gene and Chromosome 22 DiGeorge Syndrome (velocardiofacial syndrome)
bipolar affective disorder COMT gene: schizophrenia and bipolar disorder
Chromosome 13 Patau’s syndrome (trisomy) Wilson’s disease X or Y Fragile X syndrome
chromosome Lesch–Nyhan syndrome
Klinefelter’s syndrome XXY
Turners (XO) syndrome
Genetics 261
20.3.2 Edward’s Syndrome of a gene family that includes the amyloid precursor–

like proteins (APLP) 1 and 2. This may explain the link
This is caused by trisomy 18 (47, +18). between Alzheimer’s disease and Down’s syndrome (see
preceding text). The apolipoprotein E e4 allele is common
20.3.3 Patau’s Syndrome
in Alzheimer’s disease, while the e2 allele is less com-
This is caused by trisomy 13 (47, +13). mon than would be expected by chance. It may be that
the e4 allele is associated with increased accumulation of
20.3.4 Cri-du-Chat Syndrome β-amyloid protein, while the reverse is true for the e2 allele.
This partial aneusomy results from the partial deletion
of the short arm of chromosome 5. Its characteristic kit- 20.5 CELL DIVISION
ten-like high-pitched cry has been localized to 5p15.3.
Its other clinical features have been localized to 5p15.2, 20.5.1 Mitosis
known as the cri-du-chat critical region or CDCCR. This is the process of nuclear division allowing many
somatic cells to undergo cell division via the following
20.4 SEX CHROMOSOME ABNORMALITIES stages: interphase, prophase, metaphase, anaphase, and
telophase.
20.4.1 Klinefelter’s Syndrome
In this syndrome, phenotypic males possess more than one 20.5.2 Meiosis
X chromosome per somatic cell nucleus. Genotypes include
This process involves two stages of cell division and
• 47,XXY (i.e. one extra X chromosome per occurs in gametogenesis via the following stages:
somatic cell nucleus); this is the most common interphase, prophase I, metaphase I, anaphase I, telo-
genotype in Klinefelter’s syndrome phase I, prophase II, metaphase II, anaphase II, and
• 48,XXXY telophase II.
• 49,XXXXY Chromosomal division takes place once during
• 48,XXYY meiosis, so that the resulting gametes are haploid.
Recombination takes place during prophase I.
20.4.2 XYY Syndrome
In this syndrome, phenotypic males have the genotype 20.6 GENE STRUCTURE
47,XYY. Genes, the biological units of heredity, consist of
codons grouped into exons with intervening nucleo-
20.4.3 Triple-X Syndrome tide sequences known as introns. The introns do not
In this syndrome, phenotypic males have the genotype code for amino acids. Genes also contain nucleotide
47,XYY. sequences at their beginning and end that allow tran-
scription to take place accurately. Thus, starting from
20.4.4 Tetra-X Syndrome the 5′ end (upstream), a typical eukaryotic gene con-
tains the following:
In this syndrome, also known as super-female syndrome,
phenotypic females have the genotype 48,XXXX. • Upstream site–regulating transcription
• Promoter (TATA)
20.4.5 Turner Syndrome • Transcription initiation site
• 5′ Noncoding region
In this syndrome, phenotypic females have the genotype
• Exons: gene contains regions that are expressed
45,X (=45,XO).
• Introns: intervening sequences that are not
expressed in the final protein and spliced out of
20.4.6 Alzheimer’s Disease mature mRNAs
The gene for amyloid precursor protein (APP) is located on • 3′ Noncoding region, containing a poly A addi-
the long arm of human chromosome 21 and is a member tion site
20.7 DNA REPLICATION Transcription
Replication proceeds in the 5′–3′ direction with new DNA

nucleotides being added to the 3′ end. One strand,
known as the leading strand, is formed continuously,
moving into the direction of the fork (see Figure 20.2). A T G C T A G
The other strand, called the lagging strand (aka
Okazaki fragments), is formed in 100–1000 nucleotide U A C G
blocks. The process is described as semi-discontinuous A
because of the different ways in which the two DNA U
strands are synthesized. mRNA
At the end of DNA synthesis, there will be two chro-
matids for each chromosome. Each chromatid comprises Ribonucleotides
one original parental strand and one newly synthe-
sized complementary strand. This pattern of replication FIGURE 20.3 Transcription.
whereby one parental strand is retained in each daughter
cell is known as semiconservative. This is followed by splicing and nuclear transport,
so that the information (minus that from introns) then
exists in the cytoplasm of the cell on messenger RNA
20.7.1 Transcription (mRNA). The splicing out of the introns is guided by
Chromatin exists in two forms, euchromatin and het- recognition of the GT and AG dinucleotides that mark
erochromatin. Euchromatin is loosely packed, whereas the beginning and the end of the intron. A mutation at
heterochromatin is tightly condensed. Euchromatin is these two sites is called a splice-site mutation and leads
transcriptionally active and heterochromatin is generally to serious effects on the protein structure and function.
not transcriptionally active. For example, clinical features of Fragile X syndrome
Transcription is the step in gene expression in which are due to failure of FMR1 gene transcription due to
information from the DNA molecule is transcribed on to hypermethylation resulting in the absence of the FMR1
a primary RNA transcript. gene protein.
Transcription is initiated in the upstream locus con-
trol region (LCR). The transcription factors with specific mRNA
structural domains such as zinc fingers bind to the LCR. 5΄ 3΄
This process allows previously concealed strands of
DNA to be unfolded and prepared for transcription (see G A C C U A G C G A
Figure 20.3). G A U
3΄
A C G
5΄ T G DNA replication
Leading C C
strand Replication
G T
fork C
Direction of DNA A A C
synthesis A A G G C A
3΄
5΄ T T C C G
T T Ala Asp Leu
C A DNA
Lagging 3΄ G G polymerase C
strand 5΄ Newly synthesized amino acid chain C
C A
C G
C G Okazaki Incoming tRNA carrying an
3΄ fragment Ala
amino acid
FIGURE 20.2 DNA replication process. FIGURE 20.4 Translation.

Genetics 263
20.7.2 Translation
TABLE 20.2
Following transcription, splicing, and nuclear transport, Classification of Mutations
translation is the process in gene expression whereby
mRNA acts as a template allowing the genetic code to Loss-of-Function Gain-of-Function
Mutations Mutations Mutations
be deciphered to allow the formation of a peptide chain.
This process involves tRNA molecules. Impact Reduced activity or quantity Presence of an
of the gene product abnormal gene
Each tRNA contains a set of three nucleotides,
product with toxic
referred to as an anticodon, which is complementary to
effects on the cell
a set of three bases in the mRNA known as a codon (see Mode of Usually recessive Often dominant
Figure 20.4). A codon consists of three bases that code for inheritance (autosomal or X-linked) (autosomal or
a specific amino acid. With four bases, there are 4 × 4 × inheritance. Loss-of- X-linked)
4 = 64 possible codons. As there are only 20 amino acids, function mutations may not inheritance
several different codons may specify the same amino acid. have harmful effects in the
The translation is regulated by signal sequences known heterozygous state, as 50%
as the ‘stop transfer’ and the ‘start transfer’ sequences. of normal enzyme activity
The amino acid residues then form the newly synthesized is usually sufficient for
polypeptide chain. normal function
Diseases Inborn errors of metabolism Huntington’s disease
20.8 POSTTRANSLATIONAL MODIFICATION

The newly synthesized polypeptide chains can be modi- Substitution mutations resulting in silent, missense, or
fied by the addition of chemical groups. This process is nonsense mutations can be transition (purine to purine or
known as posttranslational modification. Other examples pyrimidine to pyrimidine) or transversion (purine to pyrim-
include the formation of disulfide bonds, the cleavage of idine or pyrimidine to purine) mutations. A silent mutation
transport polypeptides, hydroxylation, and phosphoryla- does not alter the amino acid residue encoded. A mis-
tion. Phosphorylation is an important event in signal trans- sense mutation results in the change of amino acid residue
duction and plays a key role in psychiatry (e.g. aripiprazole encoded, while a nonsense mutation results in the creation
increases the level of glycogen synthase kinase 3-beta of a stop codon, resulting in the premature termination
phosphorylation and offers more neuroprotective effects of the protein. Most mutations have the effect of a loss of
than haloperidol in schizophrenia) (Sham et al., 2007). function. If the number of nucleotides deleted or inserted
in an exon involves multiples of three, then the sequence of
codons or the reading frame is preserved. If it does not, the
20.9 MUTATIONS reading frame will be disrupted, resulting in a frameshift
A mutation is a change in DNA sequence that can be mutation with a truncated protein product (Table 20.2).
transmitted from the parent cell to its daughter cells.
There are two types of mutations: germline mutation 20.10 TECHNIQUES IN
refers to mutation that originates from a gamete that
MOLECULAR GENETICS
is subsequently fused with another gamete during fer-
tilization, leading to the conception of an individual 20.10.1 Restriction Enzymes
who has the mutation in every cell. A somatic mutation
occurs after fertilization and is only present in a sub- Restriction enzymes, also known as restriction endonu-
population of somatic cells. cleases, cleave DNA only at locations containing specific
Deletion involves loss while insertion involves gain nucleotide sequences. Different restriction enzymes tar-
of genetic material. Small deletions and insertions are get different nucleotide sequences, but a given restriction
caused by slippage or mispairing between complemen- enzyme targets the same sequence.
tary strands due to close homology of adjacent sequences.
Large deletions and insertions account for 5% of known
pathogenic mutations. Most large deletions and insertions
20.10.2 Gene Library
are caused by unequal crossing-over between homolo- This is a set of cloned DNA fragments representing all
gous sequences. the genes of an organism or of a given chromosome.
20.10.3 Molecular Cloning
TABLE 20.3
This technique can be used to create a gene library. It Steps Involved in Copying DNA
can be carried out by splicing a given stretch of (human)
DNA, cleaved using a restriction enzyme, into a bacte- Step Description Temperature (°C)
rial plasmid having at least one antibiotic resistance gene. 1. Denaturation DNA strands are 93
After reintroduction of the resulting recombinant plasmid separated
2. Annealing Primers attach to the 40–55
into bacteria, antibiotic selective pressure causes these
separate DNA strands
bacteria to reproduce. Multiple recoverable copies of the
3. Extension Nucleotides are added to 72
original (human) DNA are contained in the resulting bac-
make new strands: the
terial colonies. polymerase reaction
Source: Lewis, G.H. et al., Mastering Public Health: A Postgraduate

20.10.4 Gene Probes Guide to Examinations and Revalidation, London, U.K.:
These are lengths of DNA that are constructed so that they Hodder Arnold, 2008.
have a nucleotide sequence complementary, or almost com-
plementary, to that of a given part of the genome, with which,
therefore, they can hybridize under suitable conditions. 20.12 SEPARATING AND VISUALIZING
DIFFERENT DNA SEQUENCES
20.10.5 Oligonucleotide Probes
Once DNA has been replicated, for example, by PCR,
These are small gene probes that can be used to detect it can be sequenced to identify the order of nucleotides
single-base mutations. (A, C, G, or T); see Figure 20.5.
The most common method of sequencing uses chain
termination. A primer, containing DNA with tagged
20.11 POLYMERASE CHAIN REACTION
or terminator nucleotides, is added to denatured DNA
Polymerase chain reaction (PCR) is the most versatile strands. The primer bases bind to the relevant bases on
technique for cloning or making copies of DNA. PCR the DNA to form base pairs. However, every time a ter-
starts with a mixture in a buffer solution comprising of (1) minator sequence binds, it will block further synthesis
template (e.g. DNA to be copied); (2) Taq polymerase (an and the strand will not be further extended, thereby creat-
enzyme needed for DNA synthesis); (3) the four deoxyri- ing many different lengths of sequences, all ending with
bonucleotide triphosphates; and (4) DNA primers = short the same base pair (see Figure 20.6).
sequence comprising of 15–20 nucleotides that hybrid-
izes to the target sequence to be replicated but not to itself 20.13 RESTRICTION FRAGMENT
or copies of itself, for example, GATCCAG.
The process of PCR involves three steps as outlined
LENGTH POLYMORPHISM
in Table 20.3. Each three-step cycle is repeated 30–35 Restriction enzyme is a nuclease that recognizes a spe-
times (after 35 cycles more unwanted by-products cific nucleotide sequence of 4–12 bases and cleaves
are produced than useful DNA). PCR requires very the DNA within or adjacent to that sequence. A poly-
small amounts of DNA and can detect small muta- morphism can be defined based on whether the DNA
tions (<1 kb). It can be completed in less than 1–2 h. is cleaved by a restriction enzyme. Restriction frag-
Flanking DNA sequence must be known in order to ment length polymorphism (RFLP) can be used as
design the primers. DNA markers and are usually inherited in a simple
Strand to be sequenced
A
T T A G G A A
C A C T
G C
FIGURE 20.5 Strand to be sequenced. (From Lewis, G.H. et al., Mastering Public Health: A Postgraduate Guide to Examinations
and Revalidation, CRC press, Oxford, U.K., 2008, p. 197.)
Genetics 265
Prim
er T
A
A G T C
T A
A C
Primer G T
G
T C
C
C
A A G T
T T G
C
er
Prim
FIGURE 20.6 DNA sequences of varying lengths. (From Lewis, G.H. et al., Mastering Public Health: A Postgraduate Guide to
Examinations and Revalidation, CRC press, Oxford, U.K., 2008, p. 197.)
Allele 1 GAATTC... GACTTC..... GAATTC......
Fragment cut by restriction enzymes X X
Allele 2 GAATTC... GAATTC..... GAATTC......
Fragment cut by restriction enzymes X X
FIGURE 20.7 Polymorphism and restriction enzyme.
Mendelian fashion. If a nucleotide substitution changes 20.14.1 Southern Blotting

the recognition site for a restriction enzyme, one allele
will be intact (e.g. AC in allele 1) and restricted (e.g. This is a technique that allows the transfer of DNA fragments
AA in allele 2), as shown in Figure 20.7. After PCR, from gel, where electrophoresis and DNA denaturation have
the reaction products can be digested with restriction taken place, to a nylon or nitrocellular filter. It involves over-
enzyme, and the genotype will be determined after laying the gel with the filter and in turn overlaying the filter
electrophoresis. with paper towels. A solution is then blotted through the gel
Polymorphisms of the serotonin transporter gene have to the paper towels. Autoradiography can then be used to
been reported to be associated with obsessive–compul- identify the fragments of interest on the filter. The technique
sive disorder, suicidal behaviour, autism, and intense is named after its inventor, Edwin Southern (Figure 20.8).
fear. Polymorphisms of the tryptophan hydroxylase gene
have been associated with suicidal behaviour, bipolar Northern
disorder, early smoking initiation, and alcohol abuse. blotting: RNA
20.14 GEL ELECTROPHORESIS

During gel electrophoresis, DNA fragments of differ-
ent sizes move at different speeds under an electric field Western blotting:
protein
(larger fragments migrate more slowly towards a positive
Southern blotting: DNA
electric charge). Fragments carrying different genotypes
can then be identified according to their final position on
the gel. The same process can also be used with RNA and
protein fragments. FIGURE 20.8 Classification of blotting.
20.15 GENOME-WIDE STUDIES USING The closer the two loci, the less there will be recombination
MICROARRAY TECHNOLOGY between the two loci and the more likely the two will be
transmitted together. The probability of a recombination is
Microarrays or gene chips are based on sequence-specific very low for loci D and E. It is very high for loci A and G.
hybridization. In brief, different DNA sequences of inter- Recombination rate can be used as an estimate of
est are applied onto glass slides. Fluorescent-labelled DNA the distance between two points on a chromosome and
probes from the test sample will bind to the complementary this forms the theoretical basis of linkage analysis. The
target sequences on the slides that are then scanned to quan- recombination fraction is the number of recombinants
tify fluorescent signals corresponding to the specific DNA divided by the total number of offspring and it is propor-
sequences. The time for analysis of gene expression or poly- tional to the physical distance between two loci over short
morphic markers is short as several thousand hybridizations distances only. The recombination fraction is a measure
can be analysed simultaneously under the same conditions. of how often the alleles at two loci are separated during
meiotic recombination. Its value can vary from 0 to 0.5.
20.15.1 Recombination
As mentioned earlier, recombination takes place during 20.15.2 Maximum Likelihood Score
prophase I of meiosis. There is alignment and contact of
homologous chromosome pairs during prophase I, allow- This is the value of the recombinant fraction that gives
ing genetic information to cross over between adjacent the highest value for the LOD score. It represents the best
chromatids. This process of crossover or recombination estimate that can be made for the recombinant fraction
causes a change in the alleles carried by the chromatids from the given available data.
at the end of the first meiotic division.
The unit to measure genetic distance or recombination
frequency is centimorgan. Recombination, the random
20.16 LINKAGE ANALYSIS
assortment of chromosomes during meiosis, and DNA 20.16.1 Genetic Markers
mutations are the three essential processes that establish
the genetic makeup of an individual. A DNA polymorphism, such as a RFLP, if linked to a
The further apart two loci are, the more there will be given disease locus, can be used as a genetic marker in
recombination between the two loci and the less likely linkage analysis without its precise chromosomal loca-
the two will be transmitted together (see Figure 20.9). tion being known. Genetic markers can also be used in
presymptomatic diagnosis and prenatal diagnosis.
A a
20.16.2 Linkage
B b
This is the phenomenon whereby two genes close to each
other on the same chromosome are likely to be inherited
C c together.
20.16.3 Linkage Phases
D d For two alleles occurring at two linked loci in a double
heterozygote, the following linkage phases can occur:
E e
• Coupling: the two alleles are on the same

chromosome
F f • Repulsion: the two alleles are on opposite chro-
mosomes of a pair
G g
20.16.4 Linkage Analysis
FIGURE 20.9 Probability of recombination depends upon Linkage analysis is based on the principle of co-
distance. segregation of a trait (disorder) with marker gene(s)
Genetics 267
within families. The genes tend to segregate (i.e. passed

on) together from parent to offspring because the gene TABLE 20.4
causing the disorder and the marker allele are physi- Summary of Findings in Linkage Studies of Major
cally linked to each other on the same chromosome. Psychiatric Disorders
Linkage analysis is based on three principles:
Disorders Findings
Schizophrenia A genome scan meta-analysis produced
1. Affected members of a pedigree will have the
significant genome-wide evidence for linkage
same mutation on the marker allele. on chromosome 2q
2. Unaffected offspring within a family will tend Depressive disorder No consistent findings
to have the same genotype(s) on the marker. Anxiety disorders Chromosomes 7p and 1
3. Hence, affected individuals will have different Chromosomes 13 and 15q
genotypes from unaffected individuals for the Alcohol dependence A1 alleles of the dopamine D2 receptor
marker.
Figure 20.10 shows the linkage of disease-causing gene

(disease D) and allele of marker (colour blindness) on X TABLE 20.5
chromosome. If a marker is close to a disease-causing Compare and Contrast Linkage and Association
gene, alleles of the marker will tend to co-segregate with Studies
the disorder in families or be shared between affected
relatives. Linkage Studies Association Studies
The strength of linkage is expressed as logarithm of To study the association between To study the association between
the odds (LOD) score. The LOD score for a given recom- a disease and a genetic a specific allele and a disease
binant fraction is the logarithm to base 10 of the odds Use families Use cases and controls or families
with unaffected controls
P1:P2, where P1 is the probability of there being linkage
Detectable over large distances > Detectable only over small
for a given recombinant fraction and P2 is the probabil-
10 cM distances, 1 cM
ity of there being no measurable linkage. Thus the LOD
Can usually only detect large Capable of detecting small
score gives a measure of the probability of two loci being effects RR > 2 because it is effects OR < 2 but prone to
linked. The LOD score method was devised by Morton. systematic false positives
A cumulative LOD score exceeding 3 is regarded as
strong evidence for linkage while a cumulative LOD
score below −2 is regarded as strong evidence against
linkage (Tables 20.4 through 20.6).
Example of linkage analysis
A = Colour blindness gene; D = Disease D gene
20.17 QUANTITATIVE GENETICS
Father’s X chromosomes are A
D Quantitative genetics in psychiatry is concerned with
1. The mode of inheritance

2. Genetic factors as an aetiology of a psychiatric
Aa aa
illness
3. Relative contribution of genetic and environ-
mental factors
aa aa Aa Aa aa Aa aa 20.18 BASIC CONCEPTS OF
Offspring with marker A will have disease D. QUANTITATIVE GENETICS
As the genes are on the X chromosome, disease D and colour
blindness only occur in female offspring but not male offspring. 20.18.1 Pattern of Inheritance
FIGURE 20.10 Linkage of disease D gene and colour blind- In this section, R and S are dominant alleles, and r and s
ness gene. the corresponding recessive alleles.
20.19 AUTOSOMAL DOMINANT
TABLE 20.6
INHERITANCE
Summary of Findings in Association Studies
of Major Psychiatric Disorders Autosomal dominant disorders result from the presence
of an abnormal dominant allele causing the individual to
Disorders Findings
manifest the abnormal phenotypic trait. Features of auto-
Schizophrenia Dopamine D3 receptor gene and 5-HT2A somal dominant transmission include the following:
(Crocq et al., 1992; receptor gene
Williams et al., Catechol-o-methyl transferase (COMT) gene • The phenotypic trait is present in all individuals
1996) Recently discovered candidate genes, dysbindin, carrying the dominant allele.
neuregulin, G27/d-amino acid oxidase • The phenotypic trait does not skip generations—
Velocardiofacial syndrome on vertical transmission takes place.
chromosome 22q • Males and females are affected.
Depressive disorder With inconsistent results • Male to male transmission can take place.
Bipolar disorder Genes encoding for the tyrosine hydroxylase, • Transmission is not solely dependent on paren-
(Lange and Farmer, serotonin transporter, and COMT
tal consanguineous matings.
2007) Anticipation (the phenomenon whereby a
• If one parent is homozygous for the abnormal
disease has an earlier age of onset and
dominant allele, all the members of F1 will mani-
increased severity in succeeding generations)
has been described in bipolar disorder
fest the abnormal phenotypic trait.
Posttraumatic stress Serotonin transporter promoter gene Variable expressivity can cause clinical features of autoso-
disorders (Lee et al., mal dominant disorders to vary between affected individu-
2005)
als. This, together with reduced penetrance, may give the
Alzheimer’s disease Amyloid precursor gene on chromosome 21
appearance that the disorder has skipped a generation. The
Presenilin 1 gene on chromosome 14
sudden appearance of an autosomal dominant disorder
Presenilin 2 gene on chromosome 14
may occur as a result of a new dominant mutation.
Apolipoprotein E (APOE) gene on
chromosome 19
Autism Chromosome 7q 20.20 AUTOSOMAL DOMINANT DISORDERS
Hyperkinetic disorder Dopamine D4 receptor gene
(Gill et al., 1997;
20.20.1 Huntington’s Disease
Smalley et al., 1998) Huntington’s disease (chorea) is a progressive, inher-
Allele of the dopamine transporter gene ited neurodegenerative disease that is characterized by
autosomal dominant transmission and the emergence of
20.18.1.1 Law of Uniformity abnormal involuntary movements and cognitive dete-
Consider two homozygous parents with genotypes RR rioration, with progression to dementia and death over
and rr, respectively. Mating (X) results in the next (F1) 10–20 years. The huntingtin gene responsible is located
generation having the genotype shown: on the short arm of chromosome 4; this genetic mutation
consists of an increased number of cytosine–adenine–
Parents: RR x rr guanine (CAG) repeats. (The normal number of such
F1: Rr repeats at this locus is between 11 and about 34.) The age
20.18.1.2 Mendel’s First Law of onset is strongly determined by the number of repeat
This is also known as the law of segregation: units, but once symptoms develop, the rate of progression
is relatively uninfluenced by CAG repeat length.
Parents: Rr × Rr
F1: RR: Rr: rr = 1:2:1 20.20.2 Phacomatoses
20.18.1.3 Mendel’s Second Law The phacomatoses (or phakomatoses), which exhibit neu-
This is also known as the law of independent assortment: rocutaneous signs, include
Parents: RRSS × rrss • Tuberous sclerosis
F1: RrSs • Neurofibromatosis
F2: independent assortment of different alleles Æ • Von Hippel–Lindau syndrome
RRSS, RRSs, …, rrss • Sturge–Weber syndrome
Genetics 269
There are three main forms of tuberous sclerosis: • Where both parents carry one abnormal copy of
the gene, there is a 25% chance of a child inherit-
• TSC1 (tuberous sclerosis type 1), caused by a ing both mutations, hence expressing the disease.
gene on chromosome 9 • In addition, there is a 50% chance of the child
• TSC2 (tuberous sclerosis type 2), caused by a inheriting one of the mutations and be a genetic
gene on chromosome 16 carrier for the disease. When both parents are
• TSC3 (tuberous sclerosis type 3), caused by a affected, all the children will be affected.
translocation that involves chromosome 12
Examples of autosomal recessive disorder include
Neurofibromatosis is caused by an abnormality in the 1. Protein metabolism: phenylketonuria
NF-1 gene (in the region 17q11.2). 2. Fat metabolism: Niemann–Pick disease, Tay–
Sachs disease, and Smith–Lemli–Opitz syndrome
20.20.3 Early-Onset Alzheimer’s Disease 3. Mucopolysaccharidoses: Hurler’s syndrome
4. Obesity and learning disability: Laurence–
A minority of cases of Alzheimer’s disease are inher- Moon–Biedl syndrome
ited as an early-onset autosomal dominant disorder. The 5. Ataxia and learning disability: ataxia-telangiec-
mutations concerned tend to be found on chromosome 14 tasia and Marinesco–Sjögren syndrome
or chromosome 21. 6. Short stature and learning disability: Virchow–
Seckel dwarf
20.20.4 Other Autosomal Dominant Disorders
20.22 X-LINKED RECESSIVE INHERITANCE
Other disorders that can be inherited in an autosomal
dominant manner include In X-linked recessive disorders, a recessive abnormal
allele is carried on the X chromosome. All male (XY)
• Acrocephalosyndactyly type I offspring inheriting this allele manifest the abnormal
• Acrocallosal syndrome phenotypic trait. In contrast, a single recessive mutation
• Acrodysostosis for a gene on the X chromosome in women is compen-
• De Barsy syndrome sated for by the normal allele on the other X chromo-
• Early-onset familial Parkinson’s disease some so that the disease does not occur. Other features
• Periodic paralyses of X-linked recessive transmission include the following:
• Velocardiofacial syndrome • Male to male transmission does not take place.
• Von Hippel–Lindau syndrome • Female heterozygotes are carriers. A heterozy-
• Treacher Collins’ syndrome gous ‘carrier’ woman passes the allele to half
of her sons (who will express the disease), who
20.21 AUTOSOMAL RECESSIVE express it and half of her daughters (who do not).
• Males are far more likely to be affected with
INHERITANCE
X-linked recessive disorders, and females are
Autosomal recessive disorders result from the presence more likely to be carriers. Hence, the incidence of
of two abnormal recessive alleles causing the individual disease is very much higher in males than females.
to manifest the abnormal phenotypic trait. Features of
autosomal recessive transmission include the following: 20.23 AUTOSOMAL RECESSIVE DISORDERS
• Heterozygous individuals are generally carriers 20.23.1 Disorders of Protein Metabolism
who do not manifest the abnormal phenotypic
There are many disorders of protein metabolism that can be
trait.
inherited in an autosomal recessive manner. They include
• The rarer the disorder, the more likely it is that
the following:
the parents are consanguineous.
• The disorder tends to miss generations but the • Phenylketonuria (incidence 1 in 12,000). A
affected individuals in a family tend to be found reduction in phenylalanine hydroxylase causes
among siblings—horizontal transmission takes an increase in circulating phenylalanine. The
place. Guthrie test is used to screen for this disorder.
• Hartnup disorder or disease (incidence 1 in 20.23.2 Disorders of Carbohydrate

14,000). This is a renal-transport amino acid- Metabolism and Lysosomal Storage
uria in which there is reduced absorption of
neutral amino acids (including tryptophan) These disorders can be inherited in an autosomal reces-
from the alimentary canal and renal tubules, sive manner. They include the following:
causing reduced biosynthesis of nicotinic
acid. • Gaucher’s disease (incidence of type I
• Histidinaemia (incidence 1 in 18,000). This is a Gaucher’s disease is between 1 in 600 and 1
reduction in histidase causing an increased level in 2400 in Ashkenazi Jewish populations).
of histidine in the blood and urine. This is a reduction in lysosomal cerebroside
• Homocystinuria (incidence 1 in 50,000). This is β-glucosidase causing an abnormal accumulation
a reduction in cystathionine β-synthase causing of glucosylceramide.
an increased level of homocysteine in the blood • Tay–Sachs disease (incidence 1 in 4000 in
and urine. Ashkenazi Jewish populations). This is a GM2
• Maple-syrup urine disorder (incidence 1 in gangliosidosis in which a reduction in lysosomal
120,000). This is a reduction in oxoacid decar- hexosaminidase A causes an abnormal accumu-
boxylase causing the presence of branched-chain lation of GM2 ganglioside.
amino acids (valine, leucine, and isoleucine) in • Sanfilippo syndrome (or MPS type III) (inci-
the blood and urine. dence 1 in 24,000). This is a mucopolysacchari-
• Carbamoyl phosphate synthetase deficiency (or dosis. Types A, B, C, and D are recognized.
hyperammonaemia) (incidence <1 in 100,000). • Hurler’s syndrome (or MPS type I) (incidence
This is a urea cycle disorder in which hyperam- about 1 in 100,000). This is a mucopolysacchari-
monaemia occurs. dosis. A reduction in lysosomal α-l-iduronidase
• Argininosuccinate synthetase deficiency (or causes abnormal accumulation of dermatan sul-
citrullinaemia) (incidence <1 in 100,000). phate and heparin sulphate.
This is a urea cycle disorder in which there is • Metachromatic leukodystrophy (incidence about
increased citrulline in the blood and urine. 1 in 100,000). This is a sulfatidosis (sulphatidosis).
• Argininosuccinate lyase deficiency (or argini- • Sandhoff disease (incidence about 1 in 300,000).
nosuccinic aciduria) (incidence <1 in 100,000). This is a GM2 gangliosidosis in which there is an
This is a urea cycle disorder in which there is abnormal accumulation of GM2 gangliosides and
increased argininosuccinic acid in the blood and oligosaccharides.
urine. • Niemann–Pick disease (types I and II; both are
• Arginase deficiency (or argininaemia) (inci- rare). Type I is caused by a reduction in lyso-
dence <1 in 100,000). This is a urea cycle dis- somal sphingomyelinase causing abnormal
order in which there is increased arginine in accumulation of sphingomyelin.
the blood. • GM1 gangliosidoses (types I, II, and III; all are
• Cystathioninuria (incidence of about 1 in rare). Type I is the infantile type, type II is the
200,000). A reduction in g-cystathionase juvenile type, and type III is the adult type. In
causes increased cystathionine in the blood all three types, there is a reduction in lysosomal
and urine. β-galactosidase causing an abnormal accumula-
tion of GM1 ganglioside.
Further disorders are
Further disorders are
• Cystinuria
• Hydroxyprolinaemia • Fucosidosis
• Hyperlysinaemia • Galactosaemia
• Nonketotic hyperglycinaemia • Hereditary fructose intolerance
• Ornithinaemia • Krabbe disease
• Stimmler syndrome • Mannosidosis
• Type II tyrosinaemia • Pompe disease
• Oasthouse urine syndrome • Von Gierke disease
Genetics 271
20.23.3 Other Disorders • Lesch–Nyhan syndrome (incidence about 1 in

100,000)—a reduction in hypoxanthine–gua-
There are many other disorders inherited in an autosomal nine phosphoribosyltransferase causes increased
recessive manner. Many are rare or very rare. They include synthesis of urate and hyperuricaemia.
• Alexander disease • Cerebellar ataxia.
• Cerebelloparenchymal disorders • Fragile X syndrome.
• Coat disease • Lowe syndrome.
• Cockayne syndrome • Testicular feminization syndrome.
• Cohen syndrome • X-linked spastic paraplegia.
• Friedreich’s ataxia • W syndrome.
• Macrocephaly
• Oculocerebral syndrome 20.25 OTHER CONCEPTS OF INHERITANCE
• Oculorenocerebellar syndrome
• Refsum disease
20.25.1 Anticipation
• Rubinstein syndrome This refers to the occurrence of an autonomic dominant
• Turcot syndrome disorder at earlier ages of onset or with greater severity
• Wilson disease (hepatolenticular degeneration) in the succeeding generations. In Huntington’s disease, it
has been shown to be caused by expansions of unstable
20.24 X-LINKED DOMINANT INHERITANCE triplet repeat sequences.
In X-linked dominant disorders, a dominant abnormal 20.25.2 Mosaicism
allele is carried on the X chromosome. If an affected
male mates with an unaffected female, all the daugh- Abnormalities in mitosis can give rise to an abnormal cell
ters and none of the sons are affected. If an unaffected line. Such mosaicism may affect somatic cells (somatic
male mates with an affected heterozygous female, mosaicism) or germ cells (gonadal mosaicism).
half the daughters and half the sons, on average, are
affected. Again, male to male transmission does not 20.25.3 Uniparental Disomy
take place. This refers to the phenomenon in which an individual
inherits both homologues of a chromosome pair from the
20.24.1 X-Linked Dominant Disorders same parent.
Disorders that can be inherited in an X-linked dominant 20.25.4 Genomic Imprinting

manner include
This refers to the phenomenon in which an allele is dif-
• Ornithine transcarbamylase (incidence of about ferentially expressed depending on whether it is mater-
1 in 500,000)—a urea cycle disorder in which nally or paternally derived.
hyperammonaemia occurs
• Aicardi syndrome (learning disability, agenesis 20.25.5 Mitochondrial Inheritance
of corpus callosum, and early death in males)
Since mtDNA (mitochondrial DNA) is essentially mater-
• Coffin–Lowry syndrome
nally inherited, mitochondrial inheritance may explain some
• Rett syndrome
cases of disorders that affect both males and females but that
are transmitted through females only and not through males.
20.24.2 X-Linked Recessive Disorders
Disorders that can be inherited in an X-linked recessive
20.26 FAMILY STUDIES
manner include the following: Family studies investigate the degree of familial clustering
of a disorder by comparing the frequency of a disorder in
• Hunter’s syndrome (MPS type II) (incidence the relatives of affected index cases (i.e. probands) with the
about 1 in 100,000)—a mucopolysaccharidosis frequency in a representative sample drawn from a general
in which there is a reduction in lysosomal iduro- population. First-degree relatives share 50% of their genes.
nate 2-sulphatase. Second-degree relatives have, on average, 25% of the
genome in common with the proband. Depending on the • At the time of the study, some relatives may not
prevalence of disorders, there are several recruitment strat- have reached an age range during which the dis-
egies: for relatively uncommon disorders such as schizo- order manifests itself. Weinberg’s age-correc-
phrenia, probands are usually ascertained from a tertiary tion method can be used.
or specialist centre such as patients admitted to a university • Genetic factors are not separated well from
hospital or attending a specialist clinic. For relatively com- environmental factors. Twin and adoption stud-
mon disorders such as depression or anxiety, patients can be ies can be used.
recruited from GP clinics or counselling centres.
There are two types of ascertainment bias: cohort effects
20.27 MORBID RISK
and volunteer bias. Cohort effects refer to the changes in
the characteristics of a disorder over time, which may be The morbid risk (MR) (aka lifetime incidence) is used
relevant if probands have a wide age range (e.g. the clini- to express the rates of illness in relatives. It is calcu-
cal features of first episode schizophrenia of a 20-year-old lated from the number of affected relatives divided by
consist of more positive symptoms compared to chronic the total number of relatives. As not all relatives would
schizophrenia of a 50-year-old). Volunteer bias occur in have gone through the period of risk (e.g. schizophre-
studies where probands with less severe disorders (e.g. for nia symptoms may not manifest in a 5-year-old cousin),
studies of Alzheimer’s disease, mild cases of dementia) are adjustment has to be made for the effect of age of onset.
more likely to give consent and be recruited for the study. One major limitation of family studies is that it does not
distinguish between genetic and shared environmental
20.26.1 Difficulties effects (Table 20.7).
Difficulties (and possible solutions) with family studies
applied to psychiatric disorders include 20.28 TWIN STUDIES
• Psychiatric disorders need to be considered lon- The main purpose of twin studies is to identify the rela-
gitudinally. Lifetime expectancy rates or morbid tive contribution of genetic and environmental factors to
risks can be used. the aetiology.
TABLE 20.7
Summary of Morbid Risks of Major Psychiatric Disorders
MR in General
Disorders MR in First-Degree Relatives Population Other Information
Schizophrenia 3.5% (Caucasians) to 24.6% (second 0.5% Age of onset:
(Hutchinson et al., generation of Afro-Caribbean) Males = 21 years
1996) Female = 28 years
Depressive disorder 9.1% 3% Age of onset = 27 years
(McGuffin and Katz,
1989)
Bipolar disorder 5% 0.3% Unipolar depression in first-degree relatives: 11.5%
(Vallès et al., 2000) Age of onset = 21 years
Anxiety disorders 18% 3% Age of onset = 11 years
(Noyes et al., 1978)
Obsessive–compulsive 10% 1.9% Age of onset = 20 years
disorder (Paul, 2008)
Eating disorder 6%–10% 1%–2% • Family studies support familiar transmission
• Age of onset = 10–16.
Alzheimer’s disease 15%–19% 5% Most cases are sporadic cases without family history
Three times the risk of general population
Autism (Rutter et al., 3% 0.06% Autism is associated with fragile X syndrome
1990)
Attention deficit and Two times of the general population — —
hyperkinetic disorder
Genetics 273
Twin studies are based on a number of assumptions:

TABLE 20.8
1. Monozygotic (MZ) twins are genetically identi-
Twin Concordance Values for Major Psychiatric
cal because they are developed from the same
fertilized ovum. Disorders
2. MZ and dizygotic (DZ) twin pairs are assumed MZ Concordance DZ Concordance
to share environmental risk factors for the disor- Disorders (%) (%)
der to the same degree. Schizophrenia 46 14
3. The null hypothesis assumes that the risk of the Bipolar disorder 40 5
disorder is the same in MZ and DZ twins. Depressive disorder 67 20
4. The null hypothesis assumes that the risk of the Generalized anxiety 34 17
disorder is the same in twins and singletons. disorder
Panic disorder 42 17
OCD 87 47
20.28.1 Methodology Alcohol dependence 63 44
Anorexia nervosa 22 10
The rates of illness in co-twins of MZ and DZ probands Alzheimer disease 31 9
are compared. MZ twins share 100% of the genome, Autism 96 27
whereas DZ twins share, on average, 50% of their
genome. The rate of concurrence of a disorder in the co-
twin of a proband is the concordance rate: schizophrenia have higher concordance rate in MZ than
DZ pairs, which signify the importance of genetic contri-
1. Probandwise rate (asa percentage) = bution in aetiology compared to other disorders.
Twin data can be interpreted in the framework of a
(number of co-twins of probands in liability-threshold model to estimate heritability. Each
whom the disorder is concurrent)
× 100% person has an underlying liability that is determined by
(total number of co-twins) both genetic and environmental factors and the frequency
of distribution of liability follows normal distribution.
The liability distribution is set to have mean = 0 and vari-
Twin pairs are most usefully counted probandwise, that
ance = 1. Individuals below a particular threshold on this
is, if both members of an affected twin pair are ascer-
liability distribution are unaffected, while those above
tained independently, they are counted as two pairs.
the threshold are affected. In Figure 20.11, the area under
This approach allows comparison between the MR
the curve above the threshold of schizophrenics’ relatives
of the general population to develop the disorder and
is larger than general population.
the rate of the disorder in co-twins of the probands,
which is a prerequisite for model fitting and calculating
heritability.
General Relatives of
population schizophrenics
2. Pairwise rate (asa percentage) =
(number of concordant pairs of twins)

× 100%
Frequency
(total number of twin pairs)

Schizophrenic
Schizotypal
The alternative approach is to count pairwise, where

each pair is counted once. However, this rate cannot be
directly compared with the population MR.
The resemblance for the disorder in twin pairs is ini-
tially expressed as the probandwise concordance rate.
–3 –2 –1 0 1 2 3 4
Probandwise concordance is more commonly used than
Total liability
pairwise concordance. A higher concordance rate in
MZ compared to DZ pairs suggests a genetic contribu- FIGURE 20.11 Liability threshold model for transmission of
tion to the disorder. In Table 20.8, bipolar disorder and schizophrenia.
20.28.2 Difficulties
TABLE 20.9
Difficulties (and possible solutions) with twin studies Summary of Findings in Adoption Studies of Major
applied to psychiatric disorders include the following:
Psychiatric Disorders
• Pairwise and probandwise concordance rates Disorders Findings
usually give different results. Take note of the Schizophrenia In family adoption studies, the rate of
method used to determine the concordance rate. (Kety et al., 1994) schizophrenia spectrum disorders is 13%
• Zygosity was determined less accurately in among the biological relatives of affected
older twin studies. (Use modern, more accurate adoptees, 3% among biological relatives of
control adoptees, 1% among the adoptive
methods.)
relatives of affected adoptees, and 3% among
• Diagnostic variability occurred in older twin
the adoptive relatives of control adoptees
studies. (Use more detailed modern diagnostic Depressive disorder Eightfold increase in the rate for affective
criteria.) (Wender et al., disorder among the relatives of index
• Sampling bias may occur. (Use twin registers.) 1986) adoptees with affective disorder and 15-fold
• Twins are at greater risk of central nervous sys- increases in suicide rates
tem abnormalities resulting from birth injury or Alcohol dependence Increased risk of alcohol misuse and
congenital abnormalities (risk to MZ twins > dependence in the adopted-away sons of
risk to DZ twins), which may introduce errors if alcohol-dependent biological parents than
central nervous system abnormalities contribute in the adopted-away sons of non-alcohol-
to the disorder being studied. dependent biological parents
• Assortative mating may lead to a relative Hyperkinetic disorder Adoption studies show that the biological
(Van den Oord parents of children with the attention deficit
increase in the rate of illness in DZ twins com-
et al., 1994) hyperactivity disorder are more likely to
pared with MZ twins.
have the same or a related disorder than are
• Age-correction techniques may introduce the adoptive parents
errors, so do not use them.
• The environment does not necessarily affect
twins equally. Use adoption studies.
and adoptive families of unaffected adoptees.
A greater MR among biological than among
20.29 ADOPTION STUDIES adoptive family members of affected but not
unaffected adoptees would implicate genetic
20.29.1 Methodology
factors.
Individuals are studied who have been brought up by • Cross-fostering studies:
unrelated adoptive parents from an early age, instead The risk of the disorder is compared in adopt-
of by their biological parents. Types of adoption studies ees who have affected biological parents but
include the following: unaffected adopting parents and in adoptees
with unaffected biological parents but affected
• Adoptee studies: adopting parents.
It compares the adopted children of affected • Adoption studies involving monozygotic twins
and unaffected biological parents. An improved (Table 20.9).
version of this design incorporates the affection
status of the adoptive parents. If the affection
status of the biological parents is related to MR
20.29.2 Difficulties
in the adoptee, after adjusting for the affection Difficulties with adoption studies applied to psychiatric
status of the adoptive parents, then genetic fac- disorders include the following:
tors are implicated.
• Adoptee family studies: • Few cases fulfil the criteria for adoption studies.
It compares MR in the biological and adoptive • Adoption studies take a long time to carry out.
families of affected adoptees. An improved • Information about the biological father may not
version of this design includes the biological be available.
Genetics 275
• Adoption may cause indeterminate psychologi- Kessler RC, Berglund P, Demler O et al. 2005: Lifetime preva-
cal sequelae for the adoptees. lence and age-of-onset distributions of DSM-IV disorders
• The process of adoption is unlikely to be random. in the National Comorbidity Survey Replication. Archives
of General Psychiatry 62:593–602.
• In MZ twin studies, it cannot be assumed that
Kety SS, Wender PH, Jacobsen B et al. 1994: Mental ill-
the environmental influences on each twin are ness in the biological and adoptive relatives of schizo-
more or less equivalent following adoption. phrenic adoptees. Replication of the Copenhagen Study
in the rest of Denmark. Archives of General Psychiatry
51:442–455.
Lange K and Farmer A. 2007: The causes of depression. In
ACKNOWLEDGMENTS
Stein G and Wilkinson G (eds.) Seminars in General
The authors of this book would like to acknowledge Adult Psychiatry, 2nd edn., pp. 48–70. London, U.K.:
Professor Pak Sham, BA (Cantab), BM BCh (Oxon), Gaskell.
Lee HJ, Lee MS, Kang RH et al. 2005: Influence of the serotonin
MSc (Lond), PhD (Cantab), MRCPsych, Chair
transporter promoter gene polymorphism on susceptibility
Professor in Psychiatric Genomics and Department to posttraumatic stress disorder. Depression and Anxiety
Head, Department of Psychiatry, Queen Mary Hospital; 21:135–139.
the University of Hong Kong; and Dr. Ene-Choo Tan, Lewis CM, Levinson DF, Wise LH et al. 2003: Genome scan
PhD, Research Scientist in Genetics, KK Women’s and meta-analysis of schizophrenia and bipolar disorder.
Children’s Hospital, Singapore, for their contribution to Part II. Schizophrenia. American Journal of Human
this chapter. Genetics 73:34–48.
Lewis GH, Sheringham J, Kalim K et al. 2008: Mastering
Public Health: A Postgraduate Guide to Examinations
and Revalidation. Oxford, U.K.: CRC Press.
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21 Psychiatric Epidemiology*
21.1 DISEASE FREQUENCY 21.1.2.1 Units

Prevalence, being a proportion or ratio of two numbers,
21.1.1 Incidence does not have units. A given prevalence value may, how-
The incidence of a disease is the rate of occurrence of new ever, be multiplied by 100 to express it as a percentage.
cases of the disease in a defined population over a given For example, according to Jablensky and Sartorius (1975),
period of time. It is equal to the number of new cases over the annual prevalence of schizophrenia is
the given period of time divided by the total population at
risk (see the succeeding text) during the same period of time. = 0.002 – 0.004
21.1.1.1 Units = 2– 4 per 1000

The unit of incidence is T −1, that is, (time)−1. For instance,
Dunham (1965) gave the incidence of schizophrenia as = 0.2% – 0.4%
= 0.00022 year −1 (Note that the annual prevalence is a type of period

prevalence.)
= 0.00022 per year
21.1.3 Population at Risk
= 0.22 per 1,000 per year
This is the population of individuals free of a given dis-
= 22 per 100, 000 per year, etc. ease, who have not already had the disease by the time of
the commencement of a given period of time, who are at
(see Table 21.1.) risk of becoming new cases of the disease.
21.1.2 Prevalence
21.1.4 Chronicity
The prevalence of a disease is the proportion of a defined
population that has the disease at a given time: The chronicity of a disease is its average duration. It has
the units of time.
• Point prevalence. This is the proportion of a
defined population that has a given disease at a 21.1.5 Steady-State Relationship between
given point in time. Point Prevalence and Incidence
• Period prevalence. This is the proportion of a
defined population that has a given disease dur- In the steady state, in which the incidence of a disease is
ing a given interval of time. constant over a given time period and the time between
• Lifetime prevalence. This is the proportion of a caseness onset and ending is constant, the following rela-
defined population that has or has had a given tionship holds:
disease (at any time during each individual’s
lifetime thus far) at a given point in time. P = ID
• Birth defect rate. This is the proportion of live
births that has a given disease. where
• Disease rate at postmortem. This is the propor- P is the point prevalence
tion of bodies, on which postmortems are car- I is the incidence
ried out that has a given disease. D is chronicity
* This chapter may usefully be read in conjunction with Chapter 6, which deals with the principles of evaluation and psychometrics. In addition
to topics that are epidemiological in nature, this chapter also includes a few related subjects that are of value in the analysis of trial data.
277
TABLE 21.1 TABLE 21.2

Measures of Incidence Generalized Diagnostic and Test
Alternative Results
Concept Name Definition True Diagnosis
Incidence Incidence rate Number of new events during a
Test Result Positive Negative
specified time period
Cumulative Risk Proportion of a population who Positive a b
incidence develops the disease of interest in a Negative c d
defined time period
Source: Puri, B.K., Epidemiology, In: Puri,
Note: Incidence (unlike prevalence) is not affected by disease sur- B.K. and Tyrer, P.J., Sciences Basic
vival. The denominator should include those who are ‘at risk’. to Psychiatry, 2nd edn., Churchill
Livingstone, Edinburgh, U.K., 1998.
21.2 CASE IDENTIFICATION, CASE

The predictive value of a positive test result (or positive
REGISTERS, AND MORTALITY predictive value) is the proportion of the positive results
AND MORBIDITY STATISTICS that is truly positive, while the predictive value of a nega-
tive test result (negative predictive value) is the propor-
21.2.1 Case Identification
tion of the negative results that is truly negative. The
21.2.1.1 Caseness efficiency of the test is the proportion of all the results
An overall threshold is ideally defined in order to estab- that is true. In terms of the notation of Table 21.2, these
lish caseness, that is, to differentiate cases of a given psy- are given by the following expressions:
chiatric disorder from noncases. Classification systems
a
and screening can be used to help identify cases. Positive predictive value =
a+b
21.2.1.2 Classification
Classification systems that are useful in case identifica- d
tion are those that provide specific operational diagnostic Negative predictive value =
c+d
criteria as guides for making each psychiatric diagnosis.
A widely used example in psychiatry is that of DSM-5.
a+d
Efficiency = .
21.2.1.3 Screening a+b+c+d
Screening, by means of psychiatric assessment instru-
ments, can be used to identify cases. The instruments The sensitivity, specificity, predictive values, and effi-
used should have good sensitivity and specificity: ciency of a test are often expressed in terms of percent-
True + ve ages, simply by multiplying the earlier formulae by 100.
Sensitivity = Three further measures (which may also be expressed
(True + ve) + (False − ve)
as percentages by multiplication by 100) that may be
True − ve derived from Table 21.2 are
Specificity =
(True − ve) + (False + ve)
a+b
Screen prevalence =
In terms of the generalized diagnostic and test results shown a+b+c+d
in Table 21.2, the sensitivity and specificity are given by
a+c
a Disease prevalence =
Sensitivity = a+b+c+d
a+c
d a+d
Specificity = Test accuracy = .
b+d a+b+c+d
Psychiatric Epidemiology 279
21.2.1.4 Likelihood Ratio 21.2.2 Case Registers

This is a function of both the sensitivity and the specific- Examples of case registers that have proved useful in epi-
ity of a test and indexes how much the test result will demiological studies and psychiatric research generally
change the odds of having a disease/disorder: include
• The likelihood ratio for a positive result, LR+, • Swedish and Danish twin registers
is given by • Psychiatric case registers, containing records
of those who have been treated for psychiat-
Sensitivity ric disorders in certain hospitals or catchment
LR + =
1 − Specificity areas
Limitations of case registers include

• It indexes the increase in the odds of having a
disease when the test result is positive. • The registered individuals may move out of the
• The likelihood ratio for a negative result, LR−, defined geographic area.
is given by • The registers may not be kept up to date for
other reasons.
1 − Sensitivity
LR − =
Specificity
21.2.2.1 Mortality Statistics
21.2.2.1.1 Mortality Rate
• It indexes the decrease in the odds of having a
This is the number of deaths in a defined population
disease when the test result is negative.
during a given period of time divided by the population
size during that time period. This measure is also some-
21.2.1.5 Pretest Odds times referred to as the ‘crude mortality ratio’ or CMR.
The pretest odds are a function of the prevalence of the It may be expressed as a percentage by multiplying the
disease and may be calculated as follows: ratio by 100:
• Standardized mortality rate. This is the

Prevalence
Pretest odds = mortality rate adjusted to compensate for a
1 − Prevalence confounder.
• Age-standardized mortality rate. This is the
mortality rate adjusted to compensate for the
(Prevalence, in this context, is also sometimes known as confounding effect of age.
the pretest probability.) • Standardized mortality ratio (SMR). The SMR
is the ratio of the observed standardized mor-
21.2.1.6 Posttest Odds tality rate, derived from the population being
studied, to the expected standardized mortal-
The posttest odds of a disease are the odds that a
ity rate, derived from a comparable standard
patient has a disease and incorporate information
population. It may be expressed as a percentage
relating to
by multiplying the ratio by 100 (Table 21.3).
• Disease prevalence
• The patient pool 21.2.2.2 Life Expectancy
• The likelihood ratio This is a measure of the mean length of time that
• Pretest odds (i.e. risk factors for the patient) an individual can be expected to live based on the
assumption that the mortality rates used remain con-
The posttest odds are calculated as follows: stant. It is calculated from the ratio of the total time a
hypothetical group of people is expected to live to the
Posttest odds = (Pretest odds) × (Likelihood ratio) size of that group.
TABLE 21.3
Summary of Mortality Indices
Index (Commonly Expressed
per 1,000 or per 100,000) Typical Reference Period Numerator Denominator
Crude mortality rate (10.2/1000 in 1 Year Number of deaths Midyear population
the United Kingdom)
Age-specific mortality rate 1 Year Number of deaths aged X Midyear population aged X
Proportionate mortality as % of X = specific age X = specific age
total deaths of respective age
group
Case fatality rate Within a specified time period Mortality due to a condition The population of people with that
condition
Child mortality rate (0.2/1000 in 1 Year Number of deaths in children aged Midyear number of children aged
the United Kingdom) 1–4 years 1–4 years
Infant mortality rate (4.9/1000 in 1 Year Number of deaths under 1-year-old Number of live births
the United Kingdom)
Postnatal mortality rate 1 Year Number of deaths in infants aged Number of live births
4–52 weeks
Neonatal mortality rate (3.4/1000 1 Year Number of deaths in the first Number of live births
in the United Kingdom) 28 days
Stillbirth (in England and Wales, Born after 24 weeks Number of fetus born after the 24th Number of live births
there are 3000 stillbirths per week of pregnancy who does not
year; the stillbirth rate in show any signs of life
England and Wales = 5/1000)
Perinatal mortality rate (8.4/1000 1 Year Number of stillbirths + deaths Number of live births + stillbirths
in the United Kingdom) <7 days
21.2.2.2.1 Morbidity Rate

This is the rate of occurrence of new nonfatal cases of TABLE 21.4
a given disease in a defined population at risk during a Generalized 2 × 2 Contingency Table Used
given period of time: in Analytical Epidemiological Studies
• Standardized morbidity rate. This is the morbid- Outcome
Exposure to
ity rate adjusted to compensate for a confounder. Risk Factor Disease No Disease Total
• Age-standardized morbidity rate. This is the Positive a b a+b
morbidity rate adjusted to compensate for the Negative c d c+d
confounding effect of age. Total a+c b+d a+b+c+d
• Standardized morbidity ratio. The standard-
ized morbidity ratio is the ratio of the observed Source: Puri, B.K., Epidemiology, In: Puri, B.K. and
Tyrer, P.J., Sciences Basic to Psychiatry, 2nd edn,
standardized morbidity rate, derived from the
Edinburgh, U.K., Churchill Livingstone, 1998.
population being studied, to the expected stan-
dardized morbidity rate, derived from a compa-
rable standard population. It may be expressed
as a percentage by multiplying the ratio by 100. apply to the critical appraisal of, for example, prospective
cohort studies, such as the one shown in Table 21.5.
21.3 MEASUREMENTS OF RISK

21.3.1 Relative Risk
The terms described in this section can usefully be related
to the 2 × 2 contingency table shown in Table 21.4, as used In terms of analytical epidemiological studies, the rela-
in analytical epidemiological studies. Similarly, they also tive risk of a disease with respect to a given risk factor is
21.3.3 Relative Risk Increase

TABLE 21.5
Generalized Prospective Cohort This is the absolute risk increase as a proportion of the
risk in the unexposed group and is given by
Study Results
Outcome
a / ( a + b ) − c / (c + d )
Group Positive Negative Total Relative risk increase =
c / (c + d )
Cohort a b a+b
Control c d c+d
Total a+c b+d a+b+c+d
21.3.4 Absolute Risk Reduction
This is another measure of the difference in the risk
the ratio of the incidence of the disease in people exposed between the two groups being studied but this time
to that risk factor to the incidence of the disease in people indexing the risk reduction following exposure to the
not exposed to that same risk factor. In Table 21.4, this index factor. In the notation of the tables of this section,
equates to the ratio of a/(a + b) to c/(c + d). it is given by
In terms of prospective cohort studies, the relative
risk is the ratio of the probability of a positive outcome
c a
in the cohort group (exposed) to the probability of a Absolute risk reduction = −
positive outcome in the control group (not exposed). In (c + d ) ( a + b )
Table 21.5, this again equates to the ratio of a/(a + b) to
c/(c + d).
Thus, in terms of both Tables 21.4 and 21.5, 21.3.5 Relative Risk Reduction
a (c + d ) This is the absolute risk reduction as a proportion of the

Relative risk = risk in the unexposed group and is given by
c( a + b )
The relative risk does not have any units, being the ratio c / (c + d ) − a / ( a + b )
Relative risk reduction =
of two numbers, and it can take on any nonnegative real c / (c + d )
value; that is, relative risk ≥ 0.
21.3.2 Attributable Risk 21.3.6 Number Needed to Treat

This is the incidence of the disease in the group exposed The number needed to treat (NNT) expresses the benefit
to the risk factor of interest minus the incidence in the of an active treatment over a placebo. It can be used in
group not exposed to this risk factor. The attributable summarizing the results of a trial and in individualized
risk is also known as the ‘risk difference’ or the ‘absolute medical decision-making. It takes the value of the near-
excess risk’. In terms of Table 21.4, est integer (or whole number) equal to or higher than the
following expression:
= Attributable risk
1
= Risk difference c / (c + d ) − a / ( a + b )
= Absolute excess risk

21.3.7 Odds Ratio
= Absolute risk increase
If Table 21.5 is taken to refer to a retrospective study, in
which the variable consists of exposure or nonexposure
a c
= − to a given factor, while the outcome consists of being
( a + b ) (c + d ) in the disease group or the control group, the odds that
21.4 STUDY DESIGN

TABLE 21.6
Generalized Retrospective (Case–Control) 21.4.1 Hierarchy of Research Methods
Study Results Beginning with the type of research method generally
Variable considered to have the lowest credibility and in increas-
ing order of generally accepted strength of evidence, the
Outcome Exposure No Exposure Total
types of research studies that are most often used are as
Disease group a b a+b
follows:
Control c d c+d
Total a+c b+d a+b+c+d
• Case reports
• Case series
• Cross-sectional studies
• Retrospective studies
subjects in the disease group were exposed to the fac-
• Prospective studies/trials
tor are given by a/b. Similarly, the odds that subjects in
• Randomized double-blind placebo-controlled
the control group were exposed to the factor are given
clinical trials
by c/d.
• Meta-analyses (or other systematic reviews) of
These results follow from the following definition:
randomized double-blind placebo-controlled
clinical trials
Odds of an event taking place =
This hierarchical order should not necessarily be taken
Probability of that event as being set in stone. For example, case reports involving
1 − Probability of that event the first use of an innovative treatment can be of great
value.
The odds ratio is the ratio of the odds that subjects in the
disease group were exposed to the factor to the odds that 21.4.2 Confounding
subjects in the control group were exposed to the factor.
In terms of Table 21.6, we have One of the most important confounding factors in stud-
ies is age, particularly, for example, in the calculation of
morbidity and mortality rates in epidemiological studies.
ad
Odds ratio = There are various methods that may be used to compen-
bc sate for confounding variables. These include
In the case of retrospective epidemiological studies (see • Standardization (e.g. age can be compensated
Table 21.4), if the disease is relatively rare, we have for by means of age standardization)
• Stratification
a b ⇔ a+b ≈ b • Randomization
• Matching (in terms of the confounder[s]) of con-
trols with patients/subjects/index cases
and • Restriction (to restrict entry into the study
of subjects who are not affected by the
cd ⇔ c+d ≈ d confounder[s])
• Mathematical and statistical modelling
Hence, in this case, techniques
ad Summary of epidemiological findings in common psy-

Relative risk ≈ = odds ratio
bc chiatric disorders (Table 21.7 through 21.18).
TABLE 21.7
Epidemiology of Schizophrenia and Schizoaffective Disorder
Schizophrenia Schizoaffective Disorder
Incidence Approximately 15/100,000 per annum in most industrialized Incidence is not known but less common than
countries (Johnstone et al., 2004) schizophrenia
Prevalence and Adults in general population Prevalence is less than 1%, possibly in the range of
lifetime risk 1-Year prevalence: 1% 0.5%–0.8% in the United States (Sadock and
Lifetime prevalence: 1.4% Sadock, 2003)
Lifetime risk of first-degree relatives: 5%–16%
In the United Kingdom, the risk of the siblings of Afro-
Caribbean probands to develop schizophrenia is 16%. In
contrast, the risk of the siblings of Caucasian to develop
schizophrenia is 2% (Sugarman and Craufrud, 1994)
Geographic pattern Worldwide incidence is fairly similar No specific geographic pattern
Person Gender: Gender: Women > men; age of onset is later for women
• M=F than men. Male patients may exhibit antisocial
• The mortality rate in men with schizophrenia is twice of behaviour
women Age: The depressive type of schizoaffective disorder
• Men are associated with more structural brain may be more common in older than in younger
abnormalities persons. The bipolar type is more common in younger
• Women show a bimodal peak of incidence in their late adults than in older adults
20s and 50s Inheritance: There is an increased risk of schizophrenia
Age: among the relatives of probands with schizoaffective
• Onset is usually in late adolescence and young adulthood. disorder (Sadock, 2003)
• Mean onset age for men is between 15 and 25 years and
for women is between 25 and 35 years (Semple et al.,
2005)
Socioeconomic (SE) status:
• The association between schizophrenia and low social
class is now seen as a consequence rather than an
aetiology of schizophrenia
• There is social drift in people with schizophrenia as a
result of the illness, and unemployment rate can be as
high as 70%
• Low birth weight and urban birth are risk factors for
schizophrenia
• Patients in developing countries tend to have more acute
onset and better outcome than patients in developed
countries
Ethnicity:
• There is an increase in frequency of schizophrenia among
Afro-Caribbean in the United Kingdom as a result of
environmental factors (Sugarman and Craufrud, 1994)
Life events:
• Symptoms may start to appear after stressful life events
• Misuse of cannabis plays a role in people who are
homozygous for val/val in COMT gene
Disease:
• There is a negative association between rheumatoid
arthritis and schizophrenia
(continued)

Epidemiology of Schizophrenia and Schizoaffective Disorder
Schizophrenia Schizoaffective Disorder
Person Comorbidity:
• 90% are smoker (three times increase in risk as compared
to the general population) (Kelly and McCreadie, 2000)
• 60% suffer from depression
• 35%–50% misuse substances
• 10% have obsessive–compulsive symptoms (Fabisch
et al., 2001)
• 10% of schizophrenia is caused by cannabis misuse
Inheritance:
• Heritability: 82%–85% (Farmer et al., 1987; Cardno
et al., 1999)
• 40% of the first-degree relatives have abnormal smooth
pursuit eye movement
Mortality:
• At least two times higher than the general population as a
result of suicide or metabolic diseases
• Life expectancy is 10 years less than general population
• 10% commit suicide. Risk factors include male gender,
younger than 30 years, university education, paranoia,
depression, and substance abuse
Forensic aspects (Swinson et al., 2007):
• Around 50 homicides per year are committed by those in
recent contact with mental health services in the United
Kingdom. This figure represents 9% of all homicides
• 5% of homicide perpetrators have a diagnosis of
schizophrenia. This figure is much lower than the
comorbidity of alcohol and drug misuse. 60% of
homicide perpetrators have misused alcohol and drug in
the past
TABLE 21.8
Epidemiology of Mood Disorders
Depressive Disorder Bipolar Disorder Dysthymia Cyclothymia
Incidence In the United Kingdom, the 4.6/100,000 in the United One-year incidence in Unknown
incidence of depressive Kingdom adolescents is 3.4%
disorder fell from 22.5 to London: 6.2/100,000 (Garrison et al., 1997)
14.0 per 1,000 person-years Nottingham: 3/100,000
at risk (PYAR) from 1996 to Liverpool: 1.7/100,000
2006 The incidence is also increased
The incidence of depressive in people of African origin and
symptoms rose by threefold the minority ethnic groups as
from 5.1 to 15.5 per 1,000 compared with the Caucasian
PYAR (Rait et al., 2009) (Lloyd et al., 2005)
Prevalence and Prevalence in general Prevalence: In the United States, 5% of general 3%–6% of the general
lifetime risk population: 2%–5% the prevalence of bipolar I population population
Prevalence in medical disorder is 0.4%–1.6%, and the Dysthymia is more
outpatients: 5%–10% prevalence of bipolar II common than severe
Prevalence in medical disorder is 0.5% (Sadock, depressive episode in
inpatients: 10%–20% 2003) chronically medically ill
Lifetime risk for adults in the Lifetime risk for adults in the
general population general population: 1%–1.5%
Overall: 10%–20%; 1 in 4 Lifetime risk for first-degree
women and 1 in 10 men have relatives:
depressive disorder in their 4%–18% of relatives have
lifetime bipolar disorder
Lifetime risk for first-degree 9%–25% of relatives have
relatives: 20% unipolar depression
Children and adolescents: Mania in old people: 0.1%
• 0.5%–2.5% among Rapid cycling
children Rapid cycling affects
• 2%–8% among 13%–30% of bipolar patients
adolescents (Hajek et al., 2008)
Seasonal pattern:
• In the United Kingdom,
the lifetime prevalence of
major depression with a
seasonal pattern is 0.4%
• The prevalence of both
major and minor
depression with a seasonal
pattern is 1.0%
• Male gender and older
age are associated with
seasonal pattern (Blazer
et al., 1998)
Geographic People living in deprived No significant geographic No significant No significant geographic
pattern industrial areas are more pattern geographic pattern pattern
likely to be treated for Peak of admission: summer
depression than people living
in other areas
Peak of admission: spring
(continued)

Person Gender: Gender: Gender: Gender:
• F:M = 2:1 • F=M • F:M = 2:1 • F=M
Age: Rapid cycling more common Age: Age:
• The peak age of the first in women • Early onset—late • Early onset—late
onset of depression is 30 Age: adolescence or 20s adolescence or 20s
years. (>50% of depressed • The age of onset of • Late onset—30–50 • Late onset—30–50
people have their first bipolar disorder is earlier years of age, often years of age, often
depressive episode before than in unipolar disorder after a depressive after an affective
the age of 40 years) (mean age = 30 years, episode (double episode
• People younger than 40 years range: 15–50 years) depression) Life events:
are three times more likely to • The first onset is usually a SE status: • Misuse of
develop depression than older depressive episode • Common in people psychoactive
people (Coryell et al., 1992) SE status: with low income substances is a
• An older age of onset is not • Bipolar disorder is found Life events: frequent precipitant
associated with a family in occupations that require • Common in Inheritance:
history of depression creativity such as artists, unmarried • Familial aggregation
(Brodaty et al., 1991) writers, and pop stars • Early onset is in both unipolar and
Social factors: Comorbidity: associated with bipolar disorders
• Unemployment (twice the • Substance misuse: 50% childhood trauma (Stein and Wilkinson,
risk) • Attempted suicide: • Late onset often 2007)
• Separation or divorce 25%–50% occurs after a major
• Brown and Harris study: • Completed suicide: 10% depressive episode
risk factors for depression Inheritance: • Chronic life
in women: 3 or more • Genetic component plays a difficulties and
children under the age of 11 significant role in diseases (Stein and
years, unemployment, and transmitting bipolar disorder Wilkinson, 2007)
lack of confiding (Sadock and Sadock, 2003)
relationship (Brown and • Heritability: 79%–93%
Harris, 1978) (Kendler et al., 1995;
Life events: McGuiffin et al., 2003;
• Depression occurs after Kieseppa et al., 2004)
stressful life events, for Risk factors for relapse:
example, divorce, • Stopping lithium: increase in
bereavement, job loss, and risk by 28 times in 3 months
adverse childhood experience after stopping lithium)
involving loss and abuse • Substance misuse leads to
Diseases: poor response to lithium
• The first major depressive • Stressful life events
episode in old people is Mortality:
often associated with an • ↑ Risk of violent deaths by
undiagnosed neurological three times
disorder (e.g. Parkinson’s Prognosis:
disease, multiple sclerosis, • Bipolar disorder patients
cerebrovascular accident, with only manic episodes
and epilepsy) or other have better outcome than
medical disorders patients with severe
(postmyocardial infarction, depressive episode.
diabetes, and cancer) • Patients with mixed
(Robinson and Starkstein, episodes have the worse
1990) prognosis

Person Comorbidity:
• 2/3 of patients have
anxiety disorders,
substance misuse, and
personality disorders
• 1/3 of patients with
insomnia have a moderate
depressive episode
Suicide risk is increased by
20 times in patients with
depression
Inheritance:
• 55% share with the
personality trait
neuroticism
• Heritability: 33%–48%
(Kendler et al., 1992;
McGulffin et al. 1996;
Kendler and Prescott 1999)
TABLE 21.9
Epidemiology of Suicide and Deliberate Self-Harm
Suicide Deliberate Self-Harm (DSH)
Incidence • 11/100,000 for men and contribute to 2% of all male deaths 140/100,000 for men in Europe
(United Kingdom) 193/100,000 for women in Europe
• 3/100,000 for women and contribute to 1% of all female 140,000 hospital attendances per year of DSH in
deaths (United Kingdom) the United Kingdom
• Suicide accounts for 1% of all deaths in the United Kingdom
(Power, 1997)
Findings from National Confidential Inquiry into Suicide and
Homicide by People with Mental Illness (Swinson et al., 2007):
• 4500–5000 general population suicides occur per year in England
and Wales
• 160–200 psychiatric inpatients die by suicide annually; most
common method is by hanging
• 1 suicide per GP every 5 years
Prevalence and Adults: DSH among young people in the United Kingdom:
lifetime risk • Epidemiological data suggest the 12-month prevalence rate for 7%–14% (Hawton and James, 2005, Skegg,
suicide attempts is between 0.4% and 0.6% (Kessler et al., 2005)
1999, 2005) Goth subculture in the United Kingdom (Young
• 8–25 suicide attempts result in one death (Moscicki, 2001) et al., 2006):
Lifetime risk of suicide in people with alcohol misuse: 3%–4%; Lifetime self-harm: 53%
M:F = 2:1; mean age of suicide is 47 years, One-third have history 50% of people present with DSH are repeaters
of DSH and occur when patient is intoxicated with alcohol
Suicide in children and adolescents:
• Suicidal ideation: 10%
• Attempted suicide: 2%–4% of adolescents
• Suicide: 7.6 per 100,000 among the 15–19-year-olds
Goth subculture in the United Kingdom (Young et al., 2006):
• Lifetime risk of suicide attempt: 47%
Geographic and • Lithuania, Estonia, and Latvia are the countries with the highest • The rate of DSH ranges from 2% in Lebanon
temporal pattern suicide rates in the world to 20% in New Zealand
• Lithuania has the highest annual rate for men (79.3/100,000) • In England and Wales, both suicide and DSH
• China has the highest for women (17.8/100,000) (Yip and Liu, 2006) are common in the cities
• The United Kingdom has lower rate of suicide compared to other • Seasonal variation is not seen in the DSH
European countries such as France and Russia
• There are higher suicide rates in Scotland as compared to the rate
in England and Wales
• In England and Wales, suicide is more common in spring and
summer
• The suicide rate is usually reduced during war (e.g. WWII)
Person Gender: Gender:
• In the United Kingdom, the M:F ratio is 3:1 and the rate of • Women > men
women is rising Age:
• For the rest of the world, men have higher suicide rate • Peak age for women: 15–24 years
compared to women with the exception of China (Yip and Liu, • Peak for men: 25–34 years
2006). Hence, China is the only country where the M:F ratio in • The age of onset at which people first
suicide is close to 1:1 deliberately harm themselves is decreasing
Age: SE status:
• Highest suicide rates in men older than 75 years and women • More people from the lower social class
older than 65 years in England and Wales exhibit DSH
• Advancing age is a risk factor, and 90% of old people
committed suicide because of depression

Person Methods of suicide: Ethnicity and subculture:
• Psychiatric patients tend to use violent methods such as • In the United Kingdom, the rate of DSH is
hanging, shooting, and jumping from heights raised among Asian women
• 2/3 of British men and 1/3 of British women committed suicide • The Goth subculture in the United Kingdom
by hanging or vehicle exhaust fumes is strongly associated with self-harm
• Drowning is more frequent among old people Life events:
• Jumping from height is more frequent in young people who • Adverse life events (e.g. interpersonal
committed suicide conflicts) are frequently reported to have
SE status: occurred before the act of self-harm
• Poverty is associated with an increased risk of suicide Diseases:
Ethnicity: • People who deliberately harm themselves
• In the United Kingdom, immigrants from India, especially the have higher than expected incidence of
women, are at high risk physical illness and recent admissions to the
• Young Pakistani and Bangladeshi women have higher than hospital (Stein and Wilkinson, 2007)
expected suicide rates (Bhugra and Desai, 2002) DSH and suicide:
• For ethnic minorities in the United Kingdom, the most • A history of DSH is a long-term predictor of
common method of suicide is hanging suicide, and the risk of suicide is 100 times
• Violent methods are more common than among ethnic greater than that of general population
minorities as compared to the Caucasians • 15% of people attempting self-harm will have
• People of Afro-Caribbean origin who committed suicide have another episode within 1 year
the highest rates of schizophrenia (74%), unemployment, • 1% of patients eventually kill themselves in
living alone, previous violence, and drug misuse (Isabelle the year following DSH
et al., 2003) • 3%–5% of patients kill themselves in the
Social factors: 5–10 years following DSH
• Higher risk in the low and high social class Prevention:
• Low risk in the middle social class • A contact card scheme such as the Bristol
• Suicide rates in the divorced and widowed are higher than Green Card Scheme reduces the admission
people who are married rate associated with DSH
• Unemployment, low SE status, and certain occupations such
bar owners, doctors, pharmacists, artists, and farmers are risk
factors
• Institutions, for example, prisons
• Organization with easy access to firearms: army and police
• Suicide attempts occur after significant life events are
common among people with poor social support and living
alone
Diseases:
• Previous suicide attempt
• Concurrent mental disorders: severe depression, bipolar
depression, postnatal depression, postpartum psychosis, and
alcohol and drug abuse
• Young men recovered from schizophrenia and regain insight
• Chronic medical illnesses associated pain
• Anhedonia, alcohol misuse, and anxiety are short-term
predictors of suicide
(continued)

Person • Two in five people who committed suicide saw their GP in the
week preceding their suicide (Power, 1997)
• One in four contacted the mental health service in the year
before their death
Post-discharge suicide:
• In the United Kingdom, nearly a quarter of the inpatient deaths
occur within the first 7 days of admission
• 30% occur on the ward, and the most common method is hanging
• Post-discharge suicide is most frequent in the first 2 weeks
after leaving hospital, and the highest number occurred on the
first day (Meehan et al., 2006)
Inheritance:
• The tendency to attempt suicide is associated with familial
pattern through the inheritance of depressive disorder or
modelling
TABLE 21.10
Epidemiology of Anxiety Disorders
Generalized Anxiety
Disorder (GAD) Panic Disorders Social Phobia Agoraphobia
Incidence GAD: 4.3% (Beesdo et al., General population: General population: Large numbers of people in
2010) One-year incidence: 10% One-year incidence: 6% the community who have
Other anxiety disorders: For patients presenting to agoraphobia without panic
23% (phobia or panic emergency departments disorder do not seek help
disorder) (Beesdo et al., with chest pain, 25% have In the United States, about
2010) panic disorder (Ham et al., 2/1000 PYAR (Bienvenu
2005) et al., 2006)
Prevalence and General adults: General adults: Lifetime prevalence: 6% Lifetime prevalence: 4%
lifetime risk One-year prevalence: Lifetime prevalence is 8.6% Children and adolescents: (Stein and Wilkinson, 2007)
3%–8% in the United Kingdom Social phobia: 1% 6-month prevalence: 3%–6%,
Children and adolescents: (Birchall et al., 2000) Simple phobias: 2%–9% 4% for women and 2%
The prevalence is 2%. Girls First-degree relatives of Specific phobia: 3% for men
have higher rates of panic disorder:
anxiety disorders than 8%–31%
boys Children and adolescents:
Old people: <1%
The prevalence of old
people (> 65-year-old) is
5%–15%
Women > Men Women > Men The F:M ratio may be closer Women > Men
Age: Age: to 1:1 in social phobia Age:
The mean age of onset is Bimodal peak: 15–24 years Age: 25–35 years
usually in the 20s and 45–54 years First onset: 11–15 years Agoraphobia may occur
Life events: Life events: Life events: being criticized before the onset of panic
Life event is an important Recent history of divorce or or scrutinized and resulted disorder
precipitant for anxiety separation (Sadock, 2003) in humiliation SE status: common in
disorder, and it may Disease: Psychiatric comorbidity: housewives
lead to alcohol misuse Mitral valve prolapse depressive disorder and Life events: Onset usually
Comorbidity: (20%), hypertension, alcohol misuse and an follows a traumatic event
GAD is probably the most cardiomyopathy, COPD, increased rate of DSH (Sadock and Sadock, 2003)
common psychiatric and irritable bowel Inheritance: Social phobia Disease:
disorder that coexists with syndrome is more common among Half of patients have panic
another psychiatric relatives of patients with disorder as well (Sadock
disorder (e.g. social social phobia as compared and Sadock, 2003)
phobia, specific phobia, to the general population
panic disorder, and (Gelder et al., 2001)
depressive disorder)
Endocrine disorders such as
hyperthyroidism are
associated with anxiety
symptoms
(continued)

Epidemiology of Anxiety Disorders
Generalized Anxiety
Disorder (GAD) Panic Disorders Social Phobia Agoraphobia
Person Inheritance: Comorbidity: Comorbidity:
Genetic factors play a role. • Depressive disorder • Panic disorder
(70%) • Depression
• Social phobia (50%) • Other anxiety disorders
• Agoraphobia (40%)
• Alcohol misuse (30%)
Inheritance:
• Heritability: 44%
(Kendler et al., 1992)
• Risk is increased by five
times for developing
panic disorder in the
first-degree relatives of
probands with panic
disorder
TABLE 21.11
Epidemiology of OCD Spectrum Disorders and Post-Traumatic Stress Disorder
Obsessive–Compulsive Disorder Body Dysmorphic Disorder
(OCD) (BDD)/Dysmorphophobia Post-Traumatic Stress Disorder
Incidence 0.55 per 1000 person-years (Nestadt Unknown On average, about 10% of people
et al., 1998) experiencing a significant traumatic event
actually go on to develop PTSD (Kessler
et al., 1995)
Prevalence and Prevalence: 1% One-year prevalence: 0.77% Lifetime prevalence: 1 in 100
lifetime risk Lifetime prevalence: 2%–5% (Phillips, 2004) Prevalence based on circumstances:
Children and adolescents Affecting 1 in 200 people in the 1 in 5 fire fighters
2 in 100 children and adolescents community 1 in 3 teenager survivors of car crashes
1%–13% of boys 1 in 2 female rape victims
1%–11% of girls 2 in 3 prisoners of war
Person Gender: Gender: women > men Gender:
F:M = 1.5:1 Age: between 15 and 30 years old. F:M = 2:1
Women: Compulsive washing and Onset is in adolescence. Men’s trauma is due to combat experience,
avoidance are more common. SE status: People with BDD are and women’s trauma is related to assault
Men checking rituals or ruminations likely to be unmarried. or rape
(more common) Comorbidity: BDD may be comorbid Age: most prevalent in young adults
Age: Mean age of onset is around with depression (60%), SE status: low SE status and low education;
20 years (70% before 25 years, trichotillomania (26%), social phobia other factors: those single, divorced,
15% after 35 years). Men have (11%–13%), substance misuse, OCD widowed, and socially withdrawn
early age of onset (adolescence) (8%–37%), and suicide attempt Ethnicity: Afro-Caribbean/Hispanic
One of the commonest psychiatric (25%) (Phillips, 2004) Comorbidity:
disorders in children, affecting Inheritance: BDD are found in 10% Depression
1%–5% of children and of family members of the probands. Anxiety disorders
adolescents in community samples Frequencies of imagined defects Alcohol misuse
SE status: 50% of OCD patients are (Phillips, 2004): Inheritance: First-degree biological relatives
unmarried Skin 70% of persons with a history of depression have
Disease: Pediatric autoimmune Hair 55% an increased risk for developing PTSD
neuropsychiatric disorders Nose 40% following a traumatic event
associated with streptococcal Stomach/breast/eyes/thighs/teeth: 20%
infections. Postencephalitis Ugly face: 15%
Comorbidity:
Avoidance, histrionic, and
dependent personality traits (40%)
Tic disorder (40%)
Depression (60%)
Inheritance: OCD occurs in 10% of
the first-degree relatives of
patients, compared with 2% in
general population
TABLE 21.12
Epidemiology of Somatization Disorder and Hypochondriasis
Somatization Disorders (Briquet’s Syndrome) Hypochondriasis
Prevalence General population: 4% In medical outpatients: approximately 5%
Medical patients:10%–20% (Barsky et al., 1990)
Primary care: 70% of patients with emotional Transient hypochondriasis is common
disorder present in primary care with a somatic
complaint
Lifetime prevalence of somatoform pain disorder
is 10%
one in five surgery attenders has chronic somatic
symptoms longer than 2-year duration
F:M = 2:1 Men = women
Age: Age:
Between 20 and 30s; before the age of 30 years Peak incidence: 40–50-year-olds.
Comorbidity: Life events:
• Depression in 40% of people with An adverse childhood environment (e.g.
somatoform pain disorder sexual abuse, domestic violence, parental
• Substance misuse: Opioid or analgesic is upheaval) can predispose to hypochondriasis
common Comorbidity:
Diseases: • GAD (50%)
Complicated medical history with spurious • Other comorbidities: depression, OCD,
physical diagnosis and panic disorder
Family:
• Family history of psychopathy or alcoholism,
broken home, early abuse, and school refusal
• Exposure to parents who are sensitive to
body discomfort
TABLE 21.13
Epidemiology of Eating Disorders
Anorexia Nervosa (AN) Bulimia Nervosa (BN)
Incidence • 14.6/100,000 in women Incidence in primary care in the Netherlands: 11.4/100,000
• 1.8/100,000 in men (1985–1989) (Hoek, 1991)
• 20/100,000 for women aged 10–39 within primary care
Prevalence In adolescence: In adolescence:
• 0.5% of 12–19-year-olds Increased over the past three decades. Among young women: 1%
• 8–11 times more common in girls 1% of adolescent girls and young women
• Among 15-year-old school children In adults:
• 700 per 100,000 (girls) and 90 per 100,000 (boys) BN: 1%–2%
In adults:
• AN: 0.5%
• Eating problems not meeting full diagnostic criteria: 5%
F:M = 10:1 F:M = 10:1
Age: Age:
• Mean age: 15/16 years Median age = 18 years
• Median age: 17 years SE status:
SE status: All social classes are affected
• Higher social class Ethnicity:
• Certain social groups: dancers and athletes In Hong Kong, BN has become more common, and the pattern
Ethnicity: is similar to Western countries (Lee et al., 2009)
• The clinical profile of eating disorders in Hong Kong has Life events:
increasingly conformed to that of Western countries (Lee • BN seems to arise as a result of exposure to premorbid
et al., 2009) dieting and other risk factors (premorbid and parental
• AN exhibited an increasingly fat-phobic pattern obesity, innate tendency to overeat and enjoy food, critical
• Nonfat-phobic AN patients exhibited significantly lower comments about weight, shape, and eating)
premorbid body weight, less body dissatisfaction, less Other risk factors include depression, alcohol and substance
weight control behaviour, and lower EAT-26 scores than misuse during childhood, low parental contact and high
fat-phobic AN patients parental expectations, abuse, and neglect
Risk factors: Comorbidity:
• History of sexual abuse, alcohol and substance misuse, • Additional psychiatric features are common; depressive
enmeshed family relationship, and IDDM and anxiety symptoms predominate
Life events: • Patients often have problems of impulse control:
• For fat-phobic AN patients, episode of AN is precipitated self-mutilation (10%), suicide attempts (30%), promiscuity
by negative remarks made by the others on their body (10%), and shoplifting (20%)
images Genetics:
• In Singapore, some young, nonfat-phobic AN patients • Familial disposition
develop the first episode of AN before public examinations • The risk for first-degree relatives is increased fourfold
Comorbidity: Prognosis
• >80% of people with AN have additional psychiatric • 20% continue to have BN after 2–5, and a further 25% still
comorbidity during the course of their lives had bulimic symptoms
• Depression (70%) and OCD (30%) are most frequent • The use of purgative is a poor prognostic factor (Wihelm
comorbidity and Clarke, 1998)
• Suicide rate is increased by 32 times in AN patients
compared to general population
(continued)

Epidemiology of Eating Disorders
Anorexia Nervosa (AN) Bulimia Nervosa (BN)
Person Genetics:
• AN is more common in monozygotic twins compared to
dizygotic twins
• Depression and OCD are common among first-degree
relatives of AN patients (Stein and Wilkinson, 2007)
Mortality:
• The risk is increased by five times in AN patients compared
to general population
Prognosis
• 50% of patients have good recovery with normalization in
three outcome parameters: weight, menstrual pattern, and
eating behaviour
• 30% of patients have fair outcome with improvement in
one to two parameters
• 20% have poor outcome with no improvement and result in
death
• Persistent vomiting is a poor prognostic factor (Wihelm
and Clarke, 1998)
Poor prognostic factors for both AN and BN: lower initial body
weight, failure to respond to treatments, disturbed family
relationships, and severe personality disorder
TABLE 21.14
Epidemiology of Personality Disorders
Borderline Personality Disorder (BPD) Antisocial Personality Disorder (ASPD)
Prevalence Community: 0.7%–2.0% (Coid, 2003) Community: 0.6%–3.0% in the community (Coid, 2003)
Elderly: 0.8%
Psychiatric inpatients: 15% (Widiger and Weissman, 1991)
Geographic The clinical profiles of BPD in Eastern countries have increasingly • W estern societies emphasize on individualization,
pattern conformed to that of Western countries competitiveness, and rivalry between individuals that
may promote the expression of antisocial behaviours
• In contrast, collectivistic culture in Eastern societies
may put less emphasis on individualization but more
concerns of the consequence of one’s behaviour. This
leads to less antisocial behaviour in Eastern countries
• Higher rates are found in urban rather than rural
settings
• F:M = 3:1 • M:F = 6:1
• Men with BPD compared with men suffering from other Age:
personality disorders have shown more evidence of • There is a 10-fold increase in antisocial behaviours
dissociation, image distortion, frequency of childhood sexual during adolescence
abuse, longer experiences of physical abuse, and experiences Family background:
of loss at an early age • Parental criminality, parental aggression, poor
• Research suggests that men with BPD are more regularly supervision from parents, harsh and erratic discipline,
diagnosed with substance abuse problems than women and being rejected as a child
with BPD SE status:
Age: • Social adversity
• Onset is in adolescence and early 20s • Parental criminal behaviours
• Three-quarters of people with BPD are women and usually • Maternal deprivation
within childbearing age • Paternal alcohol misuse
Life events: • Low education background and association with
• Childhood physical or sexual abuse (between 40% and 70% conduct disorder
of people with BPD report having been sexually abused, often Comorbidity:
by a noncaregiver) • Alcoholism and substance misuse are common
Comorbidity • Among women, there is an association with
• Substance misuse (15%) and bulimia are common somatization disorder
comorbidity (Zimmennan and Mattia, 1999) • Inpatients have higher rates of psychiatric comorbidity
• Rapid and reactive shifts into depression are common (60%); Genetics: MZ: DZ = 60%:30% (Sadock, 2003)
affective instability, impulsive behaviour, and panic attacks
may occur (30%)
• 10% commit suicide (Work Group on Borderline Personality
Disorder, 2001)
Genetics:
• Increased prevalence of major depression and alcohol and
other substance misuse disorders is reported in first-degree
relatives
Poor prognosis:
Poor prognostic factors include sexual abuse in childhood and
victims of incest (Paris et al., 1993; Stone, 1993)
Mortality:
1 in 10 committed suicide
TABLE 21.15
Epidemiology of Substance Misuse
Alcohol misuse • Among British adults, 75% are normal drinkers, 8% are abstainers, 8% are hazardous drinkers, 5% are harmful
drinkers, and 4% are dependent on alcohol
• If the father is dependent on alcohol, the child has 80% chance to develop alcohol misuse. Hence, the risk is around four
times higher than a child whose father is not dependent on alcohol
• The lifetime risk for alcohol dependence: 10% for men and 3%–5% for women
• The prevalence of abuse: 20% for men and 10% for women
• The lifetime prevalence of psychiatric comorbidity (e.g. PTSD, depression) for women with alcohol abuse is as high as 70%
• Women are more likely to develop medical complications at a younger age as compared to men
Substance misuse • For adolescents and young adults in the United Kingdom, 50% have taken illicit drugs at some point in time. 20% used
illicit substance in the previous month. 5% used at least two substances in the past 1 month
• The peak age of substance misuse is 20 years
• M:F = 3:1
• For opiate misuse, mortality is increased by 12 times, and suicide rate is increased by 10 times
Source: Mynors-Wallis, L. et al., Shared Care in Mental Health, Oxford University Press, Oxford, U.K., 2002.
TABLE 21.16
Epidemiology of Common Psychiatric Disorders in Childhood and Adolescence
Attention Deficit and
Hyperkinetic Disorder
(ADHD) Autism Conduct Disorders School Refusal and Truancy
Incidence • <1.0% (United 5 per 10,000 (United States) 1.0%–10.0% Not known
Kingdom)
• 3.0%–7.0% of
prepubertal elementary
school children (United
States)
Prevalence • 1.7% of primary school 2/10,000 • 6.2%–10.8% among • Data from National
boys 10-year-olds Centre for Health
• 1 in 200 in the • Boys: 9% Statistics (United
population suffers • Girls: 2% States) [National Centre
severe hyperkinetic • 33%–50% among child for Health Statistics
disorders psychiatric clinic 1993]: 5 school-loss
attendees days per person
(5–17-year-olds) were
caused by acute and
chronic conditions
• 4 school-loss days per
person (5–17-year-olds)
were caused by acute
conditions only
Person Gender: Gender: Gender: Gender and ethnicity for
M:F = 2:1–9:1 M:F = 4:1–5:1 Girls with M:F = 4:1–12:1 school refusal: Caucasian
Age: autism are more likely to Age: girls have higher rate of
Symptoms present by suffer from severe learning Certain behaviours such as absence for acute reasons and
3 years of age but not disability truancy begin before the chronic reasons in
diagnosed until older than Age: age of 13 years comparison to boys of
7 years Onset is before the age of SE status: Low Afro-Caribbean origin (Berg
Comorbidity: 3 years Family environment: and Nursten, 1996)
• Conduct disorder and Disease: Harsh, punitive Age of onset (school refusal):
oppositional defiant • Association with fragile parenting, family • Between 5 and 7
disorder: 50%–80% X syndrome (≈1% of discord, lack of • At 11 years
• Academic difficulties autistic children) appropriate • Especially at 14 years and
• Anxiety and depressive • Tuberous sclerosis parental supervision, and older
disorders (up to 2%) lack of social Age of onset (truancy):
Genetics: Genetics: competence • 5% before age of 8
• First-degree biological Evidence suggests that two Genetics: More common in • Median age is 14 years
relatives are at high risk regions on chromosomes 2 children with parents (Berg and Nursten, 1996)
to develop ADHD and 7 contain genes related suffering ASPD and
to autism alcohol dependence than in
general population
(continued)

Epidemiology of Common Psychiatric Disorders in Childhood and Adolescence
Attention Deficit and
Hyperkinetic Disorder
(ADHD) Autism Conduct Disorders School Refusal and Truancy
Person • Parents of children with Prognosis: SE status (school refusal): The
ADHD show an • 40% will become rate of school refusal is
increased incidence of delinquent young adults inversely related to family
hyperkinesis, (Goodman and Scott, income (Adams and Bensen,
sociopathy, alcohol 2005) 1992)
misuse, and conversion • Early onset of conduct Life events (school refusal):
disorder disorder is associated Illnesses and family
Risk factors: Parental with higher than to problems (e.g. caring for a
exposure to alcohol, develop ASPD in young sibling, violence, and
nicotine, and maternal adulthood bullying in school)
toxaemia (Sadock, 2003) Comorbidity associated with
school refusal: Separation
anxiety (younger children),
school phobia, and
depressive disorder (older
children)
Prognosis of truancy (Berg
and Nursten, 1996):
Boys: Drug misuse (30%),
antisocial personality (25%),
and phobia (20%)
Girls: Phobia (32%), drug
misuse (25%), and antisocial
personality (11%)
TABLE 21.17
Epidemiology of Common Psychiatric Disorders in Postpartum Period
Postnatal Blues Postpartum Depression Postpartum Psychosis
Incidence 50% of women 10%–15% in the first year of the postnatal period • 1.5 per 1000 childbirths
• Affective presentation: 70%
• Schizophreniform presentation: 25%
• Confusion: 5%
Geographic pattern No geographic pattern • Lower incidence rates in some countries No geographic pattern
(e.g. Japan)
• Higher in deprived inner city areas
• In India, social status of women is lower
than men. The birth of a female infant
often leads to disappointment
Person Onset: Onset: within 6 weeks postdelivery Onset: within first 2 weeks following
The third to tenth day SE status: unemployment and lack of delivery
postpartum supportive relationship SE status: little evidence for psychosocial
Prognosis: Life events: unhappy marriage, relationship causation
Postnatal blues usually problems with partner, absence of a confiding Diseases: Some cases are caused by general
resolve in 2–3 days relationship, other young children at home, medical conditions associated with
ambivalent feelings of becoming a mother, perinatal events (infection, drug
and delivery of a premature and unwell baby intoxication, and blood loss)
Past history: Patients have often experienced Past psychiatric history: schizophrenia or
anxiety and depressive symptoms in the last affective disorders (20%–50%)
trimester of pregnancy. Past depressive Family: About 50% of affected women have
episode is also a risk factor a family history of mood disorders
Prognosis: Each episode of postnatal Prognosis:
depression lasts 2–6 months • 70%: full recovery
• 50%: risk of future psychotic episodes
• 20% risk of future puerperal psychosis
TABLE 21.18
Epidemiology of Common Psychiatric Disorders in Old People
Late Onset Psychosis/Late
Dementia Depression Suicide Paraphrenia
Incidence Risk increases with age: 1% 8.4% (Harris et al., 2006) 40 per 100 000 10–26 per 100, 000 per year
at 60 years old and doubles
every 5 years (Semple
et al., 2005)
Prevalence • 1 in 20 people older • Prevalence of depressive Not applicable • Overall: 0.1%–4%
than 65 years and 1 in 5 symptoms: 15% • First onset of
older than 80 years schizophrenia after the
develop dementia age of 60 is very rare
• Alzheimer’s disease: 50% • 2%–4% major depression
• 12%–20% minor degree
of depression
• Vascular dementia: 20% • 80% of old people who • Only 1.5% of all people
committed suicide with schizophrenia have
suffer from depression onset older than 60 years
• Lewy body • 20% of elderly • 60% of people with late
dementia: 15% inpatients fulfil the paraphrenia resemble
diagnostic criteria for paranoid schizophrenia
depression
M=F Elderly women have higher M:F = 3:2 F:M = 3:1
Age: prevalence SE status: SE status:
Risk increases with age: 2% at SE status: Financial problem is a risk • Social isolation (80% of
the age 65–70 and 20% No instrumental social factor people with late
at the age of 80 and above support, social isolation, Life events: widowhood paraphrenia are socially
Risk factors: smoking, financial difficulty, nursing Disease: Physical illness isolated)
sedentary lifestyle, home resident are less likely (e.g. chronic pain, terminal • Single and never married
high-fat/salt diet, head to be treated by GP for illness) is a major risk Comorbidity:
injury depression as compared to factor. Personality factors • Sensory
Disease: high blood adults and younger people and depression are impairment in hearing and
pressure, high cholesterol, Life events: important associated factors vision
and obesity; learning Widowhood and having • People with late
disability and Down chronic illness associated paraphrenia are four times
syndrome with functional limitation more likely to suffer from
Family: Genetic risk of and poor self-rated health hearing impairment
Alzheimer’s disease is are precipitating factors to • Neurological
associated with depression disorders are common
apolipoprotein E4 (APOE4) Genetics: Family history: Family history
allele Genetic factors are less of schizophrenia is a risk
Family history of Down important (cf depression in factor for late paraphrenia
syndrome and Parkinson’s young people) Relatives of people with late
disease also increases the Comorbidity: Depression is paraphrenia are 3.5 times
risk of dementia the most common cause of more likely to develop
obsessional symptoms in old schizophrenia as compared to
people. Depression is more the general population
common in mild dementia
than in severe dementia
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22 Biostatistics
22.1 DESCRIPTIVE AND 22.1.3.3 Simple Hypothesis

INFERENTIAL STATISTICS A simple hypothesis is one involving a single value for
the population parameter.
22.1.1 Descriptive Statistics
Descriptive statistics are ways of organizing and describ- 22.1.3.4 Composite Hypothesis
ing data. Examples include A composite hypothesis is one involving more than one
value for the population parameter.
• Diagrams
• Graphical representations
22.1.3.5 One-Sided Significance Test
• Numerical representations
• Tables A one-sided significance test is a hypothesis test involv-
ing a composite alternative hypothesis of the following
types:
22.1.2 Inferential Statistics
Inferential statistics allow conclusions to be inferred from • H1: θ > θ 0
data. An example is inferring a likely range of values for • H1: θ < θ 0
the population mean from the sample mean.
22.1.3.6 Two-Sided Significance Test
22.1.3 Hypothesis Testing: Significance Tests A two-sided significance test is a hypothesis test involv-
ing a composite alternative hypothesis of the following
A value or range of values for an unknown population type:
parameter is hypothesized. A study/experiment is then
carried out, and the value of the observed random vari- • H1: θ ≠ θ 0
able is used to test whether or not the hypothesis should
be rejected. 22.1.3.7 Critical Region
22.1.3.1 Null Hypothesis The critical region is the region of the range of the ran-
The initial hypothesis is the null hypothesis, H0, usually dom variable X such that if the observed value x falls in
representing no change: it, the null hypothesis, H0, is rejected.
H 0 : θ = θ0 22.1.3.8 Critical Value

The critical value(s) is (are) the value(s) of the test statistic
where expected from the null hypothesis, H0, that defines the
θ is the unknown parameter boundary (boundaries) of the critical region.
θ 0 is its hypothesized value
22.1.3.9 Significance Level
22.1.3.2 Alternative Hypothesis The significance level, α, is the size of the critical region
The alternative hypothesis, H1, may, for example, be one and represents the following probability:
of the following types:
• H1: θ ≠ θ 0 α = P(Type I error )

• H1: θ > θ 0
• H1: θ < θ 0 where a type I error is the error of wrongly rejecting H0
• H1: θ = θ1 when it is true.
305
22.1.3.10 Steps in Carrying Out a The two-sided central confidence interval for the
Significance/Hypothesis Test unknown parameter θ of a distribution with confidence
Hypothesis testing is carried out as follows: level (1 − α) can be derived from the random interval of
the following type:
• Formulate H0.
• Formulate H1. (θ− ( X ), θ+ ( X ))
• Specify α.
• Decide on the study/experiment to be carried out.
• Calculate the test statistic. By substituting the observation x for X, the realization of
the random interval
Test statistic (θ− ( x ), θ+ ( x ))

Appropriate statistic − Hypothesized parameter
=
Standard error of statistic is the two-sided central confidence interval for θ, in which
• θ−(x) = lower confidence limit (confidence bound)

• From the sampling distribution of the test statistic, for θ.
create the test criterion for testing H0 versus H1. • θ+(x) = upper confidence limit (confidence bound)
• Carry out the study/experiment. for θ.
• Calculate the value of the test statistic from the
sample data.
• Calculate the value of the difference, d, between
22.1.5 Advantages of Confidence
the value of the test statistic from the sample Intervals Over p Values
and that expected under H0 (the critical value(s), There has been a recent move away from simply quoting
defining the critical range). p values in psychiatric research to giving instead, or addi-
• If P(d) < α, the result is statistically significant tionally, the corresponding confidence intervals. Advantages
at the level of α (the 'p value') and H0 is rejected. of estimation over hypothesis testing include the following:
• If P(d) ≥ α, the result is not statistically signifi-
cant at the level of α and H0 cannot be rejected. • Testing the null hypothesis is often inappropriate
• If H0 is composite, the hypothesis test is designed for psychiatric research; for example, they may
so that the critical region size is the maximum reverse an investigator’s idea (for instance, that a
value of the probability of rejecting H0 when it new treatment will be more effective than a cur-
is true. rent one) and substitute instead the notion of no
effect or no difference.
• A hypothesis test evaluates the probability of the
22.1.4 Estimation: Confidence Intervals
observed study result, or a more extreme result,
From sample statistics, confidence statements can be occurring if the null hypothesis was in fact true.
made about the corresponding unknown parameters, • Proper understanding of a study result is obscured
by constructing confidence intervals. A confidence in hypothesis testing by transforming it onto a
interval can be two sided or one sided; two-sided con- remote scale constrained from zero to one.
fidence intervals need not necessarily be symmetrical • Obtaining a low p value, particularly p < 0.05, is
(central). widely interpreted as implying merit and leads
If a 100(1 − α)% confidence interval from a statistic (or to the findings being deemed important and pub-
statistics) is calculated, this implies that if the study were lishable, whereas this status is often denied study
repeated with other random samples taken from the same results that have not achieved this arbitrary level.
parent population and further 100(1 − α)% confidence • The p value on its own implies nothing about the
intervals similarly individually calculated, the overall magnitude of any difference between treatments.
proportion of these confidence intervals that included • The p value on its own implies nothing even
the corresponding population parameter(s) would tend to about the direction of any difference between
100(1 − α)%. treatments.
Biostatistics 307
• This overemphasis on hypothesis testing and If the population variances cannot be assumed to be
the use of p values to dichotomize results into equal, then the standard error is given by
significant and nonsignificant have detracted
from more useful procedures for interpreting
s12 s22
the results of psychiatric research. Standard error of difference = +
• Levels of significance are often quoted alone in n1 n2
the abstracts and texts of published papers with-
out mentioning actual values, proportions, and
22.2.1.2 Paired Samples t-Test
so on, or their differences.
• Confidence intervals do not carry with them the This procedure tests the null hypothesis that two popula-
pseudoscientific hypothesis testing language of tion means are equal when the observations for the two
significance tests. groups can be paired in some way. Pairing (a repeated
• Estimation and confidence intervals give a plau- measures or within-subjects design) is used to make the
sible range of values for the unknown parameter. two groups as similar as possible, allowing differences
• Inadequate sample size is indicated by the rela- observed between the two groups to be attributed more
tively large width of the corresponding confi- readily to the variable of interest.
dence interval. For n pairs, the appropriate standard error is given by
sd
Standard error of difference of paried observation =
22.2 SPECIFIC BIOSTATISTICAL TESTS n
22.2.1 t-Test
The t-test is used for testing the null hypothesis that two where sd is the standard deviation of the differences of the
population means are equal when the variable being paired observations.
investigated has a normal distribution in each population
and the population variances are equal; that is, the t-test
is a parametric test. 22.2.2 Chi-Square Test
The chi-square (χ2) test is a nonparametric test that can
22.2.1.1 Independent Samples t-Test be used to compare independent qualitative and discrete
This procedure tests the null hypothesis that the data are quantitative variables presented in the form of contin-
a sample from a population in which the mean of a test gency tables containing the data frequencies.
variable is equal in two independent (unrelated) groups
of cases. 22.2.2.1 Null Hypothesis
Assuming equal population variances (which can
For a given contingency table, under H0,
be checked using Levene’s test), the standard error
of the difference between two means, x–1 and x–2 , of
two independent samples (taken from the same par- (Row total)(Column total)
Expected value of a cell =
ent population) of respective sizes n 1 and n 2 and Sum of cells
respective standard deviations s 1 and s 2 , (s 1 ≈ s 2) is
given by
22.2.2.2 Calculation of χ2
The value of χ2 for a contingency table is calculated from
1 1
Standard error of difference = s +
n1 n2
 (O − E )2 
where the pooled standard deviation s is given by
χ2 = ∑ 
 E


where
(n1 − 1)s12 + (n2 − 1)s22
s= O is the observed value
(n1 + n2 − 2) E is the expected value
In order to use the χ2 distribution, the number of degrees 22.2.2.5 Goodness of Fit
of freedom of a contingency table, ν, is given by The χ2 test can be used to test how well an observed
distribution fits a given distribution, such as the normal
ν = (r − 1)(k − 1)
distribution. This can be applied to both discrete and
where continuous data and tests the hypothesis that a sample
r is the number of rows derives from a particular model.
k is the number of columns
22.2.2.3 2 × 2 Contingency Table 22.2.3 Fisher’s Exact Probability Test

A 2 × 2 contingency table has one degree of freedom This test determines exact probabilities for 2 × 2 contin-
(Table 22.1). gency tables. With the nomenclature of Table 22.1, the
For a 2 × 2 contingency table, the following formula formula used is
can be used to calculate χ2:
(az − by)2 (a + b + y + z) ( a + y )!( b + z )!( a + b )!( y + z )!

χ2 = Exact probability of table =
(a + b)( y + z)(a + y)(b + z) (a + b + y + z)!a!b!y!z!
22.2.2.4 Small Expected Values In order to test H 0, in addition to calculating the prob-
For a contingency table with more than one degree of ability of the given table, the probabilities also have
freedom, the following criteria (Cochran, 1954) should to be calculated of more extreme tables occurring by
be fulfilled for the test to be valid: chance.
• Each expected value ≥ 1.

• In at least 80% of cases, expected value > 5. 22.2.4 Mann–Whitney U Test
This is a nonparametric alternative to the independent
For a 2 × 2 contingency table, all the expected values
samples t-test. The test statistic, U, is the smaller of U1
need to be at least 5 in order to use the aforementioned
and U2:
formula; therefore, the overall total must be at least 20.
If the total is less than 20, Fisher’s exact probability test
can be used. If 20 ≤ total < 100, then a better fit with 1
U1 = n1n2 + n1 (n1 + 1) − R1
the continuous χ2 distribution is provided by using Yates’ 2
continuity correction:
1
2 U 2 = n1n2 + n2 (n2 + 1) − R2
χ2corrected =
{ az − by − 1/2(a + b + y + z)} (a + b + y + z ) 2
(a + b)( y + z)(a + y)(bb + z )
where
n1 is the number of observations in the first group
TABLE 22.1 n2 is the number of observations in the second group
Observed Values in a 2 × 2 R1 is the sum of the ranks assigned to the first group
Contingency Table R2 is the sum of the ranks assigned to the second group
— — Total For n1 ≥ 8 and n2 ≥ 8, U ≈ N (μ, σ2), where

— a y a+y
— b z b+z
n1n2
Total a+b y+z a+b+y+z µ=
2
Source: Reproduced from Puri, B.K., Statistics
n1n2 (n1 + n2 + 1)
for the Health Sciences, WB Saunders,
London, U.K., 1996. With permission. σ2 =
12
Biostatistics 309
22.2.5 Confidence Interval for the where

Difference between Two Means n1 and n2 are the sample sizes
n1 > 25
The 100(1 − α)% confidence interval for the difference n2 > 25
between two means is given by K is rounded up to the nearest integer
Difference − t1− α / 2 (Standard error of difference) The total number of possible differences is equal to n1n2.
The 100(1 − α)% confidence interval for the median
To → Difference t1− α / 2 (Standard error of difference) of these differences is from the Kth smallest to the Kth
largest of the n1n2 differences (K ∈ ℤ+).
22.2.6 Confidence Interval for the Difference If n1 and/or n2 is less than or equal to 25, then tables
based on the value of the corresponding Mann–Whitney
between Two Proportions
test statistic can be used.
For large sample sizes and population proportions not too
close to 0 or 1, the 100(1 − α)% confidence interval for the 22.2.7.2 Two Paired Samples
difference between two proportions is given by In this case, the value of K is calculated from
Difference − z1− α / 2 (Standard error of difference) n(n + 1) n(n + 1)(2n + 1)

K= − z1− α / 2
4 24
To → Difference + z1− α / 2 (Standard error of difference)
where
n is the number of paired cases
where the standard error of the difference is given by n > 50
K is rounded up to the nearest integer
pˆ 1 (1 − pˆ 1 ) pˆ 2 (1 − pˆ 2 )
Standard error of difference = + The total number of possible means of two differences
n1 n2
(including differences with themselves) is equal to n(n + 1)/2.
The 100(1 − α)% confidence interval for the median
where of these mean differences is from the Kth smallest to the
p̂1 is the sample estimate of first proportion Kth largest of the n(n + 1)/2 mean differences (K ∈ ℤ+).
p̂2 is the sample estimate of second proportion If n ≤ 50, then tables based on the value of the corre-
n1 is the sample size of the first group sponding Mann–Whitney test statistic can be used.
n2 is the sample size of the second group
22.3 MORE COMPLEX METHODS
22.2.7 Confidence Interval for the 22.3.1 Factor Analysis
Difference between Two Medians
Factor analysis is an attempt to express a set of multi-
For the following confidence intervals to be valid, the variate data as a linear function of unobserved, underly-
assumption is made that the two distributions whose pos- ing dimensions or (common) factors together with error
sible difference is being estimated have the same shape terms (specific factors). The common factors associated
but may differ in location. with each observed variable have individual loadings.
22.2.7.1 Two Unpaired Samples

22.3.2 Principal Components Analysis
In order to determine the 100(1 − α)% confidence interval
for the difference between two medians, the value of K Principal components analysis is used to produce
must first be calculated from uncorrelated linear combinations of the observed vari-
ables of a multivariate dataset. The first component has
maximum variance. Successive components account for
n1n2 n n (n + n + 1)
K= − z1− α / 2 1 2 1 2 progressively smaller parts of the total variance. Each
2 12 component is uncorrelated with preceding components.
A plot of the variance of each principal component 22.3.8 Canonical Correlation Analysis

against the principal component number is known as a
scree plot. This is an extended form of multivariate regression in
which the number of dependent variables is no longer
confined to one. The maximum correlation between the
22.3.3 Correspondence Analysis set of independent variables and the set of dependent
variables is known as the canonical correlation and gives
A correspondence analysis is similar to a principal com- information about interrelationships among the variables.
ponents analysis but is applied to contingency tables. It
allows a 2D contingency table to be presented as a 2D
graph in which one set of coordinates represents the rows 22.4 META-ANALYSIS, SURVIVAL ANALYSIS,
of the table and the other set represents the columns. AND LOGISTIC REGRESSION
Rather than partitioning the total variance, as in principal
components analysis, there is a partition of the value of χ2 22.4.1 Meta-Analysis
for the contingency table.
22.4.1.1 Definition
The term meta-analysis is used to describe the process of eval-
22.3.4 Discriminant Analysis uating and statistically combining results from two or more
existing independent randomized clinical trials addressing
This is a method of classification applied to a multivari-
similar questions in order to give an overall assessment.
ate dataset. Independent variables used to discriminate
among the groups are known as discriminating variables. 22.4.1.2 Difficulties
The discriminant function is a linear function of discrim-
Difficulties associated with meta-analysis include the
inating variables that maximizes the distance (or separa-
following:
tion) between groups.
• The existence of publication bias—trials show-
22.3.5 Cluster Analysis ing a statistically significant difference are more
likely to be published than those not finding a
This is also a method of classification applied to a statistically significant result.
multivariate dataset that derives homogeneous groups • Researchers finding 'nonsignificant' results may
or clusters of cases based on their values for the vari- be less likely formally to write up their results
able set. Hierarchical methods can be applied to the for publication.
clusters. • Arriving at selection criteria to determine which
studies to include and which not to include in the
22.3.6 Multivariate Regression Analysis meta-analysis.
• The different centres in which the different clini-
In this method, a linear multivariate regression equation cal trials have taken place may differ with respect
is fitted to a multivariate dataset. The multiple regres- to important variables in such a way as seriously
sion coefficient is the maximum correlation between the to question the validity of combining their data.
dependent variable and multiple non-random indepen- • If the meta-analysis is of clinical trials carried
dent variables, using a least-squares method. out on widely differing population groups, to
whom can the results of the meta-analysis prop-
erly be applied?
22.3.7 Path Analysis
A series of multiple regression analyses are used to
22.4.2 Survival Analysis
allow hypotheses of causality between variables to
be modelled and tested. A path diagram allows these This is a collection of statistical analysis techniques
variables and their hypothetical relationships to be that can be applied to situations in which the time to
represented graphically. It shows arrows between the a given event, such as death, illness onset, or recov-
variables, with regression coefficients (known as path ery, is measured, but not all individuals necessarily
coefficients) associated with these arrows. χ2 tests are have to have reached this event during the overall time
used to test the model. interval studied.
Biostatistics 311
22.4.2.1 Survival Function end of the treatment period, on the basis of a set of inde-
The survival function, S(t), is given by pendent variables, x1 to xn:
S (t ) = P (t s > t )
1
P(event ) =
where 1 + exp(−(α 0 + α1 x1 + + α n xn ))
t is the time
ts is the survival time
where the coefficients α 0 to α n are estimated using a max-
The survival function is also given by imum likelihood method.
S (t ) = 1 − (Cumulative distribution function of t s )
22.4.2.2 Survival Curve BIBLIOGRAPHY

This is a plot of S(t) (on the ordinate) versus t (on the Altman DG. 1991: Practical Statistics for Medical Research.
abscissa). Instead of being drawn as continuous curves, London, U.K.: Chapman & Hall.
Bryman A and Cramer D. 1994: Quantitative Data Analysis
sometimes survival curves are drawn in a stepwise fash-
for Social Scientists, revised edition. London, U.K.:
ion, with the steps occurring between estimated cumula- Routledge.
tive survival probabilities. Cochran WG. 1954: Some methods for strengthening the com-
mon χ2-test. Biometrics 10:417–451.
22.4.2.3 Hazard Function Coolican H. 2009: Research Methods and Statistics in
This measures the likelihood of an individual experi- Psychology, 5th edn. London, U.K.: Hodder Arnold.
encing a given event, such as death, illness onset, or Dunn G and Everitt B. 1995: Clinical Biostatistics: An
recovery, as a function of time. Introduction to Evidence-Based Medicine. London, U.K.:
Arnold.
Everitt B and Hay D. 1992: Talking about Statistics: A
22.4.3 Logistic Regression Psychologist’s Guide to Design and Analysis. London,
U.K.: Arnold.
This is a regression model used to predict the probability Puri BK. 2002: Statistics in Practice: An Illustrated Guide to
of a dichotomous variable, such as better/not better at the SPSS, 2nd edn. London, U.K.: Arnold.
23 Research Methodology
and Critical Appraisal
23.1 RESEARCH STUDY DESIGN crossover trial with two arms, at the time of crossover,
the subjects who had been receiving the placebo during
23.1.1 Types the first part of the study now cross over to the active
Research studies may be classified as being case–control treatment, while the subjects who had been receiving the
studies, in which patients affected by the index disease active treatment now cross over to the placebo. In con-
are compared with matched control subjects, and cross- trast, in a placebo-controlled single crossover trial with
sectional, in which subjects’ data are collected at the same two arms, at the time of crossover, the subjects who had
time (or, more usually, during the same time interval), been receiving the placebo during the first part of the
and longitudinal studies. Confounding variables that may study now cross over to the active treatment, while the
affect case–control studies include recall bias and selec- subjects who had receiving the active treatment continue
tion bias. Cross-sectional studies may be confounded by to receive the active treatment for the rest of the duration
a cohort effect whereby subjects with different ages may of the trial. A trial is double-blind if both the subjects
have different temporally influenced characteristics (e.g. and the observers are blinded to group allocation.
with respect to experiencing epidemics at different ages Table 23.1 compares and contrasts the strengths and
or different sociocultural attitudes). Longitudinal stud- weaknesses of different designs.
ies are ones in which a cohort of subjects are followed
up over time; they may be prospective, retrospective 23.1.2 Hierarchy of Evidence
(here, information bias may pose a problem), or indeed
of mixed design (in which the selection process is made See Chapter 21.
on the basis of a retrospective study, which is then fol-
lowed by a prospective study of the selected subjects). 23.1.3 Selection Process
Confounding variables that might affect longitudinal
studies may include a history effect (in which an effect The stages in the selection process for recruitment into a
is incorrectly attributed to the age of the subjects), a mor- randomized clinical trial are shown in Figure 23.1.
bidity effect (with increasing levels of certain illnesses Many major medical and scientific journals now require
occurring with age), a mortality effect (with the effect of the reporting of the results of a randomized interventional
death leading to fewer subjects over time in the cohort), trial to follow the CONSORT guidelines. CONSORT
or a practice/testing effect (because subjects will already stands for Consolidated Standards of Reporting Trials.
have experienced taking part in the testing earlier in the Such a report should include a CONSORT diagram, as
study, leading to learning). Furthermore, a Darwinian- shown in Figure 23.2.
type survival of the fittest effect may occur in a longitu-
dinal study whereby the fittest subjects survive over time,
so that some of the characteristics of the subjects who 23.2 CLINICAL TRIALS
have survived to the last part of the study may be mark-
23.2.1 Definition
edly different from those of the subjects generally who
were alive at the start of the study. Clinical trials are planned experiments carried out on
In a crossover design, the subjects act as their own humans to assess the effectiveness of different forms of
controls. For example, in a placebo-controlled double treatment.
313
TABLE 23.1
Comparing Design Strengths and Weaknesses
Cross-Sectional Case–Control Prospective
Parameter Surveys Studies Cohort Studies RCTs
Cost Low Low High High
Setup Quick and easy Quick and easy Complex Complex
Recall bias Low High Low Low
Rare diseases Impractical Practical Impractical Practical
Rare exposures Impractical Disadvantage Advantage Deliberate
Long disease course NA Advantage Disadvantage NA
Diseases with latency NA Advantage Disadvantage NA
Follow-up period None Short Long Specified
Attrition rate NA Low High Moderate
Estimate incidence NA Poor Good NA
Estimate prognosis NA Fair Good NA
Examine several possible risks NA Good Impractical Impractical
Examine several possible outcomes NA Impractical Good NA
Inference to target population Strong Less strong Strong Strong
Source: Ajetunmobi, O., Making Sense of Critical Appraisal, Arnold, London, U.K., 2002, p. 59, Table 2.1.
Note: RCTs, randomized clinical trials; NA, not applicable.
23.2.2 Classification
General population
The following classification of clinical trials is used by
the pharmaceutical industry:
Applicability of research question
• Phase I trial—clinical pharmacology and toxicity
• Phase II trial—initial clinical investigation
Target population
• Phase III trial—full-scale treatment evaluation
• Phase IV trial—postmarketing surveillance
Apply inclusion and exclusion criteria
23.2.3 Advantages of Randomized Trials

Eligible population
In a randomized trial, all the subjects have the same
probability of receiving each of the different forms of
Apply random sampling treatment being compared. The advantages of such ran-
domization include the following:
Sample population
• The effects of concomitant variables are distrib-
Randomization
uted in a random manner between the compari-
son groups; these variables may be unknown.
• The allocation of subjects is not carried out in
a subjective manner influenced by the biases of
the investigators.
Experimental group Control group • Statistical tests used to analyse the results
are on a firm foundation as they are based on
FIGURE 23.1 The selection process. (From Ajetunmobi, O., what is expected to occur in random samples
Making Sense of Critical Appraisal, Arnold, London, U.K., from parent populations having specified
2002, p. 61, Figure 2.2.) characteristics.
Research Methodology and Critical Appraisal 315
Assessed for eligibility (n = ..)
Excluded (n = ....)
Not meeting inclusion criteria (n = ..)

Refused to participate (n = ..)
Other reasons (n = ..)
Randomized (n = ..)
Allocated to intervention (n = ..) Allocated to intervention (n = ..)

Received allocated intervention (n = ..) Received allocated intervention (n = ..)
Did not receive allocated intervention (n = ..) Did not receive allocated intervention (n = ..)
give reasons give reasons
Lost to follow-up (n = ..) Lost to follow-up (n = ..)

Discontinued intervention (n = ..) Discontinued intervention (n = ..)

Analysed (n = ..) Analysed (n = ..)

Excluded from analysis (n = ..) Excluded from analysis (n = ..)
FIGURE 23.2 Example of a CONSORT diagram for an individually randomized trial. (From Stahl, D. and Leese, M., Research
methods and statistics, in: Psychiatry: An Evidence-Based Text, Puri, B.K. and Treasaden, I.H. (eds.), Hodder Arnold, London,
U.K., 2010, p. 39, Figure 4.3.)
The gold standard of clinical trials is the randomized 23.2.4.1 Concurrent Controls
double-blind controlled trial in which It is not usually possible to confirm that the different
treatment groups are comparable. Volunteer bias may
• Allocation of treatments to subjects is randomized also occur, with volunteers faring better than those who
• Each subject does not know which treatment has refuse to participate in a trial.
been received by him or her
23.2.4.2 Historical Controls
• The investigator(s) does not know the treatment
allocation before the end of the trial Here the control group consists of a group previously
given an older/alternative treatment. This group is com-
pared with suitable subjects receiving a new treatment
23.2.4 Disadvantages of Non-randomized Trials being tested. Disadvantages of using historical controls
Non-randomized trials may have concurrent or his-
torical (i.e. nonconcurrent) controls. Both types of non- • It cannot be assumed that everything apart from
randomized trials have associated disadvantages in the new treatment being tested has remained
comparison with randomized trials. unchanged over time.
• The monitoring and care of current subjects 23.3.4 Latent Traits (Constructs)

receiving the new treatment are likely to be
greater than was that of the historical controls. Psychological concepts such as attitude and intelligence
• The efficacy of the new treatment is likely to be are considered to be latent traits or hypothetical constructs
overestimated. that are believed to exist. Although not directly observ-
• The findings of such a trial may be not be widely able, constructs can be used to explain phenomena that
accepted because of the lack of randomization. can be observed and to make predictions. In the develop-
ment and use of psychometric tests, in particular, factor
analysis may be used to identify factors, corresponding to
23.3 PROBLEMS OF MEASUREMENT latent traits or hypothetical constructs, that may account
IN PSYCHIATRY for correlations observed between the scores on tests or
subtests by a large sample of subjects.
23.3.1 Aims of Measurement
The main aims of measurement in psychiatry are 23.3.5 Reliability
23.3.5.1 Definition
• To help in the diagnostic process or in other
forms of categorization The reliability of a test or measuring instrument describes
• To measure symptomatology ± its change the level of agreement between repeated measurements.
It can be expressed as the ratio of the variance of the true
scores to the variance of the observed scores:
23.3.2 Problems of Measurement
σt2
Problems in measurement in psychiatry include Reliability =
σ + σ2e
2
t
• Defining caseness
• Assessment of behaviour where
• Assessment of cognitive performance σ2t is the true score variance
• Assessment of mood σ2e is the measurement error variance
• Assessment of delusions and hallucinations
• Assessment of personality With this definition, the range of values that the reliabil-
• Assessment of psychophysiological functioning ity can take is given by
• Assessing the degree to which an individual suf-
fers from a psychiatric/psychological disorder 0 ≤ reliability ≤ 1
A low value, close to zero, implies low reliability, while a

23.3.3 Measurement Methods
high value, close to one, implies high reliability.
A range of measurement methods can be employed in
psychiatric/psychological assessments. Examples include 23.3.5.2 Interrater Reliability
Interrater reliability describes the level of agreement
• Observer-rated scales—structured and semi-struc- between assessments of the same material made by two
tured standardized psychiatric interview schedules or more assessors at roughly the same time.
• Screening instruments
• Behavioural observation studies 23.3.5.3 Intrarater Reliability
• Self-predictions Intrarater reliability describes the level of agreement
• Self-recording—for example, diaries between assessments made by two or more assessors of
• Self-rating scales for the assessment of mood the same material presented at two or more times.
• Self-rating scales for the assessment of personality
• Psychophysiological techniques 23.3.5.4 Test–Retest Reliability
• Naturalistic observations Test–retest reliability describes the level of agreement
• Psychometric measurements—for example, of between assessments of the same material made under
intelligence and personality similar circumstances but at two different times.
23.3.5.5 Alternative Forms Reliability The range of values that κ can take is
Alternative forms reliability describes the level of agree-
• κ = 1: complete agreement
ment between assessments of the same material by
• 0 < κ < 1: observed agreement > chance agreement
two supposedly similar forms of the test or measuring
• κ = 0: observed agreement = chance agreement
instrument made either at the same time or immediately
• κ < 0: observed agreement < chance agreement
consecutively.
The weighted kappa, κw, is a version of κ that takes into
23.3.5.6 Split-Half Reliability account differences in the seriousness of disagreements
Split-half reliability describes the level of agreement (represented by the weightings).
between assessments by two-halves of a split test or
measuring instrument of the same material made under 23.3.6.4 Intraclass Correlation Coefficient
similar circumstances. Since some tests or measuring The intraclass correlation coefficient, ri, is more appro-
instruments contain different sections measuring differ- priate than κ or r if agreement is being measured for sev-
ent aspects, in such cases, it may be appropriate to create eral items that can be regarded as part of a continuum or
the halves by using alternative questions, thereby main- dimension. For two raters, the value of ri is derived from
taining the balance of each half. the corresponding value of r:
23.3.6 Statistical Tests of Reliability

r =
{ ∑ (
 s + s ) − ( s − s )  r − ( x − x ) / 2}
2
1
2
2 1
 2
2
1 2
2
{( s + s ) + ( x − x ) /2}
i 2
2 2
23.3.6.1 Percentage Agreement 1 2 1 2
Measuring the percentage agreement is the simplest but

most unsatisfactory method of assessing the reliability, where
since it does not take into account agreement between r is the product–moment correlation coefficient between
observers owing to chance. the scores of the two raters
s1 is the standard deviation of the scores for the first
23.3.6.2 Product–Moment Correlation Coefficient rater
The product–moment correlation coefficient, r, may s2 is the standard deviation of the scores for the second
give spuriously high results, particularly if there is rater
chance agreement of many values. It may even give the x1 is the mean of the scores for the first rater
maximum value of one for the agreement between two x2 is the mean of the scores for the second rater
raters, even if they do not agree at all, if, for example,
one of the raters consistently rates scores on the test or It follows that
measuring instrument at twice the values rated by the
if x1 = x2 and s1 = s2
other rater.
then ri = r
else ri < r
23.3.6.3 Kappa Statistic
The kappa statistic, or kappa coefficient, κ, is a measure For more than two raters, the value of ri is derived from
of agreement in which allowance is made for chance the corresponding two-way ANOVA for (raters × subjects):
agreement. It is most appropriate when different catego-
ries of measurement are being recorded and are calcu- ns ( sms − ems )
ri =
lated from the following formula: ns sms + nr rms + ( ns nr − ns − nr ) ems
Po − Pc where
k=
1 − Pc nr is the number of raters
ns is the number of subjects
where ems is the error mean square
Pc is the chance agreement rms is the raters mean square
Po is the observed proportion of agreement sms is the subjects mean square
23.3.6.5 Cronbach’s Alpha 23.3.7.10 Divergent Validity

Cronbach’s alpha, α, gives a measure of the average cor- Divergent validity is established when measures discrim-
relation between all the items when assessing split-half inate successfully between other measures of unrelated
reliability. It thereby indicates the internal consistency of constructs.
the test or measuring instrument.
23.3.7.11 Construct Validity
23.3.7 Validity Construct validity is determined by establishing both
23.3.7.1 Definition convergent and divergent validity and is closely con-
The validity of a test or measuring instrument is the term nected with the theoretical rationale underpinning the
used to describe whether it measures what it purports to test or measuring instrument. It involves showing the
measure. power of the hypothetical construct(s) or latent traits both
to explain observations and to make predictions.
23.3.7.2 Face Validity
Face validity is the subjective judgement as to whether
a test or measuring instrument appears on the surface to 23.3.8 Type I Error
measure the feature in question. In spite of its name, it is A type I error is the error of wrongly rejecting H0 when it
not strictly a type of validity. is true. As mentioned earlier, the probability of making a
type I error is denoted by α, the significance level:
23.3.7.3 Content Validity
Content validity examines whether the specific measure- α = P(type I error)
ments aimed for by the test or measuring instrument are
assessing the content of the measurement in question.
23.3.9 Type II Error
23.3.7.4 Predictive Validity
Predictive validity determines the extent of agreement A type II error is the error of wrongly accepting H0 when
between a present measurement and one in the future. it is false. The probability of making a type II error is
denoted by β:
23.3.7.5 Concurrent Validity
Concurrent validity compares the measure being assessed β = P(type II error)
with an external valid yardstick at the same time.
23.3.7.6 Criterion Validity 23.3.10 Power

Criterion validity refers to predictive and concurrent The power of a test is the probability that H0 is rejected
validity together. when it is indeed false. It is related to β, the probability of
making a type II error, in the following way:
23.3.7.7 Incremental Validity
Incremental validity indicates whether the measurement Power = 1 − β
being assessed is superior to other measurements in
approaching true validity.
23.3.11 Sensitivity
23.3.7.8 Cross-Validity
The sensitivity of a test or measuring instrument is the
Cross-validation of a test or measuring instrument is
proportion of positive results/cases correctly identified:
used to determine whether, after having its criterion
validity established for one sample, it maintains crite-
rion validity when applied to another sample. True positive
Sensitivity =
True positive + False negative
23.3.7.9 Convergent Validity
Convergent validity is established when measures expected
to be correlated, since they measure the same phenomena, This ratio needs to be multiplied by 100 if the sensitivity
are indeed found to be associated. is to be given as a percentage.
23.3.12 Specificity Predictive value of a negative result

The specificity of a test or measuring instrument is the True negative
proportion of negative results/cases correctly identified: =
True negative + False negative
True negative
Specificity =
True negative + False positive 23.3.15 Likelihood Ratios
Likelihood ratios for tests are derived from their sensitiv-
This ratio needs to be multiplied by 100 if the sensitivity ity and specificity values. For tests in which the result is
is to be given as a percentage. binary (positive or negative), likelihood ratios are calcu-
lated as follows:
23.3.13 ROC Curve Sensitivity

Likelihood ratio for a positive result =
The receiver operating characteristic, or ROC, curve for 1− Specificity
a test is a plot of sensitivity versus (1 − specificity), as
shown in Figure 23.3. This figure shows that the closest
1− Sensitivity
point on the ROC curve to the ideal state is the best com- Likelihood ratio for a negative result =
promise between sensitivity and specificity for the test. Specificity
The area under the ROC curve represents how accurate
the test is, that is, the probability of identifying true posi- Note also the following relationships between the odds
tives and true negatives correctly. ratio (see Chapter 21) and the likelihood ratio:
Posttest odds = Pretest odds × Likelihood ratio

23.3.14 Predictive Values
The predictive value of a positive result from a research where
measure is the proportion of the positive results that is Pretest odds = (pretest probability)/(1 − pretest probability)
true positive: Note that posttest probability = (posttest odds)/(posttest
odds + 1)
Predictive value of a positive result

23.3.16 Bias
True positive
=
True positive + False positive 23.3.16.1 Selection Bias
Selection bias occurs when a characteristic associated
with the variable(s) of interest leads to higher or lower
The predictive value of a negative result from a research
participation in the research study, such as an epidemio-
measure is the proportion of the negative results that is
logical cross-sectional survey.
true negative:
23.3.16.2 Observer Bias

Ideal state; perfect sensitivity and specificity
1 In epidemiological studies, observer bias occurs when
the researcher has clues about whether the subject is in
Sensitivity
the case or comparison group, leading to a biased assess-

Nearest point on curve to ideal state ment. This is particularly likely in studies involving ret-
rospective assessments.
0 1
1 – specificity 23.3.16.3 Recall Bias
FIGURE 23.3 The ROC plot. (From Ajetunmobi, O., Making In epidemiological studies, recall bias occurs when there is
Sense of Critical Appraisal, Arnold, London, U.K., 2002, p. 74, a difference in knowledge between the subjects in the case
Figure 3.1.) and in the comparison groups, leading to a biased recall.
For example, in case–control studies, the knowledge on the BIBLIOGRAPHY

part of subjects (or, in the case of childhood disorders, their
Ajetunmobi O. 2002: Making Sense of Critical Appraisal.
parents) as to whether or not they have a given disorder London, U.K.: Arnold.
may bias their recall of exposure to putative risk factors. Altman DG. 1991: Practical Statistics for Medical Research.
London, U.K.: Chapman & Hall.
23.3.16.4 Information bias Bryman A and Cramer D. 1994: Quantitative Data Analysis for
Information bias includes both observer bias and Social Scientists, revised edition. London, U.K.: Routledge.
recall bias. Dunn G and Everitt B. 1995: Clinical Biostatistics: An Introduction
to Evidence-Based Medicine. London, U.K.: Arnold.
23.3.16.5 Confounding bias Everitt B and Hay D. 1992: Talking about Statistics: A
Psychologist’s Guide to Design and Analysis. London,
In epidemiological studies, confounding bias occurs U.K.: Arnold.
when the actual, but unexamined, underlying cause of Stahl D and Leese M. 2010: Research methods and statistics. In
the disorder being researched is associated with both the Puri BK and Treasaden IH (eds.) Psychiatry: An Evidence-
suspected risk factor and the disorder. Based Text, p. 39. London, U.K.: Hodder Arnold.
24 Physical Therapies
24.1 NEUROSTIMULATION THERAPIES • Life-threatening depression: refusal to eat.

• Depression with strong suicidal ideation.
Neurostimulation therapies are physical interventions • Psychotic depression.
that treat psychiatric disorders through delivery of elec- • Stupor.
tric current or magnetic field. • Puerperal depressive illness: the use of ECT
The following four types of neurostimulation thera- during pregnancy is known to cause complica-
pies are currently used in psychiatry: tions, but the risks associated with ECT need to
be balanced against the risks of using pharma-
1. Electroconvulsive therapy (ECT) cological treatments.
2. Repetitive transcranial magnetic stimulation
(rTMS)
3. Vagus nerve stimulation (VNS) Mania
4. Deep brain stimulation (DBS)
• Prolonged manic episode
• Treatment-resistant mania with life-threatening
24.2 ELECTROCONVULSIVE THERAPY physical exhaustion
The following are key historical points in the develop-
ment of ECT:
Schizophrenia
• During the early twentieth century, it was
hypothesized that schizophrenia and epilepsy • Catatonic schizophrenia
are more or less mutually exclusive disorders. • Schizoaffective disorder
• In 1934, Meduna, on the basis of this hypothe- • Treatment-resistant schizophrenia
sis, attempted to treat schizophrenia by inducing
seizures chemically. Other indications
• In 1938, Cerletti and Bini induced seizures
electrically. • Affective symptoms in Parkinson’s disease
• Neuroleptic malignant syndrome
24.2.1 ECT Indications and Contraindications
24.2.1.1 Indications for ECT 24.2.1.2 Contraindications against ECT
The National Institute for Health and Clinical Excellence Raised intracranial pressure is an absolute contraindica-
(NICE) guidelines recommended that ECT be used only tion to ECT. Relative contraindications include
to achieve rapid and short-term improvement of severe
symptoms after an adequate trial of other treatment • Cerebral aneurysm
options has proven ineffective and/or when the condition • Recent cerebrovascular accident
is considered to be potentially life-threatening in indi- • Recent myocardial infarction
viduals with the following: • Cardiac arrhythmia
Depression • Intracerebral haemorrhage
• Acute/impending retinal detachment
• Severe depressive illness: 60%–80% remission • Phaeochromocytoma
rate; maximum response typically attained after • Raised anaesthetic risk
2–4 weeks; relapse rate without maintenance • Sickle cell disease
antidepressant treatment after ECT is 50%–95%. • Unstable vascular aneurysm or malformation
321
24.2.1.3 Medications to Avoid before ECT Consent

• Benzodiazepines have anticonvulsant activity. If The NICE guidelines recommend the following:
there is a need for benzodiazepine before ECT,
choose a short-acting benzodiazepine such as • Autonomy: Valid consent should be obtained in
alprazolam and lorazepam. all cases in which the individual has the ability to
• Lithium may result in postictal delirium and grant or refuse consent. Consent should be obtained
confusion. without pressure or coercion, which may occur as
a result of the circumstances and clinical setting.
• Nonmaleficence: Prior to obtaining consent for ECT,
24.3 PREPARATION FOR ECT the psychiatrist must ensure that ECT is indeed indi-
cated, and the patient has the capacity to give consent.
According to the NICE guidelines, the decision as to
• Partnership: The decision to use ECT should
whether ECT is clinically indicated should be based on
be made jointly by the individual and the
a documented assessment of the risks and potential ben-
clinician(s) responsible for treatment, on the
efits to the patient, including
basis of an informed discussion. The involve-
ment of patient advocates and/or carers to facili-
• The risks associated with the anaesthesia
tate informed discussion is strongly encouraged.
• Current comorbidities
• Education: This discussion should be enabled by
• Anticipated adverse events, particularly cogni-
the provision of full and appropriate information
tive impairment
about the general risks associated with ECT and
• The risk of not having ECT
about the risks and potential benefits specific to
that individual. The psychiatrist must ensure the
Pre-ECT assessment and investigations patient understands the information provided and
address any question that the patient may have.
• Review psychiatric history, medical his- • Right to withdrawal: The individual should be
tory, drug history, and previous ECT record reminded of his or her right to withdraw consent
(to check the previous electric stimulus and at any point during the course of ECT.
response). • Second opinion: The psychiatrist should be
• Perform a physical examination with special prepared to offer the patient access to a second
focus on cardiovascular, respiratory, and neuro- opinion, should the patient request it.
logical systems. • Advance directives: In all situations in which
• Baseline MMSE is required for old people. informed discussion and consent is not possible,
• Assess the patient’s dentition, especially for advance directives should be taken fully into
old people or people who have poor dental account, and the individual’s advocate and/or
care. carer should be consulted.
• Order full blood count (FBC), urea and
electrolytes (U&E), and liver function tests
24.4 ADMINISTRATION OF ECT
(LFT).
• Order ECG and chest x-ray (CXR) for patients Bilateral and unilateral ECT
who are older than 45 years.
Electrode placement
• Consult an anaesthetist for preanaesthesia
assessment. • In unilateral ECT, the electrodes are placed on
• Consult a cardiologist if there is cardiovascular the nondominant cerebral hemisphere. The non-
risk. dominant cerebral hemisphere should be on the
• Order an x-ray for spine if there is evidence of a right side of the head for all right-handed people
spinal cord disorder. and most left-handed people. Stimulating the
• Perform CT or MRI if neurological sign is nondominant hemisphere reduces the risk of
present. cognitive side effects as compared to stimula-
• A patient receiving ECT in the morning should tion of dominant hemisphere (Figure 24.1).
remain ‘nil by mouth’ from the previous • In bilateral ECT, both cerebral hemispheres are
midnight. stimulated.
Physical Therapies 323
Second electrode or d’Elia

First electrode: 4 cm above the positioning: second electrode is
midpoint of lateral angle of eye and placed in the midpoint of the arc.
external auditory meatus The radius of arc is around 18 cm.
FIGURE 24.1 Positioning of electrodes in unilateral ECT.
Dosing/electric stimulus by (20 + 30 J)/2 = 25 J. For unilateral ECT, the

psychiatrist multiplies by 1.5 (i.e. increase by
• Seizure threshold increases with age (Table 24.1). 50%) to get 37.5 J. For bilateral ECT, the psy-
To determine seizure threshold, the psychiatrist chiatrist can add 5 J to the average value (i.e.
can use age-based dosing method. The formula 25 J) and starts at 30 J. If the seizure duration
is as follows: Dose in energy = Age divided by 2. reduces in the subsequent ECT, the psychiatrist
• For example, a 40-year-old woman requires ECT. can increase by 5 J during each session.
The initial dose is 40/2 = 20 J based in the age- • Unilateral ECT requires suprathreshold stimu-
based dosing method. The patient has no seizure lus. The electric stimulus has to exceed the sei-
at 20 J but has a seizure at 30 J. The psychiatrist zure threshold by 25%–100%.
knows that the seizure threshold is between 20 • Bilateral ECT requires a barely suprathreshold
and 30 J. Then the psychiatrist takes an average doses. The electric stimulus is just exceeding the
seizure threshold.
TABLE 24.1 Other stimulus parameters

Factors Associated with Increase or Decrease The assessment report (NICE guidelines) provides data
of Seizure Threshold that the stimulus parameters have an important influence
Increase in Seizure Threshold/ Decrease in Seizure Threshold/ on efficacy (Figure 24.2).
Decrease in Duration of Increase in Duration of The energy is determined by four stimulus parameters
Seizure Seizure (current, stimulus duration, frequency of the pulse, and
• Male gender • Caffeine
pulse width). In order to increase effectiveness, the psy-
• Baldness • Low carbon dioxide
chiatrist can consider changing the stimulus parameters
saturation of blood in the following order:
• Paget’s disease • Hyperventilation 1. Increase stimulus duration
• Dehydration • Theophylline 2. Increase the frequency
• Previous ECT
3. Increase pulse width
• Benzodiazepine
The current usually remains the same.
TABLE 24.2
Classification of Duration of Seizure
Duration of Seizure Type of Seizure
0s Missed seizure: There is no seizure activity
following delivery of electric stimulus.
The psychiatrist is advised to ensure there
are good electrode contacts and the ECT
machine demonstrates normal operation.
The psychiatrist can restimulate at 25% of
higher dose after 10 s
<15 s Short seizure: The psychiatrist is advised to
increase the energy level by 25% in the
next ECT session and not to restimulate to
prevent prolonged seizure
25–75 s Normal seizure: satisfactory response
>120 s Prolonged seizure: The anaesthetist may
FIGURE 24.2 Other stimulus parameters and usual values.
need to abort the prolonged seizure
Frequency of session and total number of treatment

Effectiveness (Table 24.2)
1. The usual frequency is twice a week for a total
of 6–12 ECT sessions. • The effectiveness of ECT is determined by
2. There is no difference in efficacy between twice the electrode placement and stimulus intensity.
a week and three times a week. Bilateral ECT was reported to be more effective
3. Maintenance ECT: The frequency ranges from than unilateral ECT.
once per week to once per month. Indications of • A barely suprathreshold unilateral ECT is inef-
maintenance ECT include fective. Raising the electric stimulus above the
a. Frequent relapse and recurrence of depres- individual’s seizure threshold was found to
sive episodes increase the effectiveness of unilateral ECT at
b. History of responsiveness to maintenance the expense of increased cognitive impairment.
ECT • For bilateral ECT, barely suprathreshold stim-
c. Patient preference uli are effective and reduce the risk of memory
d. Resistance to or intolerance of antidepressants impairment. The speed of clinical response can
be achieved by increasing the stimulus intensity.
Bilateral ECT versus unilateral ECT
Monitoring during ECT
• When deciding bilateral or unilateral ECT, there • Pulse oximetry monitors blood oxygen saturation.
are two issues to consider: memory impairment • ECG monitors heart rhythm.
and effectiveness. • EEG measures electric brain activity.
• EMG measures motor seizure activity.
Memory impairment
Anaesthesia
• Bilateral ECT is associated with greater
memory impairment as compared to unilat- 1. A muscle relaxant (succinylcholine) is adminis-
eral ECT. tered in order to prevent violent movements dur-
• Bilateral ECT has better efficacy. As a result, ing the convulsion.
bilateral ECT is preferred when there is a treat- 2. Fasciculation goes from head to toes when suc-
ment urgency (e.g. patients with high suicide cinylcholine takes effect. Fasciculation usually
risk) or when unilateral ECT fails. occurs 60–120 s after injection.
3. Atropine is administered in order to reduce 10. There may be another period of increased sym-
secretions and prevent the muscarinic actions of pathetic tone when the patient awakens from the
the muscle relaxant. Anticholinergic agent also anaesthesia.
prevents bradycardia after the seizure.
4. If there is any possibility that the patient may Interpretation of EEG strip (Figures 24.3 and 24.4)
have low or atypical plasma pseudocholinester- The NICE guidelines recommend that clinical status
ase enzymes, the anaesthetist must be informed should be assessed following each ECT session and treat-
as this could lead to prolonged muscle paralysis ment should be stopped when a response has been achieved
with the muscle relaxant. or sooner if there is evidence of adverse effects. Cognitive
5. Bilateral or unilateral (to the nondominant cere- function should be monitored on an ongoing basis and at a
bral hemisphere) ECT is administered under a minimum at the end of each course of treatment.
short-acting general anaesthetic. The NICE guidelines also recommend that a repeat
a. Thiopentone increases seizure threshold course of ECT should be considered only for individuals
and causes cardiovascular depression and who have severe depressive illness, catatonia, or mania and
apnoea. Thiopentone is commonly used. who have previously responded well to ECT. In patients
b. Propofol may shorten seizure. who are experiencing an acute episode but have not previ-
c. Ketamine is associated with the risk of hal- ously responded, a repeat trial of ECT should be under-
lucinations, tachycardia, hypertension, and taken only after all other options have been considered and
decreases seizure threshold. It is not com- following discussion of the risks and benefits with the indi-
monly used. vidual and/or where appropriate the carer/advocate.
6. A mouthpiece is placed in the patient’s mouth in
order to prevent damage from biting during the
convulsion. 24.4.1 Side Effects of ECT
7. Vagal tone is increased during and immediately
after administration of the electric stimulus. The The rate of adverse events after ECT is 0.4%.
patient may develop bradycardia. The main early side effects include
8. The sympathetic nervous system is activated
during the seizure, and there is a significant • Headache
increase in heart rate, blood pressure, and car- • Myalgia
diac output. • Nausea
9. Shortly after the seizure, there may be another • Dental damage or oral lacerations
period of increased vagal tone. The patient may • Musculoskeletal injuries
develop bradycardia and bradyarrhythmias. • Temporary confusion after ECT
Normal resting EEG

activity prior to seizure
EEG1 200 μV/cm
EEG2 200 μV/cm
After the electrical stimulus is

given, a seizure is initiated. The
EEG shows low voltage, fast activity,
and polyspike rhythms
FIGURE 24.3 EEG—at the initiation of seizure.

The EEG shows

hypersynchronous
polyspikes during full Postictal suppression occurs
seizure activity at the end of the seizure
0 b/m 0 b/m
FIGURE 24.4 EEG—at the termination of seizure.
Risk factors for post-ECT confusion • A small number of patients experience long-
lasting subjective memory impairment,
1. Bilateral ECT which is not detected objectively by cognitive
2. Coadministration of anticholinergics and lithium assessment.
3. Old age
4. Underlying cognitive impairment Outcome of memory loss
Strategies to prevent post-ECT confusion • Some specific memories of events immediately

before and after ECT are lost permanently.
1. Avoid anticholinergics and lithium before ECT. • There is some limited evidence from RCTs to
2. Reduce pulse width. suggest that the effects on memory may not last
3. Reduce the dose of electric stimulus. beyond 6 months, but this has been inadequately
4. Reduce the frequency of ECT sessions. researched.
5. Use unilateral ECT instead bilateral ECT.
ECT may cause depressed patients with bipolar mood
Memory impairment disorder to become manic.
• Anterograde (forgetting of events after the sei-
zure) and retrograde amnesia (forgetting of events
prior to the seizure) may occur after ECT. 24.5 COMPLICATIONS OF ECT
• Retrograde amnesia of events immediately pre- A complication rate of 1 per 1400 treatments and most
ceding ECT treatments may be permanent. Risk complications resolve without intervention.
factors for retrograde amnesia include bilateral Complications include
ECT, high dose of electric stimulus, and post-
ECT confusion. • Cardiac arrhythmia
• Anterograde amnesia is usually transient. It • Circulatory insufficiency
usually manifests as forgetfulness regarding • Laryngospasm
events that happened after the ECT treatment or • Prolonged apnoea
misplacing belongings after ECT. Anterograde • Prolonged seizures
amnesia usually resolves in 6 months. • Tooth damage
According to assessment report (NICE guidelines), the six In addition, rTMS with appropriate stimulation parameters
reviewed studies that used brain-scanning techniques did may result in long-term effects on synaptic efficacy.
not provide any evidence that ECT causes brain damage.
24.7.2 Mechanisms of rTMS
24.6 MORTALITY 1. TMS stimulates regions of the cerebral cortex
• The mortality rate of ECT is 2.0–4.5 deaths per by using a magnetic field generated by an elec-
100,000 ECT. tromagnet placed over the skull to induce elec-
• There was no evidence to suggest that the mortality tric currents.
associated with ECT is greater than that associated 2. rTMS delivers rhythmic pulses of electromagne-
with minor procedures involving general anaes- tism. The intensity of rTMS is usually set as a per-
thesia. The majority of deaths are related to car- centage of the patient’s motor threshold defined as
diorespiratory complications. The mortality rate is the minimum stimulus strength required to evoke
higher in patients with impaired cardiac functions. involuntary muscle movements in the hand.
• Pre-ECT oxygenation, brief anaesthesia, muscular
relaxation, and physiological monitoring reduce 24.7.3 Efficacy of rTMS
morbidity and mortality associated with ECT. • Active rTMS shows modest superiority in com-
parison to sham rTMS in treatment-resistant
24.7 REPETITIVE TRANSCRANIAL depression. (Response rate for active rTMS = 25%
MAGNETIC STIMULATION vs. sham rTSM = 9%; remission rate for active
rTMS = 17% vs. sham rTMS = 6%) (Rossini et al.,
The use of repetitive transcranial magnetic stimulation
2005; Rumi et al., 2005; Fitzgerald et al., 2008).
(rTMS) is gaining support among psychiatrists as evidence
• The combination of rTMS and antidepressant
emerges suggesting that it may provide an alternative to
may accelerate treatment response.
ECT in treating depression and other psychiatric disorders.
• MRI can provide neuronavigation technique
The following are key historical points in the develop-
that is used to guide specific site on the dorso-
ment of transcranial magnetic stimulation (TMS) and rTMS:
lateral prefrontal cortex (DLPFC), and this will
enhance response to rTMS.
• In 1896, d’Arsonval observed the occurrence of
phosphenes and vertigo when a subject’s head
is put into a coil (driven at 42 Hz) (d’Arsonval 24.8 SIDE EFFECTS
et al., 1896).
Side effects of rTMS include local discomfort, headache,
• In 1959, Kolin and colleagues stimulated the
and the risk of developing hypomania and seizure.
exposed frog sciatic nerve looped around the pole
piece of an electromagnet and caused the gastroc-
nemius to contract (driven at 60 Hz and 1 kHz)
24.8.1 ECT versus rTMS/MST
(Kolin et al., 1959). ECT is compared with rTMS in Table 24.3.
• In 1965, Bickford and Freeming successfully
demonstrated noninvasive stimulation of human
peripheral nerves (Bickford and Fremming 1965). TABLE 24.3
• In 1985, Barker (in Sheffield, England) reported A Comparison of ECT with rTMS
the first magnetic stimulation of the human
ECT rTMS
motor cortex (Barker et al., 1985).
Anaesthesia Required Not required
Seizure Required Not required
24.7.1 Indications for rTMS
Treatment frequency 2–3 per week Every day
At the time of writing, there is evidence that the adminis- Occurrence of amnesia Yes No
tration of rTMS to humans may be able to treat: Focality Relatively non-focal More focal
Tissue impedance Shunting occurs No shunting
• Depression Pulse width 0.5–2 ms 0.2 ms
• Poststroke rehabilitation for motor function
24.9 VAGAL NERVE STIMULATION 24.9.3 Efficacy of VNS

Vagal nerve stimulation (VNS) is generally carried out VNS may deliver a delayed antidepressant effect with
by surgically implanting a vagus nerve stimulator (a pulse clinical improvement over several weeks.
generator) into the subcutaneous tissues of the upper left In a 10-week randomized controlled trial, the response
chest in order to deliver pulsed electric stimulation to the rate of active VNS was 15% as compared to 10% of sham
cervical vagal trunk. VNS is of particular use in the treat- treatment (Rush et al., 2005b).
ment of epilepsy. In 10-week trial with antidepressant and VNS, the
The first use of VNS in humans was by Penry and response rate was 30% and remission rate was 15% (Sackeim
Dean (published in 1990) for the prevention of partial et al., 2001).
seizures. Later, a neurocybernetic prosthesis implant In trails with 1–2 years of VNS treatment, the response
was used in a patient with depression at the Medical rate was between 27% and 46%, and remission rate was
University of South Carolina (Charleston, the United between 16% and 29% (Maranegil et al., 2002; Nahas
States). et al., 2005; Nierenberg et al., 2008).
24.9.4 Side Effects
24.9.1 Indications for VNS
Side effects of VNS include dyspnoea, pain, cough, and
There are two major indications for VNS: voice alteration (50%).
• Epilepsy
• Treatment-resistant depression 24.10 DEEP BRAIN STIMULATION
The rationale for using VNS in treatment-resistant depres- Deep brain stimulation (DBS) involves stereotactic neu-
sion is based partly on the following findings: rosurgical implantation of electrodes under the MRI
guidance. The stimulator is implanted under the chest
• VNS has been found to reduce depressive symp- wall. Three neuroanatomical areas are stimulated:
toms in epileptic patients.
• Limbic blood flow is altered by VNS. 1. Subgenual cingulated gyrus (Brodmann area 25):
• CSF monoamine concentrations are altered by Patients who respond early to stimulation of this
VNS. area are more likely to maintain their response.
• Antiepileptic drugs may affect mood. 2. Nucleus accumbens.
3. Ventral caudate and ventral striatum.
Preliminary results with VNS appear to support its
DBS is at an investigational stage, and it may be useful
efficacy in treatment-resistant depression (Rush et al.,
for patients suffering from treatment-resistant depres-
2000).
sion. Six months after DBS, the response rate is 60% and
Patient selection and management should be offered
remission rate is 35% for depression. Twelve months after
jointly by a psychiatrist and a neurosurgeon.
DBS, the response rate is 55% and remission rate is 33%
The NICE guidelines recommend that VNS can only
for depression (Lozano et al., 2008).
be used after informing the clinical governance leads in
the respective trusts in the United Kingdom.
24.11 OTHER PHYSICAL THERAPIES
24.9.2 Mechanisms of Actions 24.11.1 Light Therapy/Phototherapy
VNS is carried out under general anaesthesia. An inci- This is treatment with high-intensity artificial light and
sion is made of the left side of the neck, and a stimulator may be used to treat patients suffering from seasonal
electrode is cuffed around the left vagus nerve. affective disorder (SAD).
The vagus nerve is stimulated periodically followed The light boxes used typically emit light of a strength
by a period of no stimulus. The stimulation frequency of around 10,000 lux. By comparison, on a sunny day,
and intensity are programmed in an external electronic the level of illumination may reach 100,000 lux, while
control. the home environment may typically be illuminated at
around 250 lux. The light spectrum used tends to be bal- 24.11.3 Psychosurgery
anced but usually with potentially harmful ultraviolet B
(UVB) frequencies filtered out. The following are key points in the history of psychosurgery:
• From 3000 to 2000 BCE, there is evidence of

24.11.1.1 Administration trepanation.
• For the strength of 2500 lux, the patient is • In the nineteenth century, Burckhardt removed
advised to receive light therapy for 2 h every postcentral, temporal, and frontal cortices from
morning. patients.
• The light exposure to eyes is important because • In 1910, Pusepp resected fibres between the
the light can alter circadian rhythm. Light ther- frontal and parietal lobes in patients with bipo-
apy reduces melatonin levels. lar mood disorder.
• Therapeutic effects are seen within a few days, • In 1936, Ody resected the right prefrontal lobe
and it usually takes 2 weeks for full therapeutic of a patient with the so-called childhood-onset
effect. schizophrenia.
• For relapse prevention, the patient is recommended • In 1935, after learning of the work of Fulton and
to receive light therapy half an hour a day starting Jacobsen involving bilateral ablation of the pre-
in autumn and continue throughout winter. frontal cortex in chimpanzees, Moniz carried out
human frontal leucotomy (work published in 1936).
24.11.1.2 Efficacy 24.11.3.1 Indications for Psychosurgery

• Fifty per cent of patients with SAD show clini- Psychosurgery is seldom performed in the United Kingdom
cally significant response to light therapy. and is a last-resort treatment in other countries for
• Chronic severe intractable depression

24.11.1.3 Side Effects • Chronic severe intractable obsessive–
• Side effects of light therapy include jumpiness, compulsive disorder
headache, and nausea (15% of patients). • Chronic severe intractable anxiety states
24.11.3.2 Psychosurgery Practise

24.11.2 Sleep Deprivation Current methods for making stereotaxic lesions include
24.11.2.1 Indications • Electrocautery
The clinical indications for sleep deprivation in mood • Radioactive yttrium implantation
disorders include • Thermocoagulation
• Gamma knife
• As an antidepressant in treatment-resistant
patients Some of the specific operations that may be used cur-
• To augment the response to antidepressants rently include
• To hasten the onset of action of antidepressant
medication or of lithium • Frontal lobe lesioning
• As a prophylaxis in recurrent mood cycles • Cingulotomy
• As an aid to diagnosis • Capsulotomy
• To predict the response to antidepressants or • Subcaudate tractotomy
ECT • Limbic leucotomy
24.11.2.2 Administration REFERENCES

In total sleep deprivation, the patient is kept awake for
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25 Advanced Psychological
Process and Treatment
25.1 SUPPORTIVE PSYCHOTHERAPY injury, massive stroke, severe dementia, acute

confusional state).
25.1.1 Objectives 3. Pathological liars, malingerers, and people with
1. Maintain and improve self-esteem of the client psychopathy.
2. Improve symptoms 4. Other forms of psychotherapies are more appro-
3. Prevent relapse priate (e.g. sensate focus therapy for sexual dys-
4. Develop adaptive and reasonable behaviour function, couple therapy for motivated couples
5. Set goals and positive thinking who have marital problems).
6. Strengthen defences and enhance adaptive capacity
25.1.6 Techniques
25.1.2 Historical Development
Open-ended question
1. Supportive psychotherapy is based on psycho-
dynamic therapy because it supports patient’s • This allows the client to respond in more than
defence mechanisms and explores conscious one word (e.g. yes or no).
problems and conflicts. • This also allows the client to take an active role
in therapy.
25.1.3 Characteristics • For example, a therapist can ask, ‘What con-
1. Supportive psychotherapy focuses on conscious cerns you today?’, in the beginning of a session.
conflicts but not unconscious conflicts.
2. There is no explicit interpretation of transfer- Observation
ence in supportive psychotherapy.
1. Pay attention to nonverbal behaviour, emotions,
25.1.4 Indications and other patterns of communication exhibited
by the client.
1. Crisis or common life problems.
2. Acute stress reaction.
Expression of interest
3. Adjustment disorder.
4. Client is not ready for more sophisticated form
1. Offer acknowledging statements, ‘I am glad that
of psychotherapy.
you make an effort to come and share with me
5. Patients with chronic medical illnesses.
about your hardship’.
2. Validate feelings (e.g. ‘I can imagine that you
25.1.5 Contraindications have gone through a lot of hardship and people
The following are contraindications for supportive psy- would feel sad in such situation’).
chotherapy. These contraindications also apply to other
types of psychotherapy in general: Set goals
1. Patient has no motivation for psychotherapy, 1. Goals are the desired outcomes of psychotherapy.
even the simplest form. 2. Goals have to be specific, measurable, realistic,
2. Acute or severe organic condition affects the and achievable in a preset time frame.
client’s ability to communicate (e.g. severe head 3. Agree on tasks to reach therapeutic goals.
331
Establish therapeutic alliance 3. Summary often links issues together and allows
transition from topic to topic.
1. Develop trust and respect between the therapist 4. Summary may enhance client’s awareness of
and the client. potential bias of their view.
2. Demonstrate empathy.
Reassurance and encouragement
Affirmation
1. Reassure the patient within limits of the thera-
1. Confirm the validity of a prior judgement or pist’s expertise.
behaviour (e.g. ‘I must say, if I were in your posi- 2. Encourage the client by instilling hope and iden-
tion, I might have a hard time dealing with those tify ‘small steps’ for improvement.
difficult people in your company’).
2. Elicit affirmative response: Rationalization and reframing
a. For example, the client has a BMI of 40. The
therapist is interested to find out his exercise 1. Rationalization involves providing a logical
level. explanation for an event, situation, or outcome.
b. ‘Do you find it difficult to do exercise?’ 2. Reframing involves providing an alternative
c. ‘Your BMI is a concern to me. How often way to look at a situation.
do you exercise?’
d. ‘ = recommended approach’; ‘ = not Avoid common pitfalls in supportive psychotherapy
recommended’.
1. Avoid attacks and criticism:
Praise a. For example, the client submitted his res-
ignation the next day without following the
1. Compliments, statements of appreciation, and therapist’s advice.
understanding: b. ‘Resignation is usually the last resort.
a. ‘Thanks for coming on time today’. Perhaps we can explore other options which
b. ‘This is a very good suggestion’. we can find satisfaction in the company’.
2. Praise the client for sincere and genuine input. c. ‘It really does not make any sense to me to
3. Reinforce positive behaviour. resign after three months just because you are
4. Seek feedback from the client to ensure accep- not happy with your boss. I cannot agree with
tance of praise. you and you never listen to my advice’.
2. Avoid overpowering statements:
Reflective listening a. ‘I hope that I have made myself clear.
There are other options which you can
1. Repeat patient’s own accounts by paraphrasing consider’.
or using words that add meaning to what the cli- b. ‘As your therapist, I am trying to get you
ent has said. to understand that resignation at this stage
2. For example, a client complains that she does is not a wise decision. Please withdraw your
not like the way her partner comments on how resignation letter’.
she handles her children. The therapist can say, 3. Avoid denigration:
‘It seems that you are a bit annoyed by your a. For example, the client wants to explain to
partner’s comment’. the therapist why he submitted the resigna-
tion letter suddenly. The therapist does not
Summary understand his explanation:
b. ‘Sorry, I do not understand. Would you
1. Summarizing, paraphrasing, and organizing of mind to explain to me again the reason for
the client’s account of issues. your sudden resignation?’
2. This indicates that the therapist is listening and c. ‘What are you trying to say? I do not
interested in the issues. understand at all’.
Advanced Psychological Process and Treatment 333
4. Avoid dismissive response: 25.2.4 Contraindications

a. For example, the client complains that
supportive psychotherapy is not working. 1. Schizophrenia
The therapist does not feel good about his 2. Delusional disorder
remark: 3. High tendency for serious self-harm
4. Severe dependence on substances
b. ‘I am sorry to hear that you find the
5. Very poor insight
psychotherapy not working. May I know in
6. General contraindications for psychotherapy
which aspects of the therapy you find not
apply (see supportive psychotherapy Section 25.1).
working?’
c. ‘It has not been a problem for most of
25.2.5 General Techniques
my clients. Most of them find the therapy
useful. May I know in which aspects of the 1. Establish a therapeutic alliance.
therapy you find unhelpful?’ 2. Set goal: the client and therapist agree to work
on an emotional or psychological problem.
3. Free association by the client.
Duration of supportive psychotherapy: several months to 4. Focus on internal conflicts since childhood.
1 year 5. Interpret transference.
6. Confrontation: an attempt to make the client
face issues that are close to consciousness but
being repressed or denied by the client.
7. Working through: draw previous maladaptive
25.2 BRIEF DYNAMIC PSYCHOTHERAPY patterns or defences to conscious awareness.
25.2.1 Historical Development 8. Enactment: play out the psychological phenom-
enon such as regression in the therapy to facili-
Psychoanalytic theories are considered in Chapter 9. tate understanding.
9. Containment of anxiety.
10. Resolution of conflicts.
25.2.2 Objectives 11. Modify and avoid maladaptive defences.
1. Improve self-understanding by developing 12. Link the past, the present, and the transference.
capacity for self-reflection. 13. Address termination issues.
2. Increase awareness of maladaptive defences and
modify such defences. 25.2.6 Subtypes of Brief Dynamic Psychotherapy
3. Understand the relationship between the past
and present. 1. Brief focal psychotherapy (Malan)
• Clarify the nature of defences and its rela-
tionship to anxiety and impulse.
2. Time-limited psychotherapy (Mann)
25.2.3 Indications • Focus on the present and chronically
1. Depressive disorder endured pain and negative self-image.
2. Anxiety disorders 3. Short-term dynamic psychotherapy (Davanloo)
3. Childhood abuse and trauma • Focus on oedipal (triangular) conflict.
4. Relationship problem
5. Personality disorder 25.2.7 Negative Reactions During Brief
6. Client’s factors
Dynamic Psychotherapy
a. Strong motivation to understand about the
influence of the past 1. Resistance: the client is ambivalent about getting
b. Adequate ego strength help and may oppose attempts from the thera-
c. Tolerance to frustration pist who offers help. Resistance may manifest
d. Capacity to form and sustain relationship in the form of silence, avoidance, or absences.
e. Psychological mindedness These can reveal a great deal about significant
f. Good response to trial interpretation relationship(s) in the past.
2. Acting out: the poor containment of strong feel- 8. Possible positive reactions from the client: grati-
ings triggered by the therapy (e.g. anger towards tude, acceptance of frustration, and demonstra-
the therapist). tion of capacity to handle grief and separation.
3. Acting in: the exploration of therapist’s personal
and private information by the client or present- Duration of treatment: 6 months to several years
ing a symbolic gift to a therapist.
4. Negative therapeutic reaction: the sudden and
unexpected deterioration or regression in appar- 25.2.9 Case Vignette
ent progression during therapy (e.g. premature A 30-year-old man presents with mixed anxiety and
termination of therapy by the client without any depression after he contracted STD from his ex-female
explanation despite a period of engagement). partner. He was recently admitted to the ward after
harming himself with self-laceration. He feels that he
is symbolically castrated by his ex-partner because all
25.2.8 Structure
ladies would avoid him. This episode reminds him of the
25.2.8.1 Initial Phase remarks made by his mother who threatened to castrate
1. Identify problem and clarification. him when he was a child. She probably ridiculed him and
2. Explore the nature and origin of the problem. tried to undermine his sense of masculinity, but the client
3. Perform a psychodynamic formulation. took her remarks very seriously. His father left the fam-
4. Establish a therapeutic alliance. ily when he was young. The client described his father
5. Establish a treatment contract. as passive and irresponsible. He wishes to see a male
psychotherapist and wants to understand the relationship
25.2.8.2 Middle Phase between the past and the present.
1. Identify defences.
2. Challenge and modify primitive, neurotic, and 25.2.10 Psychodynamic Formulation
immature defences.
3. Interpret unconscious motives and transference. A psychodynamic formulation is an account of the cli-
4. Analyse enactment and repetition of pattern. ent’s problems in the context of developmental history
5. Facilitate the working through of attachment that enables the therapist to consider the psychiatric diag-
and loss within the psychotherapy setting. nosis in the context of the client’s inner world, personal
6. Link the past and present. relationship, and past experiences. A psychodynamic
formulation of the previous case is summarized in two
25.2.8.3 Terminal Phase triangles (Figures 25.1 and 25.2).
1. Termination occurs when therapeutic endeavour
comes to a predefined end date set by the treat- 25.2.11 CASC Preparation: Explain Brief
ment contract.
Dynamic Psychotherapy to a Client
2. Termination can be a complex and powerful
event in brief dynamic psychotherapy. 1. Brief dynamic psychotherapy is useful for a cli-
3. Summarize the progress of therapy. ent who wants to understand how his or her cur-
4. Encourage the client to look forward into the future. rent difficulties may relate to past experiences
5. Address transference and countertransference based on the concepts developed by Sigmund
issues. Freud. Freud developed the model of the mind
6. Discuss possible follow-up plan and access to through psychoanalysis. Freud described that
external resources and other therapies. forces and processes in an unconscious mind
7. Possible negative reactions from the client: grief may affect how a person behaves. The content
and mourning, anger and perceptions of aban- of dreams also helps us to understand how the
donment, enactment of negative experience of unconscious mind works.
earlier separations and regression, devaluation of 2. In contrast to traditional psychoanalysis that
therapist as a result of narcissistic injury, return involves frequent meetings (typically five times
of symptoms, denial and resistance, avoidance of a week), the brief dynamic psychotherapy aims
termination, acting out, and acting in. to reduce distress reported by the client through
Symptoms: anxiety and depression
Triangle of
symptoms Underlying impulse:
Defence: denial of grief over self-harm as a result of self-hatred
the loss of relationship
FIGURE 25.1 Triangle of symptoms.
The here and now during therapy: unconscious wish to see

a male therapist to replace the missing father figure.
Triangle of
relationship
The here and now Past relationship:

outside the therapy: aggressive mother and
anger toward his partner irresponsible father
FIGURE 25.2 Triangle of relationship.
less frequent sessions over a time-limited are more likely to benefit from brief dynamic psy-
period (e.g. weekly session over a period of chotherapy. The therapist is mostly nondirective
6 months–1 year). and follows the thoughts and feelings of the client.
3. The therapist works with the client to identify
recurrent patterns. The therapist helps the cli- 25.2.12 Research and Brief
ent to draw upon feelings evoked during psy-
Psychodynamic Therapy
chotherapy. The therapist promotes reflective
thoughts and helps the client to make links with Research in brief dynamic psychotherapy faces the fol-
past experiences. The goals of therapy are to lowing challenges:
resolve conflict, to effect changes to improve
quality of life, and to enhance the client’s capac- 25.2.12.1 Structural Aspects
ity to handle frustration. 1. Psychodynamic psychotherapy is relatively
4. This process of attempting to explore the uncon- unstructured in nature. It has less clear aims,
scious mind may generate anxiety. Client often goals, or end points compared to cognitive
complains of deep-seated discomfort. Clients behaviour therapy (CBT).
who are interested in brief dynamic psychother- 2. Psychodynamic psychotherapy cannot be manu-
apy must demonstrate sufficient ego strength. alized and there is no agreement on a standard
It is because they have to be strong enough to approach. The therapy cannot be reduced to
face the process of working through and the treatment algorithms but depends on the thera-
feelings associated with conflicts. Clients have peutic alliance and analysis of transference and
to be in touch with painful memories and emo- countertransference.
tions during the therapy. They are also sub- 3. There are less psychodynamic psychotherapists
jected to the therapist’s interpretation and gentle compared to cognitive behaviour therapists.
confrontation. 4. There are funding barriers to brief dynamic
5. In general, clients who are more articulate, psy- psychotherapy research because it is often con-
chologically inclined, and able to tolerate stress ducted in private clinics.
25.2.12.2 Methodological Aspects 25.3.2 Objectives

1. There is selection bias because clients presenting 1. Alleviate symptoms such as anxiety or depres-
for brief dynamic psychotherapy are more moti- sion by helping the client to identify and chal-
vated, educated, and psychologically inclined. lenge negative cognitions.
2. Psychotherapists cannot be blinded to the inter- 2. Develop alternative and flexible schemas.
ventions, but outcome can be measured by a 3. Rehearse new cognitive and behavioural responses
trained research personnel blinded to the nature in difficult situations.
of the psychotherapeutic intervention.
3. Issues of informed consent required for research 25.3.3 Characteristics
and administering standardized questionnaires
may affect the transference and countertransfer- 1. Collaborative empiricism: engagement and col-
ence. On the other hand, issues of transference laboration between the therapist and the client.
may contaminate the client’s satisfaction on 2. Focus on specific issues.
therapy if this is an outcome measure. 3. Homework is assigned.
4. Time-limited.
25.2.12.3 Measurement of Outcomes 5. Focus on here and now.
1. There is disagreement on the universal outcomes 6. Outcome can be measured by direct observation,
in brief dynamic psychotherapy. Possible out- physiological measures, standardized instru-
comes include measures of symptom severity, ments, and self-report measures such as the
‘ego strength’, coping style, self-report in quality Beck Depression Inventory, the Beck Anxiety
of life improvement, or client satisfaction. Inventory, and the Fear Questionnaire.
2. Clients may not have a clear psychiatric diagno-
25.3.4 Indications
sis and there is often spontaneous remission of
symptoms. 1. Mood disorders: depressive disorder and bipolar
3. Statistically significant improvement in out- disorder
come may not equal to clinical improvement. 2. Generalized anxiety disorder, panic disorder,
and obsessive compulsive disorder
3. Phobia: social phobia, agoraphobia, and simple
25.3 CBT phobia
25.3.1 Historical Development of CBT 4. Eating disorders: anorexia nervosa and bulimia
nervosa
25.3.1.1 Cognitive Therapy 5. Impulse control disorders
Beck proposed that negative thinking in depression origi- 6. Schizophrenia (target at delusions and halluci-
nates from earlier assumptions that play a central role in nations, coping enhancement, enhance adher-
the maintenance of depressive symptoms. ence to treatment, and relapse prevention)
Beck’s cognitive model of depression includes the 7. Personality disorders (refer to dialectical behav-
effect of early experiences, core beliefs, underlying ioural therapy)
assumptions, cognitive distortions, automatic thoughts, 8. Substance abuse
and the negative cognitive triad. Depression can be 9. Liaison psychiatry (chronic pain, chronic
treated by modifying one of the components based on fatigue, physical illnesses)
Beck’s cognitive model. 10. Paraphilia
25.3.1.2 Behaviour Therapy 25.3.5 Contraindications

Mowrer’s two-factor model states that fear of a specific 1. Severe dementia
stimulus is acquired through classical conditioning and 2. Profound learning disability
the client tries to reduce fear by avoiding the conditioned 3. Delirium
stimulus through operant conditioning. 4. No evidence of cognitive errors
Ayllon and Azrin’s token economy model is a con- 5. No motivation or no interest for CBT
trolled environment where reinforcers were applied to 6. General contraindications for psychotherapy
systematically change a client’s behaviour. apply (see Section 25.1)
25.3.6 Techniques 25.3.8 During Each Session

25.3.6.1 Cognitive Techniques 1. Weekly update.
Cognitive restructuring helps the client to identify nega- 2. Bridge from the previous session.
tive thoughts, dysfunctional assumptions, and maladap- 3. Review homework assignment.
tive core beliefs relating to their underlying problems. It 4. Set agenda for this session.
also tests the validity of those thoughts, assumptions, and 5. Work on the agenda.
beliefs. The goal is to produce more adaptive and positive 6. Provide brief summaries.
alternatives: 7. Assign homework assignment.
8. Summarize the session and offer feedback.
1. Identify negative automatic thought (NAT) (e.g.
I am going to receive the bad news when I step 25.3.9 Structure
into by office).
25.3.9.1 Early Phase (Session 1–4)
2. Identify dysfunctional or faulty assumption
(e.g. at my workplace, people do not like me 1. Establish therapeutic relationship.
because I expressed my negative feelings last 2. Educate the client about the model of CBT and the
week). influence of thoughts on behaviour and emotion.
3. Identify maladaptive core belief and rate its 3. Set goals for psychotherapy.
strength (e.g. I am an unpopular person). 4. Identify NATs.
4. Restructure the maladaptive core belief. 5. Assessment by Socratic questioning: the use of
5. Formulate alternative positive belief. questions to reveal the self-defeating nature of
6. Rate the impact of maladaptive belief on the client’s NATs and identify cognitive triads
emotion. (automatic thoughts, cognitive distortion, and
7. Rate the impact of new core belief on emotion. faulty assumptions).
6. Case formulation.
7. Baseline measure of symptom severity by a
standard instrument.
25.3.6.2 Behavioural Techniques
RAT PAD (think of the rat in the Skinner’s box) 25.3.9.2 Middle Phase (Session 5–12)
R—rehearsal: help the client to anticipate challenges 1. Keep a dysfunctional thought diary (see
and develop strategies to overcome such difficulties. Figure 25.3).
A—assignment: graded assignment on exposure. 2. Identify cognitive errors and core beliefs
T—training to be self-reliant. through homework assignment.
P—pleasure and mastery. 3. Practice skills for reattribution by reviewing
A—activity scheduling: to increase contact with evidence and challenging cognitive errors.
positive activities and decrease avoidance and withdrawal. 4. Behaviour therapy involves identifying safety
D—diversion or distraction techniques. behaviours, entering feared situation without safety
manoeuvres, applying relaxation techniques, activ-
ity scheduling, and assertiveness training.
5. Review progress and offer feedbacks.
25.3.7 Socratic Questioning
1. What is your view of the event? 25.3.9.3 Termination (Session 13–16)
2. What is the evidence of your belief? 1. Prepare for termination.
3. Is there any alternative explanation? 2. Identify early symptoms of relapse and predict
4. What would you tell a close friend if he or she is high-risk situations leading to a relapse.
in the same situation as you? 3. Relapse prevention: develop coping strategies to
5. Are you condemning yourself based on a single overcome negative emotions, interpersonal con-
event? flicts, and pressure.
6. Do you think that you have bias? 4. Formulate a plan for early intervention if relapse
7. Have you overestimated the risk? takes place.
Situation / Date / Time Automatic Thoughts Emotion Behaviour Alternative Thoughts

(Mood score: 1–10;
1 = very depressed;
10 = very happy)
26 July 2012. ‘I can never do the things Said and angry with Said nothing, shut ‘I am too negative. This is
Thursday night right. I have no say in this myself (rated 2 out myself in a room not a catastrophe. Our
8 pm relationship. I fail of 10) relationship will get better’
My boyfriend criticised me everything in my life’
FIGURE 25.3 Dysfunctional thought diary.
5. Consolidate skills and knowledge learned in 25.4.4 Contraindications

therapy.
6. Measure severity of symptoms by a standard General contraindications for psychotherapy apply (see
instrument at the end of therapy. Section 25.1). In addition, there is a set of skill training
rules that the client must comply:
25.4 DBT 1. Client cannot miss therapy for more than 4

weeks in a row.
25.4.1 Historical Background 2. Client cannot misuse drugs or alcohol during
• Dialectical behaviour therapy (DBT) was devel- the course of therapy.
oped by Marsha Linehan who is a clinical psy- 3. Client is not allowed to discuss past suicidal
chologist from Seattle, the United States. behaviour with other clients outside therapy.
4. Client must keep information obtained from
group session confidential.
25.4.2 Objectives 5. Client must not develop private relationship with
• Borderline personality disorder (BPD) is an other clients outside therapy.
interaction between an emotionally vulnerable 6. Client must not attend the same skill training
person and an invalidating environment. As a group with his or her sexual partner.
result, the client has chronic feeling of empti-
ness and does not find his or her life worth liv- 25.4.5 Components of DBT
ing, which results in multiple self-harm. The
overall objective of DBT is to help the client 1. Individual sessions: 45–60 min on a weekly
build a life that is worth living. basis, to review diary cards in the past 1 week
• Reduces self-harm or suicidal behaviour (e.g. and discuss life-threatening behaviours.
self-laceration). 2. Skill training group by a trainer: weekly group
• Reduces and stops therapy-interfering behav- session for 2 h
iour (e.g. missing session or acting out in a. First hour: mindfulness meditation practice
therapy). and sharing of each member
• Reduces or stops serious quality of life-inter- b. Second hour: life-skill training (mindful-
fering behaviour (e.g. frequent argument with ness, interpersonal effectiveness, emotional
family members, resulting in rejection and regulation, and distress tolerance)
homelessness). 3. Brief out-of-hours telephone contact as part of
• Develop life skills. the treatment contract
4. Weekly consultation group between the indi-
vidual therapist and the skills trainer
25.4.3 Indications
25.4.6 Techniques
1. BPD: reduce self-harm behaviour, anger, num-
ber of visits of accident and emergency depart- 1. Dialectical thinking: advise the client not to
ment, and hospitalization. think linearly. Truth is an evolving process of
2. Young people with repetitive self-harm. opposing views rather than extremes.
2. Behavioural therapy with homework assignment. 3. Develop appropriate affect expression to handle
3. Mindfulness ‘how’ skills: observing and impulse control, reduction of self-harm, passive
describing events and participating without aggression, idealization, hate, and love.
self-consciousness. 4. Establish a stable representational system.
4. Mindfulness ‘what’ skills: adopting nonjudge- 5. Form a coherent sense of self.
ment stance, focusing on one thing at a time, and 6. Develop a capacity to form secure relationships.
enhancing self-effectiveness.
5. Life-skill training: Zen Buddhism: emphasize Duration: 18 months; DBT is conducted in a day hospital.
on wholeness, consider alternatives, and engulf
alternatives.
6. Use of metaphors: enhancing effectiveness of 25.6 COGNITIVE ANALYTIC THERAPY
communication, discovering one’s own wisdom,
and strengthening therapeutic alliance. 25.6.1 Historical Background
Cognitive analytic therapy (CAT) is developed by
Duration of treatment: 1 year. Anthony Ryle. CAT is a combination of cognitive and
analytic therapy.
25.5 MENTALIZATION-BASED TREATMENT
25.5.1 Historical Development 25.6.2 Objectives
1. Mentalization-based treatment (MBT) was 1. CAT aims at changing maladaptive procedural
developed by Anthony Bateman and Peter sequences.
Fonagy. 2. CAT focuses on specific patterns of thinking
and less on interpersonal behaviour.
3. CAT focuses less on transference interpretation.
25.5.2 Objectives
1. Mentalization refers to psychological minded-
ness and empathy. Mentalization is developed 25.6.3 Indications
in people who have responsive parents provid-
1. Neurotic disorders
ing secure attachment in childhood. Patients
2. Personality disorders (e.g. BPD)
with BPD have impaired mentalization. As
3. Depression
a result, they are not able to interpret their
4. Deliberate self-harm
actions or others’ actions based on the inten-
5. Abnormal illness behaviour
tional mental states such as beliefs, feelings,
and preferences. Impaired mentalization is
associated with affect dysregulation and inco-
25.6.4 Techniques
herent self.
2. MBT helps clients with BPD to develop the 1. Use open questioning and descriptive reframing
capacity to realize that a person has an agentive during the assessment.
mind and to recognize the importance of mental 2. Formulate a procedural sequence model. The
states in other people. model tries to understand the aim-directed
action (e.g. formulate an aim, evaluate environ-
mental plans, plan actions, and evaluate results
25.5.3 Indications
of actions).
1. BPD 3. Identify faculty procedures:
a. Traps: repetitive cycles of behaviour and
their consequences become perpetuation.
25.5.4 Techniques
b. Dilemma: false choices or unduly narrowed
1. Ask the client to observe his or her state of mind. options.
2. Generate alternative perspective of the experi- c. Snag: extreme pessimism about the future
ence of oneself and other people. and halt a plan before it even starts.
4. Write a reformulation letter that begins with a nar- 1. CAT is a short-term focused treatment. CAT
rative account of the client’s life story and identify involves a combination of cognitive therapy
repetitive maladaptive patterns. The letter also con- and analysis. For cognitive therapy, the thera-
tains a diagram that illustrates the reciprocal roles pist will examine your behaviours and asso-
between the client and procedural sequence model. ciated feelings. For example, if a specific
5. Change maladaptive procedural sequences and situation makes you feel depressed, an analy-
predict the likely transference and countertrans- sis of feeling may help to identify the origin of
ference feelings. Enactments become active dur- depression.
ing sessions. 2. The analytical component deals with conflict
6. Towards termination, the therapist will issue a through explanation. The therapist will try to
goodbye letter to the client that summarizes the understand your negative feelings and resolve
progress and achievement of the therapy. The cli- problematic behaviour. The client will gain more
ent may also issue a goodbye letter to the therapist. understanding through analysis and reduce the
stress levels.
Duration: 16–24 sessions. 3. In the beginning phase, the therapist will try
to understand you and formulate a model.
CASC STATION: EXPLAIN The in-depth assessment will help the thera-
CAT TO A CLIENT pist to identify any faculty pattern. You need
to write a letter to describe your life story.
Client P is a 30-year-old man. He is currently unem- The therapist will look for repetitive faculty
ployed and he worked as a graphic designer in the patterns in your life. The most important part
past. He feels hopeless after he was retrenched. His of CAT is to change maladaptive and faculty
girlfriend has recently terminated their relationship patterns.
but they are still in contact. He spends his time with 4. Prior to termination, the therapist will give you
his band and he is the band leader. He realizes that a letter that will summarize the progress and
his members have betrayed him and he has decided achievement during the therapy. You can also
to leave the band. His psychiatrist diagnosed him write a letter to the therapist to express your
with moderate depressive episode and refers him feelings (Figure 25.4).
for psychotherapy. During the assessment session,
he wants to know what has gone wrong in his work
and in the band. He hopes that the failure will 25.7 INTERPERSONAL THERAPY
not occur in his future career. He has history of
hyperthyroidism. 25.7.1 Historical Background
Task: Explain CAT to this client. Interpersonal therapy (IPT) was developed by Gerald
Klerman. IPT is based on attachment theory.
People are
His band He did not get below par
members on well with his
antagonise him. girlfriend
Disappointed
Feeling depressed More social
and build up
isolation
resentment
He will have Poor

difficulty finding interpersonal
a job function Anger
outbursts
(a) (b)
FIGURE 25.4 (a) Trap in Client P’s case. (b) Dilemma faced by Client P.
25.7.2 Objectives 25.7.4.1.2 Middle Phase

1. To create a therapeutic environment with 1. Identify 1–2 interpersonal problem areas:
meaningful therapeutic relationship and recog- a. Assess the impact of an interpersonal event
nize the client’s underlying attachment needs on mood.
2. To develop an understanding of the client’s b. Explore patient’s expectations and options
communication difficulties and attachment style in the event.
both inside and outside the therapy c. Assess the relationship between the inter-
3. To identify the client’s maladaptive pat- personal problem and underlying attach-
terns of communication and establishment of ment pattern.
insight d. Fill up an interpersonal inventory card (see
4. To assist the client in building a better social Figure 25.6).
support network and mobilize resources e. Perform communication analysis to identify
maladaptive patterns of communication.
f. The therapist can adopt three stances: neutral
stance, passive stance, and client advocate
25.7.3 Indications
stance on correcting communication patterns.
• Depressive disorder: IPT is equally effective as g. Role-play and develop strategies to handle
CBT. similar situations in the future.
• Eating disorder: bulimia nervosa. 2. For grief
• Dysthymia. a. Explore grief feelings for loss of relationship
• Other issues: interpersonal disputes, role transi- or loss of status.
tion, grief, and loss. b. Facilitate mourning of loss.
c. Develop interest and relationships to substi-
tute for the loss.
25.7.4 Techniques 3. For interpersonal disputes
a. Identify current stage of interpersonal disputes
25.7.4.1 Structure (e.g. renegotiation, impasse, or dissolution).
25.7.4.1.1 Initial Phase b. Understand role expectations.
1. Define depression and explain diagnosis. c. Modify nonreciprocal role expectations.
2. Offer an interpersonal formation (see Figure 25.5). d. Examine other interpersonal relationships.
3. Explain rationales of IPT and logistics of treat- e. Examine assumptions behind patient’s
ment such as treatment contract. behaviour and modify faculty assumptions.
4. Identify target interpersonal problem areas such 4. For role transitions
as grief, role transition, role dispute, and inter- a. Accept the loss of previous roles.
personal deficits. b. Develop positive attitude towards the new roles.
5. Assign sick role. c. Develop a sense of mastery in the new roles.
Biological factors: Psychological factors: poor Social factors: being too critical and
hyperthyroidism attachment to father often offend the others
Interpersonal crisis: Rejection by his girlfriend

and band members
Interpersonal distress and depression
FIGURE 25.5 Interpersonal formulation (using Client P under CAT as an example).

Client Name: Client P Date of Birth: 4 February 1976 Psychiatrist-in-charge: Dr. McFadzean
Date of first consultation: 26 July 2012
Name of significant person: Miss L Relationship: Ex-girlfriend
Client’s account of problems:

1. Miss L is too sensitive with unrealistic expectation.
2. Always end up in quarrel, relationship is not going anywhere.
3. Client P cannot hold his criticism and openly criticises Miss L.
4. Miss L also looks down on Client P because he is out of job.
Areas requiring further clarification:
1. Communication with band members
2. Attachment in childhood
3. Anger control
Agreed problem area:
1. Grief and loss of relationship
2. Develop more gentle way to communicate his disappointment
FIGURE 25.6 Interpersonal inventory (using Client P under CAT as an example).
5. For interpersonal role deficits distress. In order to help you to understand this
a. Reduce social isolation. concept better, I would like to give you an anal-
b. Encourage formation of new relationships. ogy. Some people like to climb to high places
c. Explore repetitive patters in relationships. as they are adventurous and enjoy the excite-
ment. For some people, climbing is frightening
25.7.4.1.3 Termination Phase and they have no confidence to do it. They are
1. Discuss the impact of termination. able to climb with assistance from a trusted and
2. Acknowledge that termination may trigger grief significant person. This significant person also
feelings. provides interpersonal reassurance. The psycho-
3. Assist patient to establish competency to han- therapy itself is like climbing the mountain, and
dle interpersonal problems independently after IPT is designed to help the client to recognize
termination. their interpersonal needs and to seek attachment
4. Identify social support resources. and reassurance in the process of improving
interpersonal relationship. More importantly,
Number of sessions: 16–20 sessions. you will be able to express those needs to other
people and promote positive responses after the
25.7.5 CASC Preparation: Explain therapy.
3. How many stages does IPT have? The therapy
IPT to a Client
has three stages. In the first stage, the therapist
1. What is IPT? IPT is a time-limited psycho- will try his or her very best to develop a good
therapy. The aim of IPT is to reduce your suf- therapeutic relationship with you and understand
fering and improve interpersonal functioning. your problem. In the second stage, the therapist
IPT focuses on interpersonal relationships as a will seek your views to work on an agreed prob-
means of bringing about change. The goal is to lem area. The information will be summarized
help you to improve your interpersonal relation- in a card. The therapist will analyse the way
ships or change your expectations on interper- you communicate with other people. The thera-
sonal relationship. pist will give you useful advice and help you to
2. What does the therapist do? The therapist will develop new skills by using role-play. The thera-
help you to improve the social support net- pist will help you to work on issues related to
work so that you can manage the interpersonal loss and develop a new role. In the final stage, the
therapist will strengthen the skills you learned relationship; to create necessary separation and
in therapy. The therapist will help to iden- independence in case of enmeshment.
tify resources for you to handle interpersonal 3. Communication problems and triangulation:
problems in the future. The whole IPT takes introduction of humour, demonstration of warmth
16–20 sessions. and empathy, role-play, and modifying both ver-
bal and nonverbal communication.
4. Role problems (e.g. family scapegoat, parental
25.8 FAMILY THERAPY child): identify problems and redefine roles. The
same-sex parent functions as primary disciplinar-
25.8.1 Historical Perspectives
ian and promotes maximum ego development by
Minuchin developed structural family therapy. He is setting limits and higher-level goals. The oppo-
interested in how families are organized in the subsys- site-sex parent functions as the facilitator or medi-
tems and in the boundaries between these components. A ator within the triangular relationship to correct
good family has clear hierarchy and boundary between inappropriate parenting from the same-sex parent.
the subsystems. 5. Task accomplishment problems (e.g. develop-
Milan developed systemic family therapy that empha- mental tasks): identifying the task, exploring
sizes that family system is more than the sum of its com- alternative approaches, taking action, evaluat-
ponents and the system as a whole is the focus of therapy. ing, and adjusting.
Symptoms of individual family members are a manifes-
tation of the way the family system is functioning.
25.8.3 Assessment Techniques
1. Ask each family member to describe his or her
25.8.2 Indications sense of the problem.
25.8.2.1 External Indicators for Family Therapy 2. Ask each individual the same question that has
been asked of other family members.
3. Ask each family member to propose a solution
1. Addition of members to the family (e.g. unplanned
to the problem.
pregnancy and birth of a young sibling).
4. Ask each individual’s reaction to what other
2. A family member is recently diagnosed with an
family members have said.
illness that can be terminal or causes significant
5. Assign homework or task that aims to solve
change in role (e.g. cancer in one parent).
problems in the family.
3. Change in financial status: for example, bank-
6. Identify nonverbal communication in the family.
ruptcy in family.
7. Identify common themes in the family.
4. Children leaving home: for example, empty nest
8. Individuals are requested to speak with ‘I’ phrases
syndrome.
but not the ‘you’ phrases during assessment.
5. Change in marital status: for example, divorced
parent remarries again, affecting the children.
6. Suprasystem problems: for example, when there 25.8.4 Types of Family Therapy
is a high crime rate in the neighbuorhood that 25.8.4.1 Structural Family Therapy (Minuchin)
affects the family, family therapy can strengthen
• Minuchin believed that families are systems that
the boundary between the family and the supra-
operate through subsystems. Each subsystem
system by working with external agencies such
requires adequate boundary and permeability.
as police or MP.
• Family problems arise when boundaries are too
loose, resulting in enmeshment. When family mem-
25.8.2.2 Internal Indicators for Family Therapy bers are too rigid, this will result in disengagement.
1. Behaviour control problems (e.g. conduct disor- • Structural family therapy identifies the set of
der in a child): engage family to deliver behav- unspoken rules governing the hierarchy, sharing
iour therapy in home environment. of responsibilities, and boundaries.
2. Boundary issues between family members • The therapist presents these rules to the family
(e.g. enmeshment): to promote communica- in a paradoxical way to bring about changes. The
tion and emotional interchange in disengaged therapist is active in control of the proceedings.
25.8.4.2 Systemic Family Therapy their parents is allowed). This therapist will
1. Milan associates often involve more than two also disqualify anyone who is an authority
therapists working in a team to maintain the sys- on the problems including the parents (e.g.
temic perspective. One therapist is always with the children are allowed to challenge their
the family while the team observes through a parents and undesired behaviour is encour-
one-way screen or video camera. The team aged. Paradoxically, change and improve-
offers input to the therapist via telephone or dur- ment will take place as family members
ing intersession breaks to discuss the family sys- cannot tolerate the paradoxical pattern).
tem. There are pre- and post-session discussions. b. Another technique is symptom prescription
2. Reframing an individual’s problem as family when symptoms are allowed to take place
problem (e.g. the borderline personality of a in specific time and place. Paradoxically,
daughter is reframed as the parental problem in symptom will disappear.
providing care to their child). An internal prob- c. Declaration of impotence by therapist
lem can be reframed as an external problem if is used when family members gang up
there are unproductive conflicts in the family and attack the therapist. Such declara-
that exhausted everyone (e.g. the family is under tion will put an end to the battle and this
the influence of anger rather than labelling a often leads to complementary relationship
family member as an angry person). between the therapist and the family. It is
3. Explore the coherence and understand the fam- paradoxical because the therapist declares
ily as an organized coherent system. impotence on the one hand but collects
4. Circular questioning is used to examine per- professional fee and planning treatment on
spective of each family member on interfamily the other hand.
member relationship. It aims at discovering and d. The therapist can pass pessimistic views
clarifying conflicting views. Hypothesis can be on the family and hope that they change
formed from the conflicting views and the thera- quickly after hearing the negative remarks.
pist can propose further changes. 4. Prescribing family rituals: Rituals refer to
membership, brief expression, and celebration.
(e.g. the therapist passes a metaphor object to
25.8.4.3 Strategic Family Therapy the family and any family member can use this
Strategic family therapy uses a complex plan rather than object to call for a meeting at home). Ritual
a simple directive to produce changes in the family. The prescription refers to setting up a timetable that
general techniques are listed as follows: assigns one parent to take charge on an odd day
and a child to take charge on an even day. Ritual
1. Positive connotation: It is a form of reframing prescription is useful for a family with parental
by ascribing positive motives to the symptom- child.
atic behaviour. 5. Other strategies include humour, getting help
2. Metaphors allow indirect communication of from a consultation group that observes through
ideas (e.g. a relationship metaphor describes the the one-way mirror to offer advice, and debate
relationship between the therapist and a family among family members.
member, and this metaphor can apply on other
relationships). Metaphorical object refers to the There are two types of strategic family therapy:
use of a concrete object to represent abstract
ideas (e.g. a blank sheet of paper in an envelope 1. Strategic approach (Haley and Madanes)
representing the family secrets). a. Clear generational boundaries are empha-
3. Paradoxical interventions sized in normal family development.
a. This method is used when direct methods b. Concerns with the family dysfunction are
fail or encounter strong resistance in some manifested by a symptom (e.g. anorexia ner-
family members. The therapist will reverse vosa in a daughter).
the vector (i.e. rather than a top-down c. Family rules usually follow a hierarchical
approach that always starts from the par- model. Improving the hierarchical and bound-
ents, a bottom-up approach from children to ary problems would prevent dysfunctional
feedback loops (e.g. the therapist focuses on was considered as a nodal point of social interac-
the hierarchy between the parents and their tions and offered deeper interpretation of hidden
daughter with anorexia nervosa. This will communication and problems in a group. He also
change the anorexia nervosa of daughter). introduced group matrix that is a total network of
d. Four types of family problems usually result communications that evolves in group therapy.
from 3. In the United States, Kurt Lewin developed the
i. Desire to be loved field theory that states that individual dynam-
ii. Desire to control and dominate ics are shaped by the surrounding social forces.
iii. Desire to love and protect other family members This concept evolves into the encounter group
iv. Desire to repent and forgive that emphasizes on self-awareness and personal
2. Mental Research Institute (MRI) strategic fam- growth (Lewin, 1943).
ily therapy 4. In 1961, Bion introduced two concepts of group
a. Define problem in behavioural term. (Bion, 1961):
b. The family members attempt to solve their a. The basic assumption group refers to the
problems by setting up a feedback loop that primitive state of mind and members gather
worsens the problems. together, which poses a threat to the group.
c. For example, if the daughter suffers from b. The work group is rational, purposeful, and
anorexia nervosa, the family has made the cooperative.
problems worse by giving harsh feedbacks.
d. In MRI strategic family therapy, the family
25.9.2 Indications
therapist focuses on correcting the daugh-
ter’s diet and eating habits. Group members require careful selection. The general
e. Then the therapist identifies the feedback inclusion criteria include
loop that prevents the daughter from eating
and sets behavioural goals. 1. High motivation
f. The family therapist helps the family by 2. Interest to explore the past issues
i. Identifying the feedback loop 3. Ability to empathize and sympathize
ii. Finding the rules that govern it 4. Positive group experience
iii. Changing the loop and the rules 5. Compatible problems: long-standing psycholog-
ical problems
25.8.4.4 Eclectic Family Therapy
• It concentrates on the present situation of the 25.9.3 Contraindications
family and examines how family members com-
municate with one another. Medical or psychiatric factors
• It is flexible and allows time for the family to work
together on problems raised in the treatment. 1. Severe head injury or other organic condition
• It is commonly used in adolescents and their family. that affects the ability to communicate
2. Paranoid schizophrenia or paranoid personality
disorder
25.9 GROUP THERAPY 3. Severe narcissistic personality disorder
4. Severe hypochondriasis
5. Severe antisocial personality disorder or people
1. In 1907, Joseph Pratt started an education group with psychopathy
for tuberculosis patients. The study of veterans
of World War I and II had great influence on the Personal factors
development of group therapy (Pratt, 1907).
2. In the second Northfield experiments, Michael 1. Poor motivation
Foulkes used the whole veteran ward as a therapeu- 2. Strong denial
tic community to increase discipline and morale 3. Inability to self-disclose
while decreasing delinquency (Foulkes, 1946). 4. Lack of empathy
He developed group analysis when the patient 5. Negative group experience
6. Problems incompatible with group therapy (e.g. b. Supportive group therapy involves empa-
marital problem) thy, encouragement, and explanation (e.g.
7. Frequent acting-out behaviour Schizophrenia Fellowship).
8. Hidden agenda (e.g. aim to develop a romantic 3. Analytic group therapy:
relationship with one of the group members) a. Analyse cyclical relational patterns.
b. Interpret transference and countertransfer-
25.9.4 Types of Group Therapy ence in interpersonal terms.
c. Interpret conflicts in a group and relate with
25.9.4.1 Classification Based on experience outside the group.
Service Administration d. Dream analysis in a group.
1. Open group therapy: allows replacement of 4. Outpatient group therapy
group members. a. It may involve a self-help group targeting
2. Closed group therapy: no replacement of group at homogenous group of clients focusing on
members is allowed. one disorder (e.g. for anxiety disorders or
3. Heterogeneous group: allows a mixture of cli- Alcoholics Anonymous, AA).
ents with different backgrounds and conditions. b. Outpatient group therapy is for short term
4. Homogeneous group: only allows group mem- and involves direct didactic instruction.
bers of the same gender, similar background, or 5. Psychodrama
same condition (e.g. anger problem). a. The group enacts the life of one member as
5. Continuous group therapy: there is no definite a role-play. The other members exchange
end date of group therapy. The therapy may last roles in the role-play and all group mem-
for years. Old members leave and new m embers bers express their views after the role-play.
join. b. Psychodrama leads to better understand-
6. Brief group therapy: there is a definite end date ing and development of strategies to handle
and members are expected to join and complete similar situations in the future.
group therapy at the same time.
7. Leadership: active or passive leadership; co-
leadership (i.e. two group leaders). 25.10 THERAPEUTIC PROCESS
25.10.1 Pregroup Therapy Assessment
25.9.4.2 Classification Based on Technique
1. Assess the client’s suitability for group therapy.
1. Milieu group therapy: Mainly developed for
2. Socialize with the client.
therapeutic community, and the whole commu-
3. Assess his or her ability to communicate and
nity (e.g. the ward) is viewed as a large group.
empathize.
Rappaport described four characteristics in
4. Set personal and interpersonal goals.
milieu group therapy:
5. Inform the rules of group therapy.
a. Democratization (equal sharing of power)
6. Discuss the common pitfalls in group therapy.
b. Permissiveness (tolerance of others’ behav-
7. Discuss strategies to reduce anxiety in group
iour outside the setting)
participation and dropouts from group therapy.
c. Reality confrontation (confront with the
8. Establish a treatment contract.
views from others)
d. Communalism (sharing of amenities)
Further details on therapeutic commu- 25.10.2 Yalom’s 11 Therapeutic Factors
nity are considered in Norton and Warren
(2009). 25.10.2.1 Early Stages
1. Instillation of hope: sense of optimism about
2. Supportive group therapy: progress and improvement.
a. For clients with chronic psychiatric disor- 2. Universality: one member’s problems also occur in
ders such as schizophrenia attending a day other members. Hence, the member is not alone.
hospital, which offers supportive group 3. Information giving: members will receive infor-
therapy. mation on their illness and associated problems.
25.10.2.2 Middle Stage 2. Bion’s basic assumption group

1. Altruism: one member feels better by helping a. Dependence
other members and sharing their solutions. b. Fight–flight
2. Corrective recapitulation of the primary family: c. Pairing
the group mirrors one’s own family and provides a 3. Resistance is an attempt to break the framework
chance for self-exploration of past family conflicts. of the group (e.g. scapegoating: subclassifying
3. Improved social skills by social learning. a group of people and attacking them and/or
4. Imitative behaviour is established by vicarious monopolizing the group).
learning or observation of the others.
5. Interpersonal learning is established by correc- Other problems of group therapy include repetitive stress
tive experience in social microcosm. injury, enhancing abnormal illness behaviour, danger
of charismatic leadership, and dissemination of false
information.
25.10.2.3 End Stage
1. Group cohesiveness occurs after intermember
acceptance and understanding. The cohesive- 25.11 COUPLE THERAPY
ness leads to the sense of safety and contain-
25.11.1 Objectives
ment of negative feelings.
2. Catharsis: group members feel encouraged and sup- 1. Couple therapy involves the therapist (or some-
ported by expressing emotionally laden materials. times two therapists) seeing two clients who are
3. Existential factors: after group therapy, group in a relationship, not necessarily in a marriage.
members have more self-understanding and
insight in responsibility and capriciousness of
25.11.2 Indications
existence.
1. Interpersonal problems in a relationship
2. Issues or difficulties related to a marriage or
25.10.3 Role of the therapist
partnership
1. The therapist can draw heavily upon a group set- 3. Grief in a couple (e.g. loss of a child)
ting to exercise the full range of therapeutic skills. 4. Sexual problems
Group therapy reduces the chance of intense
transference reactions from group members.
25.11.3 Contraindications
2. The therapist may have particular inclinations
and motivations (e.g. past experience of alcohol 1. Ongoing violent behaviour that is not under
misuse in AA groups). control
3. The therapist can encourage a combination of 2. Clear evidence that one partner is using the cou-
individual and group therapy. This will posi- ple therapy to terminate a relationship
tively integrate these two forms of therapy for
maximal benefit.
25.11.4 Issues to Be Considered Before
Arranging Couple Therapy
25.10.4 Advantages of Group Therapy
1. Therapist-related issues
1. Reduction of cost. a. Age and life experiences of the therapist are
2. The context of the group may give members essential because couples may look for ther-
value and a sense of group identity to assist them apists who are married or who have been
to cope with current problems in life. married.
b. The gender of the therapist plays a key role
as the therapist may identify with the same-
25.10.5 Countertherapeutic Process
sex client.
1. The countertherapeutic process may lead to c. Culture and religious background of the
individual disappointment, pessimism, and therapist in relation to the background of the
antagonism of therapist. couple should be considered.
d. The therapist needs to monitor his or her injunction. Provocative statements are used to stir
own countertransference (e.g. rescue fanta- up counterresponse. This response is a double-end
sies or overidentification with the client). sword because it also offers benefits by bringing
2. Therapy-related issues changes. An example is that the therapist pre-
a. The relationship between couple therapy scribes the symptom and advises one partner to
and other ongoing therapies such as indi- continue the problem behaviour. This will stir up
vidual psychotherapy counterresponse from the couple because they are
b. Confidentiality, neutrality, and triangulation uncomfortable to continue. The discomfort will
between the couple and the therapist lead to changes. System task involves making a
3. Couple-related issues timetable to allocate specific time for interaction.
a. It requires motivation from the couple to 4. Structural move: Experiment of disagreement
attend the session and it is a challenge to estab- focuses on a topic when one partner always
lish therapeutic alliance with both partners. dominates and the other habitually gives in to
b. During the course of couple therapy, there will avoid disagreement. This exercise helps the pas-
be decompensation from one or both clients. sive partner to express an opinion forcefully and
c. The therapist may face resistance and acting the other needs to value the expression. Role
out that result in early termination. reversal helps one partner to understand the
viewpoints and experiences of the other partner.
Sculpting involves one partner taking up the
25.11.5 Types of Couple Therapy position in silence and expresses his or her own
feelings without words while the other partner
Couple therapy follows one of the following psychothera-
has to guess the feelings.
peutic models:
1. The CBT model: identify reinforcement of 25.12 MOTIVATIONAL INTERVIEWING

undesirable behaviour in the couple.
2. The psychodynamic model: understand the cli- 25.12.1 Indications
ent’s emotional needs and the relationship to the 1. Substance misuse
needs of the partner. 2. Noncompliance to psychotropic medications
3. The emotionally focused model (Greenberg and
Johnson, 1988): rigid interaction patterns are
systemic in nature and result in negative emo- 25.12.2 Techniques
tional states. In this model, emotion is the target Main techniques include
and the agent of change. The therapist is a pro-
cess consultant. 1. Express empathy and establish understanding
4. The transactional model: behaviours are analysed from the client’s perspectives.
in terms of the ‘child, adult, and parent’ within a 2. Develop discrepancy in their behaviour and
client and how the client reacts with the partner. their personal goals/values.
3. Identify advantages and disadvantages of change.
4. Roll with client’s resistance by understanding
25.11.6 Techniques of Couple Therapy the client’s hesitancy to change.
1. Reciprocity negotiation: The couples develop 5. Support self-efficacy to reach personal goals and
an ability to express their offers and understand allow client to realize optimism about change.
their partner’s request. This allows an exchange 6. Provide a menu of options for change.
of positive behaviours and reactions.
2. Communication training: This encourages 25.12.3 Eye Movement and
mutual exchange of emotional messages.
Desensitization Reprocessing
3. System approaches: This approach focuses on
hidden rules and identifies underlying disagree- Eye movement and desensitization reprocessing (EMDR)
ment to resolve enmeshment. It also involves focuses on traumatic experiences, negative cognitions,
a behavioural technique called paradoxical and affective responses. The aim is to desensitize the
individual to the affective responses. This is accompa- Issues relating to the client
nied by bilateral stimulation and rapid eye movement
when the client is asked to follow the regular movement 1. Does the client feel responsible for the previous
of the therapist’s forefinger. therapist’s death (for real or imagined reasons)?
The procedural phases of EMDR include the following: 2. Comorbidity of the client (e.g. depression, panic
disorder, or substance abuse).
3. Premorbid personality of the client and coping
1. Assessment of target memory of image.
styles.
2. Desensitization by holding the target image
4. Previous experience of separations and grief
together with the negative cognition in mind.
process.
3. Bilateral stimulation continues until the mem-
5. Look for acting-out behaviour that caused the
ory has been processed with the chains of
GP to refer the case to you urgently.
association.
4. Installation of positive images.
Issues relating to the future therapy
5. Scanning of body to identify any sensations.
6. Closure and debriefing on the experience of the
1. Address new issues that are raised in the begin-
session.
ning of new therapy.
2. Explore expectations of the client to either con-
25.12.4 Grief Counselling tinue the previous form of therapy or receive
grief counselling.
Grief counselling allows the client to talk about the 3. Explore idealization of the previous therapist and
loss; to express feelings of sadness, guilt, or anger; and potential devaluation of the current therapist.
to understand the course of the grieving process. This
therapy also allows the client to accept the loss, working
through the grief process and adjust one’s life without the 25.13 BRIEF INSIGHT-ORIENTED THERAPY
deceased. Brief insight-oriented psychotherapy is based on psy-
choanalytic theory with different techniques and time
frames. Insight refers to a person’s understanding of his
CASC STATION FOR GRIEF COUNSELLING or her psychological function and personality. Treatment
framework involves the therapist assisting the client to
You are the consultant psychiatrist in charge of a
gain new and better insight into possible explanations
psychotherapy service. A 35-year-old housewife
for his or her feelings, responses, behaviours, and inter-
with agoraphobia was referred to you urgently by
personal relationships. It also expects that the client
her GP to continue psychotherapy as her previous
develops insight into his or her responses to the therapist
therapist has passed away.
and other significant relationship in the past.
Task: Assess this client’s suitability to continue
psychotherapy.
25.14 ART THERAPIES
Objective: Art therapist provides a psychotherapeutic
intervention that enables the client to effect change and
25.12.5 Approach to This CASC Station growth by using the art materials to gain insight and pro-
25.12.5.1 Issues the Candidate Needs to Explore mote the resolution of difficulties.
Issues related to the previous therapist
25.14.1 Types of Art Therapy
1. The cause of death of the previous therapist and
how the client was informed Art therapy is based on pictures and drawings. Therapeutic
2. The type and quality of the therapeutic relation- relationship progresses as art process progresses. The art
ship between the deceased therapist and client therapist acts as a facilitator and the therapist is invited in
3. The type of treatment offered (e.., CBT) the multidisciplinary team meeting to share his or her inter-
4. The stage and progress of previous therapy pretation of a client’s drawings.
Drama therapy encourages the clients to experience their Hawton K, Salkovskis PM, Kirk J, and Clarl DM. 2001:
physicality, to develop an ability to express a whole range Cognitive Behaviour Therapy for Psychiatric
of emotions, and to increase their insight and knowledge Problems: A Practical Guide. New York: Oxford
University Press.
of themselves and other people.
Hook J. 2007: Group psychotherapy. In Naismith J and Grant S.
Music therapy facilitates interaction and development of (eds.) Seminars in the Psychotherapies. London, U.K.:
insight into a client’s behaviour and emotional difficulties Gaskell.
Johnstone EC, Cunningham ODG, Lawrie SM, Sharpe M, and
through listening to music.
Freeman CPL. 2004: Companion to Psychiatric Studies.
Details of the scientific background of music therapy 7th edn. London, U.K.: Churchill Livingstone.
are considered in Puri (2009). Lackwood K. 1999: Psychodynamic psychotherapy.
In Stein S, Hiagh R, and Stein J (eds.) Essentials
of Psychotherapy, pp. 134–154. Oxford, U.K.:
Butterworth Heinemann.
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26 Schizophrenia and
Delusional Disorders
26.1 SCHIZOPHRENIA • In 1959, Kurt Schneider emphasized the impor-

tance of delusions and hallucinations in defining
26.1.1 History his first-rank symptoms (Schneider, 1959).
• In 1860, Morel used the term démence précoce • In 1960, Langfeldt sought to distinguish between
for a disorder of deteriorating adolescent psy- schizophrenia and the better-prognosis schizo-
chosis (Noll, 2011). phreniform psychoses and process versus non-
• In 1863, Kahlbaum described katatonie (Starkstein process schizophrenia (Langfeldt, 1969).
et al., 1995). • In 1972, Cooper compared patients admitted to
• In 1871, Hecker described hebephrenie (Hecker psychiatric hospitals in New York and London.
and Kraam, 2009). He found identical symptomatology, but schizo-
• In 1894, Sommer included deteriorating paranoid phrenia diagnosed nearly twice as often in New
syndromes in the concept of primary dementia. York compared to London (Gurland, 1972).
• In 1868, Griesinger believed that insanity could • In 1973, the WHO conducted the International
develop in the absence of mood disturbance, pri- Pilot Study of Schizophrenia. This study found,
mary insanity (primäre Verücktheit), and that all using narrow criteria, a 1-year incidence of
functional psychoses were expressions of single schizophrenia of 0.7–1.4 per 10,000 population
disease entity (Einheitspsychoses) (Dollfus and aged 15–54, across all countries. It was con-
Petit, 1993). firmed that psychiatrists in the United States
• In 1896, Emil Kraepelin grouped together catato- and the former USSR diagnosed schizophrenia
nia, hebephrenia, and the deteriorating paranoid twice as often as those in seven other countries
psychoses under the name dementia praecox. He (Columbia, Czechoslovakia, Denmark, Nigeria,
differentiated dementia praecox with its poor India, Taiwan, and the United Kingdom). This led
prognosis from the manic–depressive psychoses to a realization that psychiatric diagnoses had to
with their relatively better prognoses. He con- be defined operationally (Sartorius et al., 1972).
sidered dementia praecox to be a disease of the
brain (Kraepelin, 1987). 26.2 CLASSIFICATION OF SCHIZOPHRENIA
• In 1911, Bleuler introduced the term schizophre-
nia, applied it to Kraepelin’s cases of dementia 26.2.1 Schneiderian First-Rank Symptoms
praecox, and expanded the concept to include
In defining his first-rank symptoms, Schneider stated that
what today may be considered schizophrenic
in the absence of organic brain disease, the following are
spectrum disorders. He considered symptoms of
highly suggestive of schizophrenia:
ambivalence, autism, affective incongruity, and
disturbance of association of thought to be fun- • Auditory hallucinations
damental (the ‘four A’s’), with delusions and hal- • Repeat the thoughts out loud (e.g.
lucinations assuming secondary status. Bleuler Gedankenlautwerden, écho de la pensée)
was influenced by the writings of Sigmund Freud. • In the third person
He added schizophrenia simplex to Kraepelin’s • In the form of a running commentary
list (Berrios, 2011). • Delusions of passivity
• In 1931, Hughlings Jackson considered positive • Thought insertion, withdrawal, and broadcasting
symptoms as ‘release phenomena’ occurring in • Made feelings, impulses, and actions
healthy tissue; negative symptoms were attrib- • Somatic passivity
uted to neuronal loss (Jackson, 1931). • Delusional perception
351
Second-rank symptoms include perplexity, emotional 6. Formal thought disorder comprising interrup-
blunting, hallucinations, and other delusions. tions in the train of thought, incoherence, irrel-
First-rank symptoms can occur in other psychoses evant speech, or neologisms
and, although highly suggestive of schizophrenia, are not 7. Catatonic behaviour (e.g. excitement, stupor,
pathognomonic. posturing, waxy flexibility, negativism and
mutism)
8. Negative symptoms (e.g. apathy, paucity of
26.2.2 St. Louis Criteria (Feighner et al., 1972) speech, and blunted or incongruous affect)
The sufferer is continuously ill for at least 6 months, with 9. A significant and consistent change in the over-
no prominent affective symptoms, presence of delusions, all quality of some aspects of personal behav-
hallucinations, or thought disorder. Personal and family iour (e.g. loss of interest, aimlessness, idleness,
histories are taken into account (e.g. marital status, age self-absorbed attitude, and social withdrawal)
under 40, premorbid social adjustment).
Diagnostic guidelines require a minimum of one clear
symptom (two if less clear-cut) belonging to groups (1)
26.2.3 Catego (Wing et al., 1974) to (4), or symptoms from at least two of the groups (5) to
This uses the Present State Examination to generate diag- (8) should have been present for most of the time during
noses by means of a computer program. It is based on a period of one month or more.
the Schneiderian concept of schizophrenia. No account is Symptom (9) applies only to a diagnosis of simple
taken of symptom duration. schizophrenia, and a duration of at least one year is
required.
Schizophrenia is not diagnosed if extensive affective
26.2.4 Research Diagnostic Criteria symptoms are present, unless they postdate the schizo-
(Spitzer et al., 1975) phrenic syndrome. If both schizophrenic and affective
symptoms develop together and are evenly balanced, the
These are a 2-week duration, lack of affective symp- diagnosis of schizoaffective disorder is made.
toms, and presence of thought disorder, hallucinations, Schizophrenia is not diagnosed in the presence
or delusions similar to Schneider’s first-rank symptoms. of overt brain disease, or during drug intoxication or
withdrawal.
26.2.5 International Classification of Diseases, The pattern of course is classified as (1) continuous;
(2) episodic, progressive deficit; (3) episodic, stable defi-
Tenth Revision: ICD-10 (WHO, 1992)
cit; (4) episodic, remittent; (5) incomplete remission; and
There are fundamental, characteristic distortions of (6) complete remission.
thinking and perception and inappropriate or blunted
affect. There is clear consciousness. Intellectual capac- 26.2.5.1 Subtypes
ity is usually maintained, but some cognitive deficits can In ICD-10, the following subtypes of schizophrenia are
evolve over time (see Table 26.1). distinguished:
Symptoms are divided into groups:
• Paranoid schizophrenia. This is the common-
1. Thought echo and thought alienation est subtype. Hallucinations and/or delusions
2. Delusions of passivity; delusional perception are prominent. Disturbances of affect, volition,
3. Auditory hallucinations in the form of a running speech, and catatonic symptoms are relatively
commentary, or discussing the patient, or hal- inconspicuous. Auditory, olfactory, gustatory
lucinatory voices coming from some part of the and somatic hallucinations, and visual hal-
body lucinations may occur. Commonly, there are
4. Persistent delusions, culturally inappropriate delusions of control, influence, passivity, and
and impossible persecution.
5. Persistent hallucinations in any modality, • Hebephrenic schizophrenia. The age of onset
accompanied by fleeting delusions without is usually between 15 and 25 years. There is a
affective content, or by persistent over-valued poor prognosis. Affective changes are promi-
ideas, or occurring every day for weeks nent. Fleeting and fragmentary delusions and
Schizophrenia and Delusional Disorders 353
TABLE 26.1
Compare and Contrast ICD-10 and Proposed DSM-5 Diagnostic Criteria for Schizophrenia
ICD-10 (F20.) (WHO, 1992) DSM-5 (APA, 2013)
F20 Schizophrenia At least one of: 295.90 Schizophrenia
Number of symptoms Thought disturbances, passivity, hallucinatory At least two of the following: delusions, hallucinations,
voices, and persistent delusional beliefs disorganized speech, grossly disorganized or
Or two or more of: catatonic behaviour, and negative symptoms. Out of
Other persistent hallucinations, formal thought the two symptoms, at least one should be delusions,
disorder, catatonic behaviour, and negative hallucinations, or disorganized speech
symptoms At least two items of less specific symptoms
Absence of substance abuse or general medical
condition
Specify if catatonic features are present
Specify the number of episodes and remission status
(partial or full)
Deterioration in occupational It is not a compulsory criterion It is a compulsory criterion
and social function
Duration of symptoms The symptoms have to be present for at least The minimum duration of disturbance is at least
1 month for schizophrenia 6 months. The minimum duration of symptoms is at
The symptoms have to be present for at least 1 year least 1 month
for simple schizophrenia
Inclusion of simple F20.6 simple schizophrenia: 1-year of negative No mention of simple schizophrenia
schizophrenia and symptoms and deterioration in personal behaviour 295.40 Schizophreniform disorder: Duration is
schizophreniform disorder as a result of loss of drive or interest and social between 1 and 6 months; specifier includes with or
withdrawal without good prognostic factors (e.g. acute onset,
No mention of schizophreniform disorder absence of negative symptoms, confusion, good
premorbid functioning)
Other types of schizophrenia F20.0 Paranoid schizophrenia Catatonic disorder associated with another medical
F20.1 Hebephrenic schizophrenia: flatten and condition: motoric immobility (catalepsy/waxy
incongruity of affect, stereotypies, incoherent flexibility/stupor), excessive motor activity, extreme
speech, with minimal positive symptoms negativism or mutism, peculiarities of voluntary
F20.2 Catatonic schizophrenia: duration for movement (stereotypies, mannerisms), echolalia, or
2 weeks, similar to the DSM-5 criteria with echopraxia
additional symptom such as command automatism The DSM-5 does not propose subtype of
F20.3 Undifferentiated schizophrenia schizophrenia
F20.5 Residual schizophrenia: reduction in activity,
blunting of affect, lack of initiative, and poor
communication and self-care
Delusional disorder F22. Delusion disorder: 3 months in duration, no F297.1 Delusional disorder
hallucinations Duration: at least 1 month
F22.8 Other persistent delusional disorders: Not meeting the diagnostic criteria for schizophrenia,
delusional dysmorphobia, involutional paranoid but tactile or olfactory hallucinations may be present
state, and paranoia querulans Mood disturbance only lasts for a brief period of time
F22.9 Persistent delusional disorder, unspecified No significant impairment of functioning
Subtypes include
• Erotomanic type
• Grandiose type
• Jealous type
• Persecutory type
• Somatic type
• Mixed type
• Unspecified type
(continued)

Compare and Contrast ICD-10 and Proposed DSM-5 Diagnostic Criteria for Schizophrenia
ICD-10 (F20.) Proposed DSM-5
Brief psychosis F23 Acute and transient psychotic disorder: 298.8 Brief psychotic disorder: presence of one (or
symptoms not exceeding 2 weeks, with or without more) of the following: delusions, hallucinations,
associated acute stress. This disorder accounts for disorganized speech (e.g. frequent derailment or
around 10% of all psychotic disorder. 30% of incoherence), and grossly disorganized or catatonic
patients can remain in remission without behaviour. Duration is between 1 day and 1 month
medication (Philmann and Marneros, 2005) Specifier includes with stressful event, without
F23.0 Acute polymorphic psychotic disorder stressful event, and with postpartum onset
without symptoms of schizophrenia: duration < 3 Substance-induced psychotic disorder: Psychotic
months symptoms develop within 1 month of substance
F23.1 Acute polymorphic psychotic disorder with intoxication or withdrawal
symptoms of schizophrenia: duration < 1 month Psychotic disorder associated with another medical
F23.2 Acute schizophrenia-like psychotic disorder: condition: hallucination subtype, delusion subtype,
duration < 1 month and disorganized speech subtype
F23.3 Other acute predominantly delusional The number of subtypes of brief psychotic disorder
psychotic disorders: duration < 3 months proposed by DSM-5 is less than ICD-10
F23.8 Other acute and transient psychotic disorders
F23.9 Acute and transient psychotic disorder,
unspecified
Schizoaffective disorder F20.0 Schizoaffective disorder—manic type: 295.70 Schizoaffective disorder—bipolar type and
duration at least 2 weeks depressive type
F25.1 Schizoaffective disorder—depressive type: The psychosis is present for at least 2 weeks in the
duration at least 2 weeks absence of mood symptoms
F25.2 Schizoaffective disorder—mixed type: The mood symptoms account for at least 50% in the
Schizophrenia and affective symptoms are course of illness
prominent Specify the number of episodes and remission status
F25.8 Other schizoaffective disorders (e.g. partial or full)
F25.9 Schizoaffective disorder, unspecified
Post-schizophrenic F20.4 Post-schizophrenic depression Not mentioned
depression Prolonged depressive symptoms when psychotic
symptoms subside and depression occurs within
12 months of schizophrenia
Schizotypal disorder This disorder is listed under schizophrenia. Clinical This disorder is considered to be a personality
features include quasipsychotic experience, odd disorder, but DSM-5 also lists this disorder under
belief, speech, behaviour, idea of reference, excess schizophrenia. It must fulfil two core criteria for
social anxiety, paranoia, and absence of close personality disorder: impairment in self and
friends interpersonal functioning. Further details are found
in Chapter 29
hallucinations; irresponsible behaviour; fatuous, posturing, negativism, rigidity, waxy flexibility,

disorganized thought; rambling speech; and command automatism, and perseveration of
mannerisms are common. Negative symptoms, words or phrases. Catatonic symptoms alone
particularly flattening of affect and loss of voli- are not diagnostic of schizophrenia; they may
tion, are prominent. Drive and determination are be provoked by brain disease, metabolic dis-
lost, goals abandoned, and behaviour becomes turbance, alcohol and drugs, and mood disor-
aimless and empty. The premorbid personality ders. Psychomotor disturbances may alternate
is characteristically shy and solitary. between extremes; violent excitement may occur.
• Catatonic schizophrenia. One or more of the fol- It may be combined with a dreamlike state with
lowing behaviours dominate: stupor, excitement, vivid scenic hallucinations.
• Simple schizophrenia. There is an insidious 26.2.8 Liddle’s Syndromes (Liddle, 1987)

onset of decline in functioning. Negative symp-
toms develop without preceding positive symp- Liddle found that the pattern of symptoms in schizophre-
toms. Diagnosis requires changes in behaviour nia segregated into three distinguishable syndromes—a
over at least a year, with marked loss of interest, dimensional approach:
idleness, and social withdrawal.
• Residual or chronic schizophrenia. This is char- • Psychomotor poverty syndrome. There is pov-
acterized by negative symptoms. There is past erty of speech, flatness of affect, and decreased
evidence of at least one schizophrenic episode spontaneous movement.
and a period of at least 1 year in which frequency • Disorganization syndrome. There are disorders
of positive symptoms has been minimal and neg- of the form of thought and inappropriate affect.
ative schizophrenic syndrome has been present. • Reality distortion syndrome. There are delu-
There is absence of depression, institutionaliza- sions and hallucinations.
tion, or dementia or other brain disorders.
• Undifferentiated schizophrenia. General crite- A subsequent PET study of regional cerebral blood flow
ria for schizophrenia are satisfied but not con- (Liddle et al., 1992) showed that each of these three syn-
forming to the earlier syndromes. dromes is associated with a specific pattern of perfusion.
• Post-schizophrenic depression. This is a depres-
26.2.8.1 Psychomotor Poverty Syndrome
sive episode arising after a schizophrenic illness.
Schizophrenic illness must have occurred within Hypoperfusion of the left dorsal prefrontal cortex extends
the last 12 months, some symptoms still being pres- to medial prefrontal cortex and anterior cingulate cortex.
ent. Depressive symptoms fulfil at least the criteria There is hyperperfusion in the head of the caudate nucleus,
for a depressive episode and are present for at least which receives substantial projections from the dorsolat-
2 weeks. There is an increased risk of suicide. eral prefrontal cortex. Some changes are also found on the
right (laterality only a matter of degree). Hypofrontality
in schizophrenia is more often seen in chronic patients
26.2.6 Type 1 and Type 2 Schizophrenia and is associated with inactivity and catatonic symptoms.
(Crow, 1980) In normal subjects, prefrontal activity increases when
involved in internal generation of action.
Crow described a two-syndrome hypothesis of schizo-
phrenia—a categorical approach: 26.2.8.2 Disorganization Syndrome
There is hypoperfusion of the right ventral prefrontal
• Type 1 schizophrenia. This type is characterized cortex and increased activity in anterior cingulate and
by prominent positive symptoms, acute onset, dorsomedial thalamic nuclei that project to the prefrontal
good premorbid adjustment, good treatment cortex. There is relative hypoperfusion of Broca’s area
response, intact cognition, intact brain structure, and bilateral hypoperfusion of parietal association cor-
and a reversible neurochemical disturbance. tex. Evidence suggests that in primates the ventral pre-
• Type 2 schizophrenia. This type is character- frontal cortex plays a role in suppression of interference
ized by prominent negative symptoms, insidious from irrelevant mental activity. The anterior cingulate
onset, poor premorbid adjustment, poor treat- plays a role in attentional mechanisms. The suggestion is
ment response, impaired cognition, structural that these patients are engaged in an ineffective struggle
brain abnormalities (ventricular enlargement), to suppress inappropriate mental activity.
and an underlying pathology based on neuronal
loss, therefore irreversible. 26.2.8.3 Reality Distortion Syndrome
There is increased activity in the left parahippocampal
region and left striatum. This is consistent with the pro-
26.2.7 SAPS and SANS
posal that delusions and hallucinations arise from a disor-
In 1984, Andreasen developed structured scales for the der of internal monitoring resulting in failure to recognize
assessment of positive and negative symptoms: the Scale internally generated mental acts. Abnormalities of func-
for the Assessment of Positive Symptoms (SAPS) and the tion underlying schizophrenic symptoms are not confined
Scale for the Assessment of Negative Symptoms (SANS). to single loci but involve distributed neuronal networks.
26.2.9 Neurodevelopmental Classification to show morphological brain changes and cogni-

(Murray et al., 1992) tive impairment. The person is more likely to be
male and to have a poor outcome.
On the basis of genetic, epidemiological, neuropathological, • Adult-onset schizophrenia. The person is more
neuroimaging, and gender difference studies, schizophrenia likely to exhibit positive and affective symp-
has been subdivided into the following three groups: toms. The person may have a genetic predispo-
sition to manifest symptomatology anywhere
• Congenital schizophrenia. The abnormality is along a continuum from bipolar mood disorder
present at birth and may be caused by genetic to schizoaffective disorder to schizophrenia.
predisposition and/or environmental insult (e.g. • Late-onset schizophrenia. This presents after age
maternal influenza, obstetric complication, early 60 years, with good premorbid functioning. It is
brain injury, or infection). The person is more likely most common in females. It is often associated with
to have minor physical abnormalities, abnormal auditory and visual sensory deprivation. It is some-
personality, or social impairment in childhood; to times related to paranoid personality or to mood
present early; to exhibit negative symptoms; and disorder. Organic brain dysfunction is often present.
CASC STATION ON THE SYMPTOMS OF SCHIZOPHRENIA

A 17-year-old female is admitted to the psychiatric ward with a weeklong history of complaining of ‘increasing
interference to her mind’. She suffers from schizophrenia, and she has been adherent to medication. She seems
to be irritable and anxious.
Task: Take a history to establish the causes of her stress.
Approach to this station: In this station, the candidate is expected to determine whether the patient is suffering
from schizophrenia and to rule out differential diagnoses such as substance misuse, organic disorder, or affec-
tive disorder with psychotic features. Candidates who perform poorly focused only on schizophrenia and did not
consider other differential diagnoses that may lead to the patient’s described symptoms. The simulated patient
in the exam appears to be calm and denies other first-rank symptoms. However, by careful history taking, it is
possible to determine that the symptoms and presentation are most likely related to psychotic illness.
CASC Grid
Opening statement: ‘Hello, my name is Dr Ford. I would like to ask you a few questions. Would that be okay?
Can you tell me how you’ve been feeling? I understand from the nurse that you’ve been experiencing some
stress. Can you tell me more about this?’
(A) Schizophrenia (A2) Passivity

Symptoms (A1) Thought Experiences (A3) Delusions (A4) Hallucination
‘I can imagine that it is ‘Do you feel that the ‘Do you feel that people ‘Do you hear voices when
quite stressful if your thoughts are being put are talking about you or there’s no one around? If
thoughts are being into/taken out of your laughing at your yes, how do the voices
interfered with. Can you head?’ expense? Do you think address you?’
tell me more about ‘Do you feel that that people are following ‘Do the voices give you
this?’ everyone knows what’s you/out to get you?’ instructions? If yes, what
‘Are you able to think on in your mind? Do ‘Do you realize that things kinds of instructions do
clearly?’ you feel that people can happening to you have a they give?’
‘Does your mind go read your mind?’ special meaning to you?’ ‘Do you see things that
blank suddenly?’ ‘Do you feel that your (delusional perception) other people cannot see?’
thoughts are being ‘Do you feel that someone ‘Do you experience funny
broadcasted out so that wants to harm you at this sensations in your body
everyone can receive moment? If so, who is or as if something
your thoughts?’ behind it? Could it be a strange is going to
misunderstanding?’ happen to you?’
(B) Other (B4) Insight, Side

Psychiatric Effects, and Risk
Comorbidities (B1) Anxiety State (B2) Affective Disorder (B3) Substance Abuse Assessment
‘Do you feel anxious ‘How is your mood ‘Do you use recreational ‘How do you feel about
most of the time? Are today? Do you feel sad? drugs or alcohol? If so, your illness?’
there specific things/ Do you feel high, like what do you use? How ‘Do you receive any
situations that make you the top of the world?’ often do you use it? treatment at this
feel anxious? Do you ‘What is the reason When was the last moment? Do you
experience shaking/ behind your low mood? intake?’ experience any side
sweating/heart racing/ Is it because of the ‘Do you feel shaky effect?’
choking/fainting/ voices?’ without those drugs?’ ‘Do you have the feeling
dizziness?’ that life is not worth
‘How do you cope with living? Do you have
anxiety? Do you take thoughts of hurting
drug to control it?’ yourself or other
people?’
(C) Issues Related (C1) Academic (C3) Relationship with (C4) Relationship
to Young People Performance (C2) Recent Life Event Parents Problems and Peers
‘Are you in school at this ‘Did you experience any ‘Can you tell me more ‘Are you in a relationship
moment? Do you unhappy events prior to about your parents? How at this moment? If yes,
experience any admission?’ do they treat you? Are can you tell me more
academic difficulty?’ ‘Is there a change in your they overprotective?’ about your relationship?’
‘How did you do in your environment recently?’ ‘Do you feel that your ‘How about your friends?
study in the past?’ ‘Do you have any parents are critical or Do they know that you
‘Do you feel that those financial problem at this overinvolved?’ (assess are here? Do they know
voices are affecting moment?’ expressed emotion [EE]) about your illness? Are
your concentration?’ ‘What’s the family’s view they supportive?’
of your admission? Are
they concerned about
you?’
‘Do you have any family
member suffering from
similar illness?’
(D) Past Medical
History and (D4) Explain your
Background (D2) Chronic Medical (D3) Previous Traumatic Preliminary Formulation
History (D1) Recent Illness Illness Events to the Patient
‘Have you fallen sick ‘Do you suffer from Explore history of If you have identified a
recently?’ chronic disease that psychological, physical, stressor, check with the
‘Have you received any requires frequent and sexual abuse. patient and see whether
treatment such as treatment?’ ‘Do you have traumatic he or she agrees that this
antibiotics?’ Explore history of experience in the past? is the source of his or
‘Did you travel to other epilepsy, head injury, If yes, can you tell me her stress.
countries recently?’ asthma, etc. more?’
If chronic illness is
present, explore the
effect on his or her
development,
relationship with her
family, and possible
developmental lag.
26.3 EPIDEMIOLOGY OF SCHIZOPHRENIA Theories emphasizing environmental influences need

not exclude the importance of biological factors, such as
26.3.1 Statistics exposure to toxins, increased incidence of obstetric com-
• The incidence of schizophrenia is between 15 and plications, and a higher rate of infectious disease in cities.
30 new cases per 100,000 of the population per year: Social factors more common in cities include stressful
• The point prevalence is approximately 1%. life events, social isolation, and social overstimulation.
• The lifetime risk is approximately 1%.
• The age of onset is usually between 15 and 45 26.4 AETIOLOGY OF SCHIZOPHRENIA
years, earlier in men than in women.
• It is equally common in males and females.
26.4.1 Genetics in Schizophrenia
There is a higher incidence in those not married. The heritability of schizophrenia is between 82% and
• It is most common in social classes IV and V. 85% (Farmer et al., 1987: Cardno et al., 1999). Twin, fam-
• Prevalence varies geographically. Rates from ily, and adoption studies have consistently demonstrated
urban areas are generally higher than in rural areas, familial aggregation of schizophrenia, largely attribut-
with marked exceptions—the highest prevalence able to genetic factors.
measured (17.4 per 1000 population) was from a
sparsely populated rural area in the west of Ireland. 26.4.1.1 Family Studies
Table 26.2 shows the approximate lifetime risks for the
Further details on epidemiology of schizophrenia are development of schizophrenia in the relatives of patients
found in Chapter 21. with schizophrenia.
26.3.2 Theories 26.4.1.2 Twin Studies

The concordance rate for monozygotic (MZ) twins is
The following are theories accounting for geographical
approximately 45%, that for dizygotic (DZ) twins approx-
variance in the prevalence of schizophrenia:
imately 10% (Gottesman and Shields, 1972).
Studying adult offspring of 21 MZ and 41 DZ twin
• Social drift. Goldberg and Morrison (1963)
pairs discordant for schizophrenia, Gottesman and
studied fathers’ birth certificates and found
Bertelsen found the risk of developing schizophrenia was
schizophrenic males had lower social class
17% among the adult children of the MZ and DZ pro-
distribution than their fathers. They attributed
bands, 17% among the offspring of phenotypically nor-
these findings to social drift, that is, migration
mal MZ co-twins, and only 2% among the offspring of
of those affected to areas where social demands
phenotypically normal DZ co-twins. This suggests that
may be less. Men were more likely to drift into
inner city areas.
• Social residue. Healthy people migrate away TABLE 26.2
from undesirable areas, leaving schizophrenics Approximate Lifetime Risks for the
behind. Development of Schizophrenia in the Relatives
• Breeder or social causation. This theory assumes of Patients with Schizophrenia
that environmental factors either are causative or
Lifetime Expectancy Rate to
have to be present for the predisposed individual
Relationship the Nearest Percentage Point
to develop schizophrenia. Castle et al. (1993)
Parents 6
found that schizophrenic patients in Camberwell
All siblings 10
were more likely to have been born in a socially
Siblings (when one parent 17
deprived area and to have fathers with manual
has schizophrenia)
jobs. Those developing schizophrenia were
Children 13
more likely than controls to have been born into Children (when both parents 46
socially deprived households. This suggested have schizophrenia)
that some environmental factor of aetiological Grandchildren 4
importance in schizophrenia is more likely to Uncles, aunts, nephews, 3
affect those born into households of lower socio- and nieces
economic status and in the inner city.
the normal MZ co-twins carried and transmitted the rel- • Chromosome 6p22: DTNBP1 (dystrobrevin-
evant genotype without expressing it themselves. binding protein 1)
• Chromosome 6q23: TAAR6 (trace amine asso-
26.4.1.3 Adoption Studies ciate receptor 6)
When children of schizophrenic mothers have been • Chromosome 8p12: NRG1 (neuregulin)
adopted soon after birth by nonschizophrenic families, • Chromosome 8p21: PPP3CC (protein phospha-
they have a similar likelihood of developing schizophrenia tase 3 calcineurin gamma catalytic gene)
(approximately 13%) as the rates suggested by family stud- • Chromosome 13q34: G72
ies. There appears to be no such increased risk of devel- • Chromosome 22q11: PRODH (proline dehy-
oping schizophrenia in the children of nonschizophrenic drogenase (oxidase) 1), ZDHHC8, catechol-o-
parents who are similarly adopted (Kety et al., 1971). methyltransferase (COMT)
The following are possible modes of inheritance: There are problems in applying linkage methodology to
schizophrenia:
• Single major locus. Some forms possibly exist
but would account for a very small proportion of • Schizophrenia is probably genetically
observed cases. To date, no single genetic focus heterogeneous.
responsible for the development of schizophre- • Linkage analysis is usually applied to conditions
nia has been reliably demonstrated. transmitted by simpler Mendelian inheritance.
• Polygenic. There might be a threshold of gene • Diagnostic and penetrance problems prob-
numbers required for expression of schizophrenia. ably require a much higher lod score than the
• Multifactorial. There may be aetiological hetero- usual +3 before linkage for psychiatric diagno-
geneity with various genetic and environmental ses can be regarded as proved.
subtypes. There is probably a spectrum of causes
ranging from wholly genetic, through those with 26.4.2 Prenatal Factors in Schizophrenia
mixed aetiology, to the totally environmental. People developing schizophrenia as adults are born
disproportionately more often during late winter and
26.4.1.4 Linkage Studies early spring. A similar but less marked seasonal effect
Bassett and associates reported a man who presented is reported for bipolar affective disorders but not for
with schizophrenia plus minor physical abnormalities neurotic or personality disorders. Seasonally varying
both shared by his maternal uncle. Cytogenetic analysis environmental causes have been sought, and prenatal
revealed translocation of part of chromosome 5; this led infection is currently the most favoured explanation.
the writers to postulate that this segment of chromosome An excess of minor physical abnormalities is reported in
5 may be site of a putative schizophrenia gene. schizophrenics; examples are low-set ears, greater distance
Sherrington and associates collected seven extended between the eyes, and a single transverse palmar crease.
schizophrenic families from Iceland and England, probed Dermatoglyphics are determined by genes, and deleteri-
chromosome 5, and found evidence highly suggestive of link- ous events in the second trimester of pregnancy can alter
age between markers on chromosome 5 and schizophrenia. their form. Schizophrenics have deviations from normal in
However, this finding has never been replicated, and the study ridge patterns of fingers, palms, and soles. Schizophrenic
has subsequently been criticized on methodological grounds. probands of MZ twin pairs discordant for schizophrenia
The following candidate genes and chromosomes are have significantly more finger and palm epidermal ridge
implicated in the aetiology of schizophrenia: anomalies than their healthy co-twins (Bracha et al., 1991).
Structural abnormalities in the brains of many
• Chromosome 1q22: CArboxyl-terminal Pdz schizophrenics suggest a neurodevelopmental rather
ligand of neuronal Nitric Oxide synthas (CAPON) than degenerative process. Most studies investigating
• Chromosom 1q23: RGS4 I (regulator of brain morphology in schizophrenia report nonprogres-
G-protein signalling 4) sive ventricular and cortical sulcal enlargement and
• Chromosom 1q42.1: DISC1 (disrupted in schizo- structural abnormalities in the limbic areas. Structural
phrenia 1) changes reflect an early acquired hypoplasia, not degen-
• Chromosom 5q33: EPN4 eration. Cytoarchitectural changes in limbic and pre-
• Chromosome 5q34: GABA(A) receptors frontal areas are strong indicators of early disordered
brain development. Altered distribution of cortical layers 26.4.3 Personality in Schizophrenia

of NADPH-d neurons is consistent with a disturbance
of development, in which the normal pattern of pro- Only schizotypal personality disorder is aetiologically
grammed cell death is compromised, resulting in defec- related to schizophrenia. Among the schizotypal crite-
tive migration of neurons. ria, eccentricity, affect constriction, and excessive social
Murray suggests that neural dysplasia results in premor- anxiety are linked to schizophrenia. There may be a
bid cognitive deficits, abnormal personality, negative symp- milder phenotype along the schizophrenia spectrum.
toms, and abnormal CT scans in schizophrenia. Maturational
brain changes in adolescence, possibly myelination or syn- 26.4.4 Social Factors in Schizophrenia
aptic pruning, reveal immature neuronal circuitry with con-
sequent onset of hallucinations and delusions. 26.4.4.1 Rural or Urban Setting
The neurodevelopmental model of schizophrenia The higher prevalence of schizophrenia in urban areas is a
accounts for the following findings: result of interaction of genetic factors, migration, higher rates
of social deprivation, and social problems in the inner city.
• Individuals who were in their second trimester
of fetal life during the influenza epidemic in
26.4.4.2 Ethnicity
Finland in 1957 had an increased risk of later
schizophrenia (Mednick et al., 1988). Afro-Caribbean immigrants to the United Kingdom have
• The winter excess of births in schizophrenics is higher risk of schizophrenia. This phenomenon is seen in
due to a seasonal prevalence of a viral infection the second generation.
or other perinatal hazard.
26.4.4.3 Expressed Emotion
• Males have an earlier onset of schizophrenia
than females, possibly due to increased vulner- In 1968, Brown and Birley found that schizophren-
ability to neurodevelopmental damage (gener- ics had experienced significantly more independent
ally commoner in males). life events in the 3 weeks prior to onset of relapse
• The smaller proportion of male schizophren- than had controls. In 1976, Vaughn and Leff found an
ics is genetically determined; there is evidence increased relapse rate of schizophrenia in those who
that concordance rates for schizophrenia are lived with families in which the relatives displayed
lower in male than in female identical twins. high EE (critical comments, overinvolvement) (see
Figure 26.1). Changes in physiological arousal may
Obstetric complications (premature rupture of membrane, account for this effect.
premature birth (<37 weeks), and use of resuscitator or incu- There was a poverty of the social milieu of patients
bation) are more frequent in schizophrenics than in normal with chronic schizophrenia, associated with increased
controls. This is noted particularly in schizophrenics without negative symptoms, particularly social withdrawal,
a positive family history for psychosis, implying that obstet- affective blunting, and poverty of speech (Wing and
ric factors may augment or substitute for a genetic cause. Brown, 1961).
Total group
Low expressed emotion high expressed emotion
n = 71 (13%) n = 57 (51%)
< 35 h contact > 35 h contact

28% 69%
Drugs No drugs Drugs No drugs Drugs No drugs

12% 15% 15% 42% 53% 92%
FIGURE 26.1 Relapse rates of 128 schizophrenics over a 9-month period. (From Vaughn, C.E. and Leff, J.P., Br. J. Psychiatry,
129, 125, 1976.)
26.4.5 CASC Station on Schizophrenia 26.4.5.1.5 Explain the Roles of Cannabis after

and Cannabis Development of Schizophrenia
1. Self-medication
A 19-year-old man is admitted because he experiences 2. Worsening of psychotic symptoms (e.g. idea of
a psychotic episode. He smokes cannabis regularly. reference, paranoia)
His mother has browsed through the Internet and has 3. Worsening of other symptoms (e.g. agitation,
some questions for you. She wants to know the rela- confusion)
tionship between cannabis use and schizophrenia. 4. Worsening of negative symptoms
Task 26.4.5.1.6 Explain the Challenges in Dual Diagnosis

Explain to her the relationship between schizophre- 1. The difficulties of assessment: emphasize on the
nia and cannabis. Address her views, concerns, and need to be clear of the chronological sequence of
expectations. cannabis misuse and development of psychosis.
2. Other substance use such as alcohol may affect
How to fail this station: Candidates who perform well in efficacy of antipsychotics.
this station address the controversy surrounding the role 3. Amotivational syndrome, reluctance to quit can-
of cannabis in the aetiology of schizophrenia and the nabis (require motivational interviewing), and
complicating effects of cannabis on the course of illness. its effects on the therapeutic alliance.
Candidates may fail if they do not broadly describe their 4. Potential involvement of substance abuse service.
experience in clinical practice and the research evidence 5. Importance of psychoeducation to prevent fur-
relating to the association between cannabis and psychosis. ther substance use.
26.4.5.1 Approach to This Station 26.4.6 Neurotransmitters in Schizophrenia

26.4.5.1.1 Background Information
26.4.6.1 Dopamine
Cannabis leads to a twofold increase in risk of schizo-
The mesolimbic–mesocortical system is a dopaminergic
phrenia and a fourfold increase in risk of psychosis
system originating in the ventral tegmental area of the
(Arseneault et al., 2004).
brain. The mesolimbic system projects to the limbic sys-
26.4.5.1.2 Role of Genetic Factors tem, while the mesocortical system innervates the cingu-
Explain to his mother that not all cannabis users develop late, entorhinal, and medial prefrontal cortices.
schizophrenia. It depends on the COMT genotype. The dopamine hypothesis of schizophrenia asserts
People who have homozygous VAL/VAL alleles in the that the clinical features are the result of central dopa-
COMT genotype have relatively higher risk. People who minergic hyperactivity in the mesolimbic–mesocortical
are homozygous for MET/MET alleles in the COMT system. The following is put as evidence in favour of the
genotype have no increase in risk. dopamine hypothesis:
• All clinically effective antipsychotic drugs

26.4.5.1.3 Explain Effects of Cannabis occupy a substantial proportion of D2 receptors
1. Amotivational syndrome in the brain (70%–80% D2 receptor occupancy
2. Flashback phenomena in the striatum at normal doses).
3. Changes in affect • Amphetamine, a dopamine agonist, can cause a
4. Change in heart rate, red eyes, motor incoordina- state similar to that of acute schizophrenia.
tion, poor concentration, and memory problems • Dopamine agonists exacerbate psychotic
symptoms.
26.4.5.1.4 Obtain More Information About • Comparing actions of a and b isomers of flu-
Her Son’s Usage of Cannabis penthixol in patients with acute schizophrenia,
1. Duration and frequency of use only those receiving the dopamine antagonist
2. Peer influence improved (Johnstone et al., 1978).
3. Other substance use, for example, alcohol • Postmortem studies have found increased D2
4. Economic impact receptors in the basal ganglia and limbic regions
5. Predisposing factors: personality and peer pressure of schizophrenic brains.
• In animals, administration of dopamine ago- • During treatment with haloperidol, the ratio of
nists produces a behavioural picture said to be dopamine metabolite (HVA) to serotonin and
similar to human psychosis. This is reversed by noradrenaline metabolites in CSF of schizo-
giving dopamine antagonists. phrenics increased significantly and correlated
• In drug-naive schizophrenics, the number of D2 with reduction of symptoms. This supports the
receptors in the striatum was two to three times that hypothesis that interactions between different
of controls as measured by PET (Wong et al., 1986). monoamine neurotransmitters are involved in
expression of schizophrenic symptoms.
Evidence against the dopamine hypothesis includes
26.4.6.2 Serotonin (5-HT)
There is some evidence that serotonergic dysfunction
• The concentration of dopamine metabolite may be associated with schizophrenia:
homovanillic acid (HVA) in the cerebrospinal
fluid in schizophrenics has generally not been • The hallucinogen LSD (see Chapter 32) acts at
found to be higher than in control subjects. serotonin receptors.
• D2 receptor blockade caused by antipsychotics • Antipsychotic risperidone is a potent 5-HT2
is an acute effect, but the therapeutic effect is receptor antagonist (it also blocks D2 receptors,
observed 3–4 weeks later. however).
• 15%–30% of schizophrenics fail to respond to • Ritanserin, a selective 5-HT2 antagonist, reduced
dopamine antagonists. negative symptoms when given as adjunctive
• Antipsychotics have a better effect on positive therapy in neuroleptic-treated schizophrenics.
than on negative symptoms.
• Clozapine, an effective antipsychotic, has
26.4.6.3 Glutamate
less D2 blocking activity than conventional
antipsychotics. Glutamate stimulates the NMDA receptor. Phencyclidine
• Some studies have failed to replicate Wong’s (‘angel dust’—see Chapter 32) causes schizophrenic-like
findings of increased D2 receptors in striatum of effects by blocking NMDA receptors. A balance exists
brains of living schizophrenics. between excitatory glutamatergic and inhibitory dopa-
minergic terminals in the corpus striatum, regulating
GABAergic neurons. These function in the ‘thalamic
Explanations that may account for contradictory results filter’, which seems to be hypoactive in schizophrenia.
According to this theory, hypoactivity of GABA neurons
is corrected by either reducing dopaminergic activity or
• Schizophrenia is clinically complex, and the
increasing glutamatergic activity.
aetiology is heterogeneous.
• Schizophrenia may involve reduced dopaminer-
gic activity in the prefrontal cortical area and 26.4.7 Structural Cerebral Abnormalities
compensatory overactivity in subcortical or lim-
in Schizophrenia
bic areas.
• There are potential problems in patient selection Johnstone et al. (1976) conducted a CT scan study, find-
and study methodology. ing that chronically hospitalized schizophrenic patients
• Identification of D1, D3, D4, and D5 receptors has had larger lateral ventricles than controls. This has been
suggested that they alone or in addition to D2 confirmed by numerous neuroimaging studies.
receptors may be the appropriate target for anti- In 1990, Andreasen et al. conducted a large study in
psychotic drug therapy. people matched for age, sex, height, weight, and level
• Clozapine acts in part by antagonism of D1, D2, of education. The ventricle/brain ratio was greater in
and particularly D4 receptors; it is effective dur- schizophrenics than in controls. The differences were
ing long-term use in up to 60% of neuroleptic- small, and there was overlap with the normal population;
resistant patients. it was more marked in males.
• D1 antagonist alone failed to show antipsychotic MRI has shown a diffuse reduction in the volume of
efficacy. Specific D3 and D4 antagonists have not cortical grey matter in schizophrenic patients, this being
yet been studied. associated with poor premorbid function. These findings
are consistent with neurodevelopmental changes having • Hippocampal pyramidal cell disarray
taken place in such patients. • Reduced hippocampal cell numbers
The following are further structural changes in schizo- • Reduced cell numbers in the entorhinal cortex
phrenia found in some studies: • Reduced hippocampal cell size
• Disturbed cytoarchitecture in the entorhinal cortex
• Reduced size of frontal lobes or some division
thereof
• Reduced size of temporal lobe, particularly on the left
• Reduced size of hippocampus and amygdala,
26.4.9 Functional Brain Abnormalities
particularly on the left in Schizophrenia
• Reduced size of parahippocampal gyrus Hypofrontality is associated with the presence of nega-
tive symptoms and autism.
26.4.8 Neuropathological Abnormalities Combining functional imaging with task activa-
in Schizophrenia tion, Weinberger et al. (1986) measured regional
26.4.8.1 Postmortem Studies cerebral blood flow at rest and during the Wisconsin
Card Sorting Test (activates frontal lobes normally).
Compared with control subjects, the brains of schizo-
Impaired performance by schizophrenics was mir-
phrenic patients have shown the following in some studies:
rored by a smaller increase in blood flow to prefrontal
• Lower fixed brain weight cortex.
• Reduced brain length
• Reduced size of the parahippocampal gyrus
26.4.10 Deficits in Cognition in Schizophrenia
26.4.8.2 Histological Studies Cognitive impairment is common among patients suffering
Compared to controls, the brains of schizophrenics have from schizophrenia. The cognitive deficits of schizophrenia
shown the following in some studies: are summarized in Figure 26.2.
Cognitive deficits
Learning and Working memory Executive Attentional deficits Functional deficits

memory functioning
Reduction in Impairment in spatial Executive Impairment in Cognitive deficits

learning potential delayed response functioning selective attention lead to impairments
impairment occurs in (focus on one aspect in social and
Unable to use Impairment in the early phase of but ignore the other occupational
semantic categories visually oriented schizophrenia aspect of functions,
(food, animals) of working memory environmental independent living
information Performance deficits stimuli) and self care skills
Impairment in in Wisconsin card
Recall failures memory span and sorting test, Impairment in Dorsolateral lesions:
(including prompted manipulation of tasks categories test and sustained attention difficulties in
and cued recall) Tower tests delayed response
Impairment in source Impairment in rapid requiring memory
monitoring (i.e. the Lack of insight and visual processing for spatial location
patient cannot tell the unawareness of
differences between illness Reduction in Orbitofrontal lesions:
information obtained pre-pulse inhibition deficits in object
externally and that Social deficits alternation
imagined internally.
This leads to This is related to
hallucination) hypofrontality
FIGURE 26.2 A summary of cognitive deficits in schizophrenia.

26.5 MANAGEMENT OF SCHIZOPHRENIA f. Massive loading doses (rapid neurolep-

tization) should be avoided.
26.5.1 Physical Examination g. The choice of medication depends on
1. Vital signs: heart rate and temperature. the risk–benefit ratio and the potential
2. Measure BMI. side effect on a patient.
3. Neurological examination looking for side h. Where a potential to cause weight gain or
effects associated with antipsychotics such as diabetes has been identified for the atypical
extrapyramidal side effects (EPSE). antipsychotic prescribed, there should be
routine monitoring for these potential risks.
i. Use of adjunctive medication to prevent
26.5.2 Investigations harm and reduce symptoms.
B. Stabilization phase:
1. Full blood count (FBC)
a. In the early post-acute period, patients
2. Liver function tests (LFTs)
should be helped to understand their ill-
3. Renal function tests (RFTs)
ness and should be encouraged to write
4. Electrolytes
an account of their illness in their notes.
5. Thyroid function tests
b. The assessment of needs for health and
6. Fasting lipids and glucose
social care for people with schizophrenia
7. Pregnancy test β-HCG (for females)
should be comprehensive and address
8. Toxicology screen
medical, social, psychological, occupa-
9. Electrocardiogram
tional, economic, physical, and cultural
10. CT brain scan or MRI brain scan
issues.
11. Prolactin level if patient complains of galactorrhoea
c. Minimize the likelihood of relapse.
d. Enhance adaptation.
26.5.3 General Management Strategies e. Facilitate continued reduction in symp-
(Scottish Schizophrenia Guidelines toms and promote the process of recovery.
C. Maintenance phase:
and NICE Guidelines)
a. Ensure symptom remission or control.
1. Assess symptoms and establish a diagnosis b. Maintain/improve level of functioning
based on the ICD-10 or DSM-V criteria. and quality of life.
2. Establish therapeutic alliance and formulate and c. Continuation of antipsychotic drugs for 1
implement a treatment plan. or 2 years after a relapse is recommended.
3. Phase-specific management: d. Monitor adverse effects related to
A. Acute phase: treatment.
a. Community mental health teams are an e. Withdrawal of antipsychotic medication
acceptable way of organizing commu- should be gradual and monitored.
nity care. f. Following the withdrawal of drugs,
b. Crisis resolution and home treatment patients should continue to be moni-
teams should be used to manage crises tored for signs of relapse for at least 2
of patients and should augment ser- years after the last acute episode.
vices provided by early intervention and 4. Review the use of alcohol and illicit drugs
assertive outreach teams. and provision of access to specialist addiction
c. Alternatives to acute inpatient care services.
should be developed. 5. Psychosocial rehabilitation.
d. Antipsychotic therapy should be initiated 6. Assessment for the need of life and social skills
as part of a comprehensive package of care. training and a person and their carer’s need for
e. Atypical antipsychotic should be intro- psychotherapy. Cognitive behavioural therapy
duced at the earliest convenience. (CBT) and family intervention should be avail-
Atypical drugs at the lower end of the able. Cognitive remediation therapy aims to
dose range should be used in the first improve cognitive dysfunction in poor memory,
episode of schizophrenia. executive dysfunction, and attentional deficits.
26.5.4 Promoting Recovery respond better than ‘negative’ symptoms. Bear in mind

the following:
26.5.4.1 Primary Care
1. General practitioners (GPs) should develop case 1. 5%–25% of schizophrenics are unresponsive to
registers for people with schizophrenia. conventional neuroleptics.
2. GPs should regularly monitor the physical health 2. 5%–10% are intolerant owing to adverse neurolog-
of patients with schizophrenia. Particular atten- ical effects (parkinsonism, akathisia, dyskinesia).
tion should be paid to endocrine disorders, for 3. 40%–60% of schizophrenics are noncompliant
example, diabetes, hyperprolactinaemia, blood with oral medication. Possible reasons are
pressure, lipids, side effects of medication, and a. Limited insight into the disease
lifestyle risk factors, for example, smoking. b. Limited beneficial effect
3. GPs should re-refer patients to secondary care c. Unpleasant side effects
particularly if d. Pressure from family and friends
a. Treatment adherence is problematic. e. Poor communication with the medical team
b. There is poor response to treatment. Depot neuroleptics increase compliance and
c. Comorbid substance misuse is suspected. reduce relapse rates
d. Level of risk to self or others is raised. 4. Continuous therapy is superior to intermittent
e. When patient first joins the practice. treatment. It results in fewer relapses and a lower
overall dose of neuroleptics.
26.5.4.2 Secondary Care
5. Of patients who stop medication, 60%–70%
• A full assessment of health and social care relapse within a year, and 85% within 2 years,
needs should be made regularly. compared to 10%–30% of those who continue
• Carers should have their needs assessed. on active medication (Table 26.3).
26.5.5 Service Interventions
TABLE 26.3
• Assertive outreach teams should be developed
for patients who engage poorly with services, Properties of the Typical Antipsychotics
are high users of inpatient care, or are homeless. Typical
• Crisis resolution and home treatment teams Antipsychotics Properties
should be available for those in acute crisis. Typical antipsychotics 1. The most common EPSE is acute
• The Care Programme Approach (CPA) ensures in general dystonia (90%)
services are managed and integrated. 2. In acute dystonia, young men are at the
highest risk
3. In tardive dyskinesia, elderly women are
26.5.6 Hospitalization
at the highest risk
Those with acute schizophrenia often require admission to Haloperidol 1. High risk for EPSE
hospital, if necessarily compulsorily, for assessment, inves- 2. High risk for galactorrhoea
tigations, and treatment. Before discharge, Section 117 of 3. Low risk for weigh gain, postural
the Mental Health Act 1983 for detained patients, and the hypotension, or sedation
CPA for all patients, requires that an ‘assessment of needs’ Trifluoperazine 1. Low risk for weight gain or postural
hypotension
be made. A key worker should be assigned to monitor a
Sulpiride or 1. Sulpiride carries low risk of weight gain
patient’s progress and to administer depot medication.
amisulpride 2. Amisulpride carries low risk of
Attendance at a day hospital or centre may be con- dyslipidaemia, weight gain, and glucose
sidered, and there should be appropriate communication intolerance
with the patient’s GP. 3. Sulpiride and amisulpride carry low risk
Electroconvulsive therapy is used in the treatment of of postural hypotension
catatonic stupor. 4. Sulpiride and amisulpride carry low risk
of sedation
26.5.7 Drug Treatments for Schizophrenia
Source: Taylor, D. et al., The Maudsley Prescribing Guideline,
The efficacy of neuroleptics for acute symptoms has Informa Healthcare, London, U.K., 2009.
been demonstrated beyond doubt. ‘Positive’ symptoms
26.5.8 Use of Atypical Neuroleptics 26.5.9.2 Cross Sectional Measures

Atypical neuroleptics are distinguished from conven- 1. The score of Brief Psychiatric Rating Scale
tional neuroleptics by not producing catalepsy in animals (BPRS) is larger than 45.
and not elevating prolactin levels in humans. There is a 2. The score of Clinical Global Index (CGI) is
considerably lower potential for EPSE and tardive dyski- larger than 4.
nesia. EPSE occur in up to 90% of patients taking neuro- 26.5.9.3 Prospective Trials
leptic medication.
1. Trial of 4 weeks of haloperidol at 15 mg–60 mg
per day (if not tried before).
26.5.8.1 NICE Guidelines on Atypical
2. The BPRS score is larger than 35 (after the trial
Antipsychotics of haloperidol).
In the United Kingdom, the NICE issued guidelines in June
2002 with respect to the prescription of atypical antipsy- If a patient has failed to respond to a trial of three neurolep-
chotics for patients with schizophrenia. They are as follows: tics of different classes, using an adequate dose for an ade-
quate duration, an atypical agent such as clozapine can be
• The atypical antipsychotics (amisulpride, tried. Clozapine can cause agranulocytosis, so regular blood
olanzapine, quetiapine, risperidone, and counts are necessary. The incidence of agranulocytosis is
zotepine) should be considered when deciding 0.8% at 12 months and 0.9% at 18 months, with a peak risk
on the first-line treatment of newly diagnosed in the third month; it is higher in women and older patients.
schizophrenia. Kane et al. (1988) showed that clozapine was significantly
• An atypical antipsychotic is considered the better than chlorpromazine in the treatment of schizo-
treatment of choice for managing an acute phrenics previously resistant to haloperidol. Improvement
schizophrenic episode when discussion with the was observed in both positive and negative symptoms.
individual is not possible.
• An atypical antipsychotic should be considered for 26.5.9.4 Clozapine Patient Management System
an individual who is suffering from unacceptable In the United Kingdom, patients receiving clozapine are
side effects with a conventional antipsychotic. required to have their full blood counts monitored at reg-
• An atypical antipsychotic should be considered ular intervals. The CPMS is summarized in Table 26.5.
for an individual in relapse whose symptoms
were previously inadequately controlled. 26.6 MEDICATION ADHERENCE
• Changing to an atypical antipsychotic is not
Schizophrenia patients are often nonadherent to antipsy-
necessary if a conventional antipsychotic con-
chotics. The NICE guidelines recommend the following
trols symptoms adequately and the individual
interventions to enhance adherence:
does not suffer unacceptable side effects.
• Clozapine should be introduced if schizophrenia 1. Improve communication: Adapt the communi-
is inadequately controlled despite the sequential cation style to suit the patient’s needs.
use of two or more antipsychotics (one of which 2. Increase patient’s involvement: The analysis of
should be an atypical antipsychotic) each for at risks and benefits will help the patient to make
least 6–8 weeks (Table 26.4). the decision.
3. Understand the patient’s perspectives: Explore
26.5.9 Treatment-Resistant Schizophrenia about general or specific concerns (e.g. adverse
effects or worries about dependence).
Kane’s Criteria for Treatment-Resistant Schizophrenia 4. Determine the type of nonadherence: Intentional
(due to beliefs and concerns) or unintentional
26.5.9.1 Past Psychiatric History nonadherence (practical difficulties and cost).
1. In the past 5 years, the patient has no good 5. Provide information: Provide further informa-
functioning. tion in the form of leaflet.
2. In the past 5 years, two different antipsychotics 6. Monitor adherence in a nonjudgemental way:
have been tried for 6 weeks with at least 1000 The psychiatrist should explain why he or she is
mg chlorpromazine equivalent but unsatisfac- interested in patient’s adherence and let patient
tory response. understand the good intention.
TABLE 26.4
Properties of the Atypical Antipsychotics
Atypical Antipsychotics Properties
Clozapine 1. Agranulocytosis is the most common in Ashkenazi Jews
2. The most common side effect is sedation till the next morning
3. The second most common side effect is hypersalivation
4. Clozapine (like olanzapine) carries the highest risk of weight gain
5. Clozapine is least likely to cause tardive dyskinesia
Risperidone 1. Higher risk for EPSE and galactorrhoea as compared to other second-generation antipsychotics
2. Risperidone carries low risk of sedation
Paliperidone 1. Side effects include EPSE, corrected QT (QTc) prolongation, hyperprolactinaemia, metabolic
syndrome, and increase in risk of seizure
2. Renal impairment is a contraindication because paliperidone is mainly excreted by kidney
Olanzapine 1. Olanzapine carries the highest risk of weight gain among all antipsychotics
2. Olanzapine carries low risk of EPSE
3. Olanzapine carries low risk of hyperprolactinaemia
4. Olanzapine carries the lowest risk of QTc prolongation
Quetiapine 1. Quetiapine has high affinity for muscarinic receptors
2. Quetiapine carries the lowest risk for EPSE
3. Quetiapine carries the lowest risk of sexual dysfunction
4. Quetiapine carries low risk of hyperprolactinaemia
Ziprasidone 1. Ziprasidone carries low risk of dyslipidaemia, weight gain, and glucose intolerance
Aripiprazole 1. Aripiprazole carries the lowest risk of QTc prolongation
2 Aripiprazole carries low risk of sexual dysfunction
3. Aripiprazole carries low risk for EPSE
4. Aripiprazole carries low risk of dyslipidaemia, weight gain, and glucose intolerance
5. Aripiprazole carries low risk of hyperprolactinaemia
6. Aripiprazole carries low risk of postural hypotension
7. Aripiprazole carries low risk of sedation
Asenapine 1. Asenapine has less potential to raise prolactin than risperidone
2. Asenapine is associated with lower risk of weight gain
Source: Taylor, D. et al., The Maudsley Prescribing Guideline, Informa Healthcare, London, U.K., 2009.
7. Further intervention to increase adherence: If 2. Understanding and respecting patient’s views

nonadherence continues to be an issue, the psy- and decisions about treatment options and
chiatrist can suggest the patient to record his lifestyle.
or her medicine taking by multicompartment 3. Psychological interventions should be support-
medicine system. The patient can monitor the ive in nature, focus on here and now, and reality
relationship between severity of symptoms and based. To be flexible and eclectic, tailored to the
level of adherence. The psychiatrist can sim- patient’s needs as they emerge (e.g. addressing
plify the dosing regimen and offer advice to developmental issues and losses).
help the patient to cope with the side effects. 4. To foster and encourage independence and opti-
mal social and occupational functioning and
26.6.1 Psychosocial Treatments promote self-management of the illness.
for Schizophrenia
26.6.1.2 Psychoeducation
26.6.1.1 General Principles 1. The main objective is to provide the patient
1. Establishing, maintaining, and developing a with information about the illness, the range
therapeutic alliance. Engagement, rapport, and of treatments available, and the effect of using
building basic trust in a patient who may have recreational drugs such as amphetamines. The
difficulty trusting. patients are informed of the choices.
TABLE 26.5
Clozapine Patient Management System (CPMS)
Time Actions
0 1. Perform assessment and discuss with patient and carers
2. Information and advice regarding swapping to clozapine from another antipsychotic should be sought from
the pharmacy
3. Decide whether it is an inpatient or outpatient initiation. Inpatient initiation is indicated for elderly and
adolescents 16–18-year-olds, concurrent medical problems, and medication
4. Register patient with the Clozaril Patient Management System (CPMS) and obtain an initial FBC
5. Start clozapine at 12.5 mg once a green blood result is issued by the CPMS
6. For inpatient treatment, physical monitoring is required every hour for 6 h, and patient needs to be
accompanied by a carer
7. For outpatient treatment, patient and carer must be provided with emergency contact details for the first 24 h
8. Inform his or her GP on the start date
9. Baseline physical examination: weight, temperature, pulse, and BP (both lying and standing)
10. For patients with diabetes: HbA1c at baseline; for patients without diabetes: fasting blood glucose
11. Other baselines: LFTs, RFTs, lipids, and ECG
0–18 weeks 1. FBC: at least weekly for the first 18 weeks of clozapine treatment
2. Fasting plasma glucose at 1 month, then 4–6 monthly
3. LFTs, RFTs, lipids: every 6 months for the first year
4. Follow standardized clozapine initiation charts
5. A slower dose titration in the inpatient setting is required for older adults (>65’s)
6. The usual dose is 200–450 mg daily with a maximum dose of 900 mg daily. Older adults may need a lower
daily dose
7. For outpatient treatment, increments should not be done over weekend or holidays
18–52 weeks 1. FBC: at least two weekly from week 18 to week 52 of clozapine treatment
2. Fasting plasma glucose at 1 month, then 4–6 monthly
3. LFTs, RFTs, lipids: every 6 months for the first year
First to 1. FBC: at least four weekly after 1 year of clozapine treatment with stable blood results and the CPMS
second year agreement
2. LFTs, RFTs, lipids, fasting glucose every year
Second year 1. FBC: for at least 4 weeks
2. LFTs, RFTs, lipids, fasting glucose every year
Sources: Taylor, D. et al., The Maudsley Prescribing Guideline, Informa Healthcare, London, U.K., 2009; NICE, NICE Guidelines
for Schizophrenia, http://guidance.nice.org.uk/CG82 (accessed on August 1, 2012).
2. Psychoeducation for individuals with first epi- provided reprovision was well resourced with staffed
sode of psychosis or schizophrenia should homes for the more disabled, there was no increase in
encourage blame-free acceptance of illness. death rate, suicides, crime, or vagrancy at 1- and 5-year
3. Develop strategies to promote control of illness follow-up, compared to matched controls. Between dis-
by recognizing and responding to early warning charge and 5 years, negative symptoms reduced signifi-
signs and seek professional advice. cantly in response to a more stimulating environment.
Positive symptomatology remained stable.
26.6.1.3 Social Milieu
Wing and Brown (1970) found that negative symptoms
varied in intensity with social stimulation within psychi- 26.6.1.4 Grief Work on Losses
atric institutions. To work through both losses from prior to the ill-
The Team for the Assessment of Psychiatric Services ness onset and also losses arising from the disrup-
(TAPS) study (Leff et al., 1994) reported on long-stay tion, disorganization, and disability associated with
patients discharged into the community. It found that, schizophrenia.
26.6.1.5 Supportive Psychotherapy 26.6.1.8 Family Intervention

Refinements of individual supportive psychological treat- The NICE guidelines recommend the following:
ments, that is, targeted psychological treatments for spe-
cific components of illness or symptoms, developed for 1. The therapist should include the service user if
affected individual, for example, coping techniques to possible and offer at least 10 planned sessions
deal with psychotic symptoms. over a period of 3 months to 1 year.
2. Single-family intervention focusing on ‘here
26.6.1.6 Cognitive Behavioural Therapy and now’ and the family system (boundaries,
Components of CBT should involve coalitions, triangulation) is recommended.
3. Family intervention should take into account the
1. Advising the patients to keep a record to moni- relationship between the main carer and the ser-
tor their own thoughts, feelings, or behaviours vice user.
with respect to their symptoms or recurrence of 4. Therapist should establish a working relation-
symptoms ship with family and provide structure and
2. Promoting alternative ways of coping with the stability.
target symptoms 5. Cognitive techniques can be used to challenge
3. Reducing stress unhelpful attributions such as guilt.
4. Improving functioning 6. Behavioural approaches include goal setting and
5. Reducing negative symptoms by activity problem-solving.
scheduling
26.6.1.9 Art Therapy
Specific techniques targeting at auditory hallucination
The NICE guidelines recommend art therapies con-
ducted by art therapists registered by the Health and Care
1. Distraction method: Wearing headphones to
Professional Council. The objectives of art therapy include
focus attention away and the hallucinations are
extinguished with decreased reactivity.
1. Helping people with schizophrenia to experi-
2. Desensitization: Describe, record, and recog-
ence themselves differently and develop new
nize the connection between stressors and hal-
ways of relating to others
lucinations and explore what the voices mean to
2. Expressing themselves and organizing their
them.
experience into a satisfying aesthetic form
3. Accepting and understanding feeling that may
The NICE guidelines also recommend the therapist
have emerged during the creative process when
to deliver CBT on a one-to-one basis over at least 16
doing the artwork
planned sessions. The therapist should follow a treatment
manual to help the patient to establish links between
their thoughts, feelings, or actions and their current or 26.6.1.10 Rehabilitation
past symptoms. This will help them to reevaluate their 1. Objectives
perceptions, beliefs, and reasoning behind the target a. Achieve the highest possible levels of social
symptoms. and vocational functioning and well-being
for individuals with severe and persistent
26.6.1.7 Expressed Emotion mental disorders
Psychoeducational family programmes to increase medi- b. Reduce interference from symptoms and
cation compliance and coping with stressors are success- neurocognitive impairments
ful in reducing the risk of relapse. Families with high EE 2. Cognitive restructuring
were identified using the Camberwell Family Interview. a. Attention (using various computer software):
Education and family sessions in the home run in paral- to increase attention span and to improve
lel with a relatives group. The programme is aimed at the efficiency of information processing
teaching problem-solving skills, lowering criticism and b. Memory: memory notebook, mnemonics,
overinvolvement, and reducing contact between patients rehearsal
and relatives while expanding social networks. c. Executive function: to attempt remediation
3. Social skill and assertive community training 26.6.2.7 Suicide

a. Promote independent living and enhance Ten per cent of schizophrenics commit suicide, and for
social relations most sufferers, it happens early in their illness. Roy
b. Focus on food preparation, money manage- (1982) reported that suicide was more likely in the fol-
ment, personal self-care, and interpersonal lowing cases:
relationship
c. Reduce disabilities and enhance abilities • Being male
d. Reduce unacceptable community behav- • Being young
iours such as violence or substance abuse • Being unemployed
e. Crisis intervention in community and • Having chronic illness, relapses, and remissions
reduced hospitalization • Having a high educational attainment prior to
4. Supported employment and vocational onset
rehabilitation • Akathisia
a. Enhance occupational potential • Abrupt stoppage of drugs
b. Increase income and improve socioeco- • Recent discharge from inpatient care
nomic status
Finally, paranoid schizophrenics are three times more
26.6.2 Prognosis for Schizophrenia likely than nonparanoid patients to commit suicide.
Schizophrenia is a heterogeneous disorder, and there are 26.6.2.8 Violence (Bobes et al., 2009)
no reliable predictors of outcome. Approximately 25%
Violence in people with schizophrenia is uncommon,
of cases of schizophrenia show good clinical and social
but they do have a higher risk than general population.
recovery, while most studies show that fewer than a half
Prevalence of recent aggressive behaviour among outpa-
of patients have a poor long-term outcome. Factors asso-
tients with schizophrenia is 5%. The types of violence
ciated with a good prognosis include
and aggression are classified as follows: verbal aggression
(45%), physical violence towards objects (30%), violence
26.6.2.1 Sociodemographics
towards others (20%), and self-directed violence (10%).
• Being female Family members are involved in 50% of the assaults with
• Being married strangers being attacked in 20%. Psychiatrists need to be
competent in identifying patients at risk and protecting
26.6.2.2 Past History both patients and others.
• Good premorbid social adjustment
• Family history of affective disorder
• Short duration of illness prior to treatment 26.6.3 Prodrome of Schizophrenia
Prodrome refers to a range of subjective experiences
26.6.2.3 Pathology before the onset of schizophrenia (Yung and McGorry,
• No ventricular enlargement 1996).
26.6.2.4 Course of Illness 26.6.3.1 Attenuated Positive Symptoms

• An abrupt onset of the illness 1. Unusual perception.
• Later onset of the illness 2. Odd beliefs.
3. Vague and circumstantial speech.
26.6.2.5 Symptoms 4. Preoccupation with religion, occult, and philosophy.
• An affective component to the illness 5. Suspiciousness.
• Paranoid, compared with nonparanoid 6. Prepsychotic anxiety.
• Lack of negative symptoms 7. Praecox feeling refers to a subjective sense by
• Lack of cognitive impairment the clinician that the patient is odd. The patient
is usually concrete, woolly, exhibiting mild
26.6.2.6 Treatment formal thought disorder, or socially blamed or
• Good initial response to treatment reporting perceptual disturbance.
26.6.3.2 Negative Symptoms 3. Organic disorders, for example, CNS infection

1. Blunted affect 4. Epilepsy
2. Amotivation 5. Medications (ciprofloxacin)
3. Isolation and social withdrawal 6. Recreational drugs (cocaine)
7. Psychogenic catatonia
26.6.3.3 Cognitive Symptoms 8. Lethal catatonia (extreme psychotic excitement
1. Deterioration in academic, work, social func- that differs from neuroleptic malignant syn-
tioning, and self-care drome [NMS])
2. Reduced attention and concentration
26.6.3.4 General Symptoms 26.7.2 Clinical Features

1. Sleep disturbance: usually initial insomnia
1. Ambitendency.
2. Irritability
2. Automatic obedience.
3. Depressed mood
3. Mitgehen.
4. Poor hygiene
4. Mitmachen.
26.6.3.5 Interventions for Prodrome 5. Mannerism.
6. Negativism.
1. Careful observation.
7. Echolalia.
2. Consider differential diagnoses including
8. Echopraxia.
organic diagnoses.
9. Logorrhoea.
3. Consider comorbidity such as substance abuse.
10. Stereotypy.
4. Strive to minimize risk of relapse.
11. Waxy flexibility/catalepsy.
5. Aim to eliminate exposure to cannabis and
12. Gegenhalten (negativism): Patient resists the
psychostimulants by psychoeducation, enhance
attempts of examiner to move part of body in
stress management, and employ maintenance
equal strength to applied force.
antipsychotic treatment.
13. Verbigeration: morbid repetition of words.
6. Discuss prudent treatment options such as start-
ing antipsychotics and CBT.
26.6.3.6 Prognosis
26.7.3 Management
The conversion to schizophrenia is 35%. 26.7.3.1 Investigations
70% achieve full remission within 3–4 months. • Haematology: FBC
80% achieve stable remission within 1 year. • Biochemistry: RFTs, LFTs, creatinine kinase,
and blood glucose
26.6.3.7 Predictors for Further Progression • Endocrine: thyroid function tests
to Psychosis or Schizophrenia • Urine drug screen
(Cannon et al., 2008) • Heavy metal screening
1. Genetic risk with recent deterioration in function • Imaging: CT scan or MRI scan of the brain
2. Higher levels of unusual thought content • Microbiology: urine and blood culture, syphilis,
3. Higher levels of suspicion/paranoia and HIV
4. Greater social impairment • Heavy metal screening
5. History of substance abuse • Autoantibody screen
• Lumbar puncture
• Electrophysiology: ECG and EEG
26.7 CATATONIA
26.7.1 Aetiology 26.7.4 Medications
1. Schizophrenia 1. Benzodiazepines (e.g. intramuscular lorazepam
2. Depression or mania (more common than up to 4 mg per day)
schizophrenia) 2. Electroconvulsive therapy
26.7.5 Prognosis belief that his or her sexual partner is being unfaithful

and will go to great lengths to find evidence of infidel-
Two-thirds of patients improve with treatment. ity. Underclothing may be examined for semen stains,
belongings may be searched, and the partner may be
26.8 DELUSIONAL (PARANOID) DISORDERS interrogated and followed. It is more common in men.
26.8.1 ICD-10 Issues (WHO, 1992) Pathological jealousy may be associated with the fol-
lowing conditions:
According to ICD-10, a delusional disorder is an ill-defined
condition, manifesting as a single delusion or a set of related • Organic disorders and psychoactive substance
delusions, being persistent, sometimes lifelong, and not hav- use disorders (e.g. alcohol dependence, cere-
ing an identifiable organic basis. There are occasional or bral tumour, endocrinopathy, dementia, cerebral
transitory auditory hallucinations, particularly in the elderly. infection, use of amphetamines or cocaine)
Delusions are the most conspicuous or only symptom and • Paranoid schizophrenia
are present for at least 3 months. For the diagnosis, there must • Depression
be no evidence of schizophrenic symptoms or brain disease. • Neurosis or personality disorder
ICD-10 includes the previously used term late para-
phrenia, although there is some evidence that there are Treatment should be directed at the underlying disorder.
differences between persistent delusional disorder and If no primary cause is identified, pharmacotherapy with
late paraphrenia. Howard et al. (1994) showed, using MRI a neuroleptic and/or psychotherapy may be helpful. There
scans in a group of late-onset schizophrenics and late-onset may be a risk of violence to the partner, and it may be
delusional disorders, that lateral ventricle volumes in the best to recommend that the couple separate.
delusional disorder patients were much greater than those
of schizophrenics and almost twice those of controls. 26.8.3.2 Erotomania (De Clérambault’s Syndrome)
Monodelusional disorders feature a stable, encapsu- The person holds the delusional belief that someone, usu-
lated delusional system, which takes over much of a per- ally of a higher social or professional status or a famous
son’s life. The personality is preserved. personality or in some other way ‘unattainable’, is in love
with him or her. The patient may make repeated attempts
26.8.2 Epidemiology of Delusional Disorders to contact that other person. Eventually, rejections may
lead to animosity and bitterness on the part of the patient
There is a point prevalence of 0.03% and a lifetime risk towards the object of attention.
of 0.05%–0.1%. In hospital and outpatient clinical psychiatry, patients
Munro (1991) reports from his series of patients with are more likely to be female than male, whereas in foren-
monodelusional disorder: sic psychiatry, male patients are commoner. Overall,
females outnumber males.
• A mean age of onset of 35 years for males and
45 years for females 26.8.3.3 Cotard’s Syndrome
• Onset gradual and unremitting in 62% This condition, also called délire de négation, is a nihilis-
• Equal sex ratio of sufferers tic delusional disorder in which the patient believes that,
• Sufferers often unmarried, with high marital for example, all his or her wealth has gone or that rela-
breakdown and low fecundity tives or friends do not exist. It may take a somatic form
• Introverted, long-standing interpersonal difficulties with the patient believing that parts of his or her body do
• Family history of psychiatric disorder but not of not exist. It can be secondary to very severe depression or
delusional disorder or schizophrenia to an organic disorder.
• Evidence of minimal brain disorder in 16%
26.8.3.4 Capgras Syndrome
26.8.3 Specific Delusional (Paranoid) Disorders Although Capgras syndrome is also called illusion
des sosies, or illusion of doubles, it is not an illusion
26.8.3.1 Pathological (Delusional) Jealousy but a delusional disorder. The essential feature of this
This is also called the Othello syndrome, morbid jeal- rare condition is that a person who is familiar to the
ousy, erotic jealousy, sexual jealousy, psychotic jealousy, patient is believed to have been replaced by a double. It
or conjugal paranoia. The person holds the delusional is more common in females. Common primary causes
are schizophrenia, mood disorder, and organic disor- psychosis, having different aetiologies and
der. Derealization often occurs. requiring different treatments.
• Continuum theorists (e.g. Crow, Kendall) doubt
26.8.3.5 Fregoli Syndrome that there are distinct illnesses but rather that
In this very rare delusional disorder, the patient believes features of psychosis vary quantitatively along
that a familiar person, who is often believed to be the a continuum, with schizophrenia and manic
patient’s persecutor, has taken on different appearances. depression at opposing poles and schizoaffec-
Primary causes include schizophrenia and organic tive disorder somewhere in between.
disorder.
In 1991, Tsuang studied a subgroup of patients with
26.8.3.6 Induced Psychosis (Folie À Deux)
strictly defined schizoaffective disorder. It was found that
This rare delusional disorder is shared by two, or rarely the morbid risk of schizophrenia in relatives of schizoaf-
more than two, people who are closely linked emotionally. fectives was similar to that of a schizophrenic group and
One of the people has a genuine psychotic disorder; his fell between schizophrenia and affective disorder for the
or her delusional system is induced in the other person, risk of affective disorder in relatives. It was concluded
who may be dependent or less intelligent than the first that this condition was different from schizophrenia or
person. Geographical separation leads to recovery of the manic depression.
well person. In 1993, Goldstein et al. found that, among probands
with schizoaffective disorder, relatives had higher rates
26.9 SCHIZOAFFECTIVE DISORDERS of schizophrenia and unipolar depression than relatives
of males. Among relatives, males were at higher risk for
26.9.1 Types of Disorder schizophrenia spectrum disorders than females. This
The term ‘schizoaffective psychosis’ was introduced by points to a stronger relationship between schizoaffective
Kasanin in 1933 to describe a condition with both affec- disorder and schizophrenia.
tive and schizophrenic symptoms, with sudden acute In 1994, DeLisi et al. reported the following in rela-
onset after good premorbid functioning, and usually with tionship to schizophrenia and affective disorder:
complete recovery.
ICD-10 describes these as disorders in which both • At least one-third of schizophrenics have
affective and schizophrenic symptoms are prominent depressive symptoms.
within the same episode of illness, either simultaneously • Affective disorder is more frequent in the fami-
or within a few days of each other. It distinguishes vari- lies of schizophrenics than in controls.
ous types: • Unipolar depression is more common in fami-
lies of schizoaffectives than schizophrenia-only
• Manic type—the person usually makes a full probands. Bipolar disorder is as frequent in fam-
recovery. ilies of both.
• Depressive type—prognosis not as good as that • Affective disorder is frequently inherited from
of the manic subtype, with a greater chance of the same parental line as schizophrenia.
developing ‘negative’ symptoms. • Bipolar disorder is more frequent in male rela-
• Mixed type. tives, and unipolar disorder more frequent in
female relatives.
26.9.2 Relationship between Affective and It was concluded that the same genes contribute to schizo-
Schizophrenic Components phrenia and affective disorder, and sex and phenotypic
There is no consensus concerning the nosological status expression are related.
of schizoaffective disorder. Opposing views include the
Kraepelinian binary system and continuum theories:
26.9.3 Prognosis for Schizoaffective Disorders
• Binary theorists (e.g. Winokur, Kendler) hold
the traditional notion that there are two separate The prognosis of schizoaffective disorders lies between
illnesses, schizophrenia and manic–depressive that of mood disorders and schizophrenia.
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27 Mood Disorders, Suicide,
and Parasuicide
27.1 HISTORY • Mania with psychotic symptoms. The symptoms

are as mentioned earlier but with delusions and
• In 1921, Kraepelin divided the functional psy- hallucinations, usually grandiose. There may be
choses into two broad categories: dementia prae- sustained physical activity, aggression, and self-
cox and manic–depressive insanity. He thought neglect (Table 27.1).
of the latter as a disorder in which discrete epi-
sodes of illness alternated with clearly defined
well periods during which patients returned to 27.2.1.2 F31 Bipolar Affective Disorder
their previous state of health. There are repeated episodes of mood disturbance, some-
• In 1949, Cade first initiated the use of lithium, times elevated, sometimes depressed.
but it was not widely used until the 1960s. Repeated episodes of mania are classified as bipo-
• In the 1950s, tricyclic and monoamine oxidase lar (sufferers resemble those who also have depressive
inhibitor (MAOI) antidepressants were introduced. episodes in their family history, premorbid personality,
• In the 1970s, anticonvulsants were first used for age of onset and prognosis). It includes the following:
bipolar disorders. Specific psychological treat-
ments (e.g. cognitive therapy) were introduced. 1. Bipolar affective disorder with
• In the 1980s, selective serotonin reuptake inhib- a. Current episode hypomanic
itors (SSRIs) were introduced. b. Current episode manic without psychotic
symptoms
c. Current episode manic with psychotic
27.2 CLASSIFICATIONS OF symptoms
MOOD DISORDERS 2. Bipolar affective disorder with
a. Current episode having mild/moderate
27.2.1 ICD-10 Classifications (WHO, 1992) depression
27.2.1.1 F30 Manic Episode b. Current episode having severe depression
without psychotic symptoms
The fundamental disturbance is an elevation of mood to
c. Current episode having severe depression
elation, with concomitant increase in activity level. Three
with psychotic symptoms
degrees of manic episode are specified by ICD-10, all
3. Bipolar affective disorder with
used for a single manic episode only:
a. Current episode mixed
• Hypomania. There is persistent elevated mood,
increased energy and activity, feelings of well- 27.2.2 DSM-5 (APA, 2013)
being, and reduced need for sleep. Irritability
may replace elation. Work is considerably dis- 296 Bipolar I disorder
rupted. There are no hallucinations or delusions.
• Mania without psychotic symptoms. Mood is 1. Duration: at least 1 week
elevated, with almost uncontrollable excite- 2. Number of episode: at least one manic episode
ment. There is overactivity; pressured speech; 3. Manic episode: at least three or more of the fol-
reduced sleep; distractible, inflated self-esteem; lowing symptoms or four or more if only irrita-
and grandiose thoughts. Perceptual heightening bility is present
may occur. The person may spend excessively a. Inflated self-esteem or grandiosity
and become aggressive, amorous, or facetious. b. Decreased need for sleep
377

Compare and Contrast ICD-10 and DSM-5 Criteria Comparison between the ICD-10 and Proposed
on Bipolar Disorder DSM-5 Criteria for Depressive Disorder
ICD-10 (WHO, 1992) DSM-5 (APA, 2013) ICD-10 (WHO, 1992) DSM-5 (APA, 2013)
F30 Manic episode (hypomania, 296 Bipolar I disorder F32 Depressive episode 296.99 Disruptive mood
mania with and without 296.89 Bipolar II disorder (mild/moderate/severe) dysregulation disorder
psychotic symptoms) 301.13 Cyclothymic disorder F33 Recurrent depressive episode 296.2 Major depressive disorder,
F31 Bipolar affective disorder Substance-induced bipolar (mild/moderate/severe) single episode
(current episode hypomanic, disorder F34 Persistent mood disorder 296.3 Major depressive disorder,
manic with and without psychotic 293.83 Bipolar disorder (cyclothymia, dysthymia, and recurrent
features, moderate depression associated with another other persistent mood disorders) 300.4 Dysthymia (persistent
with and without somatic medical condition depressive disorder)
symptoms, severe depression with 296.80 Bipolar disorder not F38 Other mood disorders 625.4 Premenstrual dysphoric
and without psychotic features) elsewhere classified (mixed affective episode, disorder
recurrent brief depressive Substance-induced depressive
episode) disorder
293.83 Depressive disorder
c. More talkative than usual or pressure of associated with another medical
speech condition
311 Depressive disorder not
d. Flight of ideas or racing thoughts
elsewhere classified
e. Distractibility
f. Increase in goal-directed activity or psycho-
motor agitation
g. Excessive involvement in activities that
have a high potential for painful and nega- 2. There have been numerous episodes with hypo-
tive consequences (e.g. overspending, sexual manic symptoms that do not meet criteria for a
indiscretions, or foolhardy investments) hypomanic episode and numerous episodes with
4. Functional impairment and exclusion of other depressive symptoms that do not meet criteria
causes for a major depressive episode.
5. Specifiers: current or most recent episode 3. The symptoms have been present for 2 years for
manic, hypomanic, depressed, mixed features, adults and 1 year for children and adolescents.
psychotic features, catatonic features, atypical 4. Symptom-free period should be less than
features, melancholic features, rapid cycling, 2 months at a time.
with suicide risk severity, with anxiety, with
seasonal pattern, and with postpartum onset Substance-induced bipolar disorder
296.89 Bipolar II disorder 1. Manic episode develops soon after misusing a

substance which is able to cause manic symptoms
1. Duration: at least 4 days. 2. Following ingestion of substances (e.g. amphet-
2. Number of episode: one major depressive epi- amine, cannabis, and cocaine) or withdrawal of
sode and at least one hypomanic episode. substances (Table 27.2)
3. Hypomanic episode has the same requirement
of the number of symptoms as manic episode. 27.2.2.1 ICD-10 Criteria for Depressive
4. The only difference is that patients should have Episode (F32)
no impairment in functioning.
There is depression of mood, reduced energy, and
5. Specifiers are the same as manic episode.
fatiguability. Mood is pervasively depressed. Other
features are reduced attention and concentration, low-
301.13 Cyclothymia
ered self-esteem, ideas of guilt and worthlessness, pes-
1. Duration is for at least 2 years (at least 1 year in simistic thoughts, thoughts of self-harm or suicide, and
children and adolescents). disturbed sleep.
Mood Disorders, Suicide, and Parasuicide 379
Somatic changes include reduced appetite leading to 296.3 Major depressive episode, recurrent episode
weight loss (at least 5% of body weight in a month), constipa-
tion, early-morning awakening (more than 2 h before usual), 1. The presence of at least two or major depressive
diurnal variation of mood, anhedonia, loss of normal reac- episodes.
tivity of mood, reduced libido, amenorrhoea, and psycho- 2. To be considered separate episodes, there must
motor retardation or agitation. be an interval of at least 2 consecutive months in
A duration of 2 weeks is required for the diagno- which criteria are not met for a major depressive
sis. This applies to the first episode only. Severity is episode.
graded: 3. Specifiers: mild, moderate, and severe with-
out psychotic features/with psychotic features,
• Mild depressive episode chronic, mixed features.
• Moderate depressive episode
• Severe depressive episode without psychotic
symptoms 27.2.2.3 ICD-10 Criteria for Dysthymia (F34)
• Severe depressive episode with psychotic
This is a chronic, less severe depression, usually with
symptoms
an insidious onset. Symptoms include excessive guilt,
296.2 Major depressive episode, single episode difficulty in concentrating, loss of interest, pessimism,
low self-esteem, low energy, irritability, and reduced
1. At least five symptoms for 2-week duration
productivity. For the diagnosis it must be present for at
2. At least one of the following: low mood and loss
least 2 years.
of interest or pleasure
3. Other symptoms include
a. Significant weight loss or weight gain 300.4 Dysthymia (persistent depressive disorder)
b. Insomnia or hypersomnia on a daily basis
c. Psychomotor agitation or retardation 1. Similar to the ICD-10, the depressed mood
d. Low energy level should last for 2 years for adults and 1 year for
e. Feelings of worthlessness or guilt children and adolescents.
f. Poor concentration 2. Depressive symptoms include change in appe-
g. Recurrent suicidal thoughts tite, change in sleep pattern, low energy, low self-
4. Other criteria: functional impairment, no his- esteem, poor concentration and hopelessness.
tory of manic or hypomanic episode, and exclu- 3. Symptom free period should be less than
sion of other psychiatric diagnosis 2 months.
5. Subtype: mixed feature 4. No psychosis disorder or substance-abuse.
5. Significant impairment in functioning.
27.2.2.2 ICD-10 Criteria for Recurrent 6. Specifier: early onset (<21 years), late onset
Depressive Disorder (F33) (>21 years), atypical features.
There are repeated episodes of depression, without epi-
sodes of mania. Recovery between episodes is usually 625.4 Premenstrual dysmorphic disorder
complete, but a minority becomes chronic, especially in
the elderly. It includes During the final week before the onset of menses,
the patient experiences affective lability, irritability,
1. Recurrent depressive disorder with marked anxiety and other DSM-5 depressive symp-
a. Current episode mild toms. The above symptoms improve shortly after
b. Current episode moderate menses.
c. Current episode severe without psychotic
symptoms
d. Current episode severe with psychotic Substance-induced depressive disorder
symptoms
2. Recurrent depressive disorder, currently in Depressive episode develops soon after misusing a sub-
remission stance which is able to cause depressive symptoms
296.99 Disruptive mood dysregulation disorder history of mania, an earlier and more acute
onset (15 years earlier than ‘unipolars’ on aver-
1. Recurrent severe temper outbursts. age), and more episodes.
2. Frequency: three or more times per week.
3. Irritability in between temper outbursts. No difference is observed in sleep EEGs of these two groups.
4. Duration at least 12 months and symptom free
period should be less than 3 months.
27.2.3.3 Rapid-Cycling Bipolar Disorder
5. At least two different settings.
6. Age of onset: between 6 to 10 years. This refers to those patients who experience four or more
affective episodes in 12 months. It is more common in
women, predicts poorer prognosis with more lifetime
27.2.3 Other Classifications of Depression
affective episodes and a poorer response to lithium and
Depression is variously classified, and the usefulness of other treatments. Twenty per cent are induced by antide-
differing categories is still under debate. pressant drugs.
27.2.3.1 Endogenous versus Reactive Depression

27.2.3.4 Other Classes
This is a distinction drawn by Roth and the Newcastle
School in the 1950s (Richmond, 2006): 27.2.3.4.1 Double Depression
This is a major depression superimposed upon dysthymia.
1. The endogenous form (melancholia) is thought
to be of biological origin, with the following 27.2.3.4.2 Depressive Stupor
symptoms (mnemonics: MAD GRADS): The person is unresponsive, akinetic, mute, and fully
a. Motor retardation or agitation. conscious. Following an episode, the patient can recall
b. Anorexia and weight loss. the events that took place at the time. Episodes of excite-
c. Diurnal variation. ment may occur between episodes of stupor.
d. Guilt is excessive.
e. Reactivity of mood is absent. 27.2.3.4.3 Recurrent Brief Depression
f. Anhedonia. In 1990, Angst proposed diagnostic criteria for this con-
g. Distinct quality of mood. dition—dysphoric mood or loss of interest for a duration
h. Sleep is characterized by terminal insomnia. of less than 2 weeks, with at least four of the following:
2. The reactive form is thought to be of psychologi- poor appetite, sleep problems, agitation, loss of interest,
cal origin. Depression is moderate; anxiety, irrita- fatigue, feelings of worthlessness, difficulty concentrat-
bility, initial insomnia, and mood remain reactive. ing, and suicidality. One or two episodes per month for at
least a year are characteristic.
However, triggering events are present in both types.
Kendall (1965) failed to find a point of rarity in symp- 27.2.3.4.4 Masked Depression
tomatology between neurotic and psychotic depression, In masked depression, depressed mood is not always
so concluded that there are no essential differences complained of, rather somatic or other complaints. It is
between them. more common in the undeveloped world and in those
unable to articulate their emotions (e.g. those with learn-
27.2.3.2 Unipolar versus Bipolar Depression ing disability or dementia). The presence of biological
symptoms is helpful in making the diagnosis. Diurnal
This is a distinction due to Leonhard, Angst, and Perris
variation in abnormal behaviour may mirror diurnal vari-
in the 1950s (Angst and Sellaro, 2000):
ation in mood.
• Unipolar depression is more common in females.
Episodes are longer, with somatic symptoms, 27.2.3.4.5 Seasonal Affective Disorder (Lee, 2007)
anxiety, agitation, suicidal ideas, weight loss, Definition: Seasonal Affective Disorder (SAD) is a form of
and initial insomnia. recurrent depressive disorder which the sufferers consis-
• In bipolar depression a seasonal pattern and tently experience low mood in winter months. Symptoms
hypersomnia tend to be more commonly pres- include increase appetite, craving for sugar or rice, low
ent. There are more male sufferers, more family energy, increased sleep, and weight gain.
Epidemiology: 3% in Europe Bereavement reactions: Grief usually has three phases.

The stunned phase lasts from a few hours to a few weeks.
Aetiology This gives way to the mourning phase, with intense
yearning and autonomic symptoms. After several weeks
1. Melatonin/pineal gland abnormalities, replaced the phase of acceptance and adjustment takes over. Grief
by theories on disordered brain serotonin regula- typically lasts about 6 months.
tion and phase-advanced circadian rhythms.
2. Biologically vulnerable individuals are affected Atypical grief is divided by Parkes (1985) into
by the actual effect of the changes in the seasons
and specific anniversary or environmental fac- • Inhibited grief: absence of expected grief symp-
tors in winter. toms at any stage
• Delayed grief: avoidance of painful symptoms
Clinical features: The clinical features of SAD are simi- within 2 weeks of loss
lar to those of atypical depression. These include hyper- • Chronic grief: continued significant grief related
somnia, hyperphagia, tiredness, and low mood in winter. symptoms 6 months
It is important to understand the differences between

ICD-10 criteria (WHO, 1992): depression and bereavement. The following fea-
tures are more common in depression, but not in
1. Three or more episodes of mood disorder must bereavement:
occur with onset within the same 90-day period
of the year for 3 or more consecutive days. • Active suicidal ideation
2. Remission also occurs within a particular • Depressive symptoms which are out of propor-
90-day period of the year. tion with loss
3. Seasonal episodes substantially outnumber any • Feelings of guilt not related to the deceased
nonseasonal episodes that may occur. • Marked functional impairment for longer than
2 months
In SAD there is a regular temporal relationship between • Marked psychomotor changes lasting more than
the onset of depressive episodes and a particular time of a few days
year. Depressive episodes commence in autumn or winter • Preoccupation with worthlessness
months and end in the spring or summer months as the
hours of daylight increase. Management
Note that the onset of bipolar disorders may be sea-
sonal. Hyperphagia, hypersomnia, and weight gain are 1. Grief is usually managed in the outpatient set-
more frequent than in matched nonseasonal patients. ting but inpatient setting in indicated for patients
at high suicide risk.
Atypical depression: Atypical depression is more com-
2. Psychiatrist needs to assess and distinguish nor-
mon in younger individuals and in women. It is more
mal grief from the abnormal grief.
likely to have chronic course with poor inter-episode
3. Grief work is a supportive psychotherapy while
recovery. Atypical depression responds better to MAOIs.
allows expression of the loss and its meaning
The symptoms are summarized in mnemonics RAILS:
and work through the issues. It also provides
a secure base, identifies factors which block
• Reactive mood
natural grief and addressees social isolation and
• Appetite increased
spiritual issues.
• Interpersonal rejection sensitivity
4. Family involvement and psychoeducation.
• Leaden (heavy) paralysis
5. If psychotropic drug is indicated, care-
• Sleep increased
ful dosing is required to avoid side effects.
Maintenance treatment is required for severe
Mixed affective states: Kraepelin maintained that mood, prolonged grief.
cognition, and behaviour may vary independently, pro- 6. Rehabilitative efforts emphasize on stage-
ducing mixed affective states which are usually transi- appropriate tasks such as developing vocational
tional but are sometimes persistent. and social skills.
CASC STATION ON GRIEF AND BEREAVEMENT

A 50-year-old woman is referred by her GP. The referral states that she has been depressed since the sudden
death of her husband 18 months ago. She has no previous psychiatric history. She herself identifies her problem
as ‘loneliness’. She states that since her husband’s death, she has cried daily while looking at his photograph and
that the distress she felt after his death has persisted since.
Task: Take a history to assess her grief.
(A) Identify (A1) Identify the (A5) Assess Her

Details of Death Nature and (A2) Further Current Feelings
and Immediate Circumstances of Information Based on (A3) Assess Her (A4) Assess Current (Depending on
Reaction Death the Cause of Death Reactions Situation Patient’s Response)
‘How did your • Medical ‘How did you react • Assess current ‘I can imagine how
husband pass misadventure: at the time of his level of difficult it is to look
away? Was his medicolegal issues death?’ (e.g. perceived social after him for long
death sudden • Murder: progress tearful, support time before he left.
or unexpected? of police depression, • Identify the How do you feel at
Was it caused investigation disbelief, acting source of social this moment? Do
by a medical • AIDS: her out, atypical pain, support such as you feel relieved?’
misadventure? concern about or physical friends and ‘Do you feel guilty
Did he commit HIV status symptoms) relatives that you survive
suicide?’ • Civil disaster: ‘Do you also ‘Have you picked after the accident?’
‘Was his body experience up his work or ‘Did you have
found?’ symptoms interests?’ intense reaction at
• Chronic illness: which are certain period such
‘Did you look similar to those as one year after
after him for long experienced by his death?’
time before he your husband
passed away?’ before he died?’
(B3) Identify
(B1) Funeral Stage of: (B4) Assess Coping
(B) Bereavement Arrangement (B2) Mood DABDA and Support (B5) Functioning
‘Were you ‘How is your mood at ‘People usually ‘How are you ‘Are you able to
involved in this moment?’ go through the coping so far?’ resume what you
organizing his ‘How is your sleep and following stages ‘Do you turn into normally did before
funeral? Did appetite at this after their loved alcohol or his death?’
you attend his moment?’ ones passed tranquilizers?’
funeral? Did ‘Have you lost away. May I ‘Can you look after
you have a weight?’ know which yourself?’
chance to say ‘How do you find your stage are you ‘Do you have
goodbye to concentration?’ in?’ Denial, children? Do they
him?’ Angry, see you often?’
Bargaining,
Depression,
Acceptance
(C) Identify
Features
Suggestive of (C1) Prolonged (C3) Handling of (C4) Psychotic (C5) Risk
Abnormal Grief Grief (C2) Inhibited Grief Possessions Experiences Assessment
‘Is your feeling ‘Have you tried to ‘After our loved ‘Do you hear voices ‘Do you have any
as intense as avoid morning and ones passed when no one is intention to end
6 months ago?’ grieving?’ away, some around? Are the your life? If yes,
‘Is your feeling ‘Do you allow yourself people keep voices belonging why? Do you want
easily to express feeling their rooms and to your husband?’ to join him in the
triggered?’ towards his death?’ possessions as afterworld?’
if they were
still alive.
How about
yourself?’
(D) Identify (D1) Explore
Factors Past (D4) Past
Impeding Grief Relationship (D2) Explore Past Psychiatric and (D5) Seek Her
Resolution with Deceased Experience (D3) Personality Medical History Views on Treatment
‘How was your Explore childhood loss ‘Can you describe Explore past history ‘Are you keen to go
relationship and previous your character?’ of depression, low for counselling to
with him? traumatic ‘How would the self-esteem, talk about your
Were you bereavement others describe psychosis, and experience after
dependent on Look for early you a person?’ chronic physical your husband’s
him? Was disturbances in Look for illness departure?’
there any attachment: dependency,
unhappy • Affectional bonds narcissism,
experience?’ • Security excessive denial,
Identify anger, • Reciprocity or projection
violence, • Response to
conflict, separations
ambivalence, ‘Do you feel that
dependency, or history is repeating
passive itself?’
aggression
27.3 EPIDEMIOLOGY OF Broadly, depressive episodes are more common in

MOOD DISORDERS females: the annual incidence in men in the population is
between 80 and 200 per 100,000, the corresponding fig-
27.3.1 Depressive Episodes ure for women being between 250 and 7,800 per 100,000.
There is a raised incidence in those who are not married.
Problems are encountered in epidemiological studies of
The point prevalence in Western countries is 1.8%–3.2%
mood disorders because of the differing use of diagnostic cat-
for men and 2.0%–9.3% for women.
egories, screening instruments, and definitions of caseness.
The point prevalence of depressive symptoms is have a ninefold increase in lifetime bipolar disorder risk
10%–30% (women 18%–34%, men 10%–19%). In the compared to the general population. The hereditabil-
general population of Western countries, the lifetime risk ity for bipolar disorder is 85% and depression is 60%.
of suffering from depressive episodes is 5%–12% for men There are gender differences. Men are at risk of depres-
and 9%–26% for women. sion if there is family history of alcoholism and anti-
The average age of onset of depressive episodes is social behaviour. Women are at risk if there is family
around the late thirties; however, they can start at any age. history of anxiety disorder.
Brown and Harris (1978) found that 15% of urban
women had severe depressive symptoms, and there was a 27.4.1.2 Twin Studies
higher prevalence in working-class than in middle-class Twin studies compare concordance rates in monozygotic
women. (MZ) to dizygotic (DZ) twins and need twins reared apart
Bt 2030, unipolar depressive disorder is predicted to separate genetic from environmental influences. In a
to be ranked as the number one cause of global burden large Danish twin study of affective disorder (Bertelson
of diseases in terms of disability-adjusted life years et al., 1977), the concordance rate for MZ twins was 67%,
(DALYs). compared with 20% for DZ twins. The MZ to DZ concor-
dance ratio for bipolar disorder of 79:19 compared with
27.3.2 Bipolar Mood Disorder 54:24 for unipolar disorder.
The sex ratio is equal, and it is more common in the

27.4.1.3 Adoption Studies
upper social classes. The point prevalence in Western
countries is 0.4%–1.2% in the adult population. In the Adoptee studies compare the rates of illness in biological
general population of Western countries, the lifetime versus adoptive relatives of affectively ill patients which
risk of suffering from a bipolar disorder is 0.6%–1.1%. separates genetic and environmental influences. In adopt-
The average age of onset is around the mid-twenties. ees with bipolar disorder, 28% of biological parents suf-
Being unmarried is associated with higher rates of fer from a mood disorder compared with 12% of adoptive
bipolar disorder. Common comorbidities include anxi- parents. By comparison, 26% of the biological parents of
ety disorder (92%), substance misuse disorder (71%), bipolar non-adoptees were found to suffer from a mood
and antisocial personality disorder (29%) (Kessler disorder.
et al., 1997).
Further details on the epidemiology of mood disorder 27.4.1.4 Molecular Genetics (Berrettini, 2004)
are considered in Chapter 21. Linkage studies using classical autosomal markers such
as red cell types, histocompatibility antigens (HLA types)
to identify linkage with genes of disease. Early studies
27.4 AETIOLOGY OF MOOD DISORDERS showed that bipolar disorder has been cross-linked to
27.4.1 Genetic Factors colour blindness and glucose-6-phosphate deficiency.
Recent studies have demonstrated that bipolar disorder
27.4.1.1 Family Studies complex genetic heterogeneity. Multiple partially overlap-
Family studies compare the rate of affective illness in ping sets of susceptibility genes which interact with the
relatives of index cases versus relatives of controls. There environment can predispose bipolar disorder. Confirmed
are differences in morbid risk noted for unipolar (9.1%) linkages in bipolar disorder include 4p15, 12q24, 18p11,
versus bipolar disorder (11.5%) (McGuffin and Katz, 18q22, 22q11–13, and 21q22. The serotonin transporter
1989). In unipolar probands there is an increased risk (5HTT) gene has been studied, and the 5HTT promoter
of unipolar depression in first-degree relatives, but the short allele is found to have a significant association with
amount of bipolar illness is virtually the same as in the bipolar disorder.
general population (combined risk = 7%–8%). In bipolar Egeland et al. (1987) found linkage to chromosome 11
probands there is an increased risk of both bipolar and in an old-order Amish pedigree. This finding is now
unipolar disorder in first-degree relatives (combined thought to have been a statistical artefact and has not
risk = 18%–20%). Family studies have demonstrated been replicated. In linkage studies of complex diseases
that children of parents suffering from bipolar disorder such as manic–depressive disorder, spurious linkage may
be produced because of phenotypic misclassification and association. The effect of critical comments (criticism
misspecification of the disease model. index) was not mitigated by reducing the number of hours
Segregation analysis uses statistical method to exam- depressed people spent in contact with their relatives
ine pedigrees and hypothesized modes of inheritance. (unlike schizophrenia, in which it was).
There are no consistent findings in affective disorder due
to complex genetic mechanisms. Women
Recombinant DNA techniques resulting in develop- Brown and Harris (1978), in a community survey in
ment of new generation of markers. For example, the Camberwell, South London, identified vulnerability fac-
restriction fragment length polymorphisms (RFLPs) tors which increase the risk of depression in women if a
allow candidate gene approach. In bipolar disorder, can- provoking agent is present. Four vulnerability factors are
didate genes include genes encoding for tyrosine hydroxy-
lase, serotonin transporter, catechol-o-methyltransferase • Having three or more children at home under
(COMT), and brain-derived neurotropic factor (BDNF). the age of 14 years
In unipolar depressive disorder, there is lack of consis- • Not working outside the home
tent results. • Lack of a confiding relationship
• Loss of the mother before the age of 11 years
27.4.2 Personality Factors in Mood Disorder

Men (Bebbington, 2003)
27.4.2.1 Cyclothymic Personality Disorder
This is characterized by persistent instability of mood 1. Marital breakdown is an important cause of
with numerous periods of mild depression and mild ela- depression for men.
tion. It may predispose to bipolar disorder.
27.4.3.3 Recent Life Events
Excess life events occur in the 6 months before a depres-
27.4.2.2 Depressive Personality Disorder sive episode starts:
This is related to the mood disorders, overlapping sub-
stantially with them, but not congruent with them. It • Loss of a child
often coexists with mood disorders. Core phenomena are • Death of a spouse
excessive negative, pessimistic beliefs about oneself and • Divorce
others. Symptoms include unhappy, gloomy mood; low • Marital separation
self-esteem; being self-critical, brooding, negativistic, • Gaol term
and judgemental towards others; pessimism; and prone • Death of a close family member
to feelings of guilt. • Recent unemployment (three times increase in
risk)
• Suicide in relatives
27.4.3 Psychosocial Stressors in Mood Disorder
The first manic episodes are often precipitated by life
27.4.3.1 Childhood Factors
events such as bereavement, personal separation, work-
1. Childhood sexual abuse related problems, or loss of role (Ambelas, 1987). High
2. Maternal loss and disruption of bonding expressed emotion and sleep deprivation are important
3. Poor care and overprotection in parenting precipitating factors.
4. Poor relationship with adults and low intelligence Social support: Buffer of social support reduces depres-
sion. The main effect hypothesis suggests that lack of
27.4.3.2 Adulthood Factors social support leads to depression.
Vaughn and Leff (1976) showed that high expressed Vulnerability factors may operate by reducing
emotion (EE) increased the risks of relapse in depressed self-esteem.
patients. Compared to schizophrenics, depressives were Kendler et al. (1995) compared stressful life events
more sensitive to critical remarks. However, hostil- in twins with and without depression. He found that,
ity and over-involvement did not add to the significant in those with the lowest risk (MZ co-twin unaffected),
the probabilities of onset of major depression were 0.5% and levodopa), corticosteroids, anabolic steroids, and thy-
and 6.2%, respectively, for those unexposed and exposed roxine. Withdrawal from baclofen, clonidine, and fenflura-
to the life event. In those at highest genetic risk (MZ co- mine is associated with mania.
twin affected), these probabilities were 1.1% and 14.6%,
respectively. He concluded that genetic factors influ-
ence the risk of the onset of major depression in part by 27.4.5 Psychological Factors in Mood Disorder
altering the sensitivity of individuals to the depression- Seligman gave naive dogs unavoidable electric shocks
inducing effect of stressful life events. and found that, after learning that there was nothing
that could be done to influence the outcome of events,
the dogs finally developed a condition which he thought
27.4.4 Physical Illness in Mood Disorder resembled depression in humans, with reduced appetite,
Viral infection, particularly influenza, hepatitis A, reduced sex drive, and disturbed sleep. He called this
and brucellosis are sometimes accompanied or fol- condition learned helplessness.
lowed by depressed mood. More recently, a significant It has been suggested that in humans depression is
association has been found between the occurrence more likely to occur if the helplessness is perceived to be
of anti-Borna Disease Virus (BDV) antibodies and attributable to a personal source, thus leading to lowered
mood disorder (unipolar and bipolar) (Terayama self-esteem. Global stable attributions are likely to be the
et al., 2003). longest lasting.
Endocrine disorders commonly predispose to Beck et al. (1979) proposed a cognitive model of
depression. Eighty-three per cent of people with depression from which cognitive therapy has developed.
Cushing’s syndrome develop affective disorder (e.g. Three concepts seek to explain the psychological sub-
mood changes 50%, depression 30%, and mania) dur- strate of depression:
ing the course of their disorder. Depression is a fre-
1. Cognitive triad. The depressed person has:
quent (50%) and early presentation of people with
a. A negative personal view
Addison’s disease. It is also seen in hypothyroidism
b. A tendency to interpret his or her ongoing
and hypo- and hyperparathyroidism. Physical illnesses
experiences in a negative way
associated with depression include Parkinson’s disease
c. A negative view of the future
(50%), epilepsy (25%), congestive heart disease (27%),
2. Schemas. These are stable cognitive patterns form-
and hypothyroidism. Physical illnesses associated with
ing the basis for the interpretation of situations.
mania include cerebral tumour, epilepsy, AIDS, and
3. Cognitive errors. These are systematic errors
multiple sclerosis (Lange and Farmer, 2007).
in thinking that maintain depressed people’s
Cerebrovascular accident (CVA) is associated with
beliefs in negative concepts.
depression and mania. If CVA occurs in the right cere-
bral hemisphere, depression will develop especially in
Cognitive distortions include
people with past or family history of depression. If CVA
Beck’s negative triad: self, environment, and future
occurs in the left frontal part of the brain, depression
Common cognitive errors in depression: CBT SLOPS
will develop regardless of past history or family history.
out MDE
One in four people will develop a major depression after
CVA. Mania is associated with right-sided CVA, and it C—Catastrophic thinking
is commonly associated with lesions in the frontal and B—Black and white thing (dichotomous thinking)
temporal lobes, especially in patients with family his- T—Tunnel vision
tory of mania. S—Selective abstraction
Mania is associated with right-sided hemispheric L—Labelling
damage. Head injury victims are more irritable than O—Overgeneralization
euphoric. P—Personalization
Medications associated with depression include cloni- S—Should statement
dine, metoclopramide, theophylline, indomethacin, and M—Magnification and minimization
nifedipine. Medications associated with mania include anti- D—Discarding evidence or arbitrary inference
cholinergic drugs, dopamine agonists (e.g. bromocriptine E—Emotional reasoning
CASC STATION ON ASSESSING COGNITIVE DISTORTIONS

A 20-year-old cricket player presents with depressive disorder. His coach comments that he has been
absent for all the practices in the past 3 months. He missed hitting one ball which was easily thrown
and believed this single act led to the loss of the match and will eventually lead to the loss of the entire
season. The coach has read something on cognitive–behavioural therapy and hopes you can refer him for
psychotherapy.
Task: Assess his cognitive distortions.
APPROACH TO THIS CASC STATION

Opening: I wonder if you would be able to tell me how things have been for you. It sounds like you are having
a rough time in the cricket club, but tell me how you feel about yourself.
Cognitive Biases
in Beck’s Theory
of Depression Questions
Minimization Did you play a part in any success or winning of cricket games?
How do you see your role in the club?
Do you feel that you have underestimated your contribution?
Have you won any awards before? (e.g. player of the year)
Have you hit any difficult balls before? Would you say those were remarkable?
How many matches have you won?
How many points have you scored this season? Over how many games?
That sounds like a good average, what do you think?
Magnification How did you play in the match before that miss? Aren’t those successes important as well?
Will one miss lead to the loss of an entire match? What about the whole season?
Aren’t there many turns to bat in each match and many more matches for the season?
Overgeneralization How have things been outside cricket? We all have various roles outside work, as a husband, father, son, and
friend, how do you see yourself in these different roles?
Selective abstraction Based on what you’ve told me, you’ve contributed a lot to the team (points, trophies, etc.), how do you feel
about these successes?
Personalization I am sorry to hear that the team lost the game. Who do you think is responsible for the loss? (patient may say
it’s him)
Are you the only batter on the team? Cricket is a team sport. What about the other players, aren’t they
responsible as well?
It seems that you attribute failure of the team solely on yourself. Are there other factors contributing to the loss of
the game?
Arbitrary inference What do your coach and teammates think about you now? (mind-reading error)
How does this single miss affect the outcome of the season? (fortune-telling error)
Dichotomous thinking It seems that you’re either a complete success if you had hit that ball or a complete failure if you don’t. Are
there any shades in between?
Catastrophic thinking It sounds like you consider your situation to be rather depressing. Is a disaster going to happen? Will you lose
control?
Labelling What does missing this ball say about you? (patient will then label himself)
You’re calling yourself a loser. Would you call a teammate who merely missed one ball a loser?
(continued)
Schemata Questions
Underlying beliefs Did you have any unhappy experience when you were young?
In order to be happy, what must happen first?
Negative automatic Cognitive triad: How do you see yourself, the world, and your future?
thoughts How are these thoughts being triggered? Are they related to recent unhappy events in the cricket club?
Vicious cycle How do you see the relationship between your mood and negative thoughts?
Do you feel that things may change and get better? Do you think that you can be helped in anyway?
Summarizing: You have told me that things have been pretty awful for you and you feel pretty dreadful about
yourself. It seems that you have attributed failure to yourself and minimize your success. It might take some
time for us to help you, but hopefully we can figure out the best way of getting things back on track.
Acknowledgement: Dr. Terence Leong, Consultant Psychiatrist, Department of Psychological Medicine,
National University Hospital, Singapore.
27.4.6 Neurotransmitters in Mood Disorder with major depression and suicide (Lemonde

et al., 2003).
According to Schildkraut in 1965 the monoamine • The antidepressant effects of light therapy com-
hypothesis of mood disorders stated that depression was bined with sleep deprivation are influenced by
associated with a depletion, and mania with an excess, of a functional polymorphism within the promoter
central monoamine. Evidence favouring this hypothesis of the serotonin transporter gene (Benedetti
includes the following findings: et al., 2003).
• Tricyclic antidepressants inhibit the reuptake Evidence against the monoamine hypothesis includes the
of noradrenaline and serotonin by presynaptic following:
neurons, leading to an increase in the availabil-
ity of these monoamines in the synaptic cleft. • Antidepressant pharmacotherapy takes at least a
• Monoamine oxidase inhibitors increase the fortnight to effect a clinical improvement. This
availability of monoamines, by inhibiting their time interval is much greater than the relatively
metabolic degradation by monoamine oxidase. rapid onset of biochemical action.
• SSRIs increase the availability of serotonin by • Not all drugs that act as monoamine reuptake
inhibiting the reuptake of serotonin. inhibitors have a therapeutic antidepressant action
• Use of antidepressants in bipolar disorder can (e.g. cocaine).
precipitate mania. 27.4.6.1 Serotonin (5-HT)
• Amphetamine releases catecholamines from the
Additional evidence for abnormal serotonergic function
neurons; it is a central nervous system stimulant
in mood disorders includes the following:
that lifts mood.
• Reserpine, an antihypertensive drug derived • In subgroups of depressed patients, low levels of
from the Indian plant Rauwolfia, depletes cen- 5-HIAA have been reported in cerebrospinal fluid.
tral monoaminergic neuronal stores of catechol- • In depressed patients, a low density of brain
amines and serotonin. Its use can lead to severe and platelet serotonin transporter sites has been
depression and suicide. found, as well as a high density of brain and
• The cerebrospinal fluid level of the sero- platelet serotonin binding sites.
tonin metabolite 5-hydroxyindoleacetic acid • Dietary tryptophan depletion induced a prompt
(5-HIAA) is often reported as being reduced in relapse in depressed patients who had responded
depressed patients. to SSRIs.
• Impaired repression at a 5-hydroxytryptamine • There is a low plasma tryptophan in depressed
1A receptor gene polymorphism is associated patients.
• Blood platelet studies: reduced 5-HT uptake and In the dexamethasone suppression test (DST), plasma
changes in 5-HT2 receptors have been studied cortisol levels are measured following the administration
in platelets in depression in normal subjects. of the long-acting potent synthetic steroid dexamethasone
The uptake of 5-HT into platelets is reduced in the previous evening. In normal subjects, dexamethasone
depression (Lange and Farmer, 2007). leads to a suppression in the level of cortisol over the
next 24 h through negative feedback. In depressed patients
The connection of 5-HT metabolism between 5-methoxy- with biological symptoms, non-suppression of cortisol has
indole metabolism in the pineal and overlaps and impacts been reported in over 60%. The DST has not proved to be
on sleep, pain mechanisms and depression a useful laboratory test for depression because a relatively
high level of cortisol non-suppression has been found in
• There is a decreased 5-HT transporter binding
other psychiatric disorders. The DST can be affected by
density in depression.
factors such as age, bodyweight, drugs, ECT, and endo-
• Serotonin function is reduced in depression and
crinopathies. The DST is usually state-dependent and in
may be normalized with active treatment.
most subjects normalizes as the patient recovers.
27.4.6.2 Adaptive Changes in Receptors Corticotropin-releasing factor (CRH or CRF) is an
important hypothalamic peptide in the regulation of
Depression is associated with an increase in the density
appetite and eating. In the CRH stimulation test, the
of α2 adrenergic presynaptic receptors in the locus coe-
administration of CRH to normal humans leads to the
ruleus and increased density of β-adrenergic receptors in
release of corticotropin. In depression there is a consis-
the cerebral cortex.
tent reduction of corticotropin response.
During antidepressant treatment, changes take place in
The noradrenergic neurons of the locus coeruleus express
cerebral α- and β-adrenergic and serotonin receptors, show-
glucocorticoid receptors, through which corticosteroids can
ing only after 2 weeks of treatment, at the same time as the
regulate its functioning. It is hypothesized that steroids may
therapeutic effect. A decrease in the sensitivity (downregu-
be important in causing and perpetuating depression.
lation) of β-adrenergic receptors is particularly evident.
27.4.7.2 Brain–Thyroid Axis
27.4.6.3 Brain-Derived Neurotropic Factor
Thyroid-releasing hormone (TRH) causes the release of
The BDNF is associated with production of new neurons
thyroid-stimulating hormone (TSH) from the adenohy-
and important for mood regulation and memory. Both
pophysis. In normal subjects there is a circadian pattern of
serotonin and noradrenaline play roles in modulation of
TSH secretion, with a nocturnal rise which is blunted in
BDNF (Dunman et al., 1997). The levels of BDNF are
depression and returns with sleep deprivation. In the TRH
reduced in depression and causes hippocampal atrophy in
stimulation test, the TSH response to intravenous TRH is
depressed patients (Sheline et al., 1996). Antidepressant
measured. About 25% of depressed patients show a blunted
restores BDNF function.
TSH response to TRH stimulation. This does not often nor-
malize as the subject recovers from depression. Blunting
27.4.7 Neuroendocrine Factors is also found in panic disorder. TRH stimulation studies
in Mood Disorder in depression have also shown that approximately 15% of
patients have a raised TSH response; many of these patients
27.4.7.1 Brain–Steroid Axis have been found to have antimicrosomal thyroid and anti-
Disturbances of the hypothalamic–pituitary–adrenal axis thyroglobulin antibodies, indicating that depression can be
are reported in depression. In normal humans, cortisol secre- associated with symptomless autoimmune thyroiditis.
tion is episodic and follows a circadian rhythm. Peak cortisol
secretion is in the morning; between noon and 4 a.m., secre- 27.4.7.3 Melatonin
tion remains low, being lowest just after the onset of sleep. Patients with depression have disordered biological
In biological depression, there is disruption in the nor- rhythms—short REM latency (time from falling asleep to
mal circadian rhythm of cortisol secretion, the morning onset of REM sleep), early-morning awakening, and diur-
peak being increased and longer lasting. A phase shift with nal mood variation. The suprachiasmatic nucleus (SCN)
the morning peak occurring earlier has been reported. of the hypothalamus plays a major role in regulating diur-
In depressed patients, increased secretion has been nal rhythms. Information about light conditions from the
reported in corticotropin (ACTH), cortisol, β-endorphin, retina, via the retinohypothalamic pathway, controls the
and prolactin. SCN. This influences the pineal which excretes melatonin.
The biosynthesis of melatonin from its precursor, serotonin, 27.4.8.3 Functional Imaging
occurs via N-acetylation followed by O-methylation. The Depression
step involving serotonin N-acetyltransferase is probably
rate-limiting and is stimulated at night. Melatonin recep- 1. Increased blood flow in the amygdala and ven-
tors are numerous in the SCN, and parts of the hypo- trolateral prefrontal cortex in depression, and
thalamus where releasing and inhibiting hormones end. antidepressant may normalize amygdala activ-
Darkness stimulates melatonin release and light blocks its ity (Sheline, 2001; Drevets, 2003).
synthesis. When compared with normal subjects, patients 2. Reduced glucose metabolism and blood flow in
with SAD have been found to have an increased sensitiv- frontal regions.
ity of melatonin biosynthesis to inhibition by phototherapy.
Furthermore, sleep deprivation and flying overnight from 27.4.8.4 Bipolar Disorder
west to east may trigger relapse of mania.
1. Increase in amygdala activation
27.4.7.4 Water and Electrolyte Changes 2. Increased cerebello-posterior cortical metabolism
There are increases in the body’s residual sodium (which
is an index of intracellular sodium ion concentration) in
27.5 MANAGEMENT OF
both depression and mania. Erythrocyte sodium ion con-
centrations decrease following recovery from depression DEPRESSIVE DISORDER
or mania as a result of increased Na+–K+-ATPase activity. 27.5.1 Investigations
27.4.8 Neuroanatomy and Imaging 1. FBC, LFT, RFT, TFT, and ECG are required in
the assessment of the first depressive episode.
The following neuroanatomical areas are implicated in 2. CT or MRI is indicated if there are neurological
depression (Charney and Nestler, 2004): signs or symptoms.
1. Amygdala: associated with memory of emo-
tional reactions 27.5.2 Pharmacotherapy: NICE
2. Anterior cingulate cortex: associated with nega- Guidelines (Table 27.3)
tive anticipation or poor judgement
3. Cerebellum: psychomotor retardation 27.5.2.1 Unipolar Depression
4. Hippocampus: memories Categories
5. Insular cortex: process information in an emo- Frank et al. (1991) have categorized outcomes of treat-
tionally relevant context and associated with ment according to the ‘5 Rs’:
negative interpretation of events
6. Nucleus accumbens: lack of motivation • Response.
7. Prefrontal cortex: associated with impairment • Remission. This is a return to the patient’s pre-
in executive functions morbid self.
• Relapse. This is a return of depressive symptoms
27.4.8.1 Structural Imaging
in the time between initial response and recov-
Depression ery. Risk is particularly high (40%–60%) fol-
1. Ventricular enlargement lowing the withdrawal of antidepressants within
2. Sulcal widening the first 4 months of achieving a response. The
3. Hippocampus atrophy (Sheline, 2003) risk of relapse is reduced to 10%–30% by con-
4. Reduction in size in the frontal lobe, cerebellum, tinuation of pharmacotherapy.
and basal ganglia • Recovery. A patient who has achieved a stable
remission for at least 4–6 months is assumed to
27.4.8.2 Bipolar Disorder have recovered from the index episode.
1. Asymmetry in temporal lobe (Swayze et al., 1992) • Recurrence. This is a return of depression after
2. Smaller dorsolateral prefrontal cortex (Lyoo recovery from the index episode. Risk factors
et al., 2004) for recurrent depression include frequent and/or
3. Increased white matter intensities (Woods multiple prior episodes, seasonal pattern, and a
et al., 1995) family history of mood disorder.
TABLE 27.3
Pharmacological Treatment of Depressive Disorder
Stages Recommendations from the NICE Guidelines
Starting antidepressant treatment 1. Explain the following to the patient:
a. The gradual development of the full antidepressant effect
b. The importance of taking medication as prescribed and the need to continue beyond remission
c. The risk and nature of discontinuation symptoms (particularly with drugs with a shorter half-life, such
as paroxetine and venlafaxine, usually mild with duration of less than 1 week)
d. Addiction does not occur with antidepressants
2. If a person experiences side effects early in treatment, consider stopping or changing to a different
antidepressant
3. If anxiety, agitation, or insomnia is problematic, consider short-term benzodiazepine (<2 weeks)
Frequency of monitoring 1. For patients who are not considered to be at increased risk of suicide, normally see them after 2 weeks
2. For patients who are considered to be at increased risk of suicide or are younger than 30 years, normally
see them after 1 week and then frequently until suicide risk has subsided
Clinical response 1. If improvement is not occurring on the first antidepressant after 2–4 weeks, check that the drug has been
taken as prescribed
2. If antidepressant is taken as prescribed, increase the dose based on the summary of product characteristics
3. If there is improvement by 4 weeks, continue treatment for another 2–4 weeks
4. Consider switching antidepressants if the response is inadequate, there is presence of side effects, or the
patient requests to change drug
Switching antidepressants 1. Consider a different SSRI or better tolerated new generation antidepressant
2. Normally switch within 1 week for drugs with short half-life
3. C onsider at least 2-week washing period when switching: from fluoxetine to other antidepressants,
from paroxetine to TCA (because of anticholinergic side effects), from other antidepressants to new
serotonergic antidepressants or MAOI and from a nonreversible MOAI to other antidepressants
Augmentation 1. Mood stabilizers: lithium
2. Antipsychotics: aripiprazole, olanzapine, quetiapine, or risperidone
3. Another antidepressant: mianserin (be aware of blood dyscrasia) or mirtazapine
Discontinuation of antidepressants 1. Gradually reduce the dose over 4 weeks
2. Longer period is required for drugs with shorter half-life (e.g. paroxetine and venlafaxine)
3. Shorter period is required for drugs with long half-life (e.g. fluoxetine)
4. If patient experiences significant discontinuation symptoms, consider reintroducing the original
antidepressant at the dose that was effective
Acute treatment: This is initial treatment which aims to • A tricyclic antidepressant (imipramine) response
achieve a response. rate of 53%
• A MAOI (phenelzine) response rate of 30%
Continuation treatment: This begins when a patient has
• A placebo response rate of 39%
achieved a significant response to treatment. The aim is to
• An ECT response rate of 71%
prevent relapse and consolidate response into remission.
Maintenance treatment: This follows continuation treat- Drugs: The first-line treatment of depression is with antide-
ment for those patients with a history of recurrent depres- pressants. It is important that patients receive an adequate
sion. A recurrence rate of 85% is seen in those patients with dose for an adequate duration, conventionally 6 weeks.
recurrent depression within 3 years following the discontin- Antidepressants should be continued for 4–6 months
uation of pharmacotherapy. After 6 months, continuation after the amelioration of symptoms of the acute episode.
becomes maintenance treatment by arbitrary definition. Maintenance therapy usually with the same agent is used to
In an MRC trial in 1965, 269 patients with operation- treat the acute and continuation phases.
ally defined depression were randomly assigned to treat- Lithium is efficacious in preventing recurrent depres-
ment groups, with the following results at 4 weeks: sive episodes but less so than tricyclic antidepressants.
Patients maintained on the full effective treatment dose 3. The remission rate was 30% (higher than
of antidepressants have proportionately fewer relapses than expected) because of the systematic and compre-
those whose dose is cut down to a lower maintenance level. hensive approach to care.
4. One in three depressed patients who previously
did not achieve remission using an antidepres-
27.5.2.2 Sequenced Treatment Alternatives sant became symptom-free with the help of
to Relieve Depression (STAR*D) augmenting with another antidepressant. One in
Trial (Trivedi et al., 2006) four achieved remission after switching to a dif-
ferent antidepressant.
Objective of the STAR*D trial: The purpose of this trial is 5. At Level 3, 20% of participants became symp-
to determine the effectiveness of different treatments for tom-free after 9 weeks. Patients taking T3 com-
people with major depressive disorder (MDD) who have plained of fewer side effects than those taking
not responded to initial treatment with an antidepressant. lithium. The discontinuation rate for T3 was
Methodology of the STAR*D trial: The STAR*D project 10% and the rate for lithium was 23%.
enrolled 4000 outpatients (ages 18–75) diagnosed with 6. The Level 4 findings suggested that the venla-
nonpsychotic MDD in the United States. Participants faxine or mirtazapine treatment may be a better
will be initially treated (open label) with citalopram, the choice than the MAOI.
Level 1 treatment, for a minimum of 8 weeks. Patients
who experienced minimal benefit were strongly encour- Switching to or adding cognitive therapy after a first
aged to complete 12 weeks of treatment in order to maxi- unsuccessful attempt at treating depression with an
mize the chances of symptom remission (unless no benefit antidepressant medication is generally as effective as
at all is seen after 8 weeks). All participants received switching to or adding another medication. Participants
a brief depression educational programme. There were on cognitive therapy took longer to achieve remission.
four levels and participants who either did not have an
adequate response to or could not tolerate one level were
27.5.2.3 Atypical Depression
eligible to move to higher level. At each level change, par-
ticipants were asked to indicate the unacceptability of the This responds better to monoamine oxidase inhibitors
potential treatment strategies (e.g. to augment or to switch than to tricyclic antidepressants.
medications). Participants would then be eligible for ran-
dom assignment to one of the treatment options.
27.5.2.4 Psychotic Depression
The Level 2 treatment strategies include (i) switching
to other antidepressants (sertraline, venlafaxine, bupro- Spiker et al. (1985) found a superior response when an
pion) and cognitive therapy, (ii) medication and psycho- antidepressant and an antipsychotic were used in combi-
therapy augmentation, (iii) antidepressant only switch, nation, in delusional depression:
(iv) antidepressant only augmentation, (v) psychotherapy
only switch, and (vi) psychotherapy only augmentation. 1. 41% responded to amitriptyline alone.
The Level 3 treatment strategies include switching to 2. 19% responded to perphenazine alone.
(i) mirtazapine or nortriptyline or (ii) lithium or thyroid 3. 78% responded to a combination of amitripty-
hormone (T3) augmentation. line and perphenazine.
The Level 4 treatment strategies include two switch
options: (i) to tranylcypromine or (ii) to mirtazapine plus
27.5.2.5 Resistant Major Depression
venlafaxine.
Up to 20% of patients may be resistant to first-line treat-
Summary of results ment with antidepressant medication, and another 20%–
30% may have only a partial response. Patients with a
1. One-third of participants reached a remission or partial response have a significantly higher rate of relapse
virtual absence of symptoms during the initial during the first 6 months following response.
phase of the study, with an additional 10%–15% Those patients not showing a response to adequate
experiencing some improvement. first-line drug treatment may respond to augmentation
2. There were consistent findings across both stan- with various agents including lithium, T3, or tryptophan.
dard and patient-rated depression rating scales. ECT should be tried if these measures fail.
CASC STATION ON TREATMENT-RESISTANT DEPRESSION

A 40-year-old male executive suffers from depression and has failed to make a clinically significant response
after an adequate dose of amitriptyline and fluoxetine given for an adequate period of time. He has prepared a
list of antidepressants which he tried before with dosage and duration.
Task:
1. Explore the underlying reasons for poor response and explain possible management options.
2. Patient will seek your view on lithium augmentation and address his concerns.
CASC Grid
(A3) Compliance (A4) Perpetuating
(A) Causes and Tolerability of Psychosocial Factors (A5) Side Effects
of Poor (A1) Wrong (A2) Previous and Predisposing with Previous
Response Diagnosis Substance-Abuse Medication Factors Medication?
Explore the following: Explore history of ‘Are you taking the Explore marital Explore common
• Other psychiatric drug and alcohol antidepressant on a problems, work- side effects such as
diagnosis: PTSD misuse daily basis?’ related problems, nausea, headache,
• Grief reaction ‘Do you experience financial problems sexual dysfunction,
• Other medical any side effect?’ Ask about family and sedation
diagnosis: history of depression,
hypothyroidism, severity, completed
multiple sclerosis suicide, and family
• Medication: members’ responses
corticosteroid, to treatment
cardiac drugs
(B) Explain (B2) Inform the
Management Possibility of
of Possible Substitution by an (B4) Discuss
Treatment- (B1) Explore the Antidepressant Augmentation with
Resistant Dose and Duration from Different (B3) Offer Other Another (B5) Augmentation
Depression of the Current Drugs Class Treatments Antidepressant with Other Agents
‘Can you tell me For example, SNRI ECT Examples: First-line agents:
which antidepressant venlafaxine Psychotherapy such SSRI + bupropion • Add lithium
have you tried? Can as CBT or IPT SSRI + buspirone (effective in
you tell me the with medication SSRI + venlafaxine/ 50% of cases)
duration and dosage? mirtazapine • Add
Can you tell me triiodothyronine
which one works and (T3 is better
which one doesn’t’ tolerated than T4
Explore the and be aware of
possibility to the side effects)
increase the dose Second-line agents:
and duration of • Add lamotrigine
current medication • Combine
olanzapine and
fluoxetine
• Combine MAOI
and TCA
• Add tryptophan
(continued)
(C) Seek (C4)

Patient’s View (C2) Assess His (C3) Inform Duration of
on Lithium Background Inform Frequency Treatment and (C5) Risk
Augmentation (C1) Explain Lithium Knowledge of Blood Tests Explain Side Effects Assessment
The best established ‘How much ‘You need baseline ‘You need regular ‘Did you have any
augmentation information would investigation result follow-up and thyroid or kidney
strategy is the you like to know and lab test on a should carry a problem in the
addition of lithium about lithium? weekly basis for lithium card. You past?’
to a given Would it be alright 1 month. Then need to maintain ‘Are you suicidal?
antidepressant with you if I I will check lithium for 2–3 Will you take an
Lithium augmentation explain how it lithium level every years’ overdose of
with TCA has been works?’ 3–6 months. Common side effects lithium? If yes,
extensively studied, Renal, thyroid include nausea, please ask your
and lithium functions and ECT metallic taste, partner to keep
augmentation will be checked diarrhoea, frequent lithium for you’
reduces the risk of every 6 months urination, feeling ‘Do you take the
remaining depressed The dose is 400 mg thirsty, tremor, and following
per day and we muscle weakness medications which
aim at the serum Long-term side may interact with
level between 0.4 effects include lithium? (e.g.
and 0.6 mmol/L’ weight gain and diuretics, NSAIDs,
impaired kidney and ACEI,
thyroid functions carbamazepine,
‘How do you feel and alcohol)’
about lithium?’
27.5.3 Electroconvulsive Therapy and 3. Depressed mood with strong correlation with

Physical Therapies in Mood Disorder negative cognitions (Figure 27.1)
4. Mild somatoform disorders
Double-blind placebo-controlled trials have shown electro- 5. Adequate reality testing and absence of psy-
convulsive therapy (ECT) to be superior to placebo, espe- chotic feature
cially in delusional depression. It is considered the gold 6. Inability to tolerate side effects of antidepressants
standard of antidepressant therapy and is often given to
patients who have not responded to antidepressants. ECT is
also used in the treatment of resistant mania or manic stupor. 27.5.4.2 CASC Preparation: Explain CBT
ECT, repetitive transcranial magnetic stimulation (rTMS), to a Depressed Person
vagus nerve stimulation (VNS), and deep brain stimulation CBT is a structured psychotherapy with two compo-
(DBS) are mentioned in Chapter 24. nents: cognitive and behaviour therapy. Depression can be
explained by cognitive and behavioural models. According
27.5.4 Psychosocial Treatments to the cognitive model, unhelpful thoughts lead to depres-
27.5.4.1 Psychotherapies sion and unhelpful behaviours. According to the behav-
Indications to administer CBT alone without antidepres- ioural model, people with depression are often withdrawn
sant in depression include because they have no mood to socialize and do things. CBT
aims at changing unhelpful thoughts. As a result, behav-
1. Better response to psychotherapies in the past iour and mood will be improved. CBT begins with assess-
as compared to antidepressant response to ment of the client’s problems. The client is encouraged to
antidepressants keep a diary of life events and their thoughts, behaviours,
2. Reactive depression to life events and mood.
Thoughts:
‘I can never do
the things right’
Belief:
‘I’m unlovable’.
‘I must always Trigger: Behaviour: Consequence:
please Boyfriend is Depression Locks herself in Social
everybody, critical the bedroom withdrawal
especially my
boyfriend’.
Physical
symptoms:
low energy,
poor sleep
FIGURE 27.1 Cognitive model of a 20-year-old woman suffering from depressive disorder.
For cognitive therapy, the therapist helps the client to c. For relapse prevention, CBT is recommended
identify the pattern, namely, what happens before a mood for clients who have received antidepressant
change (i.e. the antecedents) and after the mood change treatment and mentalization-based CBT is
(i.e. the consequences). The therapist also helps the client to recommended for stable clients with three or
identify the negative thoughts about client, his or her views more previous episodes of depression.
about the future and the world. The client needs to challenge 2. Depression in children and adolescents: CBT is
the negative thoughts and develop new strategies of thinking. used as first-line treatment in moderate to severe
For behaviour therapy, the therapist helps the client depression for 2–3 months. If depression is unre-
to draw a list of mood-enhancing activities. The client sponsive to combined treatment, individual child
usually starts with simple activities and move on to more psychotherapy will be offered for 30 sessions.
sophisticated activities. The duration of activity will be 3. Depression in clients with chronic physical
increased in a gradual manner. health problems: individual CBT or group-
Nowadays, CBT can be administered by computer. based CBT are offered to clients with persis-
This new treatment is called computerized CBT or CCBT. tent subthreshold or mild symptoms, moderate
CCBT is commonly used in people with mild depression depression, and combined with antidepressants
or young people. New form of CBT called mindfulness- in severe depression (Table 27.4).
based CBT involves combination of meditation techniques
and CBT. The mindfulness-based CCBT aims at detach-
ing the client’s thinking process and emotions. CBT can 27.5.5 Management of Bipolar Disorder
also be offered in a group. Both CBT and antidepres- (NICE Guidelines Recommendations)
sants are of proven benefit in the treatment of depression.
CBT does not work very well for people who are very 27.5.5.1 Investigations
depressed. These patients require antidepressant first. • Evaluation of physical status. FBC, LFT, U&Es,
TFT, fasting glucose, lipid profile, and ECG
should be considered.
27.5.4.3 NICE Guidelines Recommendations • Urine pregnancy test is a must for female patients
on CBT and Depressive Disorder with bipolar disorder. STD screen should be
1. Adult depression ordered if history suggests.
a. For people with persistent subthreshold depres- • Urine drug screen will be useful to rule out the
sive symptoms or mild to moderate depression, possibility of illicit drugs causing manic-like
individual-guided self-help based on the prin- symptoms.
ciples of CBT and CCBT can be offered. • The patient may need neurological investiga-
b. For people with moderate or severe depres- tions such as lumbar puncture, EEG, and MRI
sion, combination of individual CBT or brain scan if there were neurological signs or
group-based CBT with antidepressant is symptoms which suggest an underlying neuro-
recommended. logical disorder.
TABLE 27.4
Treatment of Depressive Disorder Based on the Severity of Depression (NICE Guidelines)
Persistent subthreshold depressive symptoms Persistent subthreshold depressive Depression and chronic physical health
(mild to depressive episode) symptoms or mild to moderate depression problem
with inadequate response to initial
interventions (moderate and severe
depressive episode)
Individual-guided self-help based on CBT Antidepressant Group-based CBT: in a group of 6–8 people
principles: written materials, for 6–8 High intensity—psychological interventions with a common physical health problem over
sessions, duration over 9–12 weeks • Individual CBT: 16–20 sessions over 6–8 weeks
CCBT: explain CBT model, encourage tasks 3–4 months, 3–4 follow-up sessions Individual CBT: 6–8 weeks for moderate
between sessions, use of thought- subsequently over the next 3–6 months. depression and 16–18 weeks for severe
challenging, active monitoring of Consider 2 sessions per week for the depression
behaviour and thought patterns and first 2–3 weeks Behavioural activation: 16–20 sessions over
duration over 9–12 weeks • Interpersonal therapy: 16–20 sessions 3–4 months
Structured group physical activity over 3–4 months and 2 sessions per Behavioural couples therapy: 15–20 sessions
programme: 3 sessions per week, lasting week for the first 2–3 weeks over 5–6 months
45 min to 1 h over 10–14 weeks • Behavioural activation: 16–20 sessions
Group-based CBT: by 2 trained practitioners over 3–4 months. Consider 3–4
with 10–12 meetings of 8–10 participants follow-up sessions over next 3–6
and duration is between 12–16 weeks months. For moderate of severe
depression, consider 2 sessions per
week for the first 3–4 weeks
• For complex cases, it will involve crisis
intervention with the home treatment
team, multidisciplinary care plan, or
ECT in addition to antidepressant and
high intensity psychological
interventions
27.5.5.2 Pharmacotherapy The premature withdrawal of lithium in bipolar

If the patient is lacking insight towards bipolar disor- patients results in more than 80% of recurrences within
der, the imposition of compulsory treatment should be 36 months, a 28-fold increase compared to those left on
addressed. The treatment of acute mania is with anti- lithium. Low-dose maintenance strategies (less than the
psychotics (e.g. risperidone, quetiapine, or olanzapine). usual acute antimanic range of [0.8–1.2 mmol/L]) lead to
Lithium carbonate is used in the prophylaxis of bipo- an increased risk of relapse.
lar disorder. They can also be used in the treatment of In cases of bipolar disorder which are resistant to or
acute mania, but neuroleptics are preferred in the first intolerant of lithium, alternative prophylactic treatment
instance. It is important to ensure that antidepressant with carbamazepine or sodium valproate are effective,
is stopped because it may be the main precipitant of both as acute antimanic treatment and as prophylaxis.
mania. Short-term benzodiazepine (such as lorazepam)
can be used to control behavioural disturbance or agita- 27.5.5.3 Psychotherapy
tion. If patient is admitted to the ward, the nurses should The NICE guidelines recommend offering psychother-
avoid excessive stimulation and engage the patient in apy of at least 16 sessions over 6–9 months. It includes
structured routine. psychoeducation, general coping strategies, and CBT.
A maintenance strategy consisting of lithium carbon-
ate monotherapy in bipolar disorder is likely to result in 27.5.5.4 Relapse Prevention
sustained remission in approximately 50% of cases. The Besides medication and psychotherapy, advice (includ-
NICE guidelines recommend pharmacological treatment ing written information) on the importance of good
for at least 2 years after an episode of bipolar disorder. sleep hygiene and regular lifestyle should be given.
For those patients who work, risks of shift work 27.6 PERSISTENT MOOD DISORDERS
in triggering mania should be discussed. For those
patients who travel, the risk of flying across various ICD-10 describes persistent and usually fluctuating disor-
time zones should be informed. Families and careers ders of mood in which individual episodes are rarely suf-
often play an important role in relapse prevention. ficiently severe to warrant being described as hypomanic
Joining a support group can be useful. The GP needs or mild depressive episodes. They may last for years at
to encourage the patient to continue treatment. The a time, sometimes for the greater part of adult life and
patient is taught on identifying the triggers and early involve considerable subjective distress and disability.
warning signs of relapse. The GP helps to monitor the In ICD-10, the persistent mood disorders are classed
early signs of relapse. Treatment plan should include with the mood disorders rather than with the personality
risk management addressing risk of suicide, exploita- disorders because of evidence from family studies which
tion, self-neglect, or unprotected sex. suggests that the persistent mood disorders are geneti-
cally related to other mood disorders.
The two most important persistent mood disorders are
27.5.6 Management of Rapid Cycling cyclothymia and dysthymia.
• The NICE guidelines recommend increasing the

dose of antimanic drug or adding lamotrigine. 27.6.1 Cyclothymia
• For long-term management, the NICE guide- Cyclothymia is defined in ICD-10 as
lines recommend a combination of lithium and
valproate as first-line treatment. A persistent instability of mood, involving numerous
• Lithium monotherapy is the second-line treatment. periods of mild depression and mild elation. This insta-
• Antidepressants should be avoided and check bility usually develops early in adult life and pursues
thyroid function tests every 6 months. a chronic course, although at times the mood may be
normal and stable for months at a time. The lifetime risk
of cyclothymia is between 0.4 and 3.5%, sex ratio equal.
27.5.6.1 Prognosis for Mood Disorders First-degree relatives of patients with cyclothymia are
Depression is a chronic and recurrent condition. It has more likely than the general population to suffer from
become increasingly clear that a significant proportion of depressive episodes and bipolar disorder.
patients followed in the long term after suffering from
depression remain chronically ill, despite the previously Some are treated successfully with lithium and/or with
held belief that patients tended to recover fully between individual or group psychotherapy.
depressive episodes. Factors predicting a prolonged time
to recovery are the longer duration and the increased 27.6.2 Dysthymia
severity of the index episode, a history of non-affective Dysthymia, also called depressive neurosis, is defined in
psychiatric disorder, lower family income, and married ICD-10 as
status during the index episode.
It has been found that 15%–20% of depressed A chronic depression of mood which does not fulfil the
patients develop a chronic course of illness and 75%– criteria for recurrent depressive disorder…. The balance
80% suffer multiple episodes. The risk of relapse between individual phases of mild depression and inter-
decreases the longer the patient remains well. For a first vening periods of comparative normality is very vari-
episode of depression, an older age and a history of pre- able. Sufferers usually have periods of days or weeks
when they describe themselves as well, but most of the
vious non-affective psychiatric illness predict a shorter
time… they feel tired and depressed; everything is an
time to relapse. Continuing high levels of medication in effort and nothing is enjoyed. They brood and complain,
the first few months is associated with a higher chance sleep badly and feel inadequate, but are usually able to
of remaining well. Overall, there is a suicide rate of cope with the basic demands of everyday life.
around 15%.
The time to recovery from the index episode of Dysthymia is probably more common in women than in men.
major depression in patients suffering from double It is more common in first-degree relatives of patients with a
depression is shorter than in patients suffering major history of depressive episodes than in the general population.
depression alone, but they tend to relapse more fre- Treatment with antidepressants, individual psycho-
quently and rapidly. therapy, or cognitive therapy may be helpful.
27.7 SUICIDE AND PARASUICIDE 27.7.1.2.2 Associations

(DELIBERATE SELF-HARM) Positive associations with suicide in the general popula-
tion include
27.7.1 Suicide
27.7.1.1 Epidemiology • Being male
• Being elderly
The annual incidence of suicide in England and Wales is
• Having suffered loss or bereavement
approximately 1 in 10,000 of the population. It is more
• Being unemployed
common in men than women and also more common in
• Being retired
those aged over 45 years. The highest rates are in those
• Childlessness
who are divorced, single, or widowed. The highest rates
• Living alone in a big, densely populated town
are in social classes I and V.
• A broken home in childhood
Suicide is associated with unemployment and retire-
• Mental or physical illness
ment. Suicide rates fell in England and Wales during the
• Loss of role
First and Second World Wars.
• Social disorganization, including overcrowding,
There is a seasonal variation in suicide rates. In the
criminality, and drug and alcohol misuse
northern hemisphere, suicide rates are highest during
the months of spring and early summer. In the southern Negative associations include
hemisphere, rates are highest in the months correspond-
ing to spring and early summer. • Religious devoutness
There is evidence that the availability of method • Lots of children
affects gross suicide rates as well as the choice of • Times of war
method. Suicide rates by hanging were constant until
the 1960s when there was a rise after the abolition of 27.7.1.2.3 Risk Factors
capital punishment. A massive reduction in the num- Risk factors by psychiatric diagnosis are as follows:
ber of deaths caused by gassing followed the switch
from coal gas to the safer North Sea gas in the 1960s. • Schizophrenia. There is a 10% mortality from
A marked rise in poisoning in the early 1960s was suicide. Roy (1982) characterized schizophrenics
because of the increased availability of medicines such who commit suicide as young, male, and unem-
as barbiturates. ployed, with chronic relapsing illness. Fewer
schizophrenic patients give warning of their
intention to commit suicide than patients in other
27.7.1.2 Aetiology of Suicide diagnostic groups (23% vs. 50%). The suicide is
27.7.1.2.1 Statistics usually after recent discharge, with good insight.
Ninety per cent of people who commit suicide suffer • Affective psychosis. There is a 15% mortality
from a psychiatric disorder. Of these, approximately from suicide. Men are older, separated, wid-
50% suffer depression, 25% alcoholism, 5% schizo- owed or divorced, living alone, and not work-
phrenia, and 20% other (e.g. personality disorder, ing. Women are middle aged, middle class, with
chronic neuroses, and psychoactive substance-abuse a history of parasuicide, and threats made in the
disorders). The rate of suicide is increased by 50 times last month. Those with obsessive–compulsive
the population rate among psychiatric inpatients. There symptoms are about six times less likely to com-
is also an association with physical illnesses, particu- mit suicide than those without.
larly chronic painful illnesses, epilepsy (especially • Neuroses. Nearly 90% have a history of para-
temporal lobe epilepsy), cancer, peptic ulcer, and gas- suicide, and a high proportion have threatened
tric ulcer disease. suicide in the preceding month. There is a ten-
Following an act of deliberate self-harm, the risk of dency after a failed attempt to resort to more
completing suicide in the subsequent year is approxi- violent means. There is a high risk in depressive
mately 100 times that in the general population and neurosis and panic disorder, but a lower risk in
remains high in subsequent years. obsessive–compulsive disorder.
• Alcoholism. There is a 15% mortality from sui- to be engulfed into something wider (e.g. reli-
cide. It tends to occur later in the course of the ill- gious or terrorist suicides).
ness, and those affected are often also depressed. • Egoistic. Suicide springs from excessive indi-
Associated with completed suicide are poor phys- viduation of the individual from society.
ical health, a poor work record, previous parasui- • Anomic. This relates to how society regulates
cide, and a recent loss of a close relationship. the individual. Suicide results from the fact that
• Personality disorder. High-risk factors are labil- a human’s activities lack regulation.
ity of mood, aggressiveness, impulsivity, alien- • Fatalistic. This is a rare type of suicide, the
ation from peers, and associated alcohol and opposite of anomic, deriving from excessive
substance misuse. regulation by oppressive regimes.
27.7.1.2.4 Life Events and Suicide 27.7.1.3 Assessment of the Individual for Suicide
The risk of suicide increases, more among males than Suicidal ideation should be explored in every patient and
females, during the 5 years following the bereavement of forms a part of the routine mental state examination.
a parent or a spouse. There is no evidence that asking patients about suicidal
Compared with psychiatric patient controls, suicides thoughts increases the risk of suicide.
have experienced interpersonal losses more frequently, The majority of people who commit suicide have told
although schizophrenic suicides have experienced fewer somebody beforehand of their thoughts. Two-thirds have
losses than nonschizophrenic controls. seen their GP in the previous month. One-quarter have
Age-related variations of stressors have been described, been psychiatric outpatients at the time of death; half of
with conflict–separation–rejection more common in them will have seen a psychiatrist in the previous week.
younger age groups, economic problems in middle-aged
groups, and medical illness among the older age groups. 27.7.1.4 Management of Suicidal Ideation
Once the need for treatment has been identified, it should
27.7.1.2.5 Biochemical Disturbances be provided quickly. The interval between GP referral to
Low 5-HIAA concentration in cerebral spinal fluid is psychiatric services and consultation has been identified
associated with increased suicidal behaviour and aggres- as a danger period and should be minimized.
sion. Irrespective of the clinical diagnosis, the group If there is a serious risk of suicide, the patient should be
in which CSF concentration of 5-HIAA is low often admitted to hospital. Any psychiatric disorder from which
includes persons who have attempted a violent method of the patient suffers should be treated appropriately. If the
suicide. Serotonin may play an important role in the biol- patient is suffering from severe depression, electroconvul-
ogy of aggression and the control of impulsive behaviour. sive therapy may be required. Patients with manic depression
Postmortem ligand binding studies have found have a mortality up to three times that of the general popula-
increased numbers of 5HT2 receptors in the prefrontal tion, with suicide and cardiovascular disease being primar-
cortex of suicide victims, particularly those who used ily responsible. In patients treated with lithium prophylaxis,
violent means. Low concentrations of serum cholesterol cumulative mortality does not differ from that of the general
have been found to be prospectively associated with an population. A minimum of 2 years of lithium treatment is
increase in the risk of violent death or suicide. Biological needed to reduce the high mortality resulting from manic
mechanisms linking low serum cholesterol concentration depression. It is proposed that lithium exerts its anti-suicide
and suicide have been hypothesized. effect as a result of improved serotonergic transmission.
27.7.1.2.6 Sociological Theory

27.7.2 Parasuicide
Durkheim in 1897 used the phenomenon of suicide to
describe society (see also Chapter 7). He described four 27.7.2.1 Epidemiology
types of suicide: There is an annual incidence of about 3 in 1000, but this is
probably an underestimate. It is most common in females
• Altruistic. The individual sets no value on life and in those aged below 35 years. The highest rates are in
and renounces his or her personal being in order those who are divorced or single, among the lower social
classes, unemployed, and living in overcrowded urban Motives include interruption, attention, communication,
areas in which there are high rates of juvenile delinquency. or a true wish to die.
Ninety per cent of cases involve deliberate self-
poisoning with drugs. Forty per cent use minor tranquil- 27.7.2.3 Assessment of the Individual for Suicide
izers and a further 30% use salicylates and paracetamol.
A high degree of suicidal intent is indicated by the following:
27.7.2.2 Aetiology of Parasuicide
• The act was planned and prepared.
Compared with the general population, life events are
• Precautions were taken to avoid discovery.
more common in the 6 months before an act of parasui-
• The person did not seek help after the act.
cide. These include the breakup of a relationship, trouble
• The act involved a dangerous method.
with the law, physical illness, and the illness of a loved one.
• There were final acts such as making a will or
Predisposing factors include leaving a suicide note.
• Marital difficulties In interviewing the parasuicidal
• Unemployment
• Physical illness, particularly epilepsy • Establish rapport.
• Mental retardation • Try to understand the attempt.
• Parental neglect or abuse • Inquire about current problems.
TABLE 27.5
Prevention of Depressive Disorders and Suicide
Prevention Depressive Disorders Suicide
Primary prevention: aim to Family planning: Advise people with strong family history Close monitoring during the post-discharge
reduce incidence of the of depression to space out pregnancies to avoid poor period: young men with schizophrenia and high
disorder parenting of child education background who have regained insight,
depressed elderly with somatic complaints
Interventions in parent–child relationships with special focus Limiting supply of medication to prevent toxic
on depressed mothers to improve parenting overdose
Events centred interventions: targeting at life events Control methods of suicide: install suicide barriers
to prevent people jumping from high places and
restricting gun ownership
Reduce unemployment and poverty
Enhance social support and preventing marital
breakdown
Media report: straightforward and undramatic
factual reporting of suicide cases
Secondary prevention: early Early detection of depressive disorder by GPs or through Early detection and treatment of psychiatric
detection and treatment of public education and use of screening instruments such as disorders
hidden morbidity and general health questionnaires (GHQ), psychiatric outreach
prevent progress of the service
disease Early intervention through CCBT in mild stage
Tertiary prevention: aim to Community-based support project: help vulnerable families Better community support and psychiatric outreach
reduce disabilities arising Prevention of relapse and recurrence: continue team to identify individuals with strong suicidal
as a consequence of the pharmacotherapy (avoid premature termination), ideation and patients who are discharged from the
disorder psychotherapy such as CBT and IPT hospital after suicide attempts
Rehabilitation: restore confidence, self-esteem, and
impairment
Providing employment to depressed people who face social
adversity
Source: Paykel, E.S. and Jenkins, R., Prevention in Psychiatry, Gaskell, London, U.K., 1994.
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28 Neurotic and Stress-Related
Disorders
28.1 HISTORY 28.3.3 Mortality

• In 1869, Beard introduced neurasthenia, com- There is increased mortality in severe neurotic disorder.
prising almost all current anxiety disorders. The relative risk of death in the decade following treat-
• In 1893, Hecker subdivided neurasthenia into ment for neurosis is 1.7. The biggest cause of increased
different syndromes. risk is accidental death, particularly suicide (relative
• In 1900, Sigmund Freud (see Ref. Freud, 1953) risk = 6.1). There is also a major excess of deaths from
distinguished between nervous, circulatory, and respiratory disease. Suicide is
• Actual neuroses: somatic causation, compris- most likely in the first year after discharge.
ing neurasthenia, anxiety neurosis (general-
ized anxiety, panic disorder, and agoraphobia), 28.4 PHOBIC ANXIETY DISORDERS
and hypochondriasis
• Psychoneuroses: psychological causation, The Greek word phobos means panic or terror. In pho-
comprising hysteria and obsessions (simple bic anxiety disorders, anxiety is evoked predominantly
phobia, social phobia, and obsessive–com- by certain well-defined situations, characteristically
pulsive disorder [OCD]) avoided. Contemplation of a feared situation generates
• Libidinous impulses reaching the ego generate anticipatory anxiety.
anxiety; repression and symptom formation follow. In defining fear as phobic, the following are considered:
• Fright neurosis, not related to repressed libido,
• It is out of proportion to objective risks.
was also described, similar to current post-trau-
• It cannot be reasoned or explained away.
matic stress disorder (PTSD).
• It is beyond voluntary control.
• It leads to avoidance.
28.2 CLASSIFICATIONS OF NEUROSIS
(TABLE 28.1) Marks et al. (1993) classify adult fears as normal or
abnormal fears. The latter are grouped as follows:
28.3 GENERAL ISSUES
• Phobias of external stimuli
28.3.1 Effect of Childhood Neurosis • Agoraphobia
• Social phobia
Robins (1966) found that most children with neurotic dis-
• Animal phobia
orders do not suffer neurosis in adulthood. Adult neurot-
• Miscellaneous specific phobias
ics develop neurosis in adult life.
• Phobias of internal stimuli
In childhood, there is excess neurosis in males. After
• Illness phobia
puberty, there is excess in females.
• Obsessive phobias
28.3.2 Effect of Personality Disorder 28.4.1 Epidemiology of Phobic Anxiety Disorder

The prevalence of personality disorder in neurosis is The Epidemiologic Catchment Areas (ECA) study found
12% in primary care and 40% in psychiatric outpatients.
Psychological treatment, particularly self-help, is more • A lifetime prevalence for all phobias from 7.8%
effective in neurotic patients without personality disor- to 23.3% between sites
der. Neurotic patients with personality disorder respond • A 6 month prevalence for agoraphobia of
better to antidepressant drug treatment. 2.8%–5.8%
405
TABLE 28.1
Comparison between ICD-10 and Proposed DSM-5 Criteria
ICD-10 (WHO, 1992) DSM-5 (APA, 2013)
Phobic anxiety disorders
F40.0 Agoraphobia 300.22 Agoraphobia
F40.1 Social phobia 300.23 Social anxiety disorder
F40.2 Specific phobia 300.29 Specific phobia
• Acrophobia • Animal (e.g. spiders, insects, dogs)
• Animal phobia • Blood–injection–injury (e.g. needles, invasive medical
• Claustrophobia procedures)
• Simple phobia • Natural environment (e.g. heights, storms, water)
• Situational (e.g. airplanes, elevators, enclosed places)
• Other (e.g. situations that may lead to choking or
vomiting; in children, loud sounds or costumed characters)
Other anxiety disorders
F41.0 Panic disorder 300.01 Panic disorder
F41.1 GAD 300.02 GAD
F41.2 Mixed anxiety and depressive disorder There is no mention of mixed anxiety and depressive disorder
Other anxiety disorders
Substance-induced anxiety disorder
293.84 Anxiety disorder attributable to another medical condition
300.00 Anxiety disorder not elsewhere classified
F42 OCD 300.3 OCD
There is no mention of OCD-spectrum disorders OCD-spectrum disorders:
300.7 BDD
300.3 Hoarding disorder
312.29 Hair-pulling disorder (trichotillomania)
698.4 Skin picking disorder
Substance-induced OCD or related disorders
294.8 OCD or related disorder attributable to another medical
condition
300.3 OCD or related disorder not elsewhere classified
F43.0 Acute stress reaction 308.3 Acute stress disorder
The DSM-5 proposed 313.89 reactive attachment disorder and
313.89 disinhibited social engagement disorder
F43.1 PTSD 309.81 PTSD
F43.2 Adjustment disorder Adjustment disorder
F44.0 Dissociative (conversion) disorders Dissociative disorders
• F44.0 Dissociative amnesia 300.6 Depersonalization–derealization disorder
• F44.1 Dissociative fugue 300.12 Dissociative amnesia (localized or generalized)
• F44.2 Dissociative stupor 300.14 Dissociative identity disorder
• F44.3 Trance and possession disorder
• F44.4–7 Dissociative disorders of movement
and sensation
• F44.4 Dissociative motor disorders
• F44.5 Dissociative convulsion
• F44.6 Dissociative anaesthesia and sensory loss
• F44.7 Mixed dissociative (conversion) disorders
• F44.81 MPD
Neurotic and Stress-Related Disorders 407
• A 6 month prevalence for simple phobia of 28.4.2.3 Comorbidity

4.5%–11.8% There is overlap between anxiety disorders. For exam-
• A 6 month prevalence for social phobia of ple, 55% of agoraphobics have social phobia and 30% of
1.2%–2.2% social phobics also have agoraphobia.
Persons with major depression have 15 times the risk
The Edmonton Study (Dick et al., 1994b) found of having agoraphobia and 9 times the risk of simple pho-
bia as controls.
• A lifetime prevalence for all phobias of 8.9% Twenty-five per cent of phobics report alcohol abuse/
(females 11.7%, males 6.1%) dependence; there are higher rates in agoraphobics and
• Age of first symptoms—6 years in females, social phobics than in simple phobias.
12 years in males
• High rates of comorbidity with depression,
alcohol abuse, drug abuse, and OCD in all types 28.4.3 Management of Phobic Anxiety Disorder
of phobia
28.4.3.1 Psychological Approaches
Phobic anxiety disorders affect females more than males Behaviour therapy is the treatment of choice. Exposure
(agoraphobia 75%, simple phobia 95%), except social techniques are most widely used. Wolpe’s systematic
phobia where the sex ratio is equal. desensitization combines relaxation with graded exposure.
Reciprocal inhibition prevents anxiety from being main-
tained when exposed to the phobic stimulus while relaxed.
28.4.2 Aetiology of Phobic Anxiety Disorder Flooding entails maximal exposure to the feared
28.4.2.1 Genetic Factors stimulus until anxiety reduction occurs. This is not more
effective than other exposure techniques.
Phobic disorders or other psychiatric illnesses (neurosis,
Modelling requires the patient to observe the therapist
alcoholism, depressive illness) are more prevalent in fam-
engaging in non-avoidant behaviour when exposed to a
ilies of phobic probands.
feared stimulus.
Kendler et al. (1993a), using the twin registry, demon-
Psychoanalytic psychotherapy has proved to be
strated that familial aggregation of phobia resulted from
ineffective.
genetic liability, not from shared environmental factors.
28.4.2.2 Psychological Factors 28.4.3.2 Pharmacological Approaches

• Pavlovian classical conditioning. Watson, in Selective serotonin reuptake inhibitors (SSRIs) such as
the ‘Little Albert’ experiment on an 18-month- escitalopram, fluvoxamine, paroxetine, and sertraline are
old child, produced fear of a toy white rat by first-line treatments of phobic anxiety disorder.
presenting it repeatedly with a loud noise. Fear Monoamine oxidase inhibitors (MAOIs) are effective in
is later generalized to all furry objects (see agoraphobics and social phobics: 80%–90% of pure social
Chapter 3). phobics are almost asymptomatic at week 16, but patients
• Operant conditioning. Avoidance of a phobic withdrawn from the active drug relapse (Versiani et al., 1992).
situation is rewarded by a reduction in anxiety Benzodiazepines may help prevent the reinforcement
that reinforces avoidance. of fear through avoidance.
• Seligman’s preparedness theory. Anxiety is easily
conditioned to certain stimuli (e.g. heights, snakes, 28.4.4 Specific Phobic Disorders
spiders) and is resistant to extinction. Prepared
stimuli were dangerous to primitive man and may 28.4.4.1 Agoraphobia
have been acquired by natural selection. In 1871, Westphal first used the term to describe patients who
experienced intense anxiety when walking across open spaces.
Phobias represent a conflict leading to avoidance of situ-
ations symbolic of that conflict. ‘Little Hans’ developed a 28.4.4.1.1 ICD-10 (WHO, 1992)
phobia of horses after seeing a male horse urinate. Freud • Symptoms are manifestations of anxiety and are
believed that fear of castration by his father was displaced not secondary to other symptoms such as delu-
on to horses after this viewing. sions or obsessional thoughts.
• Anxiety is restricted to at least two of the 28.4.4.2.1 ICD-10 (WHO 1992)

following: crowds, public places, travelling
• Symptoms are manifestations of anxiety and not
away from home, and travelling alone. secondary to other symptoms.
• At least two symptoms from automatic arousal • Anxiety is restricted to or predominates in par-
symptoms, symptoms involving the chest and ticular social situations.
abdomen, and symptoms involving mental state. • The phobic situation is avoided whenever possible.
• Avoidance of the phobic situation is prominent. • Marked fear of being the focus of attention
• Two subtypes: agoraphobia without panic disor- and marked avoidance of being the focus of
der or agoraphobia with panic disorder. attention.
• At least two symptoms: blushing or shaking,
28.4.4.1.2 DSM-5 (APA, 2013) fear of vomiting, and urgency or fear of micturi-
• The agoraphobic situations are similar to ICD-10. tion or defecation.
• The fear, anxiety, or avoidance lasts for at least
6 months.
• The fear is associated with difficulty to escape 28.4.4.2.2 DSM-5 (APA 2013)
and help being unavailable. It is characterized by marked fear or anxiety about one or
• Avoidance of agoraphobic situations. more social situations in which the individual is exposed to
• The fear is out of proportion to the danger. possible scrutiny or be negatively evaluated by others. The
fear is out of proportion and lasts for 6 months or longer.
28.4.4.1.3 Course
Symptoms fluctuate, but the course is prolonged. Eighty
28.4.4.2.3 Treatment
per cent of agoraphobics are not free of symptoms after
5 years. The treatment for social phobia is similar to panic disor-
der (see succeeding text). In addition, β-blockers can be
28.4.4.2 Social Phobias used to reduce autonomic arousal, which can be particu-
Genetics: larly helpful for performance anxiety.
1. MZ/DZ = 24%:15% (Kendler et al., 1992).

2. The relatives of socially phobic probands have a 28.4.4.2.4 Course
threefold elevated risk of social phobia. The course is continuous but it may improve gradually.
Alcohol and drug abuse are common.
Imaging: Positron emission tomography (PET) scan
shows an increased blood flow in the right dorsolateral
prefrontal cortex (Gelder et al., 2006). 28.4.4.3 Isolated Phobias
Social phobias are characterized by a fear of scrutiny Isolated phobias are restricted to highly specific situa-
by others in small groups. This may progress to panic tions. The seriousness of the handicap depends on how
attacks. Avoidance is often marked (Figure 28.1). easily a feared situation can be avoided.
Thought:
‘I will make a fool of
myself ’.
Safety
Belief: Trigger: behaviour: Consequence:
‘I’m inferior and Presentation to Social phobia Avoid eye Fail to complete
a poor the CEO contact, stand the
presenter’ next to the exit presentation
Physical
symptoms:
Tremor, flushing
FIGURE 28.1 Cognitive model of a 35-year-old marketing manager suffering from social phobia.
28.4.4.3.1 ICD-10 28.5.2.2 Neurochemistry

• Symptoms are manifestations of anxiety and not • Noradrenaline (NA)
secondary to other symptoms. • Downregulation of α2-receptors and increase
• Anxiety is restricted to the particular phobic in autonomic arousal.
situation. • Electrical stimulation of the locus coeruleus
• The phobic situation is avoided whenever releases NA and generates anxiety.
possible. • Serotonin: dysregulation of the 5-HT system
• GABA: reduced GABA activity
28.4.4.3.2 Course
28.5.2.3 Endocrinology
Childhood phobias are always improved after 5 years. In
adult phobias, 20% are unchanged, 40% are better, and Thirty per cent of patients with GAD show reduced sup-
40% are worse after 5 years. pression of dexamethasone suppression test (DST).
28.5.2.4 Imaging
Structural magnetic resonance imaging (MRI) shows
28.5 GENERALIZED ANXIETY DISORDER
decreased hippocampal and medical prefrontal cortex
The diagnostic reliability of generalized anxiety disor- volumes.
der (GAD) is lower than that of other anxiety disorders. Proton MR spectroscopy shows decreased GABA in
Patients report uncontrollable worry. A negative response anterior cingulate cortex and posterior occipital cortex.
to the question ‘Do you worry excessively over minor
matters?’ virtually rules out GAD as a diagnosis (nega- 28.5.2.5 Cognitive Theories
tive predictive power 0.94). Symptoms of muscle and psy- Patients with GAD often have selective attention to nega-
chic tension are the most frequently reported by people tive details, distortions in information processing, and
with GAD. negative views on coping.
GAD is associated with the highest rates of comorbid-
ity of all anxiety disorders. 28.5.2.6 Psychoanalytic Theories
GAD represents symptoms of unresolved unconscious
conflicts, early loss of parents, overprotective parenting,
28.5.1 Epidemiology of Generalized or parenting lacking warmth and responsiveness.
Anxiety Disorder
28.5.2.7 Environmental Factors
The ECA study found
Torgersen (1983) reported that probands with GAD had lost
• A 6 month prevalence of GAD of 2.5%–6.4% their parents by death far more often than probands with
• An earlier age of onset (majority before age 20) panic disorder, suggesting that environmental factors con-
and more gradual than other anxiety disorders tribute to a higher vulnerability for the development of GAD.
Early-onset GAD is more likely to be in a female and in a 28.5.3 Diagnostic Criteria

person having a history of childhood fears and/or having ICD-10 criteria (F41.1): 6 month durations; at least four
marital or sexual disturbance. Later onset is more likely symptoms from the following category must be present:
to develop after a stressful life event.
• Core symptoms: persistent tension, worry, and
feelings of apprehension
28.5.2 Aetiology of Generalized • Autonomic arousal symptoms: palpitation,
Anxiety Disorder sweating, trembling, dry mouth
• Symptoms involving the chest and abdomen:
28.5.2.1 Genetic Factors choking sensation, nausea, difficulty in breathing
Some studies show familial aggregation of GAD, • Symptoms involving mental state: giddiness,
while others do not. Kendler et al. (1993a) concluded fear of losing control, derealization
that GAD is a moderately familial disorder with a heri- • Hot flushes or cold chills
tability of 30%. • Poor concentration, startled responses
DSM-5 (300.02) (APA, 2013)—minimum duration: 6 months 3. For CBT, it should be offered in weekly sessions
of 1–2 h and be completed within 4 months. The
• Excessive anxiety and worry (apprehensive
optimal range is 16–21 h in total. If the psycholo-
expectation) about two (or more) domains of
gist decides to offer briefer CBT, it should be about
activities or events (e.g. family, health, finances,
8–10 h with integration of structured self-help
and school/work difficulties)
material. Components of CBT include education,
• Core symptoms
problem-solving, exposure-based approaches, cog-
• Muscle tension
nitive approaches, emotion-regulation approaches,
• Fatigue
and relapse prevention. CBT is more effective than
• Irritability
relaxation training.
• Poor concentration
4. For pharmacological therapy, the psychiatrist
• Poor sleep
should consider the patient’s age, previous treat-
• Restlessness
ment response, risk of DSH, cost, and patient’s
• Four associated behaviours
preference. Inform the patient on the potential
• Marked avoidance of activities or events
side effects, possible discontinuation withdrawal,
with possible negative outcomes
and the time course of treatment. An SSRI
• Marked time and effort preparing for activities
should be offered. Examples include paroxetine,
• Events with possible negative outcomes
escitalopram, and sertraline. If one SSRI is not
• Marked procrastination in behaviour or
suitable, consider another SSRI. The psychiatrist
decision making as a result of worries
should review the patient within 2 weeks of start-
• Repeatedly seeking reassurance
ing treatment and again at 4, 6, and 12 weeks.
28.5.4 Medical Differential Diagnosis Then the psychiatrist can review the patient at
8–12-week intervals.
1. Cardiovascular disorders: arrhythmia, ischaemic 5. For GAD not responding to at least two types
heart disease, mitral valve prolapse, congestive of intervention, consider venlafaxine. Before
heart failure prescribing, the psychiatrist should consider the
2. Thyroid disorder presence of preexisting hypertension and the pos-
3. Medication such as thyroxine, antihyperten- sibility of overdose because venlafaxine is more
sives, antiarrhythmics, bronchodilators, anti- dangerous than other SSRIs. The psychiatrist
cholinergics, anticonvulsants, and NSAIDS should order an ECG to rule out cardiac arrhyth-
mias and recent myocardial infarction. The dose
28.5.5 Management of Generalized should not be higher than 75 mg per day and the
Anxiety Disorder psychiatrist should monitor the blood pressure
regularly during follow-up.
Investigations: Full blood count, renal function tests,
6. During reassessment, the psychiatrist should eval-
liver function tests, thyroid function tests, fasting glucose
uate treatment response, potential substance abuse,
and lipids, urinalysis, urine toxicology, and electrocardi-
emergence of comorbidities, day-to-day function-
ography (ECG)
ing, social networks, chronic stressors, and the role
Recommendations from the NICE guidelines:
of agoraphobia and other avoidant symptoms.
1. Benzodiazepines should not be used beyond
2–4 weeks. 28.5.5.1 Psychological Therapies (Figure 28.2)
2. For longer-term treatment, the following treat- Recommendations from the NICE Guidelines: For GAD,
ment should be considered: the recommendation is similar for panic disorder except
a. Option A: psychological therapy (e.g. the optimal range is 16–20 h in total. Briefer CBT is 8–10
cognitive–behavioural therapy [CBT]). h with integration of appropriate focused information and
b. Option B: pharmacological therapy (e.g. an self-help materials.
SSRI licensed for GAD).
c. Option C: self-help (bibliotherapy based on
the CBT principles). 28.5.5.1.1 Comorbidity and Prognosis
d. For the duration of effect, option A is longer Comorbidity: Concurrent panic disorder (25%) and
than option B; option B is longer than option C. depression (80%)
Thoughts: A lot
of worries
about her son
Belief:
Trigger: Her
‘I must worry’ Consequence:
son has not Behaviour:
‘what if my son GAD Pacing up and
rung her as Phones her son
has an accident down and
promised 10 times a day
in France?’ cannot go to
Physical work
symptoms:
Sweating,
tremor
diarrhoea
FIGURE 28.2 Example of a cognitive model of a 40-year-old mother with GAD.
28.5.5.1.2 Course 28.5.5.1.3 Prognosis (Argyropoulos et al., 2007)

Follow-up after 6 years reveals stability of diagnosis; Seventy per cent of patients have mild or no impairment
the most common change of diagnosis is to alcoholism. and 9% have severe impairment. Poor prognostic factors
Sixty-eight per cent have mild or no residual impairment; include severe anxiety symptoms, syncope, agitation,
9% have severe impairment. derealization, and suicide.
CASC STATION
Dr. Sobieski, a 50-year-old female medical doctor from your hospital, has self-referred to you. She complains of
being on the edge most of the time with palpitations and dizziness in the past 1 year. She migrated from Poland
15 years ago and describes herself as a lifelong worrier.
Task:
1. Take a history of her anxiety symptoms and explore the causes of her anxiety.
2. Inform Dr. Sobieski on your treatment plan.
CASC Grid
Approach to this station: Candidates have to differentiate the main causes of anxiety with her occupational
background.
(A) Anxiety (A1) Assess
Symptoms Based Autonomic (A2) Assess (A5) Other
on the ICD-10 Arousal Symptoms Involving (A3) Assess Mental (A4) General Nonspecific
Criteria Symptoms the Chest/Abdomen State Symptoms Symptoms Symptoms
(WHO, 1992) Palpitation Difficulty breathing Giddiness Hot flushes Exaggerated
Sweating Choking sensation Fainting Cold chills responses to
Trembling/ Chest pain Derealization or Numbness minor surprises/
shaking Nausea or stomach depersonalization Tingling/ being startled
Dry mouth churning Not being able to stop aches—muscle Persistent
worrying tension irritability
Being annoyed or irritable Restlessness Poor sleep
Fear of losing control Keyed up, on the Poor
Fear of dying or ‘going edge concentration
crazy’ Trouble relaxing Mind goes blank
Feeling afraid as if Lump in the throat
something awful may
happen
(continued)
(B1) Brief
(B) Comorbidity Screening for (B2) Assess Possible (B4) Assess (B5) Assess
and Risk Other Neurotic PTSD and OCD (B3) Assess Substance/Alcohol Fitness to
Assessment Disorders Symptoms Depression Abuse Practice
‘Do you have any ‘Do you have Assess mood and Usage of alcohol Explore cognitive
panic attack or nightmare, cognitive symptoms. and symptoms that
difficulty in flashbacks related If symptoms of GAD benzodiazepine to may affect her
breathing?’ to previous and depression are overcome work (e.g. poor
‘Do you have any trauma?’ present, a diagnosis of insomnia or other concentration,
fear? (e.g. fear ‘Do you have any mixed anxiety and recreational drugs anxiety during
of going to excessive checking depressive disorder is for medical
crowded areas or washing justified self-medication procedures)
or presenting a behaviour?’ ‘Is your anxiety
case during the worsening after
ward round?’ stop drinking or
taking
tranquillizer?’
(C) Issues
Related to the
Patient as a
Migrant Doctor (C1) Explore the (C2) The Issue of
from Eastern Issue of Self-Diagnosis and (C3) Factors that (C4) Work-Related (C5) Culture
Europe Self-Referral Self-Treatment Delay Help-Seeking Problems Issues
‘I can imagine ‘Do you recognize Explore the following Explore relationship Explore language
that it is hard that you suffer from factors: e.g. low with peers and problems in
for you as a anxiety disorder? If motivation, fear of supervisors, bullying, clinical practice,
doctor to yes, when?’ damage to her complaints from adaptation to the
disclose your ‘Have you started reputation, patients, medicolegal U.K. culture,
own illness. Do any treatment on discrimination, and her issues because of cultural clashes
you have a GP? your own?’ cultural views of negligence, medical with patients or
Did you consult mental illness errors, and multiple colleagues
him for your failures in the MRCP
anxiety exam
problems?
If not, why?’
(D1) Explore Her
(D) Other Reasons for
Background Migrating to the (D4) Developmental (D5) Past
History United Kingdom (D2) Family (D3) Personal History Issues Medical History
‘Were you a Explore her marital Explore past Explore middle-age ‘Do you have any
refugee doctor?’ status, the effect of experience of crisis and chronic medical
Explore other migration on her persecution under the stagnation in disease like
factors such as marriage, any previous communist career heart or lung
better salary, children left regime. development disease?’
well-recognized behind in Poland, Explore history of ‘Do you take
training, and the financial status personal trauma and medication on a
better job of her family, and subsequent long term
prospects past family history re-traumatization basis?’
of anxiety
disorders
(E1) Set (E4) Deliver

Boundaries for Psychotherapy in a (E5) Issue of
(E) Management Treatment and (E2) Ethical Issues, (E3) Address Medical Culturally Aware Prescribing
Plan Investigations e.g. Confidentiality Practice Issues Manner Medication
‘Would you Reassure Dr. Sobieski Suggest to take time Explore her Explain the
prefer to see a that you are trying off, offer CBT to preferences based possibility of
psychiatrist in your very best to address distorted on the cultural taking
this hospital or help her negative thought background of antidepressants
elsewhere?’ The candidate should processes, and reduce psychotherapists, and provide
Address only mention the her anxiety symptoms e.g. gender, education on the
management of issues of reporting by relaxation training cultural proper usage of
the future to the GMC if there backgrounds benzodiazepine
professional is evidence of because it can
interactions impairment in her cause
Investigations clinical practice dependence.
include FBC, Discuss
TFT, calcium, common side
phosphate, effects
glucose, and
ECG
28.6 PANIC DISORDER 28.6.2 Aetiology of Panic Disorder

This involves recurrent unpredictable attacks of severe 28.6.2.1 Genetic Factors
anxiety lasting usually for a few minutes only. There can The morbid risk for panic disorder in relatives of pro-
be a sudden onset of palpitations, chest pain, choking, bands is 15%–30%, much higher than in the general pop-
dizziness, depersonalization, and derealization, together ulation (2%). Female relatives are at higher risk than male
with a secondary fear of dying, losing control, or going relatives. There is an increased risk of alcoholism in the
mad. It often results in a hurried exit and a subsequent relatives of probands.
avoidance of similar situations; it may be followed by Kendler et al. (1993b) estimated that the heritability
persistent fear of another attack. for panic disorder with or without phobic avoidance is
35%–40%.
28.6.1 Epidemiology of Panic Disorder 28.6.2.2 Cognitive Theories

The ECA study found that 3% of the population had • Classical conditioning
experienced a panic attack in the previous 6 months. All • Negative catastrophic thoughts during panic attacks
socioeconomic groups were affected, and there was no
relationship with race or education. Women aged 25–44 28.6.2.3 Psychoanalytic Theories
years, with a family history of panic disorder, divorced, • Panic attacks arise from unsuccessful attempts
or separated were at highest risk. Other findings were to defend against anxiety provoking impulses.
• Maximum period of onset from mid-teens to

28.6.2.4 Neurochemistry (Argyropoulos
mid-thirties, rarely after the age of 40
et al., 2007)
• More common in females than males (2:1)
• A prevalence of strictly defined panic disorder 28.6.2.4.1 Noradrenaline
of 0.1%–0.4% • Hypersensitivity of presynaptic α2-receptor and
• A 1-year prevalence of 0.2%–1.2% increase in adrenergic activity.
• A lifetime prevalence of 1.4%–1.5% • Panic disorder is induced by yohimbine.
28.6.2.4.2 Serotonin • Children of probands with major depression

• Subsensitivity of 5-HT1A receptors and exagger- and panic disorder have higher rates of major
ated postsynaptic receptor response. depression and anxiety disorders.
• Panic disorder is induced by d-fenfluramine. • There is an increased rate of panic disorder but
not major depression or other anxiety disorders
28.6.2.4.3 GABA in the relatives of panic-disorder probands.
• Reduction in GABA receptor sensitivity; panic
attack is induced by flumazenil. 28.6.2.7 Life Events
There is an excess of stressful life events in the year prior
28.6.2.4.4 Others to the onset of panic disorder, especially illness or death
• Cholecystokinin (CCK) and sodium lactate of a cohabitant or relative.
induce panic attack.
28.6.2.8 Physiological Factors
28.6.2.5 Neuroimaging
Pitts and McClure (1967) provoked panic attacks in
Structural MRI shows decreased medial temporal lobe
patients with anxiety neurosis but not controls, by the
volume.
intravenous infusion of sodium lactate. There were
Functional MRI shows increased haemodynamic
higher levels of autonomic arousal in preinfusion panick-
responses in the amygdala, hippocampus, and insula.
ers compared to non-panickers.
No single biochemical or neuroendocrine finding
28.6.2.6 Comorbidity
explains lactate-induced panic. Yohimbine, a pre-
One-third develop secondary depression following the synaptic a 2-adrenergic autoreceptor blocker, induced
onset of panic disorder. If depression does occur, the panic attacks in a subgroup of individuals. This group
course is poorer. Agoraphobia usually occurs with panic showed increased noradrenergic activity and blunted
disorder but can occur separately. growth hormone response to clonidine, supporting the
There is an increased lifetime prevalence of alco- hypothesis of a dysregulation of the noradrenergic sys-
hol abuse/dependence (54%) and drug abuse/depen- tem and possibly the hypothalamus–pituitary–adrenal
dence (43%) in persons with panic disorder. Some use axis in a subgroup of panic-disorder patients. There
substances as a complication of panic disorder; others were very low rates of non-suppression during a DST
develop panic disorder as a result of withdrawal from in panic disorder.
substances. Panic attacks are associated with a reduced blood flow
Major controversy surrounds the relationship between in the frontal lobes. Panic-disorder patients not having a
anxiety disorders and depression. There is evidence sup- panic attack have reduced perfusion of the hippocampus
porting the unitary position that anxiety and depression bilaterally and an increase in blood flow to the right infe-
lie along the same continuum: rior frontal cortex.
Mitral valve prolapse occurs in 40% of panic-disorder
• High overlap of symptoms (65% of anxious patients patients compared to 9% of controls. Patients suffering
have depressive symptoms) (Roth et al., 1972) from mitral valve prolapse do not suffer more panic dis-
• Difficulty separating primary disorder in order than controls. An aetiological role for mitral valve
patients experiencing both panic attacks and prolapse in panic disorder is unlikely.
depression Panic-disorder patients have abnormal sleep breath-
• No differences in family history for anxiety and ing with increased irregularity in tidal volume during
mixed anxiety depression groups REM sleep and an increased rate of microapnoeas.
One aetiological theory of panic disorder proposes
28.6.2.6.1 Evidence Supporting Separation that patients have a hypersensitive respiratory control
• Family studies show no excess of depression in system operating at the level of brain stem chemore-
the relatives of probands suffering from pure ceptors. Their ‘suffocation’ alarm is thus at a pathologi-
panic disorder (Leckman et al., 1985). cally low set point. Enhanced CO2 sensitivity results
• Children of probands with major depression in more frequent sighing to reduce CO2 levels; this
show increased rates of major depression but not results in breathing pauses because the CO2 stimulus
anxiety disorders. for breathing is withdrawn.
28.6.3 Diagnostic Criteria 28.6.4 Differential Diagnosis

28.6.3.1 Diagnostic Criteria 28.6.4.1 Hyperventilation Syndrome (Table 28.2)
28.6.3.1.1 F41.0 Panic Disorder (ICD-10, WHO, 1992) 28.6.4.2 Medical Differential Diagnosis
• Episodic paroxysmal anxiety not confined to • Respiratory disorders: COPD, asthma, and
predictable situations. mitral valve prolapse
• Several attacks occur within 1 month. • Endocrine disorders: diabetes, hypoglycaemia,
• Discrete episode of intense fear or discomfort, thyrotoxicosis, hypoparathyroidism, phaeochro-
abrupt onset, reaches a maximum within a few mocytoma, and anaemia
minute autonomic arousal symptoms with free-
dom from anxiety symptoms between attacks.
28.6.5 Management of Panic Disorder
• Symptoms involving the chest and abdomen.
• Symptoms involving mental state (see A1–A3 of Recommendations from the NICE Guidelines:
CASC on page 407). The recommendations are similar to management on GAD.
• Hot flushes and chills.
28.6.5.1 Pharmacotherapy
28.6.3.1.2 300.01 Panic Disorder (DSM-5, APA 2013) The NICE guidelines recommend SSRI as the first-line
• Recurrent unexpected panic attacks with symp- treatment of panic disorder. Examples include citalopram,
toms similar to the ICD-10 criteria. escitalopram, fluoxetine, fluvoxamine, paroxetine, or sertra-
• At least one of the attacks has been followed by line. If an SSRI is unsuitable and there is no improvement,
at least 1 month of persistent concern or worry consider imipramine or clomipramine but not venlafaxine.
about additional panic attack and maladaptive The tricyclic antidepressants (TCAs) imipramine
change in behaviour related to the attacks. and clomipramine, MAOIs, and SSRIs are efficacious
TABLE 28.2
Compare and Contrast Panic Disorder and Hyperventilation Syndrome
Panic Disorder HVS
ICD-10 and proposed DSM-5 criteria A codable disorder. Not a codable disorder.
Overlap between the two disorders 50%–60% of patients with panic disorder 25% of HVS patients have symptoms of panic
or agoraphobia have HVS symptoms. disorder.
Aetiology Biological and psychological causes are Less well defined. Lactate, CCK, caffeine, and
well defined. psychological stressors also play a role.
Salient clinical features Panic disorder has more mental symptoms. High thoracic breathing or excessive use of
accessory muscles to breathe result in
hyperinflated lungs.
Metabolic disturbances The role of metabolic disturbances is less • Acute hypocalcaemia: positive Chvostek and
well established. Trousseau signs and prolonged QTc interval
• Hypokalaemia with generalized weakness
• Respiratory alkalosis
• Acute hypophosphataemia leading to
paraesthesias and generalized weakness
Management Acute management involves reassuring Investigation may include d-dimer and possible
patients, establish normal breathing V/Q scan to rule out pulmonary embolism.
pattern, and reduce anxiety with Acute and long-term management are similar to
anxiolytics. panic disorder. De-arousal strategy is useful.
Long-term management includes
relaxation exercise and CBT.
Sources: Johnstone, E.C. et al., Companion to Psychiatric Studies, 7th edn, London, U.K.: Churchill Livingstone, 2004; Semple, D. et al.,
Oxford Handbook of Psychiatry, Oxford, U.K.: Oxford University Press, 2005.
in the treatment of panic disorder. The downregulation 28.6.5.2.2 Course and Prognosis
of 5-HT2 receptors may be responsible for therapeutic The course is highly variable. Sixty per cent suffer mild impair-
effects, which take up to 4 weeks to appear. Increased ment. Ten per cent suffer severe disability. Poor outcome is pre-
anxiety or panic may occur in the first week of treatment. dicted by lower social class and long duration of illness.
Benzodiazepines (e.g. alprazolam in high dosage) Recurrence is common when new stressors emerge
reduce the frequency of panic attacks in the short term. in panic disorder. If a patient with panic disorder stops
There is the need to maintain treatment in the long term, the SSRI, there is more than 50% chance of recurrence
with the risk of dependency. (Taylor et al., 2009).
28.6.5.2 Psychological Treatment (Figure 28.3) 28.7 OCD

28.6.5.2.1 NICE Guidelines: CBT and 28.7.1 Epidemiology of OCD
Anxiety Disorders
1. CBT should be offered to GAD and panic disor- The ECA study found that OCD is very rare in children.
der in primary care. Rutter found no cases among 2000 10- and 11-year-olds
2. For panic disorder, CBT should be delivered by on the Isle of Wight. Other findings were
trained and supervised therapists, closely adher- • A 6-month prevalence of OCD of 1.3%–2.0%
ing to the treatment protocols. CBT should be • A lifetime prevalence of 1.9%–3.0%
offered weekly with duration of 1–2 h and be • Sex ratio equal
completed within 4 months. The optimal range • Bimodal age of onset with peaks occurring at
is 7 (brief CBT) to 14 h in total. 12–14 and 20–22 years of age (decline in onset
CBT involving the cognitive restructuring of cata- after the age of 35)
strophic interpretations of bodily experience is effica- The ECA study prevalence findings were consistently
cious in panic disorder, as are exposure techniques that higher than earlier accepted estimates.
generate bodily sensations of fear during therapy with
the aim of habituating the subject to them. Agoraphobic 28.7.2 Aetiology of OCD
avoidance is treated by situational exposure and relax-
ation techniques. 28.7.2.1 Genetic Factors
Marks et al. (1993), comparing alprazolam and expo- First-degree relatives of OCD patients have a higher than
sure therapy in patients suffering from panic disorder and normal incidence of psychiatric disorders, most com-
agoraphobia, found the effect size of exposure was twice monly anxiety, phobias, depression, and schizophrenia.
that of alprazolam; during follow-up, gains from alpra- First-degree relatives of OCD patients have higher
zolam disappeared, but exposure gains were maintained. than normal obsessional traits; the risk of OCD among
Treatment with a combination of exposure and alprazolam relatives is higher in early-onset OCD probands, suggest-
impaired improvement seen in the exposure-alone group. ing aetiological heterogeneity.
Thoughts:
‘What if I do die
of a heart
attack?’
Belief: Safety
‘Having Trigger: behaviour: Consequence:
palpitations ‘Stepping into Panic disorder Call the Admit himself
means I’ll die of the office’ ambulance for to the
heart attack!’ help emergency
department
Physical
symptoms:
Shortness of
breath, tremor
FIGURE 28.3 Cognitive model of a 45-year-old office worker suffering from panic disorder.
Twin studies suggest that monozygotic twins are more is reduced and the rituals are negatively reinforced. The
likely to be concordant than dizygotic twins for OCD use of rituals prevents the natural reduction in anxiety
(MZ/DZ = 50%–80%:25%). that would occur if exposure to the stimulus was not cut
Gilles de la Tourette’s syndrome is a familial condition short by the ritual or neutralizing thought.
with a substantial genetic basis. Twin and family studies find In a cognitive model, obsessional distortion concerns
high rates of OCD and obsessive–compulsive symptoms exaggerated the responsibility for thoughts, with a ten-
among families of patients with Tourette. This suggests thatdency to neutralize thoughts with rituals.
some forms of OCD may be related to Tourette’s syndrome. In psychoanalysis, OCD symptoms are seen as defen-
OCD is equally frequent in families of Tourette’s pro- sive responses to unconscious impulses. Obsessional
bands regardless of whether the proband has OCD. The symptoms arise from intrapsychic anxiety because of the
rate of OCD alone is higher in female relatives and the conflicts being expressed by the defence mechanisms of
rate of Tourette’s and tics is higher in male relatives of displacement, undoing, and reaction formation. The ori-
a Tourette patient’s proband. These findings suggest that gin of obsessional personality is located at the anal-train-
some forms of OCD are familial. ing stage of development; OCD is thought to represent
Probands with no relatives affected by OCD may rep- regression to this stage.
resent a sporadic form of OCD that is aetiologically dis- Neuropsychological tests suggest the presence of
tinct from the familial form. amnestic deficits with respect to nonverbal memory and
memory for actions. OCD patients also perform poorly
28.7.2.2 Neuroimaging on tests of frontal lobe function, particularly tests of
Diffusion-tensor imaging shows decreased cortico- shifting set.
striato-thalamo-striato-cortical circuitry.
Functional MRI shows increased orbitofrontal cortex,
anterior cingulate cortex, and striatum. 28.7.3 Diagnostic Criteria
28.7.3.1 ICD-10 (F42) (WHO, 1992)
28.7.2.3 Neurological Factors
Obsessional symptoms or compulsive acts are present
The reported numbers of OCD cases increased following
most days for at least two successive weeks causing dis-
the 1915 and 1926 outbreaks of encephalitis lethargica
tress or interfering with activities. Obsessional symptoms
(Foley, 2009).
have the following characteristics:
OCD patients have more abnormal births than
expected and more neurological disorders including
• The minimum duration is at least 2 weeks.
Sydenham’s chorea and encephalitis, suggestive of basal
• Recognized as the individual’s own.
ganglia dysfunction. Childhood streptococcus infec-
• At least one thought or act is resisted
tion leads to Paediatric Autoimmune Neuropsychiatric
unsuccessfully.
Disorders Associated with Streptococcus (PANDAS)
• The thought of carrying out the act must not in
that is associated with childhood-onset OCD. Flor-Henry
itself be pleasurable.
observed neuropsychological deficits implicating left
• Thoughts, images, or impulses are unpleasantly
frontal lobe dysfunction.
repetitive.
Brain-imaging techniques show morphological
• Interference with functioning by waste of time.
changes of basal ganglia structures in OCD. Frontostriatal
• F42.0 predominantly obsessional thoughts or
abnormality is present. Functional neuroimaging stud-
ruminations.
ies show increased blood flow in the basal ganglia and
• F42.1 predominantly compulsive acts.
orbital, prefrontal, and anterior cingulate cortex. Caudate
metabolic rate is reduced after treatment with drugs or
behaviour therapy in those patients responsive to treat- 28.7.3.2 DSM-5 (APA, 2013)
ment, with the percentage change in symptom ratings 28.7.3.2.1 300.3 OCD
correlating significantly with right caudate change. Obsessions are defined by
28.7.2.4 Psychological Factors 1. Recurrent and intrusive thoughts, urges, or

In learning theory, obsessions are thoughts with which images causing marked anxiety or distress
anxiety has become associated. Rituals or neutralizing 2. Attempts to suppress such thoughts, urges, or
thoughts terminate exposure to the stimulus; thus, anxiety images, or to neutralize them with compulsion.
28.7.4.2 Psychological Treatments

TABLE 28.3 NICE guidelines: Evoked response prevention (ERP) and
The Most Common Obsessions and CBT for OCD and body dysmorphic disorder (BDD)
Compulsions
The Most Common 1. For initial treatment of OCD, ERP (up to 10
The Most Common Obsessions Compulsions (in therapist hours per client), brief individual CBT
(in Descending Order) Descending Order) using self-help materials and by telephone, and
1. Fear of contamination (45%) 1. Checking (63%) group CBT should be offered.
2. Doubting (42%) 2. Washing (50%) 2. For adults with OCD with mild to moderate
3. Fear of illness, germs, or bodily fear 3. Counting (36%) functional impairment, more intensive CBT
(36%) (including ERP) (more than 10 therapist hours
4. Symmetry (31%) per client) is recommended.
5. Sexual or aggressive thoughts (28%) 3. For children and young people with OCD
with moderate to severe functional impair-
ment, CBT (including ERP) is the first-line
treatment.
Compulsions are defined by
28.7.4.3 Physical Treatments
1. Repetitive behaviours (e.g. hand washing, order- Psychosurgery may be indicated in the chronic unremit-
ing, checking) or mental acts (e.g. praying, ting OCD of at least 2 years’ duration with severe life dis-
counting, repeating words silently) in response ruption, unresponsive to all recognized forms of therapy.
to an obsession. Open, uncontrolled studies show that 65% of patients
2. The behaviours or mental acts are aimed at pre- with OCD are improved or greatly improved with cingu-
venting or reducing anxiety or distress. lotomy plus bifrontal operations. Deep brain stimulation
at the anterior limb of internal capsule may be an option
Obsessions or compulsions are time-consuming (Table 28.3). for treatment-resistant OCD.
Specifier: Good or fair insight, poor insight, and absent
insight 28.7.5 Course
Favourable prognostic factors include
28.7.4 Management of OCD
• Mild symptoms
28.7.4.1 Pharmacotherapy • Predominance of phobic ruminative ideas,
Antidepressants are effective in the short-term treat- absence of compulsions
ment of OCD. SSRIs such as fluvoxamine, fluox- • Short duration of symptoms
etine, paroxetine, and sertraline are commonly used. • No childhood symptoms or abnormal personal-
Clomipramine and SSRIs have greater efficacy than ity traits
antidepressants with no selective serotonergic proper-
ties. Concomitant depression is not necessary for sero- Poor prognostic factors include
tonergic antidepressants to improve symptoms. There
are success rates of 50%–79%. Relapse often follows • Males with early onset
discontinuation of treatment. • Symptoms involving the need for symmetry and
For treatment-resistant OCD, there is some evi- exactness
dence that adding quetiapine or risperidone to anti- • The presence of hopelessness, hallucinations, or
depressants increases efficacy, but this must be delusions
weighed against less tolerability and limited data • A family history of OCD
(Komossa et al., 2010). • A continuous, episodic, or deteriorating course
CASC STATION ON OCD

Station 1
A 26-year-old housewife is referred by her GP for psychiatric assessment. She complains of distressing obses-
sional ruminations that she may harm her 3-year-old son. According to her GP, she is evasive about the nature
of harm and becomes tearful when asked about it. She expresses shame at her thoughts. She also has grossly
time-consuming cleaning rituals in the morning after her husband has gone to work. These are associated
with thoughts about the possibility of contamination of herself or her family with the H1N1 influenza viruses.
Her illness began following the death of her father who died of colon cancer when she was 16 years old.
Subsequently, her mother died of breast cancer when she was 20. She has been married to her husband for
5 years. She had tried very hard to conceal her worries from her husband until 2 weeks ago when she could
not tolerate him coming back without taking a bath and they ended up in a quarrel. She saw the GP at her
husband’s insistence and she has never consulted a doctor for her problems. Furthermore, her GP reports that
she seems to be depressed.
Task: Take a history to establish the diagnosis of OCD.

You will speak to her husband in the next station.
CASC Grid
(A) Assess (A2) Elicit the

Obsessions and (A1) Explore the Recurrent and (A3) Explore (A4) Elicit the (A5) Explore Other
Compulsions Origin of Thoughts Unpleasant Nature Other Obsessions Unpleasant Nature Compulsions
‘I am sorry to hear ‘Do you feel that those ‘Are you concerned ‘How do you feel ‘Do you check
that you are very thoughts are about putting about your time things very often?’
concerned about the repetitive, unpleasant, things in a special consuming cleaning ‘Do you perform a
H1N1 infection’. excessive and order? Are you rituals?’ regular ritual or
‘Do those thoughts unreasonable?’ very upset by ‘Do you feel that your ceremony to
about ‘What do you think mess?’ rituals are prevent something
contamination come the chance of getting ‘Do you have unpleasurable?’ bad from
from your mind? H1N1? Have you images or doubts happening?’
Are those thoughts overestimated the keep coming to Explore other
imposed by outside risk? Do you know your mind?’ compulsive
persons or anyone who has ‘Do you like to behaviours such as
influences?’ contracted the repeat things in a checking, counting,
disease? What particular number and hoarding.
precaution have you of time? Is this
taken so far? What number bringing
did you worry prior you good luck?’
to the emergence of
H1N1?’
‘Are those thoughts
keep bothering you
that you’d like to get
rid of but can’t?’
(continued)
(B) Assess Risk, (B1) Risk

Precipitants, and Assessment to (B2) Assess Risk to (B4) Parenting (B5) Impact of Her
Impact Her Son Herself (B3) Precipitants Ability Illness
Inquire her thought of ‘How about harming Explore recent life Ask her to take you ‘Do you take a long
harming her son in an yourself?’ events that may through how she time to finish your
empathetic manner. ‘Do you feel that life lead to looks after her son daily activities?’
‘I am sorry to hear is not worth exacerbation of on a typical day. Explore the cost
that you have gone living?’ OCD symptoms. Explore the impact of incurred by her
through tremendous compulsions on her illness, e.g. high
stress. Have you parenting ability. water bills, loss of
ever thought of ‘Is there other person occupational
harming your son? helping her?’ function due to her
Can you tell me obsessional
more about this?’ slowness.
(C2) Establish the
(C) Explore Temporal (C3) Exclude
Comorbidity and (C1) Assess Relationship Between Postpartum (C5) Other
Differential Depressive OCD and Depressive Psychiatric (C4) Assess Psychiatric or
Diagnosis Symptoms Disorder Illnesses Personality Medical Conditions
Explore her current If depression is ‘Did you suffer from ‘Are you a ‘Did you have tics
mood, cognitive, and present, ask the a period of low perfectionistic before?’
biological symptoms patient ‘Does the mood after person?’ ‘Did you have any
related to depression. low mood start delivery? How ‘Are you preoccupied head injury
Pay attention to before or after your about low mood with details?’ before?’
psychotic symptoms recurrent thoughts and confusion? Did ‘Are you rigid with
such as nihilistic, of contamination?’ you hear voices rules?’
guilt-ridden asking you to harm ‘Are you a careful and
delusions and your baby? Did you thrifty person?’
mood-congruent follow the
hallucinations. command?’
(D1) Explore the
(D) Salient Meaning of ‘Never (D2) Explore (D4) Developmental (D5) Assess Her
Features of Consulted a Doctor Concealment of (D3) Assess Her Issues and Family Insight and
this Case for Her Problems’ Her Symptoms Current Marriage History Expectations
‘Would you mind to ‘May I know why ‘Is your husband Brief assessment of ‘Do you think that
tell me why you have you tried to hide supportive and developmental crises, you have a
not seen a doctor for your illness from understanding?’ e.g. separation, psychiatric illness?
your problems? Are your husband in the ‘Does he offer break-up of a If not, what are
you worried that the beginning?’ assistance when relationship, and death your views and
doctor may not ‘Is it because of your you fall sick?’ of parents. explanations?’
understand your fear of losing your ‘How is the ‘How did you cope ‘Have you read any
problem?’ husband?’ communication at with multiple losses?’ information about
‘Did you seek help ‘Are you ashamed of home? Is the ‘Are those losses and OCD?’
from other sources having psychiatric communication your fear of ‘What is your
such as self-help symptoms? How open and honest?’ contamination expectation on
book?’ about potential related?’ treatment?’
‘Why did you stigma?’ ‘Do your family ‘What type of
consult the GP this members also exhibit treatment would you
time? Were you similar concerns of prefer?’ (e.g.
prompted by your contamination and medication,
husband?’ cleaning behaviour?’ psychotherapy, or
both).
Station 2
You have performed a detailed psychiatric assessment on the patient and concluded that she suffers from severe
OCD with secondary depression and significant functional impairment. She has tried reading self-help book but
it does not work. She has been bathing her son excessively, and as a consequence, she suffers from dermatologi-
cal problems. She has history of tics. The marital relationship is poor and the couple has thought of divorce. The
patient is keen to receive treatment. You have obtained permission from the patient to speak to her husband.
Task: Discuss your approach to management.
Explain management of OCD based on the recommen- 4. Investigations: Further laboratory investiga-
dations from the NICE guidelines: tions, psychological testing, or brain imaging
may be necessary if the psychiatrist needs fur-
1. This is a potentially complex case: The fact ther information to rule out certain differential
that this is the first time the patient presents her diagnoses. You will administer a scale such
problems to her GP may indicate a poor progno- as Yale–Brown Obsessive–Compulsive Scale
sis. Other indicators of poor prognosis include a (Y-BOCS) to assess the baseline severity of her
strong conviction about rationality of her obses- OCD symptoms.
sion, prominent depression, and comorbid tic 5. Use of antidepressants (SSRI): This patient
disorder. The candidate needs to be honest to has severe OCD symptoms. She should be
her husband but provides hope that her symp- offered combined treatment with SSRI and
toms may improve with treatment. CBT, including ERP. The candidate should
2. Provide accurate information on OCD: emphasize the common pharmacodynamic
profiles of antidepressant on depression and
I am sorry to inform you that your wife suffers from OCD. The dose to treat OCD is two to three
a condition called obsessive compulsive disorder times higher than the dose for antidepressants
or OCD. Have you heard about it? Can I tell you (e.g. fluoxetine 40–80 mg or fluvoxamine 150–
more about her condition? OCD is characterized by 300 mg). There may be a delay up to 12 weeks
the presence of either obsessions or compulsions, in the onset of actions. Inform the husband
but commonly both. Symptoms can cause signifi- about the potential side effects such as worsen-
cant distress. An obsession is an unwanted intrusive
ing anxiety and nausea that will be monitored
thought, image, or urge that repeatedly enters the
person’s mind. Compulsions are repetitive behav- closely in the first few weeks of treatment. Her
iours or mental acts that the person feels driven to response will be reviewed at 12 weeks. If the
perform. These can be observable by others, such as SSRI is effective, the patient is advised to con-
her cleaning behaviour, or a mental act that cannot tinue the medication for at least 12 months to
be observed, such as her worries of getting H1N1 in prevent relapse. If her response is very poor or
her mind. It is thought that 1 in 100 of the popula- inadequate, you will offer a different SSRI or
tion have OCD. suggest clomipramine. Please note that the fol-
lowing drugs are not normally recommended
The candidate should address any concern for OCD: other TCAs, SNRIs, MAOIs, and
raised by her husband to allay his fears and to long-term anxiolytics.
assist him in adjusting to his wife’s diagnosis. 6. Use of clomipramine and management of
3. Inpatient service: Hospitalization is indicated if treatment-resistant OCD: Clomipramine can
(1) the patient poses a severe risk to her son and be used when (1) there is an adequate trial of
herself; (2) severe self-neglect; (3) extreme dis- at least one SSRI that is found to be ineffec-
tress or functional impairment; (4) complicated tive, (2) an SSRI is poorly tolerated, (3) the
comorbidity such as OCD with severe depres- patient prefers clomipramine, and (4) there
sion, anorexia nervosa, and psychosis; (5) severe has been a previous good response to clomip-
reversal of day and night patterns; or (6) very ramine. The candidate needs to carry out an
severe avoidance behaviour. ECG and a blood pressure measurement before
prescribing clomipramine. Clomipramine is a to see both patient and her husband together and
TCA (derivative of imipramine). The candidate the advantage of a joint interview is to inform and
should prescribe a small amount of tablets to educate the couple more about OCD and its man-
prevent toxicity in overdose. If the standard agement. This can only be done at the patient’s
daily dose (100–225 mg) is inadequate for agreement and there may be issues that the patient
the patient and there are no significant side does not want to be discussed. If the couple is agree-
effects, consider a gradual dose increase in able, couple therapy will involve role-playing and
line with prescription information provided coaching once her OCD symptoms have improved.
by the manufacturers. If it is still ineffective, 10. Continuity of care: ‘Many OCD patients will
clomipramine can be augmented with citalo- need ongoing follow-up over years and your
pram or adding an antipsychotic to clomip- wife is not an exception. The follow-up will
ramine or SSRI. Continue clomipramine for at enable monitoring of treatment response, side-
least 12 months if it appears to be effective and effects, and achievement of rehabilitative and
reduce the dose gradually to prevent withdraw- social reintegration goals’.
als prior to discontinuation.
7. Psychotherapy: The patient has severe func-
tional impairment, and self-help method has 28.8 OCD-SPECTRUM DISORDERS
been ineffective. She should be offered CBT 28.8.1 Body Dysmorphic Disorder
(including ERP) that also involves her hus-
band as a co-therapist. If the patient refuses 28.8.1.1 Historical Development
to come to the clinic, you will offer home- The old term for this condition is dysmorphophobia,
based treatment. If her symptoms prevent which is coined by Morselli in 1886 (Morselli, 1891).
home-based treatment, you will offer CBT by
telephone. Briefly explain to her husband that 28.8.1.2 Epidemiology (Conrado, 2009)
CBT will begin with anxiety management and 1. The prevalence of this disorder among the gen-
asking the patient to keep a diary. Then it will eral population ranges from 1% to 2%.
move onto response prevention in excessive 2. In dermatological and cosmetic surgery patients,
washing with cognitive coping and composure the prevalence is from 2.9% to 16%.
strategies. Social and occupational rehabilita-
tion will include training on housekeeping, 28.8.1.3 Aetiology
childcare, and promotion on independent 1. Genetics: family history of BDD, OCD, and
living. The psychologist will focus on her mood disorder.
residual depressive symptoms once her OCD 2. Neurochemistry: low serotonin levels.
symptoms have improved. For mild OCD, the 3. Psychodynamic theory: displacement of conflict
NICE guidelines recommend CBT to be given onto body component.
for less than 10 therapist hours. For moderate 4. Development: rejection in childhood as a
CBT, a course of an SSRI alone or more inten- result of body image problem, disharmony in
sive CBT alone (ERP and CBT for longer than family.
10 therapist hours) is recommended. 5. Culture influence: beauty equals to perfect
8. Assess social issues: Seek her husband’s view on body.
the home situation and how this may affect her
compliance to treatment. Explore from him the
ongoing difficulties in forming relationships and 28.8.1.4 Clinical Features
the future difficulties in providing care to her DSM-5 criteria (APA, 2013):
son given the nature of her OCD symptoms.
9. Improving marital relationship: Inform her hus- • Preoccupation with perceived defects or flaws in
band that the patient needs encouragement and physical appearance that are not observable to
assistance on her way to recovery. You may offer others.
• The person performs repetitive behaviours or

mental acts (e.g. comparing their appearance TABLE 28.4
with that of others) in response to the appear- Differences and Similarities between OCD
ance concerns. and BDD
• Specifiers include muscle dysmorphia, good
Differences Similarities
or fair insight, poor insight, and absent
Patients with OCD are
insight.
1. Less likely to suffer from 1. Gender ratio (M/F = 1:1)
social phobia 2. Both conditions show
2. Less likely to attempt obsessions and compulsions
Common behavioural problems: suicide 3. SSRI is the main treatment
3. Less likely to be involved 4. Both conditions cause
• Self-harm: 70%–80% in substance abuse significant distress
• Social avoidance: 30% 4. Having better insight
• Suicide: 20% 5. Have better relationship
Rituals:
• Camouflage: 90% 1. Social phobia: 38%
• Minor check: 90% 2. Substance: 36%
• Compulsion: 90% 3. Suicide: 30%
• Skin pick: 30% 4. OCD: 30%
5. Depression: 20%
Most common body sites concerned:
28.8.1.7 Management
• Hair: 63%
1. Antidepressants: SSRIs; 50% of patients respond
• Nose: 50%
to SSRIs.
• Skin: 50%
2. Antipsychotics: if patient does not respond to
• Eye: 30%
SSRIs, the psychiatrist can augment with sec-
• Face: 20%
ond-generation antipsychotics.
• Breast: <10%
3. Other pharmacological agents: clomipramine,
• Neck, forehead, and facial muscle: <5%
buspirone, and lithium.
4. For people with BDD with moderate functional
impairment, more intensive CBT (including
28.8.1.5 Differential Diagnosis ERP) is recommended based on the NICE
OCD (Table 28.4) guidelines.
CASC STATION ON BDD

A 23-year-old woman is referred by her GP. She is single and works as a disc jockey at a local radio station.
She has been worried that her nose is too large and crooked since the age of 14. She has become increasingly
worried about her nose.
Task: Take a history to establish the diagnosis of BDD.
(continued)
CASC Grid
(A) Inquire More (A2) Repeated

About Her Checking and
Concerns About the (A1) Onset and Reassurance (A3) Course of (A4) Impact of Her (A5) Explore
Nose Extent of the Problem Seeking the Illness Illness Coping Strategy
‘When did you start to ‘Are you very ‘Is there any ‘Is there any ‘How did you
become unhappy worried about fluctuation in the change in smell? Do cope in the past 10
with how you look? your appearance? intensity of your you think the defect years? Can you
If yes: what is your Do you need to concern? Is there affects the function distract yourself
concern?’ look into the time when you of your nose?’ from the nose
‘Does this concern mirror very often?’ are less ‘Why did you choose issue?’
preoccupy you? How ‘Do you do other preoccupied this job? Are you ‘Do you share your
much time do you things to monitor with your nose?’ comfortable with concerns with
spend thinking about your nose? e.g. ‘Is your concern your job your friends and
your nose?’ repeated about your nose arrangement?’ family? What do
‘Were you under measurements of is related to your ‘Does your nose they say about
scrutiny or being its size’. stress level?’ affect your social your nose?’
bullied as a result ‘Have you tried to life?’
your nose problems?’ hide your defect?’ ‘Were you rejected
‘Was there any injury ‘Do you pick at in a romantic
to your nose causing your nose or relationship
deformation?’ skin?’ because of your
nose?’
(B3) Assess
(B) Explore BDD (B1) Other Parts of (B2) Gentle Psychosis and (B5) Substance
and Comorbidity the Body Challenge Mood (B4) Assess Anxiety Abuse
‘Do you worry about ‘I am very sorry to ‘Do you have Look for generalized ‘Do you turn into
the following areas hear your worries. other unusual anxiety symptoms, alcohol or
such as your skin, hair, So far, I cannot experiences such panic attack, social tranquillizer to
body weight, breast, find any major as hearing voices phobia, and reduce your stress
eyes, teeth, legs and defect in your or seeing things agoraphobia. associated with
your face in general?’ nose. I have seen or strange Look for other your concern
If she is concerned patients who are feelings?’ compulsive about your nose?’
about her body also very ‘Can you tell me behaviours such as ‘Do you take
weight, explore concerned about a more about your repetitive checking medication to
anorexic behaviour single part of their mood? Do you and excessive reduce the size of
such as restricting bodies. Do you feel sad at this washing. the nose?’
dieting, excessive think you are over moment?’
exercise, and purging. concerned?’
(C) Past Cosmetic
Treatment and (C1) Previous (C2) Previous (C3) Financial (C4) Risk to Her (C5) Suicide and
Risk Assessment Investigations Treatment Problems Nose Self-harm
‘Did you seek medical ‘Did you go for ‘How much ‘If the doctors say ‘It seems that you
help for the nose cosmetic surgery?’ money have you that they cannot are desperate to
problems? Have you ‘If yes, for how spent on fixing offer further get your nose
seen a plastic many times?’ your nose?’ treatment to your fixed. Do you feel
surgeon? If yes, how ‘What was the ‘Do you need to nose, what would hopeless?’
many surgeons have outcome?’ borrow money you do next?’
you seen’ for treatment?’
‘What kind of ‘What is your ‘Do you plan to ‘Do you have plan to ‘Do you have
investigations did current plan for go aboard for perform the thought of
you go through?’ the nose problem?’ further operation on your harming yourself?
‘Did you consult treatment? If own?’ Have you thought
traditional healers or yes, which of ending your
alternative therapy?’ countries?’ life?’
(D) Background
History and (D2) Personality (D5) Explain
Explain (D1) Childhood and Family (D3) Past (D4) Past Diagnosis and
Diagnosis History Background Medical History Psychiatric History Seeks Her Views
Look for bullying in ‘How do you Look for chronic ‘Did you see a on treatment
school and home describe yourself medical psychologist or Emphasize that this
environment. as a person? Are problems or psychiatrist before? disorder is an
Assess temperament: you metabolic If yes, what was the excessive
‘Were you a shy perfectionistic?’ syndrome that reason?’ preoccupation
child?’ ‘How was your affects her body with an imagined
‘Did you have relationship with image. defect in
confident in your parents?’ appearance that
yourself?’ ‘Did they criticize results in
your nose before?’ time-consuming
checking.
Seek her views on
treatment issues
such as SSRI or
CBT.
28.9 HOARDING 2. 84% of hoarders reported a family history of

hoarding behaviour in first-degree relatives.
28.9.1 Historical Development 3. 37% of hoarders reported a family history of
Diogenes syndrome refers to hoarding behaviour in old OCD (Winsberg et al., 1999).
people.
28.9.1.2.2 Functional Imaging
28.9.1.1 Epidemiology (Saxena et al., 1. People with OCD and hoarding behaviour did
2004; Samuels, 2007) not have the characteristic hypermetabolism
1. Hoarding is most commonly found in people in the orbitofrontal cortex, caudate nuclei, and
with OCD. thalamus.
2. 18%–42% of people with OCD report hoarding 2. People with OCD and hoarding behaviour
and saving compulsions. showed significantly lower activity in the dorsal
3. 10%–15% of people with OCD have compulsive anterior cingulate gyrus and occipital cortex.
hoarding as their most prominent symptom. 3. Diminished activity in the cingulate cortex is
associated with poor treatment response and
28.9.1.2 Aetiology (Gaston et al., 2009) compulsive hoarding behaviour.
28.9.1.2.1 Genetics
1. The hoarding symptom shows an autosomal 28.9.1.2.3 Cognitive Theory
recessive inheritance pattern and has been asso- 1. Cognitive appraisals about possessions, trigger-
ciated with genetic markers on chromosomes 4, ing emotional responses that lead to hoarding
5, and 17 (Zhang, 2002). behaviours.
2. Hoarding behaviour is maintained through rein- 28.10 TREATMENT

forcements related to indecisiveness, concerns
over mistakes, judgements about need, and emo- 28.10.1 Psychological Treatment
tional attachment to possessions. 28.10.1.1 Cognitive Behaviour Therapy
3. Positive reinforcement is related to the pleasure (Saxena et al., 2004)
gained from acquiring and saving.
1. Introduce alternative behaviours.
4. Negative reinforcement involves avoidance of
2. Get the client organized.
grief, anxiety, and guilt.
3. Prevent incoming clutter.
28.9.1.3 Clinical Features 4. Encourage discarding of objects.
ICD-10 does not mention about this disorder.
DSM-5 criteria (300.3) (APA 2013): 28.10.2 Pharmacological Treatment
1. Persistent difficulty discarding or parting with 1. SSRI
possessions, regardless of their actual value. 2. SNRI: venlafaxine
2. This difficulty is caused by a perceived need to 3. Acetylcholinesterase inhibitors: donepezil or
save the items and distress associated with dis- galantamine
carding them.
3. The symptoms result in the accumulation of 28.10.3 Trichotillomania
possessions that congest and clutter active liv-
28.10.3.1 ICD-10 Criteria
ing areas and substantially compromise their
intended use. 1. Trichotillomania is an impulse-control disorder.
4. Specifiers include excessive acquisition, good or 2. There is persistent and recurrent failure to resist
fair insight, poor insight, and absent insight. the impulse to pull out one’s hair, resulting in
noticeable hair loss.
There are two types of hoarding: 3. The individual describes an intense urge to pull
out hair, with mounting tension before the act
1. Compulsive buying and subsequent relief.
2. Acquiring free and discarded items 4. There is no preexisting inflammation of the skin
and the hair pulling is not in response to any
28.9.1.4 Questionnaires psychotic feature.
1. The Hoarding Scale (Frost, 1993) is a 21-item
questionnaire designed to measure various 28.10.3.2 DSM-5 Criteria (312.39) (APA 2013)
aspects of hoarding behaviour. 1. Recurrent pulling out of one’s hair resulting in
2. The Clutter Image Rating Scale (Tolin, 2007) is hair loss
a pictorial scale that contains nine photographs 2. Repeated attempts to decrease or stop hair pulling
of severity of clutter representing each of three
main rooms of most people’s homes.
28.10.4 Skin Picking Disorder
28.9.1.5 Differential Diagnosis DSM-5 criteria (698.4) (APA 2013) include
Normal hoarding: The items collected are usually orga-
nized, interesting, and valuable (Melamed, 1998). 1. Recurrent skin picking resulting in skin lesions
2. Repeated attempts to decrease or stop skin picking
28.9.1.6 Psychiatric Comorbidity
1. Schizophrenia
28.11 ACUTE STRESS REACTION
2. Learning disability
3. Neurodegenerative disorders (in particular fron- This is a transient disorder developing in an individual
tal lobe dysfunction) without other mental disorder in response to excep-
4. Autism-spectrum disorders tional stress. It usually subsides within hours or days.
5. Eating disorders The risk is increased if physical exhaustion or organic
6. Impulse-control disorders factors are present.
28.11.1 ICD-10 (WHO, 1992) 28.12.1.2 Biological Factors

• There is an immediate temporal connection People with PTSD have exaggerated physiological
between the impact of an exceptional stressor responses (heart rate, skin conductance, electromyographic
and onset of symptoms, which is within minutes. response) to traumatic imagery. They have a heightened
• In addition, symptoms physiological state specific to PTSD that is difficult to sim-
• Show a mixed and changing picture—ini- ulate. This may be mediated by noradrenergic and dopami-
tial state of daze, depression, anxiety, anger, nergic neurotransmitter systems and the HPA axis. PTSD
despair, overactivity, and withdrawal may all patients have low cortisol levels after trauma. There is an
be seen, with no one symptom predominat- increase in glucocorticoid receptors in the hypothalamus
ing for long. and a reduction in peripheral cortisol (Saddock, 2003).
• Resolve rapidly, within a few hours if removal Initial mobilization and the subsequent depletion of
from the stressful environment is possible. NA following inescapable shock in animals indicate a
If stress continues, symptoms diminish after possible catecholaminergic mediation of PTSD symp-
24–48 h. toms. Drugs effective in PTSD (MAOIs, tricyclics,
• Acute stress reaction is classified as mild, mod- benzodiazepines, and clonidine) are also effective in pre-
erate, or severe. venting the development of learned helplessness in ani-
mals when infused into the locus coeruleus.
28.11.2 DSM-5 (308.3) There are similarities between PTSD symptoms and opi-
oid withdrawal, leading to speculation that opioid function is
• The duration is between 3 days and 1 month. disturbed in PTSD. Stress-induced analgesia is reversible by
• Exposure to actual or threatened death, serious naloxone in PTSD veterans exposed to traumatic stimulus.
injury, and sexual violation.
• Intrusion symptoms: recurrent distressing dreams, 28.12.1.3 Psychosocial Factors (Koenen
dissociative reactions, and prolonged stress. and Widom, 2009)
• Dissociative symptoms: inability to experience 1. Gender: female gender
positive emotions, altered sense of reality, and 2. Intelligence: low intelligence quotient (IQ) at age 5
inability to remember. 3. Previous trauma history
• Avoidance of distressing memories and external 4. Previous psychiatric history: hyperactivity, anti-
reminders. social behaviour
• Arousal symptoms including sleep disturbance, 5. Severity of trauma
irritability, hypervigilance, problems with con- 6. Perceived life threat
centration, and exaggerated startle response. 7. Peri-traumatic dissociation
8. Impaired social support
28.11.3 Management
9. Low socioeconomic status
Pharmacological treatment
28.12.2 Diagnostic Criteria
1. Beta blockers (e.g. propranolol).
2. α2-Receptor antagonist clonidine reduces night- 28.12.2.1 ICD-10 (F43.1) (WHO, 1992)
mares and emotional reactivity. • PTSD arises within 6 months as a delayed and/
or protracted response to a stressful event of an
28.12 PTSD exceptionally threatening nature.
28.12.1 Aetiology of PTSD • Symptoms include repeated reliving of the
trauma. Repetitive, intrusive memories (flash-
28.12.1.1 General Factors backs), daytime imagery, or dreams of the event
About 25% of people exposed to a potentially traumatic event must be present.
develop PTSD. Low education and social class, preexisting • Emotional detachment, persisting background
psychiatric problems, and female gender are vulnerability numbness, and avoidance of stimuli reminiscent of
factors. Viewing the dead body of a relative after a disaster is original event are often present, but are not essential.
predictive of lower PTSD. Psychopathic traits are protective. • Autonomic disturbances (hyperarousal with hyper-
Sufferers of PTSD report childhood physical sexual vigilance, enhanced startle reaction, and insomnia)
abuse more often than expected. and mood disorder contribute to the diagnosis but
are not essential. Anxiety, depression, and suicidal The NICE guidelines recommend that
ideation are not uncommon. The excessive use of
alcohol or drugs may complicate matters. 1. Trauma-focused CBT (tf-CBT) should be
offered to people with severe PTSD within
28.12.2.2 DSM-5 (309.81) 3 months of the trauma with fewer sessions in
• Exposure to actual or threatened death, serious the first month after the trauma.
injury, and sexual violation. 2. The duration of tf-CBT is 8–12 sessions with
• Intrusion symptoms: recurrent distressing dreams, 1 session per week. When trauma is discussed
dissociative reactions, and prolonged stress. in the session, it requires a longer session
• Avoidance of distressing memories and external (90 min).
reminders.
• Negative alternations in cognitions and mood
associated with traumatic events. Fluoxetine, paroxetine, sertraline, venlafaxine, and esci-
• Arousal symptoms including sleep disturbance, talopram are beneficial in PTSD. The drugs require at
irritability, hypervigilance, problems with con- least 8 weeks’ duration before the effects are evident.
centration, and exaggerated startle response. Carbamazepine, propranolol, and clonidine reduce
• Duration of disturbance is longer than 1 month. hyperarousal and intrusive symptoms; fluoxetine and lithium
• Subtypes include delayed expression, PTSD in reduce explosiveness and improve mood. Buspirone may
preschool children, and predominant dissocia- lessen fear-induced startle; it may play an adjunctive role.
tive symptoms. Alprazolam is no more effective than placebo, but
there have been some positive reports with clonazepam.
There is an almost total lack of response to placebo in
chronic PTSD.
28.12.3 Management of PTSD
A flexible, staged approach using several techniques is 28.12.3.3 Eye Movement Desensitization
advocated. Reprocessing
Involuntary multi-saccadic eye movements occur during
disturbing thoughts. It is claimed that inducing these eye
28.12.3.1 Psychological Therapy movements while experiencing intrusive thoughts stops
28.12.3.1.1 Cognitive Behavioural Therapy symptoms of PTSD. More information on eye move-
Cognitive techniques include challenging underlying ment desensitization reprocessing (EMDR) are found in
automatic thought that accidents or disasters will occur Chapter 25.
again and cognitive distortions. Cognitive restructuring,
distraction thought replacement, and thought stopping
28.12.4 Course
are useful. Assessment should include behaviour analy-
sis through diary keeping. Psychoeducation should offer Half of patients still have PTSD decades later. A dose–
explanation of PTSD symptoms. Behavioural tech- response relationship exists between the severity of the
niques include relaxation training, in vivo and in vitro stressor and the degree of consequent psychological
exposure, and desensitization to disaster or accident distress.
scenes, rehearsal, as well as assertiveness and social Most PTSD patients also have depression, anxiety dis-
skill training. orders, substance abuse, and/or sexual dysfunction.
CASC STATION ON PTSD

Station 1
A 33-year-old British army officer (Engineer Regiment) suffered a number of traumatic combat experiences in
Afghanistan. Six months ago, he was very seriously wounded by an explosive device during an operation. He lost the
eyesight of his left eye and hearing ability of his left ear. He was first treated at the deployed hospital facilities and
later sent back to the United Kingdom. Currently, he cannot work and he is disturbed by recurrent nightmares and
vivid intrusive recollections of his traumatic experiences. He avoids the news and TV programmes that remind him of
Afghanistan and he has abused alcohol since his return. He has been married for 2 years. He presents in the company
of his wife seeking treatment following his first episode of domestic violence that occurred in the setting of alcohol
intoxication and argument.
Task: Take a history to establish the diagnosis of PTSD.
You will speak to his wife in the next station.
CASC Grid
Approach to the patient: Candidates are advised to consult the patient on the volume of your voice as he has
hearing impairment.
(A) Explore (A1) Describe the (A2) Immediate (A3) E xtent of (A4) O
utcome of (A5) Psychodynamic
His Incident in Outcome of Injury and Other Soldiers in Issues
Trauma Afghanistan the Incident Suffering the Operation Associated with
the Incident
Explore his role ‘How long did Especially head ‘Were the fellow soldiers ‘I am sorry to hear
during the you wait for the injury and any killed or injured? If yes, that you cannot
operation. rescue to come?’ organic sequelae how many were see and hear well
‘Were you the ‘How did you feel such as intracerebral involved? What was nowadays. How
commander after the haemorrhage, loss your relationship with do you feel about
during the accident?’ of consciousness, them?’ it?’
operation? Were Look for the and epilepsy ‘How did you know ‘Was it the first
you assigned the symptoms of Explore other about their death?’ time you faced
duty to detect the acute stress disabling or ‘Was there any your own
bomb and ensure reactions on the disfiguring injuries. debriefing? If yes, what mortality?’
the safety of first few days ‘Did you suffer from is your view on the ‘Do you feel
others?’ after the incident. any chronic pain debriefing? Did you remorseful of
‘What was the such as low back join them?’ going to
level of threat to pain or pain related ‘Do you have guilt of Afghanistan?’
your life during to other sites of staying alive or guilt
the bomb blast?’ injury?’ of missing the bomb?’
(B) PTSD (B1) (B2) Avoidance (B3) Hyperarousal (B4) Emotional (B5) Previous
Symptoms Reexperiencing Detachment Trauma and
Personality
Identify the latency ‘How do you ‘Are you always on Look for emotional Explore other
period between spend your the edge?’ withdrawal. traumatic events
the incident and time?’ Look for anxiety ‘Are you able to in Afghanistan.
onset of his Assess the extent symptoms such as describe your ‘Do you feel
PTSD symptoms. and degree of excessive emotion?’ blunted or numb?’
‘How do those avoidance of sweating, Look for dissociative Explore previous
memories relive people, places, palpitation, panic symptoms. ‘Do you trauma (e.g.
themselves? and circumstances attacks, sleep feel that yourself or childhood trauma,
How vivid are (e.g. other army problems, the environment is road traffic
they?’ officers, army irritability, and unreal?’ accident, army
‘How often do you facilities, and poor concentration. operation).
see the images of previously Check exaggerated ‘Was this incident
the incident?’ enjoyed startle response. similar to previous
activities). unresolved
trauma?’
(continued)
‘Do you have ‘Do you have ‘Are you in shock if ‘How did the
nightmare? How difficulty to someone suddenly previous trauma
often do you have recall the details call your name?’ affect your
nightmare? Can leading to the character
you tell me more incident in development?’
about the content Afghanistan?’
of nightmare?’
(C) Risk (C1) Suicide (C2) (C3) Substance (C4) Depression (C5) Other
Assessment Dangerousness Abuse Common
and to Others Comorbidities
Comorbidity
Assess suicidal Assess the level Assess his alcohol Assess his current Look for symptoms
ideation and the and quality of intake before, mood, biological, and of adjustment
level of dangerousness to during, and after the cognitive symptoms of disorder, OCD,
dangerousness if his wife and the deployment. depression. and psychosis.
he has a suicidal others. Explore the type of
plan. ‘Would you alcohol and the
Look for extreme perform amount he drinks
pessimism dangerous act every day.
because he lost when you are Explore the purpose
his occupational angry? If yes, of alcohol usage
ability at this age. what would you (e.g. to reduce the
do?’ anxiety level).
Explore misuse of
benzodiazepines,
analgesics, or
cannabis.
(D) (D1) Vulnerability (D2) Marital (D3) Compensation (D4) Support and (D5) Background
Background to PTSD Relationship and Treatment from History
History and Entitlements the Army
Compensation
Issues
Candidate needs to ‘Can you tell me ‘Have you discussed ‘Did they refer you to ‘Why did you join
explore what more about the with the Ministry of see other specialists the army in the
made him relationship with Defence on the for your visual and first place?’
vulnerable to your wife?’ arrangement of hearing problems?’ ‘How does this
PTSD, ‘Does the compensation and ‘Did they refer you to incident affect
e.g. low education, relationship veterans allowance?’ counselling?’ your original
maladaptive change before, ‘What is your Assess his insight to his intention of being
coping style, during, and after expectation? Are blindness, hearing an army officer?’
personality, low your deployment you satisfied with impairment, and PTSD.
resilience, and to Afghanistan?’ the amount being ‘Do you cooperate with
childhood trauma offered?’ treatment?’
Station 2
After assessment of the patient, it is concluded that he suffers from PTSD with severe depression and anxiety. The onset
of PTSD symptoms was 4 months after the trauma. He is not keen to receive psychiatric help from the army psychiatric
service and prefers to be treated in the civilian setting. The patient is deemed to have high risk for future violence and
suicide as he cannot guarantee safety and he still wants to drink. He has given you the permission to talk to his wife.
Task: Inform his wife about your management plan and address her concerns.
Explain management of PTSD based on the NICE guide- Explore her views on patient’s intention to serve
lines recommendations. the army, his deployment to Afghanistan, and
When symptoms are mild and have been present less the bomb blast incident.
than 4 weeks after the trauma, the NICE guidelines rec- 3. Emergency issues in regard to his high risk
ommend watchful waiting but this is not appropriate for of violence and suicide: You should propose
this patient who has symptoms for 2 months. to admit patient to the hospital for safety rea-
The NICE guidelines classify two intervention sons and for further assessment of his physi-
strategies when symptoms have been present for more cal and psychiatric status. You may advise
than 3 months or less than 3 months after a trauma. further laboratory investigations such as liver
As this patient developed PTSD symptoms 4 months function tests.
after the trauma, the psychotherapy arrangement will 4. Detoxification: You will try to enhance the
follow the recommendations stated on the right side of motivation of the patient to quit alcohol and ini-
Table 28.5: tiate a detoxification programme when he stays
in the hospital.
1. Address the referral process: Explore the dif- 5. During the hospitalization, you may commence
ficulty encountered by his wife to bring the short-term hypnotic medication to reduce his
patient in to see a doctor. anxiety and ease his alcohol withdrawal. After
2. Assess the impact of the violent episode on his stabilization, you will offer the psychological man-
wife: Demonstrate empathy to her sufferings. agement of PTSD. The psychologist can take this
TABLE 28.5
Psychological Treatment for PTSD
Less Than 3 Months after a Trauma More Than 3 Months after a Trauma
Types of psychotherapy Offer trauma-focused psychological treatment, Offer trauma-focused psychological treatment
tf-CBT (tf-CBT). (tf-CBT or EMDR) on an individual outpatient
basis.
Do not routinely offer non-trauma-focused
interventions (such as relaxation or nondirective
therapy) that do not address traumatic memories.
Time frame between the With severe PTSD within 1 month after the event It should be offered regardless of the time elapsed
traumatic event and therapy or who present with PTSD within 3 months of since the trauma.
the event
Length of the session Usually 60 min. When the trauma is discussed, Usually 60 min. When the trauma is discussed,
longer treatment sessions (90 min) are usually longer treatment sessions (90 min) are usually
necessary. necessary.
Duration of therapy Consider offering 8–12 sessions of tf-CBT (or Consider offering 8–12 sessions of tf-CBT
fewer sessions about 5—if the treatment starts psychological treatment when the PTSD results
in the first month after the event). from a single event.
Consider extending trauma-focused psychological
treatment beyond 12 sessions if there are multiple
traumatic events, traumatic bereavement, chronic
disability results from the trauma, significant
comorbid disorders, or social problems.
Frequency of therapy Regular and continuous (usually at least once a Regular and continuous (usually at least once a
week). week).
Therapist requirements Delivered by the same person. Delivered by the same person.
No improvement after Consider the following drug treatment for sleep Consider an alternative form of trauma-focused
psychotherapy disturbance: psychological treatment or pharmacological
1. Hypnotic medication for short-term use treatment in addition to trauma-focused
2. A suitable antidepressant for longer-term use psychological treatment.
opportunity to establish contact and therapeutic 28.13 ADJUSTMENT DISORDERS

alliance to prepare for long-term psychotherapy.
6. Explain psychotherapy: The patient may need States of distress and emotional disturbance arise in the
more than 12 sessions as he experienced mul- period after a stressful life event. Individual predisposi-
tiple traumatic events in Afghanistan. If his tion plays a greater role than in other stress-induced con-
wife requests for other forms of psychological ditions, but this condition would not have arisen without
treatment (e.g. supportive therapy, nondirective a stressor.
therapy, hypnotherapy, psychodynamic, or sys- Manifestations vary. They include depressed mood,
temic psychotherapy), inform her that there is no anxiety, worry, an inability to cope, and some inability
convincing evidence for a clinically important to manage the daily routine. Conduct disorders may be
effect. associated, especially in adolescents. Regressive phe-
7. Drug treatment for PTSD: Candidate should nomena in children are frequently seen.
not offer drugs as routine first-line treatment Onset is within 1 month of the stressor. The duration is
for PTSD patients. The patient may need anti- usually less than 6 months, except for prolonged depres-
depressant as he is severely depressed. You sive reaction.
would recommend paroxetine or mirtazapine. Grief reactions considered abnormal because of their
Antidepressant is used before psychotherapy if form or content are included in this category.
the patient prefers not to engage in a tf-CBT or he
cannot start psychological treatment because of
serious threat of further trauma. Antidepressant 28.13.1 ICD-10 (F43.2) (WHO, 1992)
is indicated for PTSD patients who have gained
The following adjustment disorders are outlined in
little or no benefit from a course of tf-CBT.
ICD-10:
Antidepressant can be used as an adjunct to
tf-CBT. After initiation of the antidepressant,
• Symptoms must occur within 1 month of expo-
monitor potential side effect such as akathisia,
sure to an identifiable psychosocial stressor.
increased anxiety, and suicidal ideation. If the
• F43.2 brief depressive reaction—less than
patient responds to the antidepressant treat-
1 month.
ment, continue the medication for 12 months.
• F43.21 prolonged depressive reaction—less than
Discontinuation of antidepressant would require
2 years.
gradual reduction over a 4-week period.
• F43.22 mixed anxiety and depressive reaction.
8. Addiction service: Candidate should consider
• F43.23 predominant disturbance of emotions
referring the patient to the local addiction ser-
and/or conduct.
vice and encourage him to attend Alcoholics
Anonymous or other appropriate support
groups. It is important to liaise with his GP.
9. Medicolegal aspects: The candidate should
28.13.2 DSM-5 (APA 2013)
offer help (e.g. writing a medical report) to the
patient because he may need to put his case • The development of emotional or behavioural
forward to the Ministry of Defence or other symptoms in response to an identifiable stressor
related bodies for compensation or entitlement occurring within 3 months of the onset of the
application. stressor
10. Couple therapy: Counselling of his wife and/or • Do not represent normal bereavement
couple therapy will be offered after discharge if
both patient and his wife are interested in couple Other subtypes:
therapy.
11. Long-term management: The patient is advised • With depressed mood
to participate in a rehabilitation programme • With anxiety
with the aim to resume or maintain employ- • With mixed anxiety and depressed mood
ment, recreational activities, and social inter- • With disturbance of conduct
action, with the support of the British Veterans • With mixed disturbance of emotions and
Association. conduct
28.14 DISSOCIATIVE (CONVERSION) • There is amnesia for the duration of the

DISORDERS fugue, but self-care and social interaction are
maintained.
28.14.1 ICD-10 (WHO, 1992) • It lasts for hours to days, but recovery is abrupt
and complete.
Dissociative (conversion) disorders are presumed to be
psychogenic in origin. They are associated with traumatic
events, insoluble problems, or disturbed relationships. 28.14.2.3 Dissociative Stupor
The unpleasant affect associated with these conflicts is • The sufferer is stuporose, with no evidence of a
transformed (converted) into symptoms. physical or other psychiatric cause.
Diagnostic guidelines are as follows: • Onset is sudden and stress related.
• The person sits motionless for long periods,
• No evidence of physical disorder that may speech and movement absent. Muscle tone, pos-
explain symptoms ture, breathing, and eye movements indicate that
• Evidence for psychological causation—a clear the individual is neither asleep nor unconscious.
association in time with stressful events
28.14.2.4 Trance and Possession Disorders
28.14.2 Specific Dissociative Conditions • There is a temporary loss of personal identity
and awareness of surroundings.
28.14.2.1 Dissociative Amnesia • Attention and awareness are limited to one or
• Loss of memory of an important event is not due to two aspects of the immediate environment.
organic disorder, fatigue, or ordinary forgetfulness. • There are repeated movements, postures, or
• Partial and selective amnesia is usually centred utterances.
on traumatic events.
• The extent varies from day to day. A persistent This includes only an involuntary or unwanted trance,
core cannot be recalled while awake. occurring outside the culturally accepted situation.
• Perplexity, distress, or calm acceptance may
accompany the amnesia. 28.14.2.5 Dissociative Disorders of
• It begins and ends suddenly, following stress. Movement and Sensation
It rarely lasts more than a couple of days, and
• There is loss of movement or sensations, usually
recurrence is unusual.
cutaneous, with no physical cause.
• It is more common in young adults but rare in
• Symptoms often reflect the person’s concept of
the elderly.
disorder, which may be at variance with physi-
• Recovery is complete.
ological or anatomical principles (e.g. glove and
28.14.2.1.1 DSM-5 (300.12) (APA, 2013) stocking anaesthesia).
• The resulting disability helps the person to
An inability to recall important autobiographical infor-
escape conflict or express dependency or resent-
mation, usually of a traumatic nature, that is inconsistent
ment indirectly.
with normal forgetting and memory function.
• There is calm acceptance (la belle indifférence),
There are two primary forms of dissociative amnesia:
not common and not diagnostic. This is also
seen in normal people facing serious illness.
1. Localized or selective amnesia for a specific event
• Premorbid personality and relationships are
2. Generalized amnesia for personal identity and
often abnormal.
life history
28.14.2.2 Dissociative Fugue 28.14.2.6 Dissociative Convulsions

• There are all the features of dissociative amne- • Pseudoseizures mimic epileptic seizures, but
sia (see preceding text), plus an apparently pur- tongue biting, serious bruising, and inconti-
poseful journey away from home. A new identity nence of urine are uncommon.
may be assumed. • Loss of consciousness is absent or replaced by
• It is precipitated by severe stress. stupor or trance.
28.14.2.7 Dissociative Anaesthesia pelvic pain, substance abusers (40%), patients with eating
and Sensory Loss disorders, and those with a history of childhood abuse.
• There are patches of sensory loss that do not IQ is negatively correlated.
correspond to anatomical dermatomes.
• Visual loss is rarely total. 28.14.4 Aetiology of Dissociative Disorder
• General mobility is well preserved.
Sigmund Freud introduced the term conversion to
• Dissociative deafness and anosmia are uncommon.
describe the unconscious rendering of innocuous of
28.14.2.8 Other Dissociative Disorders threatening ideas by conversion into physical symptoms,
which have symbolic significance. This results in the
28.14.2.8.1 Ganser Syndrome
relief of emotional conflict (primary gain) and the direct
This is a complex disorder described by Ganser, charac- advantages of assuming a sick role (secondary gain).
terized by approximate answers and usually accompanied The spectrum of dissociation (MPD is most extreme)
by several dissociative symptoms, often in circumstances with increasingly complex and symptomatic forms is
that suggest psychogenic aetiology. related to increasingly severe childhood trauma.
The five main features of Ganser syndrome are the Levels of psychological distress are highly correlated
following: with dissociative experiences.
Of 100 substance-dependent subjects, 39 had dissocia-
• Approximate answers (vorbeireden) tive disorder and 43 reported childhood abuse. Patients with
• Clouding of consciousness dissociative disorder may use substances to block out more
• Somatic conversion severe abuse memories and suppress dissociative symptoms.
• Pseudohallucinations (often)
• Subsequent amnesia
28.14.5 Management of Dissociative Disorder
28.14.2.8.2 Multiple Personality Disorder Do not confront the individual. Complete physical investiga-
Controversy exists about whether multiple personality tions and emphasize that serious illness is excluded. Minimize
disorder (MPD) is iatrogenic or culture specific. There the advantages of a sick role, and praise healthy behaviour.
is an apparent existence of two or more distinct person- Allow the patient to discard symptoms without losing face.
alities within an individual, of which only one is evident The main treatment of MPD is long-term psychoana-
at any time. Each personality is complete, with its own lytic psychotherapy aimed at the unification of divided
memories, behaviour, and preferences. mental processes.
One personality is dominant. It does not have access
to memories of the other and is unaware of the existence 28.14.6 Course
of others. The change from one personality to another is Dissociative states tend to remit after a few weeks or
sudden and associated with stress. months. Chronic states of more than 1 or 2 years are
Psychoanalysis views MPD as a complex, chronic often resistant to therapy. Those with acute, recent onset,
developmental dissociative disorder related to severe, a good premorbid personality, and resolvable conflict
repetitive childhood abuse or trauma, usually beginning have a better prognosis.
before the age of 5 years. Dissociative defences are used In a classic paper, Slater (1965) reported on a 9-year
to handle subsequent traumatic experiences. follow-up of 85 patients who were diagnosed as hyster-
Additionally, mass hysteria presents with abnormal ill- ics by senior psychiatrists and neurologists. He found
ness behaviour transmitted in close communities spread- that 33% developed definite organic illness, 15% had a
ing from individuals of high status down the hierarchy. major mental illness, and 12 patients died, 4 from suicide
Affected individuals are suggestible. Couvade syndrome of whom 2 had demyelinating neurological conditions
presents in males whose partners are pregnant, with symp- and 8 from natural causes that could have accounted for
toms of morning sickness, abdominal pain, and anxiety. their original presentations. Of the original sample of 85,
he was left with 7 young patients who had experienced
acute psychogenic reactions in the form of a conversion
28.14.3 Epidemiology of Dissociative Disorder
syndrome and 14 who were suffering from lasting per-
Relatively high frequencies of dissociative experiences sonality disorders. Slater concluded that the diagnosis of
are reported in patients with PTSD, women with chronic hysteria should not be made.
28.15 DEPERSONALIZATION– Foley PB. 2009: Encephalitis lethargica and the influenza virus.
II. The influenza pandemic of 1918/19 and encephali-
DEREALIZATION tis lethargica: Epidemiology and symptoms. Journal of
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Freud S. 1953: The Standard Edition of the Complete Psychological
The presence of persistent or recurrent depersonalization, Works of Sigmund Freud. London, U.K.: Hogarth.
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Depersonalization: Experiences of unreality, detach- of compulsive indecisiveness. Behaviour Research and
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bei Neurasthenie. Centralblatt für Nervenheilkunde
During the depersonalization and/or derealization
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29 Personality Disorders
29.1 HISTORY 29.2.1.1 Cattell’s Trait Theory

• Hippocrates described four temperaments: mel- Cattell identified 20,000 words describing personality.
ancholic, sanguine, phlegmatic, and choleric. Using factor analysis, he derived 16 first-order personality
• In 1801, Pinel described manie sans délire factors (PFs). Cattell’s 16-PF test was devised on the basis
(Campbell, 1996). of this work. Second-order factor analysis resulted in
• In 1835, Prichard described moral insanity three broad dimensions similar to Eysenck’s dimensions:
(Kaplan, 1952).
• In 1906, Kraepelin described psychopathic per- • Sociability (extra/intra)
sonality: excitable, unstable, eccentric, liars, • Anxiety
swindlers, antisocial, and quarrelsome subtypes • Intelligence
(Koizumi et al., 1964).
29.2.1.2 Eysenck’s Theory
• Schneider (1958) subsequently extended the
concept of psychopathic personality to include Factor analysis of rating scale data yields orthogonal
suffering to the self as well as to society. dimensions, assumed to be normally distributed:
• In 1938, Stern coined the term ‘borderline’, which
signified a new disorder that is at the border • Neuroticism/stability
between schizophrenia and neurosis (Stern, 1938). • Extroversion/introversion
• In 1939, Henderson’s psychopathic states included • Psychoticism/stability
three subtypes: aggressive, inadequate, and cre- • Intelligence
ative psychopaths (Henderson, 1939).
• In 1955, Cleckley described sociopathy: unre- Personality inventories have been used to measure these
liable, untruthful, lacking remorse, poor moti- traits. The Maudsley Personality Inventory (MPI) was
vation, and antisocial behaviour (Hare and superseded by the Eysenck Personality Inventory (EPI),
Neumann, 2008). which in turn was superseded by the Eysenck Personality
• In 1967, Kernberg introduced the concept of border- Questionnaire (EPQ)—measuring psychoticism and con-
line personality organization and use of primitive taining a lie scale.
defences (Kernberg, 1975).
• In 1978, Eysenck called for a dimensional rather 29.2.1.3 Minnesota Multiphasic
than a categorical approach to the description of Personality Inventory
personality (Eysenck and Eysenck, 1975). In this lengthy inventory, the subject answers ‘true’,
‘false’, or ‘cannot say’. It is empirically constructed and
Details of personality development are considered in measures traits. It is widely used.
Chapter 5.
29.2.1.4 Rorschach Inkblot Test
29.2 CLASSIFICATION AND MEASUREMENT This is a projective test analysing fantasy material.
29.2.1 Dimensional Approach 29.2.1.5 Rotter’s Internal–External

Personality disorder differs from normal variation only Locus of Control
in terms of degree. It assumes that universal traits are Individuals vary along a continuum in their percep-
present in all people in differing degrees. Personality tion of the locus of control of events. Those attributing
traits of some individuals are sufficiently maladaptive events to an internal source are more confident about
and abnormal as to constitute personality disorder. changing their life and environment.
437
29.2.2 Categorical Approach 1. Impairments in self-functioning (a or b)

a. Identity: confused boundaries between self
This approach groups people into discrete categories. It and others; distorted self-concept; emo-
is simple and widely used, but most individuals do not tional expression often not congruent with
conform to categories: context or internal experience
b. Self-direction: unrealistic or incoherent
• Kretschmer linked body-build with personality: goals: no clear set of internal standards
• Pyknic—sociable and relaxed 2. Impairments in interpersonal functioning (a or b)
• Asthenic—self-conscious and solitary a. Empathy: pronounced difficulty under-
• Athletic—robust and outgoing standing impact of own behaviours on oth-
• Sheldon also linked build with personality: ers; frequent misinterpretations of others’
• Endomorphic—viscerotonic personality motivations and behaviours
• Ectomorphic—cerebrotonic personality b. Intimacy: marked impairments in develop-
• Mesomorphic—somatotonic personality ing close relationships, associated with mis-
trust and anxiety
The DSM-5 continues to classify personality disorders

29.3 ICD-10 AND PROPOSED
under cluster A, cluster B and cluster C personality
DSM-5 CLASSIFICATIONS disorders as in DSM-IV-TR. The cluster system is a
These are primarily categorical classifications, but they good way to classify personality disorder.
incorporate a dimensional approach, allowing the record-
ing of personality traits subthreshold for a diagnosis of
29.4 STATISTICS
personality disorder (Table 29.1).
The DSM-5 proposes criterion A for all personality A gradient exists in the prevalence of personality disor-
disorder, which includes the following (Table 29.2): ders from community to inpatient setting (see Table 29.3).
TABLE 29.1
Comparison between the ICD-10 and Proposed DSM-5 Criteria
ICD-10 (WHO, 1992) DSM-5 (APA, 2013)
General criteria • Individual’s characteristic and experience and • Impairments in cognition, affectivity, interpersonal
behaviour as a whole deviate markedly from the function and impulse control
culturally expected and accepted range in cognition, • Inflexible and enduring pattern for long duration
affectivity, control over impulses, and manners • The impairments in personality functioning and
of relating to other people. personality trait expression are not better understood
• No emphasis on personality trait as normative for the individual’s developmental stage
or sociocultural environment
Criteria on stability • The behaviour must be inflexible and maladaptive • The impairments in personality functioning
• Dysfunctional across a broad range of personal and the personality trait expression are stable across
and social situations time and consistent across situations
• The deviation is stable and of long duration, having
its onset in late childhood and adolescence
Exclusion criteria • Other adult mental disorders • Direct physiological effects of a substance
• Organic brain disease, injury, and dysfunction (e.g. a drug of abuse, medication)
• General medical condition (e.g. severe head trauma)
Criteria on functioning • Not emphasize on functioning • Significant impairments in self (identity
or self-direction) and interpersonal (empathy
or intimacy) functioning
Personality Disorders 439
TABLE 29.2
Comparison and Contrast between the Types of Personality Disorders Listed
in ICD-10 and DSM-5
ICD-10 (WHO, 1992) DSM-5 (APA, 2013)
F60.0 Paranoid personality disorder Cluster A Personality disorders
F60.1 Schizoid personality disorder 301.0 Paranoid personality disorder
F60.2 Dissocial personality disorder 301.2 Schizoid personality disorder
301.22 Schizotypal personality disorder
F60.3 Emotionally unstable personality disorder (.30 impulsive Cluster B Personality disorders
type; .31 borderline type) 301.7 Antisocial personality disorder
301.83 Borderline personality disorder
301.5 Histrionic personality disorder
301.81 Narcissistic personality disorder
F60.4 Histrionic personality disorder Cluster C Personality disorders
F60.5 Anankastic personality disorder 301.82 Avoidant personality disorder
F60.6 Anxious (avoidant ) personality disorder 301.6 Dependent personality disorder
301.4 Obsessive-compulsive personality disorder
F60.7 Dependent personality disorder Other Personality disorders
F60.8 Other specific personality disorders (eccentric, haltlose, 310.1 Personality change due to another medical
immature, narcissistic, passive-aggressive, and psychoneurotic) condition
F60.9 Personality disorder unspecified 301.89 Other personality disorder
The following are the approximate prevalences of per- The American Epidemiologic Catchment Area (ECA)
sonality disorder: study found, using a diagnostic interview schedule, a prev-
alence of personality disorder in the community of 6%.
• Community 10%
• General practice 20%
29.5 CLUSTER A PERSONALITY DISORDERS
• Psychiatric outpatients 30%
• Psychiatric inpatients 40% • Cluster A: paranoid, schizoid, and schizotypal
personality disorders—odd or eccentric
Common defence mechanisms: projection, fantasy, and

TABLE 29.3 denial
Prevalence of Personality Disorders in Different
Settings
29.5.1 Schizoid Personality Disorder
Prevalence
29.5.1.1 Epidemiology
Personality Disorder Community Outpatients Inpatients
Paranoid 0.5%–2.5% 2%–10% 10%–30% • Prevalence: 0.5%–1.5%
Schizoid 0.5%–1.5% Uncommon • Gender ratio: M/F = 2:1
Schizotypal 3%
Antisocial 3% in males 3%–30%
29.5.1.2 Aetiology
1% in females
Borderline 1%–2% 10% 20% • Genetics: Schizoid personality disorder is
Histrionic 2%–3% 10%–15% more common among the first-degree relatives
Narcissistic 0.4%–0.8% 2%–16% of schizophrenia patients. The heritability of
Avoidant 0.5%–1.0% 10% schizoid personality disorder is 0.55.
Dependent 1%–1.7% • Development: Parents are experienced as cold
Obsessive–compulsive 1.7%–2.2% 3%–10% and neglectful, leading to the belief that rela-
tionships are not worth pursuing.
stereotypical behaviours in comparison to

TABLE 29.4 people with autism and Asperger’s syndrome.
ICD-10 Criteria and Mnemonics for Schizoid 3. Schizophrenia
Personality Disorder • People with schizoid personality disorder do
not exhibit first-rank symptoms.
Mnemonics
ICD-10 Criteria (Robinson, 2001)
• People with schizotypal disorder are more
eccentric with disturbed perception and
Met general criteria for personality disorder SIR SAFE
thought form.
and ≥4 symptoms
Affect Solitary lifestyle 29.5.1.6 Management
1. Emotional coldness, detachment, or Indifferent to praise
1. Most individuals rarely seek treatment because of
flattened affectivity and criticism
2. Limited capacity to express either warm, Relationships: no
poor insight into associated problems. They have
tender feelings, or anger towards others interest low capacity for relationship and motivation.
3. Appear to be indifferent to either praise or Sexual experience: 2. Supportive psychotherapy is useful to establish
criticism no interest therapeutic alliance. As trust increases, the ther-
Behaviour Activities: solitary apist may be able to access fantasies.
1. Few, if any, activities provide pleasure Friendships: few 3. Medications: Low-dose antipsychotics and anti-
2. L
ittle interest in having sexual experiences friends depressants have been used with varied outcomes.
Emotions: cold and
with another person (taking into account age)
detached
3. Consistent choice of solitary activities 29.5.1.7 Course
4. N
o desire for or possession of any close friends Schizoid personality disorder has an early onset with
or confiding relationships (or only one)
stable course.
Cognition
1. Excessive preoccupation with fantasy and
introspection 29.5.2 Schizotypal Disorder
2. M
arked insensitivity to prevailing social norms
and conventions (which is unintentional) 29.5.2.1 Epidemiology
Prevalence: 3%
Gender ratio: male > female
29.5.1.3 Diagnostic Criteria
(See Table 29.4.) 29.5.2.2 Aetiology
• Kety et al. (1971) in an adoption study demon-
29.5.1.4 Elicit Schizoid Personality in CASC strated that abnormalities were more common
• Do you care about what other people say about in the biological relatives of schizophrenics than
you? How do you feel if other people criticize you? in adoptive relatives or controls (‘schizophre-
• Are you in touch with your emotion? nia spectrum disorders’). From this derived the
• Do you tend to enjoy being around with people operational criteria for schizotypal personality
or do you prefer to be alone? disorder. Almost all studies of the families of
• How many friends do you have in your whole life? schizophrenic probands have found an excess of
• What kind of activity do you prefer? Do you both schizophrenia and schizotypal personality
have intimacy with other people? disorder among relatives (22% in the biological
relatives of schizophrenics vs. 2% of adoptive
29.5.1.5 Differential Diagnosis relatives and controls).
1. Other personality disorders • The heritability is 0.72.
• People with paranoid personality disorder • Common biological abnormalities shared by
are easier to be engaged, and they are more schizophrenia and schizotypal disorder:
resentful than people with schizoid person- 1. Dopamine dysregulation: raised CSF HVA
ality disorder. concentrations
2. Pervasive developmental disorders 2. Reduction in temporal lobe volumes
• People with schizoid personality disor- 3. Impaired smooth pursuit eye movements
der have better communication and fewer 4. Impaired tests of executive functioning
TABLE 29.5
ICD-10 Criteria, Proposed DSM-5 Criteria, and Mnemonics for Schizotypal Disorder
ICD-10 Criteria DSM-5 Criteria Mnemonics
ICD-10 considers schizotypal disorder under Psychoticism UFO IDEA
schizophrenia, schizotypal, and delusional disorder a. Eccentricity: odd, unusual, or bizarre Unusual perception
rather than personality disorder. behaviour or appearance Friendless except first-degree family
Duration: 2 years b. Cognitive and perceptual dysregulation Odd beliefs and speech
Appearance Odd or unusual thought processes; Ideas of reference
a. Eccentric appearance odd sensations Doubt about motives of other people
b. Odd behaviour c. Unusual beliefs and experiences: unusual Eccentric appearance and behaviour
experiences of reality Affect: inappropriate or constricted
Cognitive
a. Odd beliefs or magical thinking that Detachment
influences behaviour and inconsistent a. Restricted affectivity: constricted
with subcultural norms emotional experience and indifference
b. Rumination without inner resistance b. Withdrawal: avoidance of social contacts
c. Vague, circumstantial, metaphorical, overelaborate, and activity
or stereotyped thinking Negative affectivity
Affect or emotion a. Suspiciousness: expectations
a. Inappropriate or constricted affect of and heightened sensitivity to signs
of interpersonal ill-intent or harm; doubts
Perception
about loyalty and fidelity of others; feelings
a. Unusual perceptions and experiences
of persecution
b. Occasional transient quasipsychotic
episodes with intense illusions, auditory or other
hallucinations, and delusion-like ideas
Relationship
a. Socially withdrawn
b. Suspicious or paranoid
29.5.2.3 Clinical Features a. Paranoid and schizoid personality disorder:

(See Table 29.5.) People with paranoid and schizoid personal-
ity disorder do not have perceptual or cogni-
tive disturbances.
29.5.2.4 Elicit Schizotypal Disorder in CASC b. Borderline personality disorder: People
• Can you share me some of your ideas at this with borderline personality disorder may
moment? have brief psychotic experiences, which are
• Do you feel that you have some special powers? closely related to their affective states.
How about magical power? c. Avoidant personality disorder: People with
• Do you have any unusual experience? How do avoidant personality disorder may seek
you experience it (e.g. by seeing or hearing)? closeness with other people.
• Do you have friends? Can you trust people? 3. Pervasive development disorder: autism and
• How do other people find you? Do they find you Asperger’s syndrome
odd?
29.5.2.6 Management
29.5.2.5 Differential Diagnosis 1. Supportive therapy and social skill training.
1. Delusional disorder, schizophrenia, and severe 2. Antipsychotic drugs (e.g. risperidone or olan-
depressive disorder with psychotic features zapine) may lead to mild to moderate improve-
2. Other personality disorders ment in psychotic symptoms.
TABLE 29.6
ICD-10 Criteria and Mnemonics for Paranoid Personality Disorder
ICD-10 Criteria Mnemonics (Robinson, 2001)
At least four of the following GET FACT
Behaviour Grudges are held without justification
1. Tendency to bear grudges (feeling resentful about something) persistently Excessive sensitivity to setbacks
Cognition: Threats and hidden meanings are read into benign remarks
1. Excessive sensitivity to setbacks and rebuffs Fidelity of spouse is unjustifiably doubted
2. Suspiciousness and a pervasive tendency to distort experience by Attacks on character or reputation are perceived
misconstruing the neutral or friendly actions of others as hostile or Confides reluctantly because of fears of betrayal
contemptuous Trustworthiness of others is doubted without due cause
3. Combative and tenacious sense of personal rights out of keeping with the
actual situation
4. Recurrent suspicions, without justification regarding sexual fidelity of
spouse/sexual partner
5. Persistent self-referential attitude, associated particularly with excessive
self-importance
6. Preoccupation with unsubstantiated ‘conspiratorial’ explanations
of events immediate either to the person or in the world at large
29.5.2.7 Course and Prognosis 29.5.3.3 Clinical Features

1. Schizotypal disorder has a relatively stable (See Table 29.6.)
course, with only a small proportion (10%) of
individuals going on to develop schizophrenia. 29.5.3.4 Elicit Paranoid Personality
2. Clinical features such as magical thinking, para- Disorder in CASC
noid ideation, and social isolation are associated 1. How do you find other people in general? Can
with an increased risk to develop schizophrenia. you trust them?
2. Have you encountered any setback recently? What
is the reason behind it? Do you think that there is a
29.5.3 Paranoid Personality Disorder conspiracy that purposely screws you up?
3. How do you feel about your spouse or partner?
Is he or she loyal to you?
• Prevalence: 0.5%–2.5% 4. How do you feel about your neighbours? Are
• Gender ratio: male > female they doing something behind you?
5. Why do you think all these people are against
29.5.3.2 Aetiology you? Is it because you are an important person
1. The heritability is 0.69. and they screw you up on purpose?
2. Paranoid personality disorder is more common
among the first-degree relatives of schizophre- 29.5.3.5 Differential Diagnosis
nia patients. • Delusional disorder: People with delusional dis-
3. There is a lack of protective care and support in order have their delusions well encapsulated and
childhood. Excessive parental rage and humili- systematized, but people with paranoid person-
ation cause feelings of inadequacy resulted in ality disorder do not have well-formed delusions.
projection onto others of hostility and rage. • Schizophrenia: People with schizophrenia
4. Temperament is characterized by nonadaptability exhibit first-rank and negative symptoms.
and tendency to hyperactivity and intense emotions. • Severe depressive episode with psychotic fea-
5. Sensory impairments: impaired vision and hear- tures: mood congruent delusions such as delu-
ing and victims of traumatic brain injury. sions of guilt or nihilistic delusions.
6. Social factors: new immigrants and ethnic • Substance misuse: for example, amphetamine or
minority. cannabis.
• Other personality disorders • Age of onset: adolescence or early adulthood

• Borderline personality disorder: Transient • Suicide rate: 9%
paranoia is common but not as persistent as
in paranoid personality disorder. 29.6.1.2 Aetiology
• Schizoid personality disorder: appears to be 29.6.1.2.1 Biological Factors
more indifferent. • Family studies show the risk of relatives of bor-
• Narcissistic personality disorder: Paranoia derline personality disorder to develop the same
may occur as a result to the threat of an disorder is five times higher as compared to the
imagined success. general population.
• Avoidant personality disorder: They tend to • Concordance rate of monozygotic (MZ) versus
avoid other people as a result of lack of self- dizygotic (DZ) twins: 35% versus 10%.
confidence or fear of embarrassment. • Borderline personality disorder is more com-
mon in first-degree relatives of patients with
29.5.3.6 Management
depression.
1. Supportive psychotherapy or problem-solving • Some studies demonstrate abnormal dexameth-
therapy. asone suppression test result, decreased REM
2. Cognitive–behavioural therapy (CBT) latency, decreased thyrotropin response, and
a. Cognitive therapy targets at the core beliefs abnormal sensitivity to amphetamine in patients
such as others are malicious and deceptive. with borderline personality disorder.
Patient needs to realize that there is a need • Specific marker for impulsivity: decreased CSF
to reduce suspiciousness. 5HIAA, which is a metabolite of serotonin.
b. In behaviour therapy, patient is involved in role • Chronic trauma leads to decreased hippocam-
play to handle hostility and personal attacks pal volume, decreased hemispheric integration,
in daily life. Patient is advised to record their and hyperactive hypothalamic–pituitary–gonadal
ideas in the dysfunction thought diary. (HPA) axis.
3. Psychotropic medications: Antidepressants and • Goyer et al. (1994) in a PET scanning study of
antipsychotics are indicated to treat mood and personality-disordered subjects found a sig-
psychotic symptoms. nificant inverse correlation between a history of
29.5.3.7 Course and Prognosis aggressive impulse difficulties and regional cere-
bral metabolic rates in the frontal cortex. Those
1. The hypersensitivity results in poor peer rela-
subjects with borderline personality disorders had
tionships and eccentricity.
significantly reduced frontal cortex metabolism.
2. Paranoid ideas may intensify when patient is
• Increased bilateral activity in amygdala after
under stress.
exposure to emotionally aversive stimuli.
3. Some patients with paranoid personality disor-
• Orbitofrontal cortex abnormalities lead to
der may develop agoraphobia.
reduction in cortical modulation of amygdala.
Such abnormalities are associated with impul-
29.6 CLUSTER B PERSONALITY DISORDERS sivity, affect dysregulation, chronic feeling of
emptiness, and decreased mentalization.
• Cluster B: antisocial, borderline, histrionic, and
narcissistic personality disorders—dramatic, 29.6.1.2.2 Early Development
emotional, or erratic • Borderline personality is the result of a lack of
stable involved attachment during development.
Common defence mechanisms: splitting, dissociation, This leads to an inability to maintain a stable
denial, acting out, and projective identification sense of self or others without ongoing contact.
The child will have limited capacity to depict
29.6.1 Borderline Personality Disorder feelings and thoughts in self and other people.
This capacity is known as mentalization.
29.6.1.1 Epidemiology • Family environment is characterized high con-
• Prevalence: 1%–2% flict and unpredictability. The caregiver is not
• Gender ratio: M/F = 1:2 emotionally available.
• Emotionally vulnerable temperament interacts Behaviour

with an invalidating environment.
• Early separation or loss. 1. Marked tendency to act unexpectedly and with-
• History of parental substance misuse or forensic out consideration of consequences
history in parents. 2. Marked tendency of quarrelsome behaviour and
conflicts with others, especially when impulsive
29.6.1.2.3 Past Trauma and Abuse acts are thwarted or criticized
• Childhood trauma: Borderline personality 3. Difficulty in maintaining any course of action
results from early traumatic experiences occur- that offers no immediate reward (Table 29.7).
ring within a context of sustained neglect result-
ing in enduring rage and self-hatred. 29.6.1.4 Elicit Borderline Personality
• Physical or sexual abuse. Disorder in CASC
29.6.1.2.4 Defence Mechanisms 1. Do you have problem with your anger control?
How often do you get into quarrels?
• Splitting—adopting a polarized or extreme view
2. How often do you feel empty inside yourself?
of the world where people are either all good or
What would you do when you feel empty?
all bad and fail to see that each person has good
3. How is your relationship with other people?
and bad aspects. For example, a patient with
4. How do you feel if your friend or partner left you?
borderline personality disorder tries to classify
Do you have a strong feeling of abandonment?
the doctors of the ward into two groups, good
5. Do you think that your friends would view you
doctors and bad doctors. The patient fails to see
as a moody person?
the strengths and weaknesses of each doctor.
6. How often do you hurt yourself (e.g. cutting or
• Projective identification—the patient uncon-
burning)? Why do you cut yourself? Do you
sciously projects a figure onto the other people.
want to reexperience the pain in the past?
For example, a man does not like his father
and projects a bad father figure onto the male
doctor (projection) and accuses the doctor as 29.6.1.5 Differential Diagnosis
a noncaring individual. As a result of counter- 1. Depressive disorder: People with border-
transference, the male doctor tries to avoid the line personality disorder may present with
patient as if he does not care about the patient depression, but people with depressive dis-
(identification). order do not demonstrate primitive defence
mechanisms such as splitting or projective
29.6.1.3 Clinical Features identification.
The ICD-10 classifies emotionally unstable personal- 2. Bipolar disorder: Both borderline personality
ity disorder into impulsive and borderline type. The disorder and bipolar disorder may present with
DSM-5 does not propose the concept of emotionally mood swings. People with borderline personal-
unstable personality disorder and only has borderline ity disorder refer mood swings as fluctuations in
personality disorder. mood from normal to irritability without hypo-
mania or mania.
29.6.1.3.1 Emotionally Unstable Personality 3. Post-traumatic stress disorder (PTSD): People
Disorder: Impulsive Type (ICD-10) with PTSD usually present with flashbacks,
The patient met the general criteria for personality dis- hypervigilance, and nightmares of the trau-
order and at least three of the following symptoms of matic event but do not exhibit primitive defence
impulsive type: mechanisms.
4. Schizophrenia: Both borderline personality
Affect disorder and schizophrenia may present with
psychotic symptoms. People with borderline
1. Tendency to outbursts of anger or violence, with personality disorder present with transient psy-
inability to control the resulting behavioural chosis or visual illusions. Negative symptoms
explosions and first-rank symptoms are uncommon in bor-
2. Unstable and capricious mood derline personality disorder.
TABLE 29.7
Comparison of the ICD-10 Criteria, the Proposed DSM-5 Criteria, and Mnemonics for Borderline
Personality Disorder
ICD-10 Criteria DSM-5 Criteria Mnemonics (Robinson, 2001)
Borderline type (ICD-10) 1. Negative affectivity I RAISED A PAIN
The borderline type requires the person a. Emotional lability: unstable emotional Identity disturbance
to meet the diagnostic criteria of impulsive experiences and frequent mood changes Relationships: unstable
type and an additional two symptoms b. Anxiousness: intense feelings of nervousness Abandonment: fear of impulsivity
in the following: or panic in reaction to interpersonal stresses Self-harm
and fears of losing control Emptiness
Affect
c. Separation insecurity: fears of rejection Dissociative symptoms
1. Chronic feelings of emptiness
by or separation from significant others Affective instability
Behaviour and associated with fears of excessive Paranoid ideation
1. Liability to become involved in intense dependency and complete loss of autonomy Anger
and unstable relationships, often leading d. Depression: frequent feelings of being down, Idealization and devaluation
to emotional crises miserable, or hopelessness Negativistic – undermine the efforts of
2. Excessive efforts to avoid abandonment 2. Disinhibition self and others
3. Recurrent threats or acts of self-harm a. Impulsivity: acting on the spur of the
Cognition moment in response to immediate stimuli;
1. Disturbances in and uncertainty about acting on a momentary basis without a plan
self-image, aims, and internal or consideration of outcomes; difficulty
preferences (including sexual) establishing or following plans; a sense
of urgency and self-harming behaviour
under emotional distress
b. Risk taking: engagement in dangerous, risky,
and potentially self-damaging activities
3. Antagonism
a. Hostility: persistent or frequent angry
feelings; anger or irritability
5. Other personality disorders to special treatment because they suffered in

a. Dependent personality disorder: People the past. People with narcissistic personality
with dependent personality disorder are disorder feel that they are entitled to special
less chaotic in affect regulation and less treatment because of their special status.
impulsive. e. Identity confusion in normal adolescence
b. Antisocial personality disorder: People with development.
antisocial personality disorder have history
of forensic problems and do not concern Comorbidity: depression, PTSD, substance misuse, and
about the safety of other people. bulimia nervosa
c. Histrionic personality disorder: People with
histrionic personality disorder want to be 29.6.2 Management
the centre of attention but usually demon-
strate less self-harm, emptiness, and affec- 29.6.2.1 Inpatient Treatment and
tive instability. Therapeutic Communities
d. Narcissistic personality disorder: People This is controversial. Currently, there is a trend away from
with narcissistic personality disorder see long-term admissions for borderline patients, probably
rejection as humiliating. People with bor- driven by cost containment. There is evidence to support the
derline personality disorder see rejection as value of therapeutic communities such as the Henderson or
abandonment. People with borderline per- the Cassel Hospital. The therapeutic community approach
sonality disorder feel that they are entitled is a multicomponent treatment programme, incorporating
individual therapy, ward groups, and patient participation personality disorder. Details of DBT and men-
in the maintenance of the community. talization-based treatment are considered in
Indications for admission include (Paris, 2004) Chapter 25.
3. The NICE guidelines recommend that thera-
1. Life-threatening suicide attempt pists should use an explicit and integrated
2. Imminent danger to other people theoretical approach and share this with their
3. Psychosis clients.
4. Severe symptoms interfering with functioning 4. The guidelines also recommend that the thera-
that are unresponsive to outpatient treatment pists should set therapy at twice per week and
should not offer brief psychological interven-
The risks of hospitalization to the patient include tions (less than 3 months duration).
5. Other psychotherapies
• Stigma a. Supportive psychotherapy: diminish sui-
• Disruption of social and occupational roles cidal behaviour and impulsive acts while
• Loss of freedom awaiting a remission since the long-term
• Hospital-induced behavioural regression prognosis of this disorder is good.
b. CBT: Cognitive therapy focuses on mal-
Some consider the drawing up of a contract between the adaptive cognitions about oneself and other
patient and doctor essential to the success of inpatient people. Behaviour therapy improves social
care. Miller (1989) considers a good treatment contract to and emotional functioning.
incorporate the following: c. Schema-focused therapy: aims at modifying
schemas (e.g. fear of abandonment), reduc-
• Mutual agreement by all involved parties. ing self-harm behaviour, and improving
• Specific, focused, achievable goals with strate- interpersonal relationship.
gies to achieve them. d. Transference-focused therapy: aims at cor-
• Specific responsibilities of patient and staff. recting distorted perceptions of significant
• Provision of the minimum degree of structure others and decreasing symptoms and self-
necessary. destructive behaviour.
• Patient foregoing his or her usual means of man- e. Family therapy is frequently offered to bor-
aging intolerable feelings; alternative strategies derline adolescent patients and is regarded
are provided. by many as the treatment of choice for these
• Positive reinforcement of desirable behaviour. patients.
• Not being drawn up when staff have unresolved f. Social skill training.
punitive wishes towards the patient.
• Strictly enforced, but room for negotiated
modification. 1. The psychiatrist can prescribe an SSRI (e.g.
fluoxetine) to treat mood lability, rejection sen-
sitivity, and anger.
The alternative approach of brief admissions at the time
2. If the second SSRI is not effective, the psy-
of crisis is increasingly popular.
chiatrist can consider adding a low-dose anti-
The NICE guidelines recommend the following:
psychotic (e.g. quetiapine) for anger control
or an anxiolytic (e.g. clonazepam) for anxiety
29.6.2.2 Psychotherapy control.
1. Long-term outpatient psychotherapy is rec- 3. Mood stabilizers such as sodium valproate and
ommended because patients can handle chal- carbamazepine can be added if the aforemen-
lenges in daily life with the support from tioned medications are not effective.
psychotherapists. 4. It is recommended not to use psychotropic med-
2. Dialectical behaviour therapy (DBT) and ications that have narrow therapeutic index such
mentalization-based therapy are recom- as lithium or tricyclic antidepressants, which are
mended treatment for people with borderline toxic during overdose.
29.6.2.4 Course and Prognosis

1. Impulsivity improves significantly over time. TABLE 29.8
Affective symptoms have the least improvement. Percentages of Convictions in Male Adoptees
2. A 15-year follow-up of 100 borderline personality- and the Biological and Adoptive Parents
disordered patients found that 75% were no lon- Conviction Rate
ger diagnosed as borderline. All scales showed a
Neither biological nor adoptive parent convicted 13.5%
reduction of symptomatic behaviour, with a clear
Adoptive parents convicted. 14.7%
functional improvement. However, there is a high Biological parents not convicted
risk of suicide, with 8.5% completing suicide in Adoptive parents not convicted 20.0%
the 15-year follow-up period. Those patients with Biological parents convicted
chronic depression, good motivation, a psycho- Adoptive and biological parents convicted 24.5%
logical attitude, low impulsiveness, and a stable
environment are most responsive to treatment.
3. Poor prognosis is associated with early child- MZ to DZ concordance rates for adult criminality are
hood sexual abuse, early first psychiatric contact, 52%:22%. This suggests a definite genetic contribution.
chronicity of symptoms, high affective instabil- However, concordance rates of 87%:72% for juvenile
ity, aggression, and substance use disorder. delinquency are suggestive of a familial but not a genetic
component to aetiology.
Within a family that has a member with antisocial
29.6.3 Dissocial Personality Disorder personality disorder, males more often have antisocial
29.6.3.1 Epidemiology personality disorder and substance-related disorders,
whereas females more often have somatization disorder.
• There is a lifetime prevalence of 2.3%–3.6%.
However, in such families, there is an increase in the
• The male-to-female sex ratio is 7:1.
prevalence of all of these disorders in both males and
• It is twice as prevalent in inner cities compared
females compared with the general population.
to rural areas.
It is suggested that family background plays a part in
• Antisocial behaviours usually start at age 8–10
subsequent criminality but only when there is already
years. They do not develop after age 18.
a genetic predisposition. The risk of criminality is
• The highest lifetime prevalence is in the
increased in those with prolonged institutional care and
25–44-year-old group, followed by the 18–24-year-
multiple temporary placements and those where the
old group.
socioeconomic status of their adoptive home is low:
• Subjects are less likely to be married and less
well educated. • Dysfunctional serotonin: low 5HIAA in CSF and
associated with hostile and aggressive behaviour.
29.6.3.2 Aetiology • Imaging findings
29.6.3.2.1 Biological Causes • Structural MRI shows reduction in volume
Genetic causes: Most twin and adoption studies suggest of temporal lobes but not frontal lobes. The
that antisocial personality disorder has a partial genetic reduction of temporal lobe volumes is asso-
aetiology (see Table 33.2). The heritable form of crimi- ciated with violent and sexually aggressive
nality is associated with petty recidivism and property behaviour.
offences rather than violent crime (Table 29.8). • Functional MRI shows reduction in cerebral
Mednick et al. (1984) studied 14,427 adoptees and blood flow (CBF) in the prefrontal cortex,
their biological and adoptive parents. The effect was orbitofrontal cortex, and amygdala. The
stronger when the biological mother was convicted than reduction in CBF in amygdala is associated
if the biological father was convicted. Association was with callous and unemotional trait.
for property offences only, playing a significant role in • EEG studies in antisocial personality disor-
repeat offences; it did not apply to violent offences. ders demonstrate abnormalities that have led to
Robins (1966) found that the father’s criminal behav- speculation that psychopathic behaviour reflects
iour was the single best predictor of antisocial behaviour cortical immaturity. Abnormalities found in this
in a child. group more often than in normal include
• Generalized widespread slow (⊖) wave activity 29.6.3.2.3 Psychological Causes

• ‘Positive spike’ abnormality over temporal • Temperament: high novelty seeking, low
lobes harm avoidance, low reward dependence, and
• Localized temporal slow-wave activity uncooperativeness
These abnormalities are more likely to occur in highly 29.6.3.3 Clinical Features
impulsive and aggressive psychopaths. (See Table 29.9.)
29.6.3.2.2 Developmental Causes 29.6.3.4 Elicit Dissocial Personality

• Parental deprivation and antisocial behaviour. Disorder in CASC
For example, witnessed abuse when the patient 1. How do you see the authority? Are you upset if
was young. people give you order? What would you do to
• Inconsistent or harsh parenting. the authority if you are upset with them?
• Frequent moves or migration, large family size, 2. How do you see other people? Are you often
and poverty. involved in fights with others? Are you con-
• Childhood risk factors include cruelty to cerned about safety of other people?
animals, enuresis, innate aggression, and 3. How do you see about commitment or obliga-
fire setting. tion? Are you able to keep your promise?
TABLE 29.9
Comparison of the ICD-10 Criteria, the Proposed DSM-5 Criteria, and Mnemonics for Dissocial
Personality Disorder
ICD-10 Criteria DSM-5 Criteria Mnemonics
ICD-10 criteria Antagonism CALL ASPD
Affect a. Manipulativeness: frequent use of Conduct disorder before age 15
1. Very low tolerance to frustration and a low subterfuge to influence or control others Antisocial activities
threshold for discharge of aggression, b. Deceitfulness: dishonesty and fraudulence Lies frequently
including violence or misrepresentation of self Lack of superego
2. I ncapacity to experience guilt or to profit c. Callousness: lack of concern for feelings Aggression
from adverse experience, particularly punishment or problems of others; lack of guilt or remorse Safety of others being ignored
d. Hostility: persistent or frequent angry Planning failure
Behaviour
feelings; anger or irritability in response to minor Denial of obligation
3. Incapacity to maintain enduring relationships,
insults
though no difficulty in establishing them
4. Marked proneness to blame the others or to offer Disinhibition
plausible rationalizations for the behaviour that a. Irresponsibility: failure to honour obligations
has brought the individual into conflict or commitments and lack of follow-through on
with society agreements and promises
b. Impulsivity: acting on the spur of the
Cognition
moment in response to immediate stimuli; acting
5. Callous unconcern for the feelings of others
on a momentary basis without a plan or
Gross and persistent attitude of irresponsibility
consideration of outcomes; difficulty establishing
and disregard for social norms, rules, and
and following plans
obligations
c. R isk taking: engagement in dangerous,
risky, and potentially self-damaging
activities, unnecessarily and without regard
for consequences; boredom proneness and
thoughtless initiation of activities to counter
boredom; lack of concern for one’s
limitations and denial of the reality of
personal danger
4. Do you tell lies if there is a chance? impact of antisocial behaviour. Behaviour ther-
5. Have you ever been arrested or pulled over by apy targets at reduction of antisocial behaviour.
the police? 3. Pharmacological interventions should not be
routinely used for the treatment of dissocial per-
29.6.3.5 Differential Diagnosis sonality disorder.
1. Temporary antisocial behaviour (e.g. vandalism 4. Pharmacological interventions may be con-
or riot), focal behaviour, not exploitive, and with sidered in the treatment of comorbid disorders
conscience preserved. such as depression and anxiety (e.g. SSRIs)
2. Psychopathy is different from dissocial person- and aggression (e.g. low-dose antipsychotics or
ality disorder in the following: mood stabilizers).
a. People with psychopathy encounter more
difficulty for inhibiting antisocial and vio- 29.6.3.7.1 Lithium
lent behaviour (e.g. empathy, guilt, and close In male convicts with a pattern of recurring easily trig-
emotional bonds). gered violence, a marked reduction in infractions resulted
b. Psychopathy is associated with higher risk from treatment with lithium. The reduction in aggressive
of recidivism and violence. The presence of episodes requires lithium levels above 0.6 mmol/L. Major
deviant sexual behaviour in psychopaths is infractions such as assault or threatening behaviour are
associated with violent behaviour. responsive to lithium in about 60%; minor infractions are
c. EEG: Psychopaths have lower cortical unresponsive.
arousal, measured by slower cortical evoked Lithium is helpful in a small number of patients with
potentials. Autonomic arousal is also lower, diverse personality disorders. Affective features, a fam-
leading to speculation that sensation-seek- ily history of affective disorder, or alcoholism may help
ing behaviour may be an attempt to increase selected subjects. A 2 month trial of lithium may be nec-
cortical arousal. essary to establish responders.
3. Substance misuse, for example, stimulants, PCP,
and ketamine. 29.6.3.7.2 Carbamazepine
4. Mania/hypomania—antisocial behaviour (e.g. Impulsive aggression is the most serious symptom of per-
reckless driving or violence) as a result of sonality disorder. In patients with behavioural dyscon-
impaired judgement and irritability. trol, aggressive acts are reduced by about two-thirds, and
the severity of the outburst is improved. It is helpful even
29.6.3.6 Comorbidity in the absence of epileptic, affective, or organic features.
There is a highly significant correlation between antisocial Not all patients with dissocial personality disorder are
personality disorder and drug and alcohol dependence. suitable for psychotherapy. Contraindications to psycho-
A high proportion (90%) have at least one lifetime therapy include
psychiatric diagnosis (e.g. somatization disorder, depres-
sion, and substance misuse). 1. History of violence causing injury
2. Absence of remorse over violent act
29.6.3.7 Management 3. Obvious secondary gain through therapy (e.g.
Recommendations from the NICE guidelines avoidance of responsibility)
4. Superior intelligence with poor insight or very
1. Consider offering cognitive and behavioural low intelligence
interventions in order to address problems such 5. Lack of significant relationship in the past and
as impulsivity, interpersonal difficulties, and historical incapacity to develop attachments
antisocial behaviour. For people with foren- 6. Offering threats to therapist
sic history, the CBT should focus on reducing 7. Intense countertransference experienced by
offending and other antisocial behaviours. multiple therapists
2. When providing CBT to people with dissocial
personality disorder, it is important to assess risk 29.6.3.8 Course and Prognosis
regularly and adjust the duration and intensity of • Early onset of childhood conduct disorder
the programme accordingly. Cognitive therapy (<10 years) is the most predictive of dissocial
targets at cognitive bias such as minimization of personality disorder.
• In those with antisocial personality disorders, • Kernberg proposed that narcissistic person-
there is a significant association between the ality disorder is part of borderline personal-
ability to form a relationship with the therapist ity disorder; idealization is a defence against
and treatment outcome. In confined settings envy and self is highly pathological.
such as prison or in the military, confrontation • Temperament: high novelty seeking and reward
by peers may bring changes in social behaviour. dependence.
• Prevalence seems to decrease with increasing
age. Spontaneous remission may occur in mid- 29.6.4.3 Clinical Features
dle age. There is a correlation between increas- (See Table 29.10.)
ing age and remission rate.
Types of Narcissist (Gabbard, 2000)
• In general, people with dissocial personality dis-
order have reduction in impulsivity and increase 1. The oblivious narcissist: arrogant, self-absorbed,
in awareness of the consequences of reckless centre of attention, sender in a social network
behaviour over time. They continue to be diffi- (e.g. Facebook), not sensitive to reaction to oth-
cult people, resulting in interpersonal problems. ers, and not affected by criticisms from others
• 5% of people with dissocial personality disorder 2. The hypervigilant narcissist: shy, seeking
commit suicide, and suicide risk is increased by attention from others, avoiding to be centre of
four times compared to the general population. attention, receiver tends to detect criticism in
• There is increase in mortality as a result of acci- messages, sensitive to reaction to others, and
dents, drug overdose, and victims of homicide. easily humiliated by others
3. Mixed oblivious and hypervigilant narcissist
Positive prognostic factors include
29.6.4.4 Elicit Narcissistic Personality
• Show more concerns and guilt of antisocial Disorder in CASC
behaviour 1. How do you see other people? Do you feel that
• Ability to form therapeutic alliance they are not up to your standard? What would
• Positive occupational and relationship record you do to them? Do you feel sorry for them?
2. How do you compare yourself with others? Do
you feel superior? If yes, in which aspect? Do
29.6.4 Narcissistic Personality Disorder
you feel people are jealous of you?
29.6.4.1 Epidemiology 3. Do you have fantasy? If yes, would you mind to
The prevalence is between 0.4% and 0.8%. tell me the content of your fantasy? Do you like
Gender ratio: men = women to dream about success or power?
4. What would happen if other people criticize
29.6.4.2 Aetiology you? Do you see this as a blow to your ego?
Do you feel angry about that?
29.6.4.2.1 Psychological Causes
• Parenting: parental deprivation, pampering, and
spoiling by parents. TABLE 29.10
• Most theories state that people with narcissis- Comparison of the DSM-5 Criteria and Mnemonics
tic personality disorder develop narcissism in for Narcissistic Personality Disorder
response to their low self-esteem. People with DSM-5 Criteria Mnemonics
narcissistic personality disorder have inflated
self-esteem and seek information that confirms Antagonism, characterized by GAME
a. Grandiosity: Feelings of entitlement, either Grandiose fantasy
their illusory bias.
overt or covert; self-centredness; firmly of self-importance
• Psychodynamic theories
holding to the belief that one is better than Arrogant
• Kohut proposed that narcissistic personality others; condescending towards others Manipulative
disorder is different from borderline per- b. Attention seeking: Excessive attempts to Envious of others
sonality disorder; idealization is a normal attract and be the focus of the attention of
development for missing psychic structure; others; admiration seeking
self is nondefensive and normally arrested.
5. How do you find your physical appearance? 29.6.5.2.2 Developmental Causes

Do you think that you are physically attrac- • Freud: Histrionic personality results from dif-
tive? Do you like to look at yourself in the ficulties in the Oedipal phase of psychosexual
mirror or pictures repeatedly? Do you admire development.
your own self? • Significant separations in the first 4 years of life.
• Association with authoritarian or seductive
29.6.4.5 Differential Diagnosis
paternal attitudes during childhood.
1. Other cluster B personality disorders, for exam- • Low cohesion but high control in family.
ple, histrionic personality disorder • Favouritism towards boys or male gender in a
2. Adjustment disorder with depressive features or family (if patient is a woman), which leads to
depressive disorder with narcissistic defences power imbalance in family.
3. Hypomanic episodes • Traumatic childhood.
4. Substance misuse • Chronic physical illness in childhood and atten-
tion seeking by physical complaints.
• Absence of meaningful relationships in life.
1. Anorexia nervosa
2. Depression or dysthymia 29.6.5.2.3 Defence Mechanisms
3. Hypomania • Dissociation
4. Substance misuse • Denial
29.6.4.7 Treatment 29.6.5.3 Clinical Features
1. People with narcissistic personality disorder (See Table 29.11.)
are often ambivalent about treatment, and they
tend to feel that it is the others who need to 29.6.5.4 Elicit Histrionic Personality
change. Disorder in CASC
2. People with narcissistic personality disorder 1. How do you interact with other people? Do
may come to seek help when they are depressed you frequently find yourself being the centre of
after narcissistic injury. attention?
3. Psychotherapies such as dynamic psychotherapy
and CBT are useful. TABLE 29.11
Comparison of the ICD-10 Criteria and Mnemonics
for Histrionic Personality Disorder
1. Depression is perpetuated by continuing frus-
tration and disappointment and reduced boost- Mnemonics
ers for narcissism. ICD-10 Criteria (Robinson, 2001)
2. Patients may encounter difficulty with ageing Affect CRAVE SIN
as a result of high value placed on self-image 1. Self-dramatization, theatricality, Centre of attention
and unrealistic strength. They may not be able or exaggerated expression of emotions Relationship: viewed to be
to satisfy with life achievements. 2. Shallow and labile affectivity closer to others than
Behaviour actually is
3. Suggestibility (he or she is easily Appearance: very important
29.6.5 Histrionic Personality Disorder Vulnerable to suggestions
influenced by others or
from other people
29.6.5.1 Epidemiology circumstances)
4. Continual seeking for excitement Exaggerate expression of
Prevalence: 2%–3% emotion
and activities in which the individual
Gender ratio: M = F Seductive
is the centre of attention
5. Inappropriate seductiveness in Impressionistic speech but
29.6.5.2 Aetiology no substance in the speech
appearance or behaviour
29.6.5.2.1 Psychological Causes Cognition
Novelty seeking
• Emotional, hypersensitive, extraversion, and 6. Overconcern with physical
reward dependence attractiveness
• Tendency towards attention seeking
2. How do you find your physical appearance? Do 29.6.5.8 Course and Prognosis
you feel that people from the opposite gender 1. In general, people with histrionic personality
often find you attractive? disorder have less functional impairments com-
3. Do you find yourself good in acting or pared to other personality disorders.
pretending? 2. Some people with histrionic personality disor-
4. How do you find your emotion? Does your emo- der improve with age as a result of maturity.
tion fluctuate much? 3. Sensation seeking may lead to substance misuse.
5. Do you tend to seek excitement from time to
time?
29.7 CLUSTER C PERSONALITY DISORDERS
• Hypomania/mania: characterized by episodic • Cluster C: avoidant, dependent, and obsessive–
mood disturbances with grandiosity and elated compulsive personality disorders—anxious or
mood, which should not be found in histrionic fearful
personality disorder.
• Somatization/conversion disorder: people with Common defence mechanisms: isolation, passive aggres-
histrionic personality disorder are more dra- sion, hypochondriasis, and undoing
matic and attention seeking.
• Substance misuse.
• Other personality disorders 29.7.1 Anankastic Personality Disorder
• Borderline personality disorder: more 29.7.1.1 Epidemiology
self-harm, chaotic relations, and identity
29.7.1.1.1 Prevalence
diffusion.
• Dependent personality disorder: more Prevalence in the community: 1.7%–2.2%. Anankastic
impairment in the decision-making process. personality disorder is the most common personality dis-
• Narcissistic personality disorder: people order in the community in the United Kingdom.
with narcissistic personality disorder need More common in eldest children, Caucasians, and
attention for being praised, and they are high socioeconomic status
very sensitive to humiliation. Gender ratio: M > F
29.6.5.6 Comorbidity 29.7.1.2 Aetiology

• Somatization disorder 29.7.1.2.1 Biological Causes
• Alcohol misuse 1. More common in the first-degree relatives of
patients of obsessive–compulsive personality
29.6.5.7 Treatment disorder.
1. Dynamic psychotherapy may be useful for 2. The heritability is 0.78.
people with histrionic personality disor-
der. Patients may see power and strength as
a male attribute based on their childhood
experience and feel inferior about one’s own 1. Early development: Excessive parental control
gender. As a result, they need to seek atten- and criticism cause insecurity. This insecurity
tion. Dynamic therapy can help the patients is defended by perfectionism, orderliness, and
to analyse their deep-seated views and under- control.
stand how their childhood experiences affect 2. Psychodynamic theories
perception and personality development. The a. Freud: fixation at the anal stage of psycho-
therapists should help the patients to develop sexual development
their self-esteem. b. Erikson’s development: autonomy versus
2. CBT can challenge cognitive distortions and shame
reduce emotional reasoning.
3. Psychotropic medications: SSRIs target at 29.7.1.3 Clinical Features
depressive symptoms. (See Table 29.12.)
TABLE 29.12
Comparison of the ICD-10 Criteria, DSM-5 Criteria, and Mnemonics for Anankastic Personality Disorder
ICD-10 Criteria DSM-5 Criteria Mnemonics (Robinson, 2001)
Affect Compulsivity PERFECTION
1. Feelings of excessive doubt and caution Rigid perfectionism on everything being flawless, Preoccupation with details, rules, and plans
Behaviour perfect, and without errors or faults, including Emotionally constricted
1. Perfectionism that interferes with task one’s own and others’ performance; sacrificing of Reluctant to delegate tasks
completion timeliness to ensure correctness in every detail; Frugal
2. Excessive conscientiousness and believing that there is only one right way to do Excessively devoted to work
scrupulousness (extremely careful) things; difficulty changing ideas; preoccupation Controlling of other people
3. Excessive pedantry (adherence to rules and with details, organization, and order Task completion hampered by perfectionism
forms) and adherence to social conventions Miserly spending style and failure to discard old Inflexible
items Overconscientious in morals, ethics,
Cognition
Rigidity at tasks long after the behaviour has and values
1. Rigidity and stubbornness
ceased to be functional or effective; Not able to discard old items and
2. Undue preoccupation with productivity to
continuance of the same behaviour despite hoards objects
the exclusion of pleasure and interpersonal
relationships repeated failures
29.7.1.4 Elicit Anankastic Personality 3. Somatoform disorders.

Disorder in CASC 4. Hypochondriasis.
1. How do you describe yourself? Are you a per- 5. 30% of people with anankastic personality dis-
fectionistic person? Does it slow you down? order suffer from OCD but not vice versa.
2. What is your view on rules and morals? Are you
strict with moral principles? 29.7.1.7 Management
3. Are you a careful person? Do you pay a lot of 1. Psychodynamic psychotherapy is useful. It
attention to details? involves an active therapist who challenges
4. Do you like to spend money? isolation of the affect and helps the patient to
5. Are you able to throw away old items? If not, increase emotional awareness. The therapist also
where do you keep them? helps to modify harsh superego. Patient needs to
develop the capacity to accept that he or she is
29.7.1.5 Differential Diagnosis a human being and cannot be p erfectionistic in
Obsessive–compulsive disorder (OCD): People with OCD all areas.
present with clearly defined obsessions and compulsions. 2. CBT is useful to enhance tolerance of imper-
People with anankastic personality disorder are more ego- fection and errors. Patients should label the
syntonic with their behaviour, and hence, they are less anxious. tasks as completed once the result is good
Generalized anxiety disorder (GAD): People with enough.
GAD present with excessive worries related to common
life events. 29.7.1.8 Course and Prognosis
Schizoid personality disorder: People with anankastic Adolescents with anankastic personality traits may grow
personality disorder may present with constricted affect out of the diagnosis.
because they want to maintain control. People with schiz-
oid personality appear to be emotionally cold because
there is a fundamental lack of capacity to express emotion. 29.7.2 Anxious (Avoidant) Personality Disorder
29.7.1.6 Comorbidity 29.7.2.1 Epidemiology
1. Depressive disorder. Prevalence in the community is 0.5%–1.0%.
2. Anxiety disorders. Gender: male = female
29.7.2.2 Aetiology 2. Are you an anxious person?

29.7.2.2.1 Biological Causes 3. Do you mix around with other people? Do you
worry that other people may not like you?
1. The heritability found in anxious personalities
4. Do you try to avoid social interaction? Are you
is probably related to trait anxiety, in obses-
concerned about criticism?
sional personalities to a more general neurotic
5. Do you participate in any activity that you find
tendency as measured by the EPI, and in hysteri-
pleasurable?
cal personalities to extroversion.
2. The heritability is 0.28. 29.7.2.5 Differential Diagnosis
3. Anxious personality disorder and social phobia 1. Social phobia: People with social phobia show
may be genetically related. more impairment and distress in social situa-
29.7.2.2.2 Psychological Causes tions. Their low self-esteem is lower compared
1. Temperament: neuroticism and introversion. to people with avoidant personality disorder.
2. Parenting: Parents tend to be inconsistent, absent, 2. Agoraphobia: People with agoraphobia have fre-
and less in demonstrating parental love. Parents quent panic attacks.
are discouraging and rarely show pride in their 3. Depressive disorder: Negative self-evaluation is
children. Rejection and isolation often occur. As a a result of low mood.
result, maladaptive avoidance develops as a defence 4. Other personality disorders
against shame, embarrassment, and failure. a. Dependent personality disorder: People
3. Anxious attachment: The patient wants to have with avoidant personality disorder avoid
close relationship, but he or she is fearful of contact, while people with dependent per-
rejection. sonality disorder focus on being cared for.
b. Schizoid personality disorder: isolated but
29.7.2.3 Clinical Features emotionally cold.
(See Table 29.13.) c. Paranoid personality disorder: People with
paranoid personality disorder are isolated
29.7.2.4 Elicit Anxious (Avoidant) because of lack of trust in other people.
Personality Disorder in CASC
1. How do you see yourself? Do you often see 29.7.2.6 Comorbidity
yourself inadequate? 1. Social phobia
TABLE 29.13
Comparison of the ICD-10 Criteria, DSM-5 Criteria, and Mnemonics for Anxious Personality Disorder
ICD-10 Criteria DSM-5 Mnemonics
Affect Detachment AVOID
1. Persistent, pervasive tension, and apprehension a. Withdrawal: reticence in social situations; Avoid involvement
avoidance of social contacts and activity Very anxious
Behaviour
b. Intimacy avoidance: avoidance of close Overconcern about criticism
2. Unwilling to be involved with people unless
or romantic relationships and interpersonal Inhibited in interpersonal situations
certain of being liked
attachments Disapproval expected at work
3. Restricted lifestyle due to need for physical security
c. Unwilling to get involved unless being liked
4. Avoidance of social or occupational activities
involving significant interpersonal contact because Negative affectivity
of fear of criticism, disapproval, or rejection a. Worry about criticism and view oneself as
socially inept
Cognition
5. Belief that one is socially inept, personally
unappealing, or inferior to others
6. Excessive preoccupation with being criticized
or rejected in social situations
29.7.2.7 Treatment
1. CBT is more useful and effective as compared TABLE 29.14
to brief dynamic psychotherapy to help patients Comparison of the ICD-10 Criteria and Mnemonics
to overcome avoidance. for Dependent Personality Disorder
2. Assertiveness and social skill training is useful ICD-10 Criteria Mnemonics
to help patients to make and refuse request.
Affect FEARS
3. Distress tolerance skill is important to help 1. Uncomfortable or helpless Fear of being left alone
patients to handle anticipatory anxiety in social when alone due to exaggerated Expression of disagreement is
situations. fears of inability to self-care limited
Behaviour Avoid decision-making and
29.7.2.8 Course and Prognosis 2. Encourages or allows others to responsibility
1. People with avoidant personality disorder may make most of one’s Relationship is sought urgently
do well in familiar environment with known important life decisions with other relationship ends
people. 3. Subordination of one’s own Self-confidence is lacking
2. Shyness tends to decrease when the patients get needs to those of others on
older. whom one is dependent, undue
3. People with avoidant personality disorder and compliance with their wishes
4. Unwilling to make even
comorbid depressive disorder may have high
reasonable demands on the
dropout rate in treatment.
people one depends on
Cognition
5. Preoccupation with fears of
29.7.3 Dependent Personality Disorder
being left to care for oneself
29.7.3.1 Epidemiology 6. Limited capacity to take
everyday decisions without an
The prevalence in the community is between 1% and 1.7%.
excessive amount of advice and
reassurance from others
29.7.3.2 Aetiology
29.7.3.2.1 Biological Causes
• Twin studies suggest a biological component to 3. In situations when you do not agree with other
submissiveness. people, are you able to express yourself?
• The heritability is 0.57. 4. What would happen if you are left alone? Would
you be fearful?
• Dependent personality traits are thought to
1. Depressive disorder
result from parental deprivation and indulgent
2. Agoraphobia
parents who prohibit independent activity.
3. Social phobia
• Dependent personality results from fixation at
4. Other personality disorders
the oral stage of psychosexual development.
a. Borderline personality disorder: Both bor-
• Hostile dependency: dependency as a way to
derline personality disorder and dependent
manage anger and aggression.
personality disorder share fear of rejection
• Insecure attachment.
and abandonment. People with borderline
personality disorder show more anger, emp-
29.7.3.3 Clinical Features
tiness, and dramatic responses. People with
(See Table 29.14.) dependent personality disorder are more sub-
missive and clinging. People with dependent
29.7.3.4 Elicit Dependent Personality personality disorder want to be controlled, but
Disorder in CASC people with borderline personality disorder
1. Can you describe your character? Are you a react strongly to the efforts to be controlled.
dependent person? People with borderline personality disorder
2. How do you feel about making a decision? show more rage and chaotic relationship.
b. Avoidant personality disorder: People with

avoidant personality disorder show low explore the presence of any other chil-
self-esteem, need for reassurance, and high dren and her views towards motherhood.
sensitivity for rejection. People with avoid- Finally, the candidate should explore the
ant personality disorder react by avoiding, reason why she does not want to look after
while people with dependent personality her baby (e.g. complications or illness
disorder seek out for relationship. in the infant, extreme social adversity,
c. Histrionic personality disorder: People with unstable emotion). The candidate should
histrionic personality disorder are more inquire the mode of feeding (e.g. breast-
seductive, flamboyant, and manipulative to feeding) and the care of the baby (e.g. the
get attention. availability of friends or others who are
looking after the baby). The candidate
29.7.3.6 Treatment should explore her coping mechanisms
1. CBT and social skill training. and substance misuse during the antenatal
2. Therapy targets at increasing self-esteem, self- and postnatal periods.
confidence, sense of efficacy, and assertiveness. 2. Candidates need to explore how the border-
3. Explores fear of autonomy. line personality affecting the way a depres-
4. Family or couple therapy. sive episode would present in this patient.
For example, the effect of chronic empti-
ness and feeling of abandonment may affect
CASC STATION ON BORDERLINE quality of low mood. Patients with border-
PERSONALITY DISORDER line personality disorder may have transient
psychosis, and candidates should explore
A 28-year-old woman is referred by an obstetrician
possible delusions or hallucinations, which
for assessment of postnatal depression. She delivered
may pose harm to the baby. Has patient
a baby boy 6 weeks ago, and she claims that she does
used ‘acting out’ (e.g. severe self-injury) as
not want to look after her baby. She has a past history
a means of presentation to the obstetrician?
of borderline personality disorder. The obstetrician
Explore the biological (e.g. insomnia) and
has made a note stating that she behaves like a child.
cognitive symptoms of depression.
Take a history to assess the reasons of distress
3. Risk assessment includes assessment on
and the impact of borderline personality disorder
suicidality, frequency of self-mutilation,
on her mood and parenting ability.
and infanticide risk.
Approach to This CASC Station 4. Candidates are advised to take a back-
ground history to assess the degree of
1. Explore her reasons for distress by impairment (e.g. duration of unemploy-
empathic open questioning including vali- ment) and severity of the borderline
dating statements to identify the onset and personality disorder (e.g. number of hospi-
the course of the current problems. The talizations). Look for common comorbidity
patient may have gone through a lot of such as PTSD and eating disorders. Assess
difficulties during the antenatal period. her development and its relationship to
It is important to hear from her views of her current regression. An understanding
childbirth and explore her thoughts and of interpersonal issues and relevant crises
feelings during pregnancy. The candidate including coping responses is important.
should assess the impact of her borderline 5. The candidate should also hear from the
personality disorder on motherhood (e.g. patient about her unmet needs and prefer-
was this pregnancy unplanned and based ence for treatment. The candidate should
on a short intense relationship with a man? also explore treatment (e.g. psychother-
Assess her current relationship with the apy) received in the past and the outcomes
father of the baby.) The candidate should of various treatment interventions. If the
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30 Cross-Cultural Psychiatry
30.1 BASIC CONCEPTS 30.1.1 Cultural Assessment

Culture is defined as the learned way of life of a group The DSM-5 (APA, 2013) has a section on cultural for-
of people bound together by a common social heritage. mulation interview. Selected and modified questions are
People of the same cultural group behave, think, and give listed as follows:
meaning to their life in a similar way and share a set of
values and beliefs. 1. Cultural definition of the problem: Patients often
Ethnicity is defined as the specific patterns of a group understand their problems in their own way based
of people by a common genetic background, country of on their cultural background. The understanding
origin, and language. Ethnicity is one of the aspects of may be similar or different from Western medi-
culture. cine. How would you describe your problem?
Race is defined as the biological features of a group 2. Culture perceptions of cause: What do you
of people by similar skin colour and other physical think are the causes of your problems based on
characteristics. your own cultural belief? Could it be related to
Cultural consciousness is defined as the personal con- bad things in life, interpersonal problems, or
sciousness of his or her own cultural identity. Cultural spiritual issues?
consciousness is developed in the following stages: 3. Cultural identity: Do you see your cultural
It starts with naivety and the individual has no aware- background causing the current problems? Do
ness of his or her own cultural identity. Then the person members from your cultural group offer help to
comes into acceptance of his or her own cultural identity cope with the current situations?
and becomes resistance to other cultures. As the patient 4. Help seeking from own culture: Do you seek
matures, he or she redefines and reflects on his or her help from traditional healers or therapists? In
own cultural consciousness and leads to multiperspective comparison to Western medicine, which type of
internalization. treatment was most helpful or most unhelpful?
Acculturation is defined as the decision made by 5. Doctor–patient relationship: Based on our cul-
an individual to adopt cultural values from a domi- tural background, do you find it difficult for the
nant culture and undergo changes. For example, doctor to understand you? Do you feel discrimi-
a Chinese immigrant to the United Kingdom finds nated as a result of your cultural background?
his or her children adopt the British culture and not Do you feel psychiatric services in the trust suit
interested in the Chinese culture after migration to people sharing the same culture with you?
the United Kingdom. Acculturation has four compo-
nents: assimilation, integration, marginalization, and
separation. 30.2 INTERNATIONAL COMPARISONS
Alienation is defined as the sense of powerlessness,
social isolation, and entrapment because the person is not
30.2.1 Schizophrenia
belonging to a culture and not feeling welcome. This may Kraepelin delineated dementia praecox and manic
occur in immigrants that have newly arrived in a foreign depression. In 1904, he visited the asylum of Buitenzorg
country. in Java to examine the similarities and differences
Assimilation is defined as the process of adjustment between European patients and those from another cul-
when two different cultures come into contact with each ture. He was satisfied that he could recognize cases of
other over a long period of time. For example, the colo- dementia praecox in Java, giving credence to his diagnos-
nial Hong Kong demonstrates assimilation of British and tic distinction. This represents one of the first investiga-
Chinese culture. tions in transcultural psychiatry.
459
30.2.1.1 International Pilot Study of Schizophrenia To identify the cause of the good prognosis for schizo-
This study (WHO, 1973) was devised to determine whether phrenia in the less-developed world, Leff et al. (1990)
schizophrenia could be recognized as the same condition in determined the levels of expressed emotion (EE) in a sub-
a wide variety of cultural settings. Nine centres (Columbia, sample of the Chandigarh cohort of first-contact schizo-
Czechoslovakia, Denmark, India, Nigeria, Russia, Taiwan, phrenic patients from the WHO determinants of the
the United Kingdom, and the United States) participated. outcome study. At 1-year follow-up, a dramatic reduction
The Present State Examination was translated into seven had occurred in each of the EE components. No rural rel-
languages, and psychiatrists trained in its use interviewed ative was rated as high EE at follow-up. It was concluded
1200 patients. Diagnoses were then generated using the that the better outcome of this cohort of schizophrenic
computer program CATEGO. The main findings were patients is partly attributable to tolerance and acceptance
by family members.
• When narrow criteria of Schneider’s first-rank
symptoms were applied, an incidence of schizo- 30.2.2 Neurosis
phrenia was found, which did not differ significantly
across cultural settings. Therefore, schizophrenia is Using standardized interviewing and case-finding tech-
recognizable as the same condition across a wide niques, the prevalence rates for neurosis in developing
variety of cultures. countries are comparable with or higher than those
• Broadly defined, schizophrenia has an incidence found in the West, contrary to what was previously
that differs significantly from one country to believed.
another. In many Third World countries, hysteria represents a
• The outcome of schizophrenia was found to high proportion of psychiatric practice. In the West, there
vary inversely with the social development of has been a substantial decrease in the numbers of patients
the society. Those from developing countries with hysteria and a compensatory rise in the incidence of
had a better prognosis than those from the devel- anxiety and depression. It is suggested that this can be
oped world. seen as a shift from a somatic to a psychological mode
of communication of emotional distress. The tendency
to express distress in a psychological form is associated
30.2.1.2 Determinants of Outcome Study with higher social class and education. Catatonia could
This study (Sartorius et al., 1986) extended its case- similarly be viewed as a nonverbal manifestation of
finding techniques to include rural primary health-care schizophrenia.
centres, traditional healers, police stations, and prisons as Orley and Wing (1979) investigated the rates of psy-
well as the more conventional psychiatric settings. More chiatric illness in two villages in East and West Africa.
than 1300 cases were interviewed in 12 centres across 10 The rates of depression and anxiety showed large differ-
countries. The main findings were ences (22% and 10%, respectively). Compared to rates
in Western countries (10%–12%), these rates are high.
• The incidence of narrowly defined schizophre- Communities in the developed and undeveloped world
nia was stable across a wide range of cultures, are heterogeneous, a point emphasized by the ‘new cross-
climates, and ethnic groups, confirming findings cultural psychiatry’ (see succeeding text).
of the International Pilot Study of Schizophrenia In comparing the psychopathology of Jewish and
(IPSS). The form of presentation of schizophre- gentile East London depressives, hypochondriasis and
nia varied across cultures. tension are much more common in the Jewish group,
• Catatonic schizophrenia was a common form of whereas guilt is more common in the gentiles. Guilt is
presentation in the underdeveloped world but has culturally determined and more common in Christians.
become much rarer in the West. Catatonia pre- Somatic symptoms of depression appear to be uni-
sented in 10% of cases in developing countries but versal, but the concept of depression of mood is not rec-
in only a handful of those in developed countries. ognized in all cultures; many cultures do not have the
• Hebephrenic schizophrenia was diagnosed in language to express the feeling of depression as described
13% of cases from developed countries but in in the West. Instead, such terms as ‘sinking heart’ or
only 4% of cases from developing countries. ‘soul loss’ are found. In China, 87% of people suffering
• In developing countries, acute schizophrenia was from neurasthenia fulfil the criteria for major depression
diagnosed more often than in developed countries. and respond to treatment with antidepressants.
Cross-Cultural Psychiatry 461
30.2.2.1 New Cross-Cultural Psychiatry 30.2.2.3 Classificatory Systems

Kleinman (1977) described the ‘new cross-cultural psy- Europe and North America have greatly influenced the
chiatry’. He criticized as a category fallacy the assump- models of mental illness and the classification of mental
tion that Western diagnostic categories were themselves illness over the last century. ICD-10 has been criticized
culture-free entities. in cross-cultural terms. The international group of psy-
Anthropologists have criticized the older transcultural chiatrists involved in drawing up the first draft consisted
epidemiological research for imposing Western concepts of 47, only 2 of whom were from Africa. Thus, condi-
of psychopathology on non-Western people. These stud- tions encountered in many other cultures that do not
ies have also been criticized on the grounds of translation resemble Western categories have been assigned the title
difficulties, the poor quality of questionnaire-generated ‘culture-bound’ conditions or ‘masked’ representations
diagnosis, a disregard for various understandings of the of ‘real’ illness.
self, and for ignoring the cultural variation for broadly
defined illness. 30.2.2.4 Culture-Bound Syndromes
Beliefs about the mechanisms of illness among people
Debate exists about what constitutes a culture-bound
in the underdeveloped world have been divided into three
syndrome. The term is used to describe disorders that
main ideas:
are considered unique to a given culture (cultural deter-
minist view). However, the question of whether the clas-
• Object intrusion. This is illness caused by a
sically described ‘culture-bound syndromes’ are actually
physical object being intruded into the person’s
unique to the given culture, or are in fact universal phe-
body.
nomena merely influenced by culture (universalist view),
• Spirit intrusion. A spirit is believed to take pos-
has not been settled. The following syndromes are fre-
session of the person’s body.
quently cited.
• Soul loss. The soul of the person is believed to
have been stolen by spirits.
30.3 CULTURE-BOUND
30.2.2.2 Translation and Validity of Rating Scales SYNDROMES IN ASIA
In the translation of rating scales, five types of problem
30.3.1 Amok
in validity arise:
Occurring in Malays, amok consists of a period of with-
• Content validity. The content of instruments drawal, followed by a sudden outburst of homicidal
must be relevant in the culture into which the aggression in which the sufferer will attack anyone
instrument is translated. For example, coca within reach. The attack typically lasts for several hours
paste abuse is common in Peru, so the substance until the sufferer is overwhelmed or killed. If alive, the
abuse schedule should reflect this. person typically passes into a deep sleep or stupor for
• Semantic validity. Words used in the origi- several days, followed by amnesia for the event. It almost
nal and new instruments must have the same always occurs in men.
meanings. It was first described in Malays in the mid-sixteenth
• Technical validity. Where languages are not century. It is believed to have originated in the cultural
written or illiteracy rates are high, answering a training for warfare among Malay warriors. Later it
questionnaire may elicit answers that represent a became a personal act by an isolated individual, appar-
misunderstanding of the intention. ently motiveless, but the motive could be understood as
• Criterion validity. Do responses to similar the restoration of self-esteem or ‘face’.
items measure the same concept in two cul- It was very common in Malaya at the beginning of the
tures? For example, in American Indians, hal- nineteenth century, but the incidence was reduced when
lucinations normally occur during the course the British took over the administration of Malaya. Today
of bereavement, but this is not the case in it has virtually disappeared.
North Americans generally; this must thus be It is most common in Malays, but reports of amok
accommodated. from other countries exist, questioning its position as a
• Conceptual validity. This requires that responses culture-bound syndrome; it is clear, however, that there is
relate to a theoretical construct within the culture. a strong cultural element.
Among Malay cases in mental hospitals, the most passing of semen in urine as a consequence of excessive
common diagnosis is schizophrenia. Depression, acute indulgence in masturbation or intercourse.
brain syndrome, and hysterical dissociation have also Patients are typically from a rural area, from a family
been found in some cases. The majority do not have with conservative attitudes towards sex and of average or low
a mental illness. Attacks are often preceded by inter- socioeconomic status. Literacy and religion are unimportant.
personal discord, insults or personal loss, and social Bhatia and Malik (1991) studied male patients attend-
drinking. ing a sexual problems clinic in New Delhi. They found
that 65% arrived with a primary complaint of dhat syn-
drome. Twenty-three per cent of these also complained of
30.3.2 Latah
impotence or premature ejaculation. The age of presenta-
This usually begins after a sudden frightening experi- tion is early twenties, with about 50% unmarried. Most
ence in Malay women. It is characterized by a response are literate. Although some suffered from depression and
to minimal stimuli with exaggerated startles, coprolalia, anxiety, those with dhat syndrome differed from the oth-
echolalia, echopraxia, and automatic obedience. It has ers only in the relative absence of depression and anxi-
been suggested that this is merely one form of what is ety. Treatment with anxiolytics or antidepressant drugs
known to psychologists as the ‘hyperstartle reaction’ and resulted in significant improvement, however.
is universally found. Dhat syndrome is considered by many to be a true
culture-bound condition. The belief in the precious prop-
erties of semen is ingrained in Indian culture.
30.3.3 Koro
This is common in Southeast Asia and China; it 30.3.5 Frigophobia
may occur in epidemic form. It involves the belief of
genital retraction with disappearance into the abdo- Frigophobia is common in China and Southeast Asia.
men, accompanied by intense anxiety and the fear of Patients believe that excessive cold results in illness and
impending death. they compulsively dress in heavy or excessive clothing.
Cases of a similar condition have been described in
non-Chinese subjects. In these cases, the syndrome is 30.3.6 Taijinkyofusho
often only partial, such as the belief of genital shrinkage,
Taijinkyofusho is common in Japan. The patient fears that
not necessarily with retraction into the abdomen; it usu-
he or she offends the other people or makes them uncom-
ally occurs within the context of another psychiatric dis-
fortable through inappropriate behaviour or self-presenta-
order and resolves once the underlying illness has been
tion (e.g. offensive odour or physical blemish). Differential
treated.
diagnosis such as social phobia should be considered.
Debate about the cultural specificity of this disorder
continues. Some argue that the culturally determined
syndrome is clearly different from the symptom of geni- 30.4 CULTURE-BOUND
tal retraction occurring in some non-Chinese psychotic SYNDROMES IN AMERICA
subjects.
The development of koro has been associated with 30.4.1 Piblokto
psychosexual conflicts, personality factors, and cultural This dissociative state is seen among Eskimo women.
beliefs in the context of psychological stress. The patient tears off her clothing, screams, cries,
and runs about wildly, endangering her life by expo-
30.3.4 Dhat sure to the cold. It may result in suicidal or homicidal
behaviour.
This is commonly recognized in Indian culture and is
also widespread in Nepal, Sri Lanka, Bangladesh, and
30.4.2 Susto
Pakistan. Dhat was prevalent in Europe in the nineteenth
century because masturbation was prohibited by religion Susto literally means the loss of soul. This syndrome is
and emission was a sin. It includes vague somatic symp- common in Mexico and Central and South America. The
toms (fatigue, weakness, anxiety, loss of appetite, guilt, aetiology of susto includes organic causes, stress, and
etc.) and sometimes sexual dysfunction (impotence or social inadequacy. Patients usually present with both psy-
premature ejaculation), which the subject attributes to the chiatric and physical symptoms. Psychiatric symptoms
include depression, anxiety, and paranoia. Organic symp- Sufferers of brain fag syndrome are resistant to psy-
toms include indigestion and anaemia. chological interpretation of their condition. It is suggested
that brain fag syndrome is a form of depression in which
30.4.3 Windigo depressive features are not articulated in Western psycho-
logical terms.
This is described in North American Indians and ascribed
to depression, schizophrenia, hysteria, or anxiety. It is a dis-
order in which the subject believes he or she has undergone 30.5.3 Ufufuyane
a transformation and become a monster who practises can- Ufufuyane is common in South Africa. Clinical fea-
nibalism. However, it has been suggested that windigo is in tures include anxiety, convulsions, repeated neologisms,
fact a local myth rather than an actual pattern of behaviour. paralysis shouting, sobbing, trance-like stupor, and loss
of consciousness. Patients may complain of nightmares
30.4.4 Uqamairineq with sexual themes and temporary blindness.
Uqamairineq is common in Inuits living within the
Arctic Circle. Prodromal symptoms include transient 30.5.4 Nerfiza
auditory or olfactory hallucinations. Patients with uqa- Nerfiza is common in Egypt, Northern Europe, Greece,
mairineq present with sudden paralysis in semi-sleeping Mexico, and Central and South America. Clinical features
states, anxiety, agitation, and hallucinations. include depression, anxiety, and fearfulness. Patients
present with somatic complaints such as headache and
30.5 CULTURE-BOUND muscle pain, appetite loss, agitation, nausea, giddiness,
SYNDROMES IN AFRICA insomnia, fatigue, and tingling sensation.
30.5.1 Bouffee Delirante
30.6 PSYCHIATRY AND BLACK AND ETHNIC
Bouffee delirante is common in West Africa and Haiti. MINORITIES IN BRITAIN
Patient presents with sudden outburst of agitation, aggres-
sion, and auditory and visual hallucinations. Bouffee Britain is a multiracial society. In some large cities, eth-
delirante resembles acute and transient psychosis. nic minorities represent 30% or more of the total popula-
tion. Ethnic minority groups are of two types:
30.5.2 Brain Fag Syndrome • Immigrants
This is a widespread low-grade stress syndrome described • Second- or third-generation residents
in many parts of Africa and also in New Guinea. It is com-
monly encountered among students, probably because of The stresses incurred by these two groups are different.
the high priority accorded to education in African society, Ethnic minority groups are heterogeneous in terms of
and is particularly prevalent at examination times. religion and cultural background.
Five symptom types have been described as compris-
ing brain fag syndrome: 30.6.1 Immigrants
• Head symptoms—aching, burning, crawling People migrate for various reasons, and so adjustment
sensations will depend on many factors including those operating
• Eye symptoms—blurring, watering, aching before migration, the reasons for migration, and factors
• Difficulty in grasping the meaning of spoken or operating in the host society.
written words
• Poor retentivity 30.6.1.1 Types of Migrants
• Sleepiness on studying • Settlers are likely to be prepared for a new way
of life.
Guinness (1992) found the rates to be highest in rural • Exiles have been forced to migrate. This may
areas serving peasant populations (34% of students), com- result in grief reaction for their old way of life.
pared to peri-urban schools (22%) and schools for the pro- They may have suffered torture or other atroci-
fessional élite (6%). ties before migration.
• Migrant workers are less likely to put down these criticisms. Harvey et al. (1990) studied consecutive
roots in the host country. They may be support- Afro-Caribbean and white British psychotic inpatients
ing their family financially at home. prospectively and found no differences in the course of
• Others: students, business people, etc. illness or the pattern of symptoms. This caused them to
reject the hypothesis that misdiagnosis accounts for the
30.6.1.2 Stresses Involved in Migration higher rates of schizophrenia in this group.
There are various social stresses: Schizophrenia as defined by operational research cri-
teria is more common in people of Afro-Caribbean ori-
• Culture shock and readjustment to the host society gin living in the United Kingdom.
• Downward social mobility, poor housing, unem- Sugarman and Craufurd (1994) found a lifetime
ployment or job dissatisfaction, unfulfilled aspi- morbid risk of schizophrenia in the parents of Afro-
rations, and lack of opportunities Caribbean subjects to be the same as the risks to par-
• Racial prejudice and discrimination in the host ents of British white schizophrenic subjects (8.9% and
society 8.4%, respectively). However, for the siblings of Afro-
• Loss of extended family support Caribbean probands, the risk was 15% compared to
• Intergenerational difficulties as children inte- 1.8% for white siblings. Among the siblings of U.K.-born
grate, bringing cultural conflict into the home Afro-Caribbean probands, the risk was even higher at
27.3%. These observations suggest that schizophrenia in
In a 3-year follow-up study of Vietnamese boat people given Afro-Caribbean patients is no less familial than the rest
asylum in Norway, Hauff and Vaglum (1995) found there of the population (as evidenced by the similar risks to
was no decline in psychological distress over time. One in parents) but that the increased risk is caused by environ-
four suffered psychiatric disorder and the prevalence of mental factors capable of precipitating schizophrenia in
depression at 3 years was 18%. Female gender, extreme trau- those who are genetically predisposed to it.
matic stress in Vietnam, negative life events in Norway, and The environmental factor postulated has not been
chronic family separation were the predictors of psychopa- identified to date. There is no evidence of increased rates
thology. Thus, the effects of war and persecution were long of schizophrenia in the West Indies and therefore no evi-
lasting and compounded by adversity in exile. dence that Afro-Caribbeans carry a greater genetic load-
Some studies have found that the mental health of ref- ing for schizophrenia.
ugees improves over time, and it is possible that adverse Admission rates for Asians are similar to Europeans,
factors in the host environment have significant effects on except for the 16–29-year age group, who tend to have
the readjustment and mental health of refugees. lower psychiatric admission rates than Europeans. This
gives rise to concerns that services are not reaching this
30.6.2 Mental Illness among Ethnic Minorities particular group.
30.6.2.1 Schizophrenia
The higher than expected rates of schizophrenia among 30.6.2.2 Suicide
Afro-Caribbean people born in Britain have been noted 30.6.2.2.1 The United Kingdom
since the 1960s. Studies of hospital admissions have Raleigh and Balarajan (1992) reported suicide rates
demonstrated high rates of schizophrenia in this group among British ethnic minority groups compared to the
compared to British whites and Asians. indigenous British white population:
The highest rates of schizophrenia in the Afro-
Caribbean group occur in U.K.-born second-generation • Suicide rates were high among young Indian
subjects (up to nine times that among Europeans). women (age-specific standardized mortality
Differences persist even when age and socioeconomic rates (SMRs) of 273 and 160 at ages 15–24 and
status are taken into account. 25–34, respectively) but low among Indian men
These results have caused controversy, with criticisms (SMR 73).
of misdiagnosis due to unfamiliar culturally determined • Suicide rates were low in Caribbeans (SMRs 81
patterns of behaviour, acute psychotic reactions being and 62 in men and women, respectively).
mistaken for schizophrenia, or racism accounting for the • Suicide rates were high in East Africans (SMRs
observed differences. However, well-designed studies 128 and 148 in men and women, respectively) and
dealing with methodological problems fail to substantiate were largely confined to the younger age groups.
• Immigrant groups had a higher rate of sui- 30.6.2.4 Child and Adolescent

cide by burning, with a ninefold excess among Psychiatric Presentations
Indian women. Second-generation Afro-Caribbean children present-
• Goth youth culture in the United Kingdom (Young ing to child and adolescent psychiatric services dif-
et al., 2006): Goth refers to subgenre of punk with a fer in their patterns of presentation when compared to
dark and sinister aesthetic, distinctive clothing, and British white children of comparable age and socioeco-
taste in music. The prevalence of self-harm in Goth nomic status.
youth culture is 53% (cf. 7%–14% of self-harm Psychotic and autistic disorders are overrepresented
among young people in the United Kingdom). The in Afro-Caribbean children compared to whites, with
prevalence of attempted suicide is 47%. psychotic disorders present in 3.4% and 0.8%, respec-
tively, and autistic disorders present in 3.4% and 0.6%,
30.6.2.3 Other Countries respectively. Studies also find that the autistic children
Aboriginal people in Australia: The gender ratio is 7:1. of immigrant parents are more likely than their white
Hanging is the most common method. Causes include counterparts to be severely or profoundly mentally handi-
marginalization, purposeless in life, poor social support, capped. Mental handicap is also overrepresented in Afro-
poor education, and alcohol abuse. Caribbean children (19% vs. 11%).
Afro-Caribbean children present with a significantly
China: Half of all female suicides in the world come higher rate of conduct disorder (35% vs. 25%) and a sig-
from China. Rural women attempt suicide by pesticide nificantly lower rate of emotional disorder (18% vs. 27%)
ingestion. when compared to white counterparts.
Hong Kong: Dramatic increase of suicide by charcoal
burning in airtight space (age: 25–54 years). Common
causes include debts and financial difficulty. 30.6.3 Use of Psychiatric Services
by Ethnic Minorities
India: High suicide rates among young Indian women
are reported within India and in countries where Indian Young, male, black, schizophrenic Afro-Caribbeans
immigrants have settled. High expectations of academic have high psychiatric admission rates compared to white
and economic success, the stigma of failure, the authority British and a higher rate of compulsory admissions. In
of their elders, and the expected unquestioning compli- inner-city London, the ratio of black Afro-Caribbeans
ance of younger family members are thought to predis- to whites among admissions is higher than the equiva-
pose to suicide in this culture. Among Indian women, lent proportion in the population (three times higher in
these pressures are accentuated by expected submission Hammersmith and Fulham).
and deference to males and elders. Rates of suicide and Part of the explanation for this is the higher rates of
attempted suicide in this group are not greatly different schizophrenia in black Afro-Caribbeans. Bebbington
from those in the country of origin, suggesting that the et al. (1994) concluded that ethnicity was not of major
increased rates are not particularly related to issues of importance in decisions to use the Mental Health Act
migration. In India, dowry-related self-burning is well in two regions in London. The use of compulsion was
known. The common causes of suicide by burns in young strongly linked with challenging behaviour and diagnosis
women include marital problems and interpersonal dif- of schizophrenia but not with ethnicity per se.
ficulties with other family members. In contrast, sui- Dunn and Fahy (1990), studying police admissions
cide rates among older Indian women are low, which is under Section 136 of the Mental Health Act 1983 to a
thought to accord with the greater respect given to them South London psychiatric hospital, found an excess of
by virtue of their age. admissions of blacks. However, clinicians judged that
more than 90% of detained black and white subjects were
Japan: Responsibility-driven suicide is often committed
suffering from a psychiatric disorder and were therefore
by middle-aged men. Elderly accounts for 24% of suicide
appropriately detained. The judgement of the police in
and associates with depression and somatic complaints.
this study was not biased towards apprehending black
Māori (indigenous peoples) in New Zealand: There has people as a result of unconscious racist attitudes, as pre-
been recent increase of suicide among young Māori men. viously suggested by some.
Depression and suicidal ideation are common among Cole et al. (1995) found that for first-episode patients,
Māori adolescents. the route to psychiatric care in Haringey (North London)
was different from those for chronic patients. While com- REFERENCES
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31 Liaison, Organic, and
Neuropsychiatry
31.1 LIAISON PSYCHIATRY somatoform disorders. Changes in physical symptoms

mirrored changes in emotional arousal.
31.1.1 Somatization Disorder
Social learning: Somatizers were more likely to report
There are multiple, recurrent, frequently changing physi- parental physical illness and to have had more physi-
cal symptoms. Most patients have multiple contacts with cal illness themselves in childhood. Emotionally dis-
primary and specialist medical services; there are many ordered subjects reported more parental lack of care.
negative investigations. Gastrointestinal and skin symp- It was hypothesized that physical illness in childhood
toms are most common. Sexual and menstrual complaints lessened the distress of lack of care, resulting in somatic
are also common. Onset after the age of 40 may indicate rather than emotional responses as a means of attract-
the onset of affective disorder. ing care or lessening hostility, which endures into adult
life. Somatic symptoms represent a way of communi-
cating emotions.
There is a 0.2%–0.5% prevalence in the United Kingdom:
1. Three per cent of repeated gut clinic attenders
ICD-10 requires the presence of all the following:
have somatization disorder.
2. Using abridged criteria (four unexplained symp-
• Two years of multiple and variable physical
toms in males, six in females), the prevalence is:
symptoms, with no physical explanation found
a. Community—4.4%
• Persistent refusal to accept the advice of several
b. Patients with medically unexplained
doctors
symptoms—32%
• Impairment of functioning attributable to symp-
3. It is far more common in women than men
toms and resulting behaviour
(F:M = 5:1).
4. It is more common in people with lower educa-
The possibility of developing an independent physical
tion and from lower socioeconomic class.
disorder should be considered.
5. It usually starts in early adult life except somato-
The emphasis on symptoms and their effects distin-
form pain disorder that starts later in life.
guishes this from hypochondriacal disorder (see follow-
31.1.1.2 Aetiology ing text) where the emphasis of concern is on possible
underlying disease.
Genetic factors: Torgersen (1986) reported an MZ to DZ
Briquet’s syndrome or St. Louis hysteria is a multiple
concordance in somatoform disorder of 29:10. This sug-
somatization disorder.
gests that somatoform disorder has a familial transmis-
Somatization disorder is renamed as somatic symptom
sion. There is an increased rate of dissocial personality
disorder in the DSM-5 (APA, 2013). Patients suffer from
disorder among first-degree relatives.
somatic symptoms that cause distress and result in signifi-
Environmental factors: The South London somatization cant disruption in life. Patients also have disproportionate
study reported by Craig et al. in 1993 was a longitudinal and persistent thoughts about the seriousness of somatic
study in primary care; it compared somatizers with those symptoms. The symptoms lead to high level of anxiety.
with pure emotional disorder and those with pure physical As a result, excessive time and energy are devoted to the
disorder. The physical symptoms of somatizers were less symptoms concerned. The duration is at least 6 months.
likely to improve; one-third went on to develop chronic Specific feature includes predominant pain.
469
31.1.1.3.1 Comorbidities earlier, this significantly reduces the use of resources.

Comorbidities include depressive disorder, anxiety disor- However, depression and anxiety are often present and
ders (e.g. generalized anxiety disorder, panic disorder, and may require treatment. Prognosis is poor and 80% of
social phobia), adjustment disorder, psychotic disorder, patients continue to suffer from somatization disorder
histrionic personality disorder, dissocial personality dis- after 5 years.
order, substance misuse, and other somatoform disorder.
31.1.2 Somatoform Autonomic Dysfunction
31.1.1.3.2 Management
Engage the patient and spouse. Conduct no more inves- Symptoms are presented as if caused by a disorder of
tigations but listen empathically. Elicit childhood expe- a system or organ largely under autonomic control (e.g.
rience of illness and parental disability. Link physical cardiac neurosis, psychogenic hyperventilation, gastric
symptoms to relevant life events (the reattribution neurosis, nervous diarrhoea).
model of Goldberg). Reduce all medication apart from ICD-10 (WHO, 1992)
antidepressants for the depressed. Limit the expecta-
tions of cure. • There are persistent and troublesome symptoms
Psychotherapies are useful in the treatment of somati- of autonomic arousal.
zation disorder: • Symptoms are referred to a specific organ sys-
tem, with no evidence of organ pathology.
• There is distress about the possibility of disorder
1. Cognitive therapy: Cognitive therapy is use- of the organ system, not responsive to repeated
ful in the treatment of somatization disorder reassurance.
by helping the patient to establish the con-
nection between emotions and somatic symp-
toms. Dysfunction thought diary records 31.1.3 Persistent Somatoform Pain Disorder
somatic symptoms and emotionally significant This presents with persistent, severe, distressing pain, not
life events causing the somatic symptoms. explained by physical disorder. Pain occurs in association
Psychologist can help the patient to review with emotional conflict and results in increased support
thoughts and beliefs focusing on somatic com- and attention.
plaints and advise the patient to consider alter- The prevalence of persistent pain is 3%. The onset
natives. The goal of cognitive therapy is to help of somatoform pain disorder is usually between 40
the patient to reattribute physical symptoms and 50 years. The female to male ratio is 2:1. Acute
to underlying psychological state (e.g. stress, pain (<6 months) is associated with anxiety disorder.
depression). Chronic pain (≥6 months) is associated with depres-
2. Behaviour therapy: Enhance activity level, sive disorder. The onset of somatoform pain is usually
encourage positive coping behaviours, and abrupt. Treatment involves antidepressants (e.g. dulox-
develop alternative ways to express emo- etine, nortriptyline), gradual withdrawal of analgesics,
tions and not to focus on somatic symptoms in cognitive–behavioural therapy (CBT) (challenges cog-
communications. nitive and behaviour activation) and relaxation tech-
3. Family support: Educate the partner or other niques. In general, acute pain carries a better prognosis
family members on how to respond to patient’s than chronic pain.
somatic complaints.
31.1.4 Hypochondriacal Disorder
Alexithymia (limited ability to describe emotions ver-
bally) is common in somatoform disorder. Traditional 31.1.4.1 Epidemiology
psychotherapy with alexithymic individuals is difficult. The prevalence of hypochondriacal disorder in the
A more reality-based educational and supportive general population is 1%. The prevalence among
approach is better. medical patients is 5%. The onset was between 20 and
30 years. It occurs in both men and women, with no
31.1.1.3.3 Course and Prognosis familial characteristics. Hypochondriacal disorder is
The course is chronic and fluctuating. Treatments use dis- associated with lower economic status and history of
proportionate health resources. If engaged as mentioned medical illnesses.
Liaison, Organic, and Neuropsychiatry 471
31.1.4.2 Aetiology 2. Behaviour therapy: Self-monitoring of worries,

The aetiology of hypochondriacal disorder includes social negative thoughts, and illness-related behaviours. It
learning theory and patients may adopt a sick role to also involves exposure and response prevention and
avoid obligations. From the psychodynamic perspectives, reducing repeated reassurance-seeking behaviours.
aggression is transformed into hypochondriacal ideas. 3. Relaxation techniques.
ICD-10 (WHO, 1992)
• There is a persistent belief in the presence of The course of hypochondriacal disorder is usually epi-
at least one serious physical illness, despite sodic and patients may present with different hypochon-
repeated investigations revealing no physical driacal idea each time. Around 30%–50% of patients
explanation of presenting symptoms, or persis- have good prognosis. Good prognostic factors include
tent preoccupation with presumed deformity. good past health, high socioeconomic status, and sudden
• There is a persistent refusal to accept the advice onset of hypochondriacal ideas.
of several different doctors that there is no phys-
ical illness underlying the symptoms. 31.1.4.6 Conversion Disorder and Body
Dysmorphic Disorder
Attention is usually focused on one or two organ systems Conversion disorder and body dysmorphic disorder are con-
only. Anxiety disorders (e.g. generalized anxiety disorder, sidered in Chapter 28.
obsessive–compulsive disorder [OCD]) and depressive dis-
order are common comorbidity. If depressive symptoms
31.2 FACTITIOUS DISORDER
are prominent and precede the onset of hypochondriacal
ideas, then depressive disorder may be primary. AND MALINGERING
31.2.1 Factitious Disorder
31.1.4.3 DSM-5
The DSM-5 proposed to rename hypochondriasis as illness In factitious disorder, the patient intentionally produces
anxiety disorder (APA, 2013). In order to fulfil the diagnos- physical or psychological symptoms but the patient is
tic criteria, the patient is preoccupied with having a serious unconscious about his or her underlying motives. The
illness that is clearly excessive or disproportionate. Somatic patient may have working experience in the healthcare
symptoms are usually not present and only be present mild setting and equip with basic medical knowledge. Common
in intensity. The person also exhibits high level of anxiety presenting signs and symptoms include bleeding, diar-
and easily be alarmed about health and performs excessive rhoea, hypoglycaemia, infection, impaired wound heal-
health-related behaviours (e.g. repetitive checking). The ing, vomiting, rashes, and seizures. The patient often has
duration of illness is at least 6 months. There are two types poor prognosis and refuse to receive psychotherapy.
of illness anxiety disorder, the care-seeking subtype that is
associated with increased rate of medical consultation and 31.2.2 Factitious Disorder by Proxy
the care-avoidant subtype that is associated with avoidance
of medical consultation and treatment. In factitious disorder by proxy, the patient intention-
ally produces physical signs or symptoms in another
31.1.4.4 Management person (usually an infant or a child) who is under the
Psychiatrists should advise medical colleagues or general patient’s care.
practitioners to gradually reduce the frequency of visits
and unnecessary investigations by increasing the dura-
31.2.3 Malingering
tion between appointments.
Antidepressant such as SSRI is useful. In malingering, the patient intentionally produces physi-
Psychotherapies are useful to treat hypochondriacal cal or psychological symptoms and the patient is fully
disorder: aware of his or her underlying motives. As a result, the
patient does not want to cooperate for further assessment
1. Cognitive therapy: Reattribution and develop and evaluation because the marked discrepancy between
alternative explanations of symptoms and con- the severity of symptoms reported and the objective
cerns of serious illness. Cognitive restructuring physical findings will be revealed. The patient may suffer
can modify dysfunctional assumptions. from antisocial personality disorder (Table 31.1).
TABLE 31.1
Compare and Contrast Factitious Disorder, Malingering, and Somatization Disorder
Factitious Disorder Malingering Somatization Disorder
Motivation Assume the sick role External gain (e.g. false claim Internal psychological
from an insurance company, motivation
avoid legal responsibility)
Signs or symptoms Intentional production or Intentionally produced Unintentional and
feigning signs or symptoms involuntary
Attitude towards Provide a vague and Poor cooperation in evaluation Frequent medical
medical professionals confusion history and treatment consultation to seek relief
Patient may go from hospital of symptoms
to hospital seeking
hospitalization
31.3 CARDIOLOGY AND PSYCHIATRY The relationship between depression and ischaemic heart
disease (IHD):
The relationship between stress and the cardiovascular
system (Wise and Rundell, 2002): 1. Twenty per cent of patients with IHD have
comorbid depression.
1. Stressful life events lead to appraisal of the current 2. Major depression as an independent risk factor
situation. Primary appraisal assesses the threat- for IHD.
ening nature of a life event. Secondary appraisal 3. After an acute myocardial infarction, major
assesses the adequacy of coping strategies. depression predicts mortality in the first
2. There will be three phases of responses. Phase 6 months. The impact of a depressive episode is
1 is an alarm reaction, phase 2 is the resistance equivalent to the impact of a previous infarct.
stage, and phase 3 is the exhaustion stage.
3. The sympathetic system is activated by stress- The impact of depression on heart diseases:
ful life events. Patient will experience dilation
of pupils, dry mouth, palpitations, and sweating. 1. Poor compliance to cardiac treatment.
4. Chronic mental stress–associated ordinary 2. Autonomic disturbances in depression may lead
life events are the most common precipitant of to heart rate changes and arrhythmias.
myocardial ischaemia in patients with coronary 3. Serotonin dysfunction in depression: platelet
artery disease. Type A behaviour (e.g. aggres- activation and thrombosis.
siveness, impatience, and hostility) is associ-
ated with the incidence of recurrent myocardial
infarction and cardiac death in patients with pre- 31.3.1 Antidepressant Trials in Patients
vious myocardial infarction. Twenty per cent of
Suffering from IHD
people with acute myocardial infarction suffer
from depressive disorder (Friedman et al., 1987). 1. Sertraline Antidepressant Heart Attack
5. Psychosocial stress increases the levels of adrena- Randomized Trial (SADHART)
line and noradrenaline, which causes an increase This study found sertraline to be a safe treat-
in peripheral vascular resistance, resulting in ment for depression after myocardial infarction,
hypertension and hypertrophy of the heart. but there was little difference in depression sta-
6. An acute emotional trigger such as provoking tus between groups receiving sertraline and pla-
anger is the immediate precipitant of arrhyth- cebo after 24 weeks of treatment. However, the
mias in patients who are in a chronic state of effect of sertraline was greater in the patients
helplessness. Helplessness is an underlying with severe and recurrent depression. This study
sense of entrapment without possible escape. was not designed to assess the effects of treat-
Arrhythmias can lead to sudden cardiac death. ment on cardiovascular prognosis, but severe
TABLE 31.2
Use of Psychotropic Drugs for Patients Suffering from Atrial Fibrillation
Mood
Antipsychotics Antidepressants Stabilizers Hypnotics Dementia
Recommended Aripiprazole Mirtazapine (patients Lithium Benzodiazepines Rivastigmine seems
with AF often take Valproate to be the best
NSAIDs and warfarin)
Not recommended Clozapine Olanzapine Tricyclic antidepressants Nil Nil Avoid other
Paliperidone acetylcholinesterase
inhibitors in
paroxysmal AF
cardiovascular events during the 6-month treat- Advanced uraemia causes lethargy, asterixis, myoclo-
ment tended to be less frequent in the sertra- nus, deterioration in total intelligence, and impairment in
line group. The effect of sertraline on chronic working memory.
depression was not evaluated. The differential diagnosis of neuropsychiatric symp-
2. ENhancing Recovery in Coronary Heart Disease toms in CRF patients includes hypercalcaemia, hypo-
(ENRICHD) Study (Berkman et al., 2003) phosphataemia, hypo- or hyperglycaemia, hypo- or
In this trial, the effects of CBT on depression hypernatraemia, drug intoxication, and central nervous
and cardiac outcomes were evaluated. No sig- system (CNS) pathologies such as meningitis, encepha-
nificant difference in the cardiac outcomes was litis, subdural haematoma (SDH), and hypertensive
found between the intervention and the care as encephalopathy.
usual arms. Although substantial improvement Uraemic encephalopathy is associated with nonspe-
in the severity of depression was observed cific EEG changes.
6 months after initiation of CBT, the differ-
ence between both arms diminished over time
and was no longer present after 30 months. 31.4.2 Psychiatric Aspects of Dialysis
3. Myocardial INfarction and Depression—
Intervention Trial (MIND–IT) (Van Melle et al., Psychiatrists are often asked to assess patients with
2007) chronic renal failure refusing dialysis.
Antidepressant treatment did not alter the Assessment should include
course of chronic depression after myocardial
infarction status or improve the cardiac out- 1. Capacity to make decisions: capacity is reduced
comes (Table 31.2). as a result of uraemia; previous views or advanced
directives should be sought and dialysis should
continue to optimize the patient’s condition to
31.4 NEPHROLOGY AND PSYCHIATRY make decisions
31.4.1 Psychiatric Aspects of 2. Presence of depression, hopelessness, and sui-
cidal plan
Chronic Renal Failure
3. Misconception and misunderstanding of dialysis
Chronic renal failure is a result of irreversible loss of glo-
merular filtration rate (GFR). Progressive loss of GFR Dialysis improves uraemic encephalopathy but sexual
leads to end-stage renal failure. dysfunctions and impaired quality of life continue
The most common causes of CRF in the United throughout the course of dialysis. Dialysis dementia is
Kingdom include autosomal dominant polycystic kidney characterized by progressive encephalopathy, stuttering,
disease, diabetes mellitus (DM), chronic pyelonephritis, dysarthria, dysphasia, impaired memory, depression,
glomerulonephritides (IgA nephropathy), hypertension, paranoia, myoclonic jerk, triphasic EEG abnormality, and
obstructive uropathy, and vascular disease. seizures (Tables 31.3 and 31.4).
TABLE 31.3
Use of Psychotropic Drugs for Patients Suffering from Renal Impairment
Mood
Types Antipsychotics Antidepressants Stabilizers Hypnotics
Recommended First-generation antipsychotic drug: Citalopram Valproate Lorazepam
haloperidol 2–6 mg/day Sertraline Carbamazepine Zopiclone
Second-generation antipsychotic drug: Lamotrigine
olanzapine 5 mg/day
Not recommended Sulpiride Tricyclic antidepressant Lithium Diazepam
Amisulpride (because of (long
Avoid highly anticholinergic agent. anticholinergics effects) half-life)
TABLE 31.4
Summary of Electrolyte Disturbances and Psychiatric Manifestations
Low Levels High Levels
Sodium Causes: antidepressants, lithium, carbamazepine, diuretics, Causes: dehydration, diarrhoea, CNS lesions, and severe
SIADH, and compulsive water drinking burns
Neuropsychiatric features: anorexia, fatigue, headache Neuropsychiatric features: reduced consciousness (Na > 160),
confusion, and convulsion (if Na < 115) confusion, stupor, and coma if sodium is very high
Potassium Causes: vomiting, nausea (in bulimia nervosa), laxative Causes: excessive consumption of NSAIDS, potassium
addiction, diuretics, hypomagnesaemia, renal tubular acidosis, supplements, acute and chronic renal impairment, tumour
and Cushing’s disease lysis syndrome
Neuropsychiatric features: muscular weakness, lethargy, and Neuropsychiatric features: weakness, sensory perception
drowsiness. deficits, and delirium
Calcium Causes: hypoparathyroidism, phenytoin, secondary Common causes: hyperparathyroidism, malignancy, chronic
hyperparathyroidism renal failure, dehydration
Neuropsychiatric features: weakness, depression, delirium, and Less common causes: milk-alkali syndrome, sarcoidosis,
seizure thiazide diuretics, and vitamin D
Neuropsychiatric features: anorexia, vomiting, nausea; late
stage: drowsiness, depression, delirium, and seizure
Magnesium Causes: starvation, chronic alcoholism, and acute intermittent Causes: renal failure, magnesium-containing oral
porphyria medication
Neuropsychiatric features: weakness, depression, delirium, Neuropsychiatric features: drowsiness, weakness, and coma
seizure, and hallucination
Metabolic acidosis Metabolic alkalosis
Acid–base Causes: starvation, alcohol, diabetic ketoacidosis, renal failure, Causes: vomiting and chloride depletion
balance and severe sepsis Psychiatric features: irritability, hypoventilation, lethargy,
Psychiatric features: fatigue, anorexia, hyperventilation, and confusion when pH > 7.55
laboured breathing (Kussmaul respiration), coma, and
convulsions
Source: Maxwell, P. H., Medical Masterclass—Nephrology, Blackwell Science, London, U.K., 2001.
31.5 HEPATOLOGY AND PSYCHIATRY early as 3 years of age. Features include hepatic dysfunc-
tion (40%); psychiatric symptoms such as depression,
31.5.1 Hepatic Encephalopathy cognitive impairment, abnormal behaviour, and person-
Hepatic encephalopathy is caused by hyperammonaemia ality change (35%); and renal, haematological, and endo-
and an increase in GABA neurotransmission. crine symptoms. Cirrhosis and fulminant hepatic failure
The stage of hepatic encephalopathy is summarized are well-described complications. Ocular saccades are
as follows: slowed in Wilson’s disease (ocular saccades are also slow
in Huntington’s disease and supranuclear palsy). Other
Stage 0—Subclinical, psychomotor test abnormalities neurological features include dysphagia, drooling, slow-
Stage 1—Lethargy, confusion, excitation, sleep ness, flexed postures, a gaping mouth, dysarthria, coarse
disturbance, and decreased attention tremor, dystonia, rigidity, and chorea. The characteristic
Stage 2—Somnolence, inappropriate behaviour Kayser–Fleischer rings nearly present in all patients with
Stage 3—Stupor but arousable, speech neuropsychiatric symptoms and slit lamp examination
incomprehensible can be performed to verify the diagnosis. Cirrhosis usu-
Stage 4—Coma ally takes two or three decades to develop.
The diagnosis is established by low serum cerulo-
The first step in management of hepatic encephalopathy plasmin, an increased level of copper in the urine (>100
is to identify the underlying cause. Daily dietary protein μg/24 h), and an elevated hepatic copper level (>250 μg of
intake is reduced to 40 g or less, preferably restricted to copper/1 g of liver by dry weight). The CSF urate levels
high biological value protein. Patients will be given laxa- parallel serum levels and these levels are low in Wilson’s
tives, enemas, lactulose, and antibiotics (e.g. neomycin). disease.
Pharmacological treatment includes d-penicillamine
and oral zinc. Liver transplantation is indicated for
31.5.2 Wilson’s Disease (Lishman, 1997) patients with fulminant hepatitis or advanced cirrhosis.
Wilson’s disease is an autosomal recessive disorder
of hepatic copper metabolism. The incidence is 1 in 31.5.3 Use of Psychotropic Drugs for
200,000. The gene responsible for this disorder has been Patients Suffering from Liver Diseases
located on chromosome 13 and encodes a copper-bind-
ing, membrane-spanning protein with ATPase that regu- The general principle includes fewer drugs, lower dose,
lates metal transport proteins. and monitoring of side effects. Avoid drugs that are hepa-
Patients usually present with liver disease during totoxic, sedative, and cause constipation that increases
adolescence; however, clinical onset may be detected as the risk of hepatic encephalopathy (Table 31.5).
TABLE 31.5
Use of Psychotropic Drugs for Patients with Liver Impairment
Types Antipsychotics Antidepressants Mood Stabilizers Hypnotics
Recommended Low dose of haloperidol Paroxetine Lithium Lorazepam
Sulpiride or amisulpride: no Citalopram Oxazepam Temazepam
dosage reduction is required Zopiclone
if renal function is normal
Not recommended Avoid antipsychotic drugs Avoid tricyclic antidepressant Avoid carbamazepine Avoid diazepam that
that have extensive hepatic that is associated with because it induces has long half-life
metabolism such as constipation hepatic metabolism
chlorpromazine that is Avoid fluoxetine because of Avoid valproate because it
associated with long half-life and the risk of is highly protein bound
anticholinergic side effects accumulation of metabolites and metabolized by liver
31.6 ENDOCRINOLOGY AND Rare causes include congenital agenesis, dyshormono-

PSYCHIATRY (GURNELL, 2001) genesis, tumour infiltration, and secondary hypothyroid-
ism with TSH deficiency.
31.6.1 Hyperthyroidism
31.6.2.2 Neuropsychiatric Symptoms
Clinical example: A 30-year-old woman is referred to
Twenty per cent of patients present with psychiatric symp-
your clinic. She is quite edgy and complains that any
toms. Fatigue accompanied by mental and physical slow-
overindulgence has resulted in severe facial flushing. She
ing is a central psychiatric feature. Depression and anxiety
has also been troubled by watery diarrhoea. She has lost
are very common. Cognitive assessment is important.
a significant amount of weight despite good appetite and
Myxedema causes psychotic symptoms (paranoid
her periods have stopped. Thyroid function test shows
delusions, auditory or visual hallucinations) and delirium.
T4 = 250 mmol/L and TSH = 0.2 mU/L.
Epidemiology: Hyperthyroidism affects 2%–5% of all 31.6.2.3 Investigations
women mostly between the age of 20 and 45 years, with Electroencephalogram: One-third of patients show slow-
a F:M ratio of 5:1. ing of the dominant rhythm and a reduction of the back-
ground activity.
Aetiology: Common causes include Grave’s disease
(presence of thyroid antibodies), toxic multinodular goi- 31.6.2.4 Treatment
tre, solitary adenoma, thyrotoxicosis factitia, and drugs
Lithium-induced goitre has been found in 4%–35% of
such as amiodarone and exogenous iodine.
patients and the goitre is reversible after stopping lithium
Rarer causes include thyroid carcinoma, pituitary
for 1–2 months.
tumour, ovarian teratomas, and acute thyroiditis (viral or
Thyroxine replacement therapy may reverse psychiat-
postirradiation). Stress can precipitate Grave’s disease.
ric symptoms. If there is no response by 1 month, psy-
Neuropsychiatric aspects: 50% present with psychiat- chotropic medication such as antidepressant is required.
ric symptoms. Anxiety and depression are common.
Depressive symptoms are not linearly related to thyrox-
31.6.3 Cushing’s Syndrome
ine levels. In the thyroid crisis, delirium will occur (3%–4%).
Psychosis is rare in hyperthyroidism (1%). Clinical example: A 25-year-old woman with long-stand-
ing irregular menses presents with gradually worsening
Treatment: Antithyroid medication, radioactive thy-
hirsutism and weight gain. She has acnes on her faces and
roxine, or thyroid surgery is able to reverse psychiatric
she feels depressed. Her supervisor complains that the
symptoms. If there is no response by 1 month, psycho-
customers do not like her physical appearance because
tropic medication such as antidepressant is required.
she works in a boutique.
Aetiology: Cushing syndrome is most commonly caused
31.6.2 Hypothyroidism
by exogenous administration of corticosteroids. Other
Clinical example: A 45-year-old woman is no longer able causes include ACTH-dependent causes (e.g. Cushing’s
to meet the demands of her job, complaining of excessive disease, ectopic ACTH-producing tumours, and ACTH
tiredness, lethargy, and constipation. The only past medi- administration), non-ACTH-dependent causes (e.g. adre-
cal history is the history of palpitations that are now well nal adenomas or carcinomas), and alcohol-dependent
controlled on amiodarone. pseudo-Cushing’s syndrome.
Neuropsychiatric symptoms: 50%–80% suffer from
Epidemiology: Hypothyroidism is one of the most com-
depression with moderate to severe symptoms. Depression
mon endocrinopathies in the United Kingdom with a
will resolve with the control of hypercortisolism. Suicide
prevalence of 1.4% in females but rarer in men (0.1%).
has been reported in between 3% and 10% of patients.
31.6.2.1 Aetiology Cognitive impairment such as amnesia and attentional
deficits are common.
Common causes include autoimmune hypothyroidism,
Hashimoto’s thyroiditis, postsurgical and postirradia- Investigation: In dexamethasone suppression test, the
tion hypothyroidism, antithyroid, and other drugs such as cortisol level is expected to be less than 50% of the base-
lithium and amiodarone and in mountainous area, iodine line value in Cushing’s disease but not other causes of
deficiency. Cushing’s syndrome.
Psychiatric side effects associated with steroid: emo- 31.6.6 Psychogenic Polydipsia

tional lability (e.g. euphoria, anxiety, depression, hypo-
mania), distractibility, insomnia, auditory and visual Psychogenic polydipsia causes dilutional hyponatraemia
hallucinations, delusions, intermittent memory impair- and reduction in serum osmolality. Unlike SIADH, patients
ment, and mutism. Higher risk if the dose of prednisolone with hysterical polydipsia produce diluted urine. Water
is higher than 40 mg per day and more prone in women. deprivation test under careful monitoring of fluid status is
diagnostic and helps to distinguish psychogenic polydipsia
from SIADH. Psychogenic polydipsia is controlled by lim-
31.6.4 Addison’s Disease iting fluid intake. Management involves offering reassur-
Clinical example: A 30-year-old woman presents with ance to patients and relatives and fluid restriction.
weakness, dizziness, anorexia, weight loss, and gastrointes-
tinal disturbance. On physical examination, there is general- 31.6.7 Diabetes Mellitus
ized hyperpigmentation of the skin and mucous membrane.
She also has postural hypotension and loss of pubic hairs. Clinical Examples
Epidemiology: 75% of adrenocortical insufficiency is 1. A 60-year-old woman suffers from depression.

caused by Addison’s disease. Female to male ratio is 2:1. She has informed you that she has become thirsty
Neuropsychiatric Symptoms and having to pass urine very often. Routine uri-
nalysis shows glycosuria and ketones.
1. Fatigue, weakness, and apathy are common in 2. A 50-year-old man with history of schizophrenia
early stage. and DM is prescribed with clozapine. He com-
2. Ninety per cent of patients with adrenal disor- plains of sudden abdominal pain. Mental state
ders present with psychiatric symptoms. examination reveals that he appears to be agitated
3. Memory impairment is common. and confused. This is an example of clozapine-
4. Depression, anxiety, and paranoia tend to have a induced hyperglycaemia and diabetic ketoacidosis.
fluctuating course with symptom free intervals.
Introduction: DM refers to a group of metabolic disor-
5. Psychosis occurs in 20% of patients.
ders characterized by hyperglycaemia, resulting from
6. Adrenal crisis may lead to delirium.
inadequate production and/or impaired action of insulin.
Type I DM is caused by autoimmunity governed by
31.6.5 Syndrome of Inappropriate Antidiuretic
the HLA class II genes. Environmental factors such as
Hormone Hypersecretion viruses (Coxsackie, rubella, mumps, cytomegalovirus,
Clinical example: A 20-year-old man is referred from the Epstein–Barr virus [EBV]), infants fed on bovine serum
GP for nausea, confusion, and mild irritability. A routine albumin in cow’s milk, and stress.
electrolyte check shows that the serum Na is 120 mmol/L Type II DM is strongly associated with obesity. The risk
(normal range: 135–145 mmol/L). Physical examination to develop type II DM is 40 times higher in people with
reveals no evidence of dehydration and fluid overload. BMI> 35 as compared to those with BMI < 23. Type II DM
Subsequent investigation reveals urine Na excretion of 40 is caused by insulin resistance and defects of insulin secre-
mmol/L (normal range <20 mmol/L), plasma osmolality of tion. Type II DM has high identical twin concordance rate.
250 mOsmol/kg, and urine osmolality of 800 mOsmol/kg.
Chronic hypoglycaemia may cause psychotic symptoms.
Aetiology: Causes include various tumours (e.g. small
Investigations: Glycosuria may suggest the presence of DM
cell carcinoma of the lung), chest infections, CNS causes
but requires blood test to confirm. The diagnosis of DM is
(e.g. tumours, brain abscess, head injury, meningitis),
made on the basis of fasting plasma glucose level of ≥7.0
porphyria, alcohol withdrawal, and a number of drugs
mmol/L that should be confirmed on a second occasion.
such as carbamazepine, chlorpropamide, and vincristine.
Investigations: Syndrome of inappropriate antidiuretic 31.6.8 Diabetes Insipidus
hormone hypersecretion (SIADH) leads to water reten-
tion and low serum sodium level. To make the diagno- Clinical example: A 60-year-old woman has informed you
sis, other causes of dilutional hyponatraemia such as that she has become thirsty and passes urine very often.
diuretic use and excess water intake should be excluded. She has low urine osmolality and high plasma osmolality.
Cranial diabetes insipidus (DI) is caused by post head lability, inattention, intellectual deterioration, and
injury, cranial surgery, radiotherapy, craniopharyngioma, dementia. Prognosis for dementia is unpredictable. Skull
and CNS infection. x-ray may show symmetrical calcification in the basal
Treatment of cranial DI includes symptomatic relief ganglia.
by the synthetic vasopressin analogue desmopressin. Secondary hypoparathyroidism is more common than
Desmopressin is administered orally or more conve- primary hypoparathyroidism. It is often caused by thy-
niently via a nasal spray. roid surgery and associated with acute delirium. Other
psychiatric features include depression, psychosis, mania,
Nephrogenic DI is caused by renal disorders, hypercal-
anxiety, and irritability. The prognosis for psychiatric
caemia, hypokalaemia, and lithium.
symptoms is favourable.
Treatment of nephrogenic DI: Thiazide diuretic (e.g. hydro- Pseudohypoparathyroidism is caused by end-organ
chlorothiazide) and sodium restriction are often effective. unresponsiveness to circulating parathyroid hormone
as a result of familial calcification of basal ganglia. It is
31.6.9 Hyperparathyroidism associated with learning disability with poor response to
treatment.
Clinical example: A 57-year-old woman presents with
thirst, polyuria, constipation, anorexia, malaise, and Physical features: Tetany, cramps, cataracts, and general-
depression. She has history of renal calculus. ized seizures. In the aforementioned clinical example, the
latent tetany is known as Trousseau’s sign. The contrac-
Hypercalcaemia is caused by primary hyperparathyroid-
tion of the facial muscles is known as Chvostek’s sign.
ism and contributes to psychiatric morbidity.
Neuropsychiatric symptoms include the following: 31.7 ONCOLOGY AND PSYCHIATRY
1. Disturbance of mood and drive is prevalent. Tumours induce release of a number of pro-inflammatory
Depression may progress to psychosis and suicide. markers from macrophages and inflammatory cells such
2. Delirium is caused by high calcium levels or as the TNF-α that causes weight loss, fatigue, and consti-
parathyroid crisis. tutional symptoms.
3. Cognitive impairment: impaired attention, men- Symptoms include
tal slowing, and impaired memory.
4. Psychosis (5%–20%): mainly persecutory delu- 1. Pain
sions and hallucinations. 2. Nausea (25% of patients receiving chemotherapy)
3. Fatigue
Treatment: Correction of serum calcium usually results 4. Cognitive impairment
in reversal of psychiatric symptoms. 5. Depression and anxiety (25% of people with
cancer suffer from depressive disorder)
31.6.10 Hypoparathyroidism
Metastatic brain tumours occur in patients suffering from
Clinical example: A 35-year-old woman is referred to primary renal, pancreatic, gynaecological, prostate, and
the liaison team because of acute confusion. She also bladder cancer. Leptomeningeal disease is caused by
complains of muscle cramps and loss of sensation in her non-Hodgkin’s lymphoma and adenocarcinoma of lung.
extremities. Her partner reports that the muscle cramps Effects of direct neurological insults of metastatic brain
are caused by exercise. She had a thyroid surgery 1 month tumours include
ago. On physical examination, a latent tetany is provoked
by inflating a sphygmomanometer cuff to 10–20 mmHg 1. Complex partial seizures
greater than her systolic blood pressure. In addition, tap- 2. Delirium
ping her facial nerve in front of the ear induce a brief 3. Dementia
contraction of her facial muscles. 4. Mania
Epidemiology: More common in women. Common causes of delirium in cancer patients include
Types of hypoparathyroidism. 1. Hypercalcaemia
Primary hypoparathyroidism is rare and associated with 2. Hypomagnesaemia
insidious onset. Psychiatric features include emotional 3. Hyperviscosity syndromes
31.7.1 Side Effects of Chemotherapeutic Agents 31.7.2.3.2 Endocrine Changes

Neuropsychiatric Side Effects of Chemotherapeutic Agents 1. Abnormality in hypothalamic–pituitary–adre-
nal axis
1. Cognitive impairment/dementia as a result of 2. Hypocortisolism
leukoencephalopathy (e.g. cytosine arabinoside,
methotrexate) 31.7.2.4 Diagnostic Criteria
2. Acute confusion (associated with most chemo- The American use of the CDC criteria emphasizes the
therapeutic agents) presence of at least four symptoms (e.g. muscle pain,
3. Manic and depressive symptoms (e.g. steroid, sore throat, headache, shortness of breath, chronic
interferon) cough, visual problems, and difficulties in maintain-
4. Psychosis (e.g. procarbazine) ing upright position) from a list of eight symptoms.
5. Personality change (e.g. cytosine arabinoside) In contrast, the British emphasize less on the somatic
6. Fatigue (e.g. fluorouracil, interleukin, interferon) symptoms but put more emphasis on physical and
7. Seizures (e.g. vincristine, vinblastine, alkylating mental fatigue instead.
agents) Neurasthenia (ICD-10 F48.0): CFS is the functional
8. Anorexia (associated with most chemotherapeu- medical syndrome that is the approximate equivalent of
tic agents) neurasthenia in psychiatry.
9. Neuropathies and sexual dysfunction
10. Cataracts (e.g. steroids)
11. Anticholinergic side effects (e.g. antiemetic agents) 1. Either of the following must be present:
a. Persistent and distressing complaints of
31.7.2 Chronic Fatigue Syndrome feelings of exhaustion after minor mental
(Wessely et al., 2003) effort.
b. Persistent and distressing complaints of
31.7.2.1 Epidemiology feelings of fatigue and bodily weakness
In the United Kingdom, prevalence of chronic fatigue after minor physical effort.
syndrome (CFS) ranges from 0.8% to 2.6% and only 2. At least one of the following symptoms must be
0.1% fulfil the Centres for Disease Control (CDC) (1988) present:
criteria. The female to male ratio is 3:1. The age of onset a. Feelings of muscular aches and pains.
is between 29 and 35 years. People with CFS may have b. The patient is unable to recover from the
lower occupational status and educational background. symptoms in criterion 1 or 2 by means of
rest, relaxation, or entertainment.
31.7.2.2 Aetiology c. The duration of the disorder is at least
1. Persistent viral infection: EBV. EBV is the most 3 months.
common viral cause and attributes to 9%–22% d. Exclusion: organic emotionally labile dis-
of CFS. Enteroviruses (e.g. Coxsackie B) also order, postencephalitic syndrome, postcon-
cause CFS. cussional syndrome, mood disorders, panic
2. Immune dysfunction: abnormal immune disorder, or generalized anxiety disorder.
responses with reduced or enhanced responses
after acute infection. Fibromyalgia is characterized by tenderness at trigger
3. Electrolyte imbalance: low intracellular magnesium. points affecting mainly the cervical and thoracic areas.
4. Chronic candidiasis: chronic intestinal over- Other features include fatigue, poor sleep, joint stiffness,
growth of Candida albicans produces fatigue numbness, and cognitive dysfunction. It is commonly
via toxins or allergic response. associated with depression and anxiety.
31.7.2.3 Pathology
31.7.2.3.1 Immunological Changes 31.7.2.5 Investigations
1. Increase in expression of activation markers on For all patients: FBC, ESR, CRP, U & Es, LFTs, TFTs,
the surface of T lymphocytes urine protein, and glucose.
2. Increase in number of CD 8+ cytotoxic T cells For selected patients: EBV serology, toxoplasmosis serol-
3. Decrease in number of natural killer cell function ogy, cytomegalovirus serology, human immunodeficiency
virus (HIV) serology, CXR, creatinine phosphoki- 31.7.2.7 Prognosis

nase, rheumatoid factor, and cerebral MRI (look for 1. Between 20% and 50% of CFS patients seen in
demyelination). specialist care improve in the medium term, but
fewer than 10% return to premorbid functioning.
31.7.2.6 Management 2. The prognosis is better in children and in
1. Pharmacological treatment: a nonseda- patients in primary care.
tive SSRI such as fluoxetine may be help- 3. The principal predictors of poor outcome or
ful for patients with CFS and depression. treatment response include intensity of focus on
Essential fatty acids may be beneficial. Avoid symptoms of CFS, psychiatric morbidity, poor
benzodiazepine. sense of control, being passive with treatment,
2. Psychological treatment: CBT with graded underlying secondary gain (e.g. disability ben-
activity programme, anxiety management, and efits), and old age.
interpersonal therapy. 4. There is no increase in mortality (with the
3. Rehabilitation: exercise programme. exception of suicide).
CASC STATION ON CHRONIC FATIGUE SYNDROME

Name: Mr. D
Age: 33 years old
Occupation: Accountant
Marital status: Married with two children
Mr. D complains of tiredness, lethargy, and intermittent, vague, generalized muscle pains, which he dates from
when he had glandular fever (infectious mononucleosis) 1 year ago. Mr. D is referred to you by his GP, who has
conducted the following investigations: FBC, U & Es, LFTs, TFTs and urine analysis, all of which are within
normal limits. He has been avoiding contact with his usually extensive social network. Mr. D now does not
entertain any possibility of returning to his previous level of occupational functioning. His wife also says that
she is not coping. The marital relationship is under significant strain.
Task: Take a history to establish the diagnosis.
CASC Grid
(A) (A2) Onset, (A5) Functional

Diagnostic Course and the Impairment and
Criteria of Nature of (A3) Biological (A4) Cognitive Understanding of
CFS (A1) Explore about Fatigue Fatigue Symptoms Symptoms Symptoms
‘Can you tell me more about ‘Besides Explore the Explore the Besides his work,
the fatigue?’ glandular following: following: assess the impact of
‘When did the fatigue start?’ fever, was 1. Sore throat 1. Mental fatigue fatigue on him as a
‘How long have you been there any 2. Muscle and 2. Impaired husband and father.
fatigue?’ (expected to be psychosocial joint pains but memory and ‘What do you think
longer than 6 months) stressor?’ no joint concentration the underlying
‘Do you know your body ‘Is the fatigue swelling 3. To prompt the causes of the fatigue?
weight prior to the onset of persistent or 3. Presence of patient to How do you cope?’
fatigue?’ (exclude fluctuating?’ lymph nodes describe other
premorbid obesity) 4. Unrefreshing symptoms,
‘Do you have any other sleep ‘Are there any
chronic medical illnesses 5. Post-exertional other
prior to the onset of fatigue, malaise (more symptoms you
e.g. diabetes?’ (exclusion tired after have not told
criteria for diagnosis) exercise and not me about?’
relieved by rest)
(B) Exclude
other Causes (B2) General (B3) Neuromuscular (B4) Psychiatric (B5) Drugs and
of Fatigue (B1) Infections Conditions Disorders Causes Substances
1. Infectious 1. Autoimmune 1. Myositis 1. Depression 1. Alcohol
mononucleosis disease 2. Multiple sclerosis (explore suicidal 2. Solvents
is caused by 2. Endocrine 3. Myasthenia thoughts) 3. Side effects of
Epstein–Barr disorders gravis 2. Adjustment medications
virus (EBV) (Addison’s 4. Fibromyalgia: disorder 4. Exposure to
2. Other viral disease, muscle pain in 3. Anxiety and heavy metals
infections include hypothyroidism) bilateral occiput, hyperventilation (e.g. mercury)
Q fever, 3. Cardiac, lower cervical, 4. Somatoform and
toxoplasmosis, respiratory trapezius, disorders irradiation
and CMV; disease, and renal supraspinatus, 5. Hypochondriasis
influenza and failure second rib, 6. Neurasthenia
enteroviruses; 4. Asthma greater 7. Psychosis
chronic active trochanter, and 8. Eating disorder
hepatitis B and knees 9. Narcolepsy and
C; HIV sleep apnoea
3. Lyme disease
4. Cryptococcal
meningitis
(C) Background (C2) Personal History (C3) Current Social (C4) Sick Role and (C5) Social
History (C1) Family History and Personality Situation Employment History
‘Do your family Explore childhood Explore current marital ‘Are you on sick Explore:
members or trauma, unhelpful relationship (why the leave at this 1. Social support
relatives have parenting, long marital relationship is moment? If so, 2. Social
strong ideas about absence from school, strained and what granted by which networks
illness and what repeated episodes of kinds of treatment (if doctor?’ 3. Financial
should be done?’ glandular fever. any) have the couple ‘Is your company problems
‘Do they have Explore personality: received?), difficulties keeping your job?’
difficulty expressing ‘How do you in previous ‘Are you keen to
emotions (i.e. describe yourself as relationships, and return to the current
alexithymia)? Do a person?’ social supports company?’
they express their
emotions through
body symptoms?’
31.8 ORGANIC PSYCHIATRY By convention, the following disorders are excluded from
the category of organic mental disorders and considered
In ICD-10, organic mental disorders are grouped on the separately:
basis of a common demonstrable aetiology being present
in the form of cerebral disorder, injury to the brain, or • Psychoactive substance use disorders (including
other insult leading to cerebral dysfunction, which may be brain disorder resulting from alcohol and other
• Primary—disorders, injuries, and insults affect- psychoactive drugs)
ing the brain directly or with predilection, such • The causes of learning disability (mental
as Alzheimer’s disease retardation)
• Secondary—systemic disorders affecting the
31.8.1 Organic Mental Disorders
brain only in so far as it is one of the multiple
organs or body systems involved (e.g. hypothy- The treatment, course, and prognosis for the following dis-
roidism) (Table 31.6) orders are essentially those of the underlying pathology.
TABLE 31.6
Summary of the Organic Causes of Dementia
Degenerative
Diseases of the
Central Nervous Intracranial Endocrine Vascular
System Intoxication Causes Disorders Metabolic Disorders Causes
Alzheimer’s Alcohol Space-occupying Addison’s disease Hepatic failure Multi-infarct
disease Heavy metals such lesions such as Cushing’s syndrome Renal failure (vascular)
Pick’s disease as lead, arsenic, tumours, chronic Hyperinsulinism Respiratory failure dementia
Huntington’s thallium, and subdural Hypothyroidism Hypoxia Cerebral artery
disease mercury haematomas, Hypopituitarism Renal dialysis occlusion
Creutzfeldt– Carbon monoxide aneurysms, and Hypoparathyroidism Chronic uraemia Cranial arteritis
Jakob disease Withdrawal from chronic abscesses Hyperparathyroidism Chronic electrolyte imbalance Arteriovenous
Normal-pressure drugs Infections (↑Ca2+, ↓Ca2+, ↓K+, ↑Na+, malformation
hydrocephalus Withdrawal from Head injury ↓Na+) Binswanger’s
Multiple alcohol punch-drunk Porphyria disease
sclerosis syndrome Paget’s disease
Lewy body Remote effects of carcinoma or
disease lymphoma
Hepatolenticular
degeneration (Wilson’s disease)
Vitamin deficiency (thiamine,
nicotinic acid, folate, B12)
Vitamin intoxication (A, D)
31.8.1.1 Organic Hallucinosis

Organic hallucinosis is defined as being a disorder of per- TABLE 31.7
sistent or recurrent hallucinations, in any modality but Causes of Organic Hallucinosis
usually visual or auditory, that occur in clear conscious- Psychoactive Alcohol abuse (alcoholic hallucinosis)
ness without any significant intellectual decline and that substance use Amphetamine and related sympathomimetics
may or may not be recognized by the subject as such; Cocaine
Hallucinogens, e.g. LSD
delusional elaboration of the hallucinations may occur,
Flashback phenomena following the use of
but often insight is preserved. The causes of organic hal-
hallucinogens
lucinosis are shown in Table 31.7. Intoxication Drugs—amantadine, bromocriptine,
ephedrine, levodopa, lisuride
31.8.1.2 Organic Mood Disorder
Intracranial causes Brain tumour
Organic mood disorder is a disorder characterized by a Head injury
change in mood, usually accompanied by a change in Migraine
the overall level of activity, caused by organic pathol- Infections, e.g. neurosyphilis
ogy. Table 31.8 gives the main causes of organic mood Epilepsy, particularly temporal lobe epilepsy
disorder. Sensory deprivation Deafness
Poor vision, e.g. cataract
31.8.1.3 Organic Anxiety Disorder Torture, e.g. in prisoners of war
Organic anxiety disorder is characterized by the occur- Endocrine Hypothyroidism—‘myxedematous madness’
Huntington’s disease
rence of the features of generalized anxiety disorder and/
or panic disorder caused by organic pathology. Some Source: Reproduced from Puri, B.K. et al., Textbook of Psychiatry,
of the symptoms of anxiety, which include tremor, par- 2nd edn., Churchill Livingstone, Edinburgh, U.K., 2002.
aesthesia, choking, palpitations, chest pain, dry mouth, With permission.
nausea, abdominal pain, loose motions and increased
The stuporose symptoms may include complete mutism,

TABLE 31.8 negativism, and rigid posturing, while excitement mani-
Causes of Organic Mood Disorder fests as gross hypermotility. Other catatonic symptoms
Psychoactive substance Amphetamine and related include stereotypies and waxy flexibility. Important
use sympathomimetics causes of organic catatonic disorder include encephalitis
Hallucinogens, e.g. LSD and carbon monoxide poisoning.
Medication Corticosteroids
Levodopa 31.8.1.5 Organic Delusional or
Centrally acting antihypertensives— Schizophrenia-Like Disorder
clonidine, methyldopa, reserpine, and
Organic delusional or schizophrenia-like disorder is
rauwolfia
Alkaloids
defined as a disorder in which the clinical picture is
Cycloserine dominated by persistent or recurrent delusions, with or
Oestrogens—hormone replacement without hallucinations. The delusions are most often per-
therapy, oral contraceptives secutory, but grandiose delusions or delusions of bodily
Clomiphene change, jealousy, disease, or death may occur. Memory
Endocrine disorders Hypothyroidism, hyperthyroidism and consciousness are unaffected. Causes are listed in
Addison’s disease Table 31.9.
Cushing’s syndrome
Hypoglycaemia, diabetes mellitus 31.8.1.6 Organic Personality Disorder
Hyperparathyroidism In ICD-10, organic personality disorder is defined as being
Hypopituitarism
characterized by a significant alteration of the habitual
Other systemic disorders Pernicious anaemia
patterns of behaviour displayed by the subject premor-
Hepatic failure
bidly. Such alteration always involves more profoundly the
Renal failure
Rheumatoid arthritis
expression of emotions, needs, and impulses. Cognition
Systemic lupus erythematosus may be defective mostly or exclusively in the areas of
Neoplasia, particularly carcinoma of planning one’s own actions and anticipating their likely
the pancreas, Carcinoid syndrome personal and social consequences. The causes of organic
Viral infection, e.g. influenza, personality disorder are summarized in Table 31.9.
pneumonia, infectious mononucleosis
(glandular fever), hepatitis
Intracranial causes Brain tumour
Head injury TABLE 31.9
Parkinson’s disease Causes of Organic Delusional/Schizophrenia
Infections, e.g. neurosyphilis Disorder and Organic Personality Disorder
Source: Reproduced from Puri, B.K. et al., Textbook of Psychiatry, Causes of Organic Delusional/ Causes of Organic Personality
2nd edn., Churchill Livingstone, Edinburgh, U.K., 2002. Schizophrenia Disorder Disorder
With permission. Psychoactive substance use Intracranial (particularly
• Amphetamine and related affecting the frontal or temporal
substances lobes)
frequency of micturition, are secondary to hyperventila- • Cocaine • Head injury
tion. Secondary cognitive impairment may occur. Table • Hallucinogens • Tumours
31.4 shows the main causes of organic anxiety disorder; Intracranial causes affecting the • Abscesses
of these, it is particularly important to exclude hyper- temporal lobe (e.g. tumours, • Subarachnoid haemorrhage
epilepsy) • Neurosyphilis
thyroidism, phaeochromocytoma, and hypoglycaemia in
Huntington’s disease • Epilepsy
clinical practice.
Huntington’s disease
Hepatolenticular degeneration
31.8.1.4 Organic Catatonic Disorder
(Wilson’s disease)
Organic catatonic disorder is defined as being a disor- Medication (e.g. corticosteroids)
der of diminished (stupor) or increased (excitement) psy- Psychoactive substance use
chomotor activity associated with catatonic symptoms; Endocrinopathies
the extremes of psychomotor disturbance may alternate.
31.9 NEUROPSYCHIATRIC ASPECTS OF • Intravenous drug use and mother-to-child HIV

HUMAN IMMUNODEFICIENCY infections have made relatively smaller contribu-
tion to the HIV epidemic in the United Kingdom
VIRUS INFECTION AND ACQUIRED
when compared to other developed countries.
IMMUNODEFICIENCY SYNDROME
(CITRON ET AL., 2005)
31.9.2 Human Immunodeficiency Virus
31.9.1 Introduction
The HIV is a lentivirus and a type of retrovirus. The HIV
31.9.1.1 Epidemiology of HIV/AIDS is composed of an outer envelope and an inner core. The
in the United Kingdom outer envelope is made up of knoblike glycoproteins (gp
• Approximately 33.5 million people worldwide 120s) that bind to the CD4 molecules of susceptible host
are living with HIV/AIDS and 95% of them are cells. The HIV is detected in the CNS within 14 days of
living in developing countries. infection.
• In the United Kingdom, around 92,636 people
were infected by HIV by the end of 2010 and one- 31.9.3 Diagnosis of HIV Infection
quarter of them are unaware of their infection.
and Counseling
• The introduction of combination antiretroviral
treatment has resulted in a rapid decline in the HIV infection is confirmed by the presence of anti-HIV
number of acquired immunodeficiency syn- antibodies in the serum. Acute infection is detected by
drome (AIDS) cases and deaths reported each the appearance of immunoglobulin G (IgG) and immu-
year since the mid-1990s. By the end of 2010, noglobulin M (IgM) within 3 months of infection, P24
there have been 26,791 diagnoses of AIDS in the antigen, or HIV RNA by PCR. As immunodeficiency
United Kingdom. The number of deaths among becomes more severe, the IgG titer to the core protein
people living with HIV/AIDS has remained begins to fall and P24 antigenaemia starts to surge.
constant, averaging around 400–500 deaths per The cluster of differentiation 4 (CD4) is a glycoprotein
year in the United Kingdom. expressed on the surface of T-helper cells. The CD4 to
• Heterosexual sex represented 42% of all HIV CD8 ratio is a marker of disease progression.
diagnoses in 2010. Most new cases contracted After the confirmation of diagnosis, the patients may
HIV by heterosexual sex outside of the United undergo tremendous psychological stress because they may
Kingdom, particularly in Africa. need to reveal information related to the HIV status and
• The number of new HIV infections among the mode of transmission (e.g. history of unprotected sex with
male homosexual group has increased in the commercial sex workers, homosexuality, or intravenous drug
United Kingdom steadily (Dougan et al., 2007). misuse) to their sexual partners and spouses (Table 31.10).
TABLE 31.10
Pretest and Posttest Counseling
Pretest Counseling Posttest Counseling
1. Help the person to analyse the reasons for testing and to evaluate 1. Ensure privacy and confidentiality.
the likelihood that he or she is infected. 2. Explore the feelings of the patient while waiting for the test
2. Explain to the person that the test is not expected to provide a result.
diagnosis of AIDS, any information concerning the severity of the 3. Presenting the results in a sensitive but honest manner.
infection, the infectiousness, and prognosis. 4. If a patient is confirmed to be infected with HIV, then inform the
3. Explain to the person that false positive or negative results may person about HIV and AIDS, avoiding any unwarranted estimate
occur. of survival and definite prognosis.
4. Inform the person about the possible consequences of a positive 5. Prompt the person to talk about their concerns and worries.
result, individual psychological reactions, interpersonal problems, 6. Encourage the person to fight against the infection and seek help
possible stigma, and difficulties in purchasing medical insurance. from infectious disease specialist.
5. Provide education about mode of transmission and prevention 7. Inform the person about the resources available in the community.
strategies. 8. Provide education on safe sex techniques.
TABLE 31.11
Summary of Clinical Progression and CD4 Count
200 Cells/mL < CD4 Count 50 Cells/mL < CD4 Count < 200 CD4 + Counts < 50
< 500 Cells/mL Cells/mL Cells/mL
Patients are at risk for developing AIDS-defining conditions including Patients are at increased
symptomatic but non-AIDS-defining opportunistic infections, neoplasm risk for fatal HIV-related
conditions associated with decreased (primary non-Hodgkin’s illness.
immunological functions. lymphoma), and AIDS-related
HIV infection affects the brain within the first dementia occur.
few months of infection and leads to minor Toxoplasma gondii cause changes
cognitive impairment. Weight loss, fatigue, in cognition and affect.
and thrush (oral candidiasis) may occur in
the early stage of the illness.
The most common opportunistic infections in the 31.9.5 Psychiatric Disorders and HIV Infection
CNS are Cryptococcus neoformans and Toxoplasma
gondii (Table 31.11). 31.9.5.1 Acute Stress Reaction
Acute stress reaction is common immediately after the
diagnosis of HIV infection. The patient may present in a
31.9.4 Antiretroviral Treatment state of shock with depersonalization and derealization.
The highly active antiretroviral therapy (HAART) is Other psychological reactions include anger, withdrawal,
composed of the following: guilt, denial, fear of death, and despair. Counselling with
infectious disease nurse is often useful.
• Nucleoside analogue reverse transcriptase inhibi-
tors (NARTIs): zidovudine (AZT), didanosine 31.9.5.2 Adjustment Disorder
(ddI), zalcitabine (ddC), and lamivudine (3TC) Adjustment disorder may present with depression,
• Pharmacodynamics: phosphorylation to tri- anxiety, somatic complaints, obsessions, and compul-
phosphate and incorporated into growing sions. Adjustment disorder is common in patients who
DNA chain and blocks further DNA chain face family estrangement, overconcern of loved ones,
expansion unemployment, and financial difficulties. Supportive
• Nonnucleoside analogue reverse transcriptase psychotherapy by infectious disease nurse or CBT by
inhibitors (NNARTIs): nevirapine and efavirenz psychologist is often useful.
• Protease inhibitors (PIs): indinavir, ritonavir,
31.9.5.3 Depressive Disorder
and saquinavir
31.9.5.3.1 Epidemiology of Depression
In general, the common neuropsychiatric side effects of in HIV-Infected Patients
antiretroviral drugs include depression, mania, psycho- • The prevalence of depression in people living
sis, vivid dreams, and suicidal ideations. with HIV is around 30%.
Specific neuropsychiatric side effects of each medica- • Depressive disorder is more frequent in the period
tion are listed as follows: following the identification of seropositive; HIV
infection or in the initial stages of HIV dementia.
• Efavirenz: decreased concentration, depression,
nervousness, and nightmares 31.9.5.3.2 Aetiology
• Interferon: fatigue and depression 31.9.5.3.2.1 Biological Causes
• Interleukin-2: depression, disorientation, confu- 1. Association with chemotherapy for malignant
sion, and coma lymphoma
• Steroids: mania or depression 2. Endocrine and metabolic disturbances
• AZT: mania and depression 3. Occurrence of opportunistic infections or
• Vinblastine: depression and cognitive impairment neoplasm
TABLE 31.12
Application of Antidepressants in HIV-Infected Patients
Selective Serotonin Reuptake Inhibitors Tricyclic Antidepressants Electroconvulsive Therapy
(SSRIs) Novel Antidepressants (TCAs) (ECT)
SSRIs are suitable for patients infective with Bupropion (75–150 mg bid) TCAs are indicated for the ECT is used successfully in
HIV because SSRIs do not affect the CD4 Avoid in patients with following purposes: HIV-infected patients
count. Most SSRIs are equally effective. advanced HIV, epilepsy, and Anti-diarrhoea ECT is useful for patients who
SSRIs demonstrate 70%–90% response rate AIDS-related dementia Sedation are too ill to tolerate
and placebos only demonstrate 50% Venlafaxine (75–150 mg bid) Anti-nausea antidepressants, severely
response rate Low protein binding, low Anti-anxiety suicidal, psychotic, and
Fluoxetine (10–60 mg/day) affinity for cytochrome Analgesics for neuropathic exhibit treatment resistance
Highly protein bound, long half-life and P450 mixed-function pain ECT is associated with an
inhibition of CYP 2D6 oxidase system increase in risk of confusion
Paroxetine (10–40 mg/day) Mirtazapine (7.5–45 mg/day)
Highly protein bound, anticholinergic side Low affinity for cytochrome
effects and most potent inhibitor of CYP 2D6 P450 mixed-function
Sertraline (25–200 mg/day) oxidase system and
Highly protein bound and shortest half-life associated with sedation
Citalopram (20–40 mg/day) and weight gain
Least protein bound and least interaction of
cytochrome P450 mixed-function oxidase
system, associated with prolonged QTc
Source: American Psychiatric Association (APA), Desk Reference to the Diagnostic Criteria from DSM-5, American Psychiatric Association
Press, Washington, DC, 2013.
31.9.5.3.2.2 Psychosocial Causes 31.9.5.3.3 Management

1. Low level of education. The following investigations are required before initia-
2. Multiple and frequent bereavements. tion of antidepressant treatment: FBC, RFT, LFT, TFT,
3. History of mood disorders. and ECG (Table 31.12).
4. History of substance abuse appears to be the
most important predictor for depression in 31.9.5.4 Mania
patients infected with HIV. 31.9.5.4.1 Epidemiology
5. Unemployment. The prevalence of mania in HIV-infected patients is around
6. Unresolved grief and multiple losses. 1.5%. The prevalence increases as the disease progresses.
31.9.5.4.2 Aetiology
31.9.5.3.2.3 Clinical Characteristics If mania presents early in the course of HIV infection, it
1. Biological depressive symptoms (e.g. fatigue, is usually associated with social problems. If mania pres-
anorexia, weight loss, sleep disorders, and loss ents late in the course of HIV infection, it is usually asso-
of libido) are similar to somatic manifestations ciated with HIV dementia. Other causes of mania include
of AIDS.
2. Cognitive depressive symptoms (e.g. memory 1. Side effects of antiretroviral agents such as AZT
disturbance, poor concentration, slowing of and lamivudine
mental processes) are similar to AIDS-related 2. Direct effect of the HIV infection on the CNS
dementia. 3. Metabolic disturbance
3. Psychiatrists should focus on the following 4. CNS opportunistic infection (e.g. toxoplasmosis
symptoms such as low mood, guilt, suicidal ide- cerebritis, cryptococcal meningitis)
ation, hopelessness, and loss of interest when 5. CNS opportunistic tumours from non-Hodgkin’s
assessing severity of depression. lymphoma
31.9.5.4.3 Treatment (See Tables 31.13 and 31.14) • Motor symptoms include loss of balance, poor
31.9.5.4.4 Prognosis coordination, clumsiness, and leg weakness.
• Later stage: Global deterioration of cognitive
Mania in patients infected with HIV indicates poor prog-
functions is manifested by word finding diffi-
nosis and affects adherence to antiretroviral drugs as a
culties. Patients may exhibit psychomotor retar-
result of unrealistic optimism in the disease condition.
dation and mutism. Speech becomes slow and
31.9.5.5 Cognitive Impairment and Dementia monotonous. Neurological examination may
reveal that the patient has difficulty in walking
31.9.5.5.1 Epidemiology
as a result of paraparesis. Patients may lie in bed
• Early cognitive impairment occurs in 20% of and appear indifferent to the illness and sur-
patients infected with HIV. It can be classified roundings. Bladder and bowel incontinence are
into cognitive, behavioural, and motor symptoms. common at this stage. Myoclonus and seizures
• Cognitive symptoms include poor memory, may occur.
concentration impairment, and mental slowing. • The prevalence of dementia in patients suffering
The patient may need a written reminder to help from AIDS is around 25%.
them to recall. • The onset of AIDS-associated dementia is
• Behavioural symptoms include apathy, reduced insidious and occurs later in the course of ill-
spontaneity, and social withdrawal. Depression, ness when there is significant immunosuppression
irritability or emotional lability, agitation, and (Table 31.15).
psychotic symptoms may occur.
TABLE 31.13
Application of Mood Stabilizers in HIV-Infected Patients
Lithium Carbonate Sodium Valproate Carbamazepine
1. Poorly tolerated, especially 1. Effective in treating mania in 1. Elevated risk of pancytopenia in
in HIV nephropathy. patients infected with HIV. HIV-infected patients.
2. Monitor closely for 2. Require regular monitoring 2. Monitor FBC on a weekly basis when
neurotoxicity and of liver functions. given concomitantly with zidovudine.
gastrointestinal side effects.
3. Serum levels can easily be 3. Coadministration with 3. Carbamazepine induces its own
altered due to diarrhoea or zidovudine may increase the metabolism and decreases its own levels
poor fluid intake. serum levels of zidovudine. as well as the levels of other drugs.
Source: American Psychiatric Association (APA), Desk Reference to the Diagnostic Criteria from DSM-5, American
Psychiatric Association Press, Washington, DC, 2013.
TABLE 31.14
Summary of Pharmacokinetic Interactions among Antidepressants, Mood Stabilizers,
and Antiretroviral Drugs
CYP 2B6 CYP 2D6 CYP 3A4 Glucuronidation
Psychotropic Bupropion TCA Benzodiazepine Sodium valproate
drugs SSRI Buspirone Lamotrigine
Mirtazapine Mirtazapine Opiate analgesics
Antiretroviral PIs (e.g. ritonavir) PIs (e.g. ritonavir) NNRTIs (e.g. nevirapine) PIs (e.g. nelfinavir)
drugs inhibit CYP 2B6 inhibit CYP 2D6 induce CYP 3A4 induce glucuronidation
Abbreviations: NNRTI, nonnucleotide reverse transcriptase inhibitor; PI, protease inhibitor.

TABLE 31.15
Diagnostic Criteria of HIV-Associated Cognitive Impairment and AIDS-Associated
Dementia
HIV-Associated Cognitive Impairment AIDS-Associated Dementia
Two or more of the following for at least 1 month: Acquired abnormality in at least two of the following cognitive
• Impaired attention or concentration abilities for at least 1 month:
• Mental slowing/cognitive inefficiencies • Attention/concentration
• Impaired memory • Speed of information processing
• Slowed movements • Abstraction/reasoning
• Poor coordination • Visuospatial skill
• Personality change, irritability • Memory/learning
• Must be accompanied by mild functional • Speech/language
impairment (e.g. work or activities of daily At least one of the following:
living). Emotional lability • Presence of neurological sign, e.g. abnormality in motor function
• Decline in motivation or emotional control or change in behaviour
• Moderate to severe functional impairment
Absence of clouding of consciousness or delirium
No evidence of other etiological factor of dementia
Source: American Psychiatric Association (APA), Desk Reference to the Diagnostic Criteria from DSM-5, American
Psychiatric Association Press, Washington, DC, 2013.
31.9.6 Differential Diagnosis 31.10 NEUROPSYCHIATRIC ASPECTS

The differential diagnoses include OF PARKINSON’S DISEASE
31.10.1 Introduction
1. Opportunistic infections: cryptococcal menin-
gitis, CMV encephalitis, herpes simplex enceph- 31.10.1.1 Pathophysiology of Parkinson’s Disease
alitis, and cerebral toxoplasmosis. Parkinson’s disease (PKD) is characterized by the loss of
2. Neoplasm and cerebral lymphoma. dopaminergic neurons in the substantia nigra. The loss
3. Metabolic encephalopathy. of the dopaminergic neurons and subsequent reduction in
4. HIV encephalitis or leukoencephalopathy. dopamine neurotransmission in the globus pallidus and
subthalamic nuclei results in classical signs of PKD such
The presentations of the aforementioned differential as tremor, rigidity, bradykinesia, and postural changes. In
diagnoses are more acute as compared to AIDS dementia 18 F-dopa PET scanning in patients with PKD, decreased
complex. uptake of 18 F-dopa has been observed. Intraneuronal
α-synuclein inclusions cause neuronal death and gliosis.
An interaction between tubulin and α-synuclein acceler-
31.9.7 Management
ates α-synuclein aggregation in diseased brains, leading
31.9.7.1 Investigations to the formation of Lewy bodies that are eosinophilic
In patients suffering from AIDS-associated dementia, intracytoplasmic inclusions in neurons. In general, tubu-
MRI and CT scans usually show the cerebral atrophy and lin mutation affects microtubule function and may play
white matter abnormalities. The CSF β2-microglobulin is an important pathological role in dementia or neurode-
a sensitive marker that indicates severity of dementia. generative process.
31.9.7.2 Treatment 31.10.1.2 Clinical Features of PKD

There is no specific medication but antiretroviral treat- The clinical features of PKD are summarized by a mne-
ment may be useful. monic TRAPPED (Bentley, 2008).
Tremor: PKD is characterized by a unilateral, resting, 31.10.2 Psychiatric Disorders and PKD

and pill-rolling tremor of 4–6 Hz. The tremor is wors-
ened by stress and reduced by relaxation. 31.10.2.1 Depression
Rigidity: PKD is characterized by lead-pipe and cog-
• Prevalence of major depressive disorder is 20%.
wheel rigidity.
• Prevalence increases to 40% if dysthymia and
Akinesia: PKD is characterized by reduction in frequency minor depression are included.
and speed of movement. • Two-thirds of depressed PKD patients have
comorbid anxiety.
Perservation: Patient continues to blink after glabellar tap.
Postural instability: PKD is characterized by stopped 31.10.2.1.2 Aetiology
posture with festination and shuffling gait. 31.10.2.1.2.1 Biological Factors
• Family history of depression
Expression: PKD is characterized by masklike face and
• History of left brain injury and right
reduction in blinking.
hemi-parkinsonism
Depression or dementia. • Hypometabolism in striatal–thalamic–frontal
circuits
• Low dopamine levels in the mesolimbic system
31.10.1.3 Treatment of PKD
and reduction in motivation and drive
31.10.1.3.1 Pro-Dopaminergic Drugs
1. Levodopa (l-dopa): Examples include carbi- 31.10.2.1.2.2 Psychosocial Factors
dopa and benserazide. Neuropsychiatric side • Past psychiatric history of depression
effect includes dyskinesia, on and off phenom- • Presence of cognitive impairment
enon, insomnia, and psychosis. • Loss of functional independence
2. Dopamine agonists: Examples include ergoline 31.10.2.1.2.3 Clinical Features
(e.g. cabergoline) and nonergoline (e.g. rop- • Depression in PKD has bimodal onset. Patients
inirole). Dopamine agonists delay the time to may become depressed at the time of diagnosis.
require l-dopa and not as effective as l-dopa. It Depression occurs late in the course and associ-
may cause confusion in old people. ated with severe bradykinesia and gait disturbance.
3. MAO-B inhibitors: Examples include selegi- • Depressive symptoms precede motor symptoms
line and rasagiline. MAO-B inhibitors delay the in 30% of cases.
time to require l-dopa. • Psychiatrists should focus more on low mood,
4. COMT inhibitors: Examples include entacapone irritability, pessimism, and suicidal thoughts
and tolcapone. COMT inhibitors are given with when assessing depression in patients suffering
l-dopa to increase its bioavailability. from PKD.
• Comorbidity with anxiety occurs in two-thirds
31.10.1.3.2 Other Treatments
of cases.
5. Anticholinergic agent: Example includes ben-
zhexol. Anticholinergic agent is indicated for 31.10.2.1.2.4 Treatment
tremor. Confusion is a common neuropsychiat- • Exclude underlying organic causes such as
ric side effect. hypothyroidism.
6. Indirect dopamine agonist and anticholin- • Optimize treatment of motor symptoms.
ergics agent: Example includes amanta- • SSRI is the first-line treatment for depression in
dine. Amantadine is indicated for dyskinesia. PKD.
Confusion is a common neuropsychiatric side • Bupropion is an alternative antidepressant.
effect. • Avoid tricyclic antidepressants that may cause
7. Neurosurgery: Examples include thalamot- confusion and cognitive impairment.
omy, subthalamotomy, pallidotomy, implanta- • If SSRI and bupropion fail, psychiatrist can con-
tion of subthalamic nuclei stimulators and fetal sider ECT. ECT causes transient improvement
cell grafts. Stimulation of subthalamic nuclei in motor symptoms. Side effects include post-
may increase suicide risk and sexual drive. ECT confusion.
• Augmentation with direct and indirect dopa- 31.10.2.3.2.3 Clinical Features

mine agonists (e.g. amantadine). Dopamine ago- • Anxiety symptoms are more common dur-
nists have antidepressant properties. ing the ‘off’ periods (predominantly nonmotor
• Pallidotomy and deep brain stimulation may symptoms such as breathing difficulties).
reduce depression.
31.10.2.3.2.4 Treatment
31.10.2.2 Mania • Optimize treatment of PKD.
• Consider SSRI, SNRI, or mirtazapine.
• Acetylcholinesterase inhibitors (e.g. rivastig-
• The prevalence of mania is 1%. mine) may reduce anxiety.
• The prevalence of euphoria is 10%. • Benzodiazepine may worsen motor symptoms
because GABA further reduces dopamine levels
31.10.2.2.2 Aetiology in the striatum.
31.10.2.2.2.1 Biological Factors • Pallidotomy and deep brain stimulation may
• Dopamine agonists and anticholinergic agents reduce anxiety.
can cause euphoria and mania.
• Stimulation of subthalamic nuclei may cause 31.10.2.4 Psychosis
high sexual drive and disinhibition. 31.10.2.4.1 Epidemiology
• The prevalence of psychosis is between 20%
31.10.2.2.2.2 Clinical Features
and 30% in PKD patients receiving treatment.
• Mania usually occurs during the ‘on’ period
• A small percentage of patients have hallucinations
(e.g. predominantly motor symptoms) of PKD.
before initiation of l-dopa or dopamine agonists.
31.10.2.2.2.3 Treatment 31.10.2.4.2 Aetiology
• Exclude other organic causes of mania.
31.10.2.4.2.1 Biological Risk Factors
• Reduce the dose of dopamine agonists and anti-
• Stimulation of subthalamic nuclei
cholinergic agents.
• Severe PKD
• Optimize the environment to reduce stimulation.
• Presence of REM sleep disturbance
• Low-dose quetiapine is the best tolerated anti-
• Associated with sensory deficits
psychotic to treat mania.
• High doses of l-dopa and dopamine agonists
• Combination of medications (e.g. augmentation
31.10.2.3 Anxiety
of dopamine agonist with amantadine)
• The prevalence of anxiety disorders (e.g. 31.10.2.4.2.2 Psychosocial Risk Factors
generalized anxiety disorder, panic disor- • Presence of depression
der, social phobia, and simple phobias) is • Associated with cognitive impairment and dementia
between 25% and 50% of patients suffering • Staying in a nursing home
from PKD.
• Around 90% of PKD patients suffering from 31.10.2.4.2.3 Clinical Features
anxiety disorder have comorbid depression. • Visual hallucination is common and occurs in
20%–40% of PKD patients receiving anti-PKD
31.10.2.3.2 Aetiology medications.
31.10.2.3.2.1 Biological Factors • 10% of PKD patients who receive treatment expe-
• Altered locus coeruleus activity. rience both auditory and visual hallucinations.
• Low dopamine levels causes release of nor- • 5% of PKD patients who receive treatment
adrenaline and anxiety symptoms. experience delusions. Delusions are often com-
• Reduction of cortical GABA. plex and persecutory in nature.
• Loss of insight occurs when the course of PKD
31.10.2.3.2.2 Psychosocial Factors and cognitive impairment progresses.
• Past psychiatric history of anxiety disorder • Psychotic symptom is a significant contributor
• Loss of functional independence to caregiver stress.
31.10.2.4.2.4 Treatment
• Exclude other organic causes of psychosis.
• Reduce the dose of dopamine agonists.
• It is not necessary to treat infrequent hallucina-
tions or delusions.
• Low-dose quetiapine is the best tolerated
antipsychotic.
• If comorbid dementia exists, consider adding an
acetylcholinesterase inhibitor.
• ECT is indicated for psychomotor symptoms.
• For treatment-resistant psychosis, low-dose clo-
zapine (e.g. 25 mg/day) is often effective. Side
effects of clozapine include blood dyscrasia.
31.10.2.5 Sleep Disturbances
• 60%–90% of PKD patients suffer from sleep
disturbances.
31.10.2.5.2 Clinical Features
• REM behaviour disorder (e.g. periodic limb
movement, restless leg syndrome)
• Nightmares
• Obstructive sleep apnoea
31.10.2.6 Cognitive Impairment and Dementia FIGURE 31.1 Anterior cerebral artery infarction.
E—elderly
• 20%–40% of patients suffering from PKD suf- M—malformations (e.g. arteriovenous malformation)
fer from dementia. A—autoimmune causes (e.g. vasculitis)
• 65% of patients suffering from PKD develop T—toxins (e.g. cocaine, amphetamine)
dementia by age of 85 years. O—occlusions (e.g. cerebral venous thrombosis)
M—metastases (e.g. lung, thyroid, and renal
31.11 NEUROPSYCHIATRIC ASPECTS OF cancer)
CEREBROVASCULAR ACCIDENT A—accident (e.g. head injury)
31.11.1 Introduction 31.11.1.2 Psychiatric Disorders and

31.11.1.1 Types of Cerebrovascular Accident Cerebrovascular Accident
Ischaemic stroke: 88% 31.11.1.2.1 Depression
31.11.1.2.1.1 Epidemiology
• Lacunar infarct: 25% • The prevalence of major depressive disorder is
• Atherosclerotic cerebrovascular disease: 20% 30% among patients suffering from cerebrovas-
• Cardiogenic embolism: 20% cular accident (CVA).
• Cryptogenic type: 30% • The incidence of depression is lower among
• Other causes: 5% patients suffering from an occlusion of the pos-
Haemorrhagic stroke: 12% terior cerebral arteries in comparison to occlu-
Causes of haemorrhagic stroke are summarized by a mne- sions in anterior and middle cerebral arteries.
monic ‘HAEMATOMA’ (Bentley, 2008) (Figures 31.1
31.11.1.2.1.2 Aetiology
through 31.5 and Tables 31.16 and 31.17):
• CVA in the left hemisphere (e.g. left lateral frontal
H—hypertension lobe) has a stronger association with depression in
A—aneurysm comparison to CVA in the right hemisphere.
FIGURE 31.4 Subarachnoid haemorrhage with blood in the

sulci, third ventricle and the posterior horn of the left lateral
FIGURE 31.2 Middle cerebral artery infarction. ventricle.
Subdural
haematoma
FIGURE 31.3 Posterior cerebral artery occlusion. FIGURE 31.5 Subdural haematoma.
TABLE 31.16
Type of CVA, Clinical Example, and Neuropsychiatric Sequelae
Type of CVA Clinical Example Neuropsychiatric Sequelae
Anterior cerebral A 66-year-old man with history of type II diabetes mellitus Neuropsychiatric sequelae of anterior
artery infarction. presented with a sudden onset of bilateral lower limb cerebral artery infarction:
(see Figure 31.1) weakness and numbness 3 days ago. Occlusion of the anterior cerebral artery
Physical examination revealed both distal and proximal may result in global dementia and frontal
weakness of both legs with impaired pinprick sensation, lobe personality changes.
which spared the arms and the face. Grasp reflex and
sensory neglect were evident on the left side. The patient
was extremely emotional when being asked for a physical
examination.
Middle cerebral A 55-year-old woman with history of hypertension Neuropsychiatric sequelae of middle
artery infarction. presented with an acute onset of left-sided weakness and cerebral artery infarction:
(see Figure 31.2) blurring of vision. Physical examination revealed Nondominant middle cerebral artery
weakness and sensory loss involving the left half of the occlusion may cause confusional states,
face and the left upper and lower limbs. Left homonymous sensory loss, inattention, and
hemianopia and left-sided neglect were also evident. anosognosia.
Posterior cerebral A 58-year-old housewife presented with an acute onset of Neuropsychiatric sequelae of posterior
artery occlusion. dizziness, nausea, and posterior cranium headache 5 days cerebral artery infarction:
(see Figure 31.3) ago. She sought medical attention before she found that Posterior cerebral artery occlusion causes
she could not read half of the page of her story book. cortical blindness and denial of disability
Physical examination revealed homonymous hemianopia, and sometimes alexia without agraphia.
loss of pinprick sensation in her left face and arm, and Occlusion of rostral basilar artery can
severely impaired short-term memory. result in bizarre hallucinations,
disorientation, and somnolence.
TABLE 31.17
Type of Hemorrhage, Clinical Example, and Neuropsychiatric Sequelae
Subarachnoid A 40-year-old right-handed man complained of Neuropsychiatric sequelae of subarachnoid
haemorrhage. insidious onset of dizziness, nausea, and vomiting for haemorrhage:
(see Figure 31.4) 5 days. He also got generalized headache, which was Persistent memory impairment: 40%.
precipitated by lying down. The headache itself was Depression and anxiety: 25%.
neither throbbing in nature nor associated with any Severe personality impairment: 20%.
phobic symptoms, limb weakness, or numbness. Two Dysphasic disability: 10%.
days before admission, he experienced diplopia, Worsening cognitive sequelae after subarachnoid
which was more severe on looking downwards, on haemorrhage is caused by normal-pressure
and off chills, and low-grade fever. hydrocephalus.
The Glasgow coma scale (GCS) was 15/15. Cranial A severe amnesic syndrome resembling Korsakoff’s
nerves were intact including the range of eye gaze. syndrome may emerge in the days or weeks
No focal neurologic sign was elicited. Planter reflex following subarachnoid haemorrhage.
was downgoing on both sides. Fundoscopy did not
reveal any papilledema.
Subdural An 87-year-old woman was found lying on the floor Neuropsychiatric sequelae of subdural haematoma:
haematoma. unconscious, after a fall. Physical examination Cause: Head injury.
(see Figure 31.5) revealed unequal pupils, increased tone on her left Clinical presentation:
side, and upgoing plantar reflex on the left side. 1. Acute presentation with stupor or coma together
with some evidence of localizing signs.
2. Chronic presentation with headache, poor
concentration memory loss, and fluctuating course.
• Patients who develop depression after right- 31.11.1.2.3.2 Clinical Features

sided CVA is associated with family history of • Post-CVA mania usually occurs 3–9 months
depression. after stroke.
• The volume of the lesion is directly proportional • The first episode can be mania or depression.
to the severity of depression.
31.11.1.2.3.3 Treatment
31.11.1.2.1.3 Treatment
• Mood stabilizer such as lithium is indicated.
• SSRI is indicated.
31.11.1.2.2 Mania 31.11.1.2.4 Cognitive Impairment and Dementia
31.11.1.2.2.1 Epidemiology 31.11.1.2.4.1 Epidemiology
• The prevalence of mania is 0.5%–1% among • 30% of patients suffering CVA develop severe
patients suffering from CVA. cognitive impairment.
31.11.1.2.3 Aetiology
Vascular dementia is considered in Chapter 39.
31.11.1.2.3.1 Biological Factors
• CVA in the right hemisphere (e.g. right orbitofron-
tal lobe) has a stronger association with mania in
comparison to CVA in the left hemisphere. 31.12 NEUROPSYCHIATRIC
• Family history of bipolar disorder. ASPECTS OF EPILEPSY
• Post-CVA mania is associated with cortical and
31.12.1 Introduction
subcortical lesions.
• CVA in the thalamus is associated with mania. 31.12.1.1 Classification of Epilepsy (Figure 31.6)
Axis I: ictal phenomenon; Axis II: seizure type; Axis III: type of
epileptic syndrome; Axis IV: aetiology; Axis V: impairments.
Partial seizures (seizures Generalised seizures (bilaterally Unclassified epileptic seizures

beginning locally) symmetrical and without lead (inadequate or incomplete data)
onset)
1. Absence seizures Thalamocortical relays on a

2. Atypical absence seizures hyperexcitable cortex in a typical
3. Myoclonic seizures absence seizure. Atypical absence
4. Tonic−clonic seizures seziure is associated with temporal
5. Atonic seizures lobe epilepsy, frontal lobe epilepsy or
Lennox-Gastaut syndrome
It is not associated with aura
Combination of absence seizure and
tonic−clonic seizure increases the risk
of psychosis
Simple partial seizures (consciousness is Complex partial seizures (with impairment of

preserved) consciousness)
1. With motor symptoms Complex partial seizure begins as a simple partial seizure
2. With somatosensory or special sensory and progresses to impairment of consciousness. It
symptoms involves aura and automatism. Duration is from 30 s
3. With autonomic symptoms to 2 min. Causes include mesial temporal lobe epilepsy
4. With psychic symptoms and febrile convulsion in childhood
FIGURE 31.6 International league against epilepsy classification.

31.12.1.1.1 Absence Seizure 31.12.1.1.2 Nonepileptic Seizures

Characteristics of absence seizure include Psychiatrists should rule out organic causes of seizure
(drug or medication induced, infection, substance mis-
• Abrupt onset and offset use/withdrawal) before the diagnosis of nonepileptic
• Short duration (usually <10 s) seizure.
• Eyes: glazed, blank stare, slight blinking, and Classical features of nonepileptic seizure
eye-rolling
• Normal intelligence, physical examination, and • Presence of past psychiatric disorders, for
imaging finding example, affective disorders, dissociative states,
• Clonus and automatism may occur when the deliberate self-harm, family history of psychi-
duration of seizure increases atric disorders, sexual maladjustment, hysterical
• EEG: 3 Hz spike and wave with photosensitivity personality, and good past health (e.g. absence
of head injury, CNS infection, and thromboem-
Special clinical features associated with epilepsy (5As): bolic phenomenon)
• Precipitants including intense current psychoso-
• Aura: rising epigastric sensation, déjà vu, and cial stressors
olfactory or auditory hallucinations • Characteristics of nonepileptic seizure: occur-
• Autonomic signs: change in skin colour, tem- ring in daytime when other people are around,
perature, and palpitations gradual onset, wide range of atypical presenta-
• Absence seizure: motor arrest and motionless stare tion, pelvic thrusting, lack of tonic and clonic
• Automatism: lip-smacking, chewing, swallow- movements, one-sided somatosensory symp-
ing; fumbling, and walking toms, and reactive papillary light reflex
• Amnesia: amnesia of the entire seizure • Underlying motives: presence of primary and
secondary gains
Frequency of partial seizures according to neuroanatomi- Investigation
cal areas (Table 31.18):
• EEG is normal during and after the seizure.
• Temporal lobe epilepsy: 75% Video telemetry further examines the very
• Frontal lobe epilepsy: 15% stereotyped (and therefore probably epileptic) or
• Parietal lobe epilepsy: 5% the very nonstereotyped (and probably nonepi-
• Occipital lobe epilepsy: 5% leptic) nature of seizure.
TABLE 31.18
Characteristics of Epilepsy According to Neuroanatomical Locations
Frontal Lobe Epilepsy Temporal Lobe Epilepsy
Nonspecific ‘cephalic’ aura. Predisposing factors: history of birth injury
Motor automatisms—‘fencing’ posture, versive eye and and infantile febrile convulsions.
head movement, speech arrest, and bizarre vocalization Aura: complex and varied. It may present as
(e.g. singing). The duration of automatism usually less lip-smacking, forced thinking, visual
than 5 min. hallucinations, and tinnitus.
Bilaterally coordinated limb movements (e.g. clapping). Behaviour: hyperemotionality and
Contralateral clonic Jacksonian march when supplementary hyposexuality.
motor area is involved.
Brief, frequent, dramatic, nocturnal seizures with
immediate recovery.
Frontal lobe epilepsy is often misdiagnosed as ‘hysterical’.
Prolactin levels remain the same after frontal lobe epilepsy.
Frontal lobe epilepsy is associated with phonation
(i.e. speech during seizure).
Serum prolactin should be taken within 20 min after the 31.13.1.2.1.1.3 Clinical Features of Ictal Violence
seizure. The interpretation of prolactin levels is listed as 1. Lack of motivation
follows: 2. Sudden paroxysmal onset
3. Nonselective victims including close family member
• Generalized seizure: 1000 IU/mL 4. Brief duration
• Partial seizure: 500 IU/mL 5. Impaired consciousness reported by witness
• Pseudo-seizure: 0 IU/mL 6. Little attempt to conceal violent act
7. Amnesia for the event
Treatment
8. Subsequent genuine remorse
• If patient stays in the ward, regular nursing 31.13.1.2.1.1.4
Investigation and Treatment of Ictal
monitoring is required. Violence
• Psychotherapeutic exploration (by abreaction: • Consult a neurologist who is experienced in this
a drug-assisted interview using diazepam or field.
sodium amylobarbitone may be helpful). • Look for aggression during epileptic automa-
tism during video–EEG telemetry.
31.13 PSYCHIATRIC ASPECTS OF EPILEPSY • Carbamazepine (400–800 mg/day) is indicated
for episodic dyscontrol and violence.
31.13.1 Epidemiology
31.13.1.2.1.1.5 Personality Change
31.13.1.1 Psychiatric Comorbidity of Epilepsy • In general, patients with epilepsy are more emo-
1. Depression: the prevalence of depression is tional and irritable.
9%–22% and it is 17 times more likely than gen- • Left temporal epilepsy is associated with rumi-
eral population. native tendency.
2. Suicide: the percentage of death by suicide is • Idiopathic generalized epilepsy is not related to
11.5% and the risk of suicide is four to five times any particular personality type.
higher than general population.
3. Psychosis or schizophrenia: patients suffering 31.13.1.2.1.1.6 Cognitive Function
from epilepsy are two to four times more likely • Left temporal epilepsy is associated with verbal
to develop psychosis or schizophrenia. The memory deficits.
prevalence of schizophrenia among temporal • Other causes include drug intoxication, noncon-
lobe epilepsy patients is 3%. vulsive status, and hippocampal spike activity.
4. Pathological aggression: 4%–50% of patients • Postictal amnesia is common but epileptic
suffering from epilepsy exhibit pathological dementia is rare.
aggression.
5. Criminal offences: patients suffering from epilepsy Ictal and postictal psychiatric phenomenon (Tables 31.19
are three times more likely to commit criminal and 31.20).
offences in comparison to the general population.
31.13.2 Psychotropic Medications and Epilepsy
31.13.1.2 Psychiatric Conditions and Epilepsy (See Table 31.21.)
31.13.1.2.1 Violence
31.13.1.2.1.1 Aetiology of Violence in Epileptic Patients 31.14 NEUROPSYCHIATRIC ASPECTS
31.13.1.2.1.1.1 Biological Factors OF HEAD INJURY
• High serum cortisol following seizure
• Sedation and disinhibition 31.14.1 Epidemiology
• Presence of neurological signs
• Associated with episodic dyscontrol 31.14.1.1 Head Injury
• 10% of all visits to the emergency department.
31.13.1.2.1.1.2 Psychological Factors • Incidence of head injury: 1,500 per 100,000.
• Cognitive deficits in attention, memory, and • 130 per 100,000 suffer from persistent cognitive
motor speed deficits after head injury.
• Childhood history of impulsive behaviour • Males to females = 2:1.
TABLE 31.19
Summary of Ictal and Postictal Neuropsychiatric Phenomenon
Ictal Postictal Interictal
Confusion or Automatisms are simple, repetitive Postictal phenomenon may occur Occurs in temporal lobe epilepsy
psychosis movements. It may involve immediately upon the occurrence (especially the left temporal lobe).
wandering with confusion and of a fit or within a week. It may Chronic interictal psychosis is more
clouded consciousness. occur in a background of clouded common than postictal psychosis.
Automatisms usually last less than consciousness. Risk factors:
5 min. Two typical postictal phenomenon: • Hamartomas.
Nonconvulsive features: absence 1. Fugues: prolonged episode of • An aura of fear.
status, myoclonic flickering eyelids. wandering, altered behaviour, • Left-handed.
Complex partial features: mental amnesia, and impaired • Mesial temporal focus.
confusion, psychosis, fluctuating consciousness, which may last • Onset of epilepsy in adolescence.
levels of consciousness, complex for hours or days. Classical presentation:
automatisms, episodic 2. Twilight states: abnormal Chronic paranoid hallucinatory psychosis
hallucinations, and marked mood subjective experiences with the presence of the first-rank
changes. (perceptual and affective) and symptoms.
Underlying cause of ictal are also associated with Onset: 10–15 years after the first episode
phenomenon: ongoing paroxysmal cognitive impairment and of epilepsy.
brain discharges. perseveration. Patients may This occurs in 2% of patients with
have paranoid delusions. temporal lobe epilepsy.
EEG: slow-wave changes that may Visual hallucinations or illusions are
last up to a few hours. more common in lesions associated
ECT may lead to dramatic with the right temporal lobe.
improvement. The person is usually in clear
Spontaneous remission is common. consciousness when psychosis occurs.
Differences from schizophrenia:
1. No family history of schizophrenia.
2. Good premorbid personality.
3. Less personality deterioration.
4. Warmer affect.
5. Presence of neurological
abnormality on examination.
Mood or anxiety Fear is the most common anxiety Depression and anxiety are Depression is caused by psychosocial
symptoms symptom. common (15%–45%). factors such as stigma associated with
Sudden severe depression may occur. Reduced monoaminergic activity epilepsy.
Elation or mania is rare. causes depression.
TABLE 31.20
Acute and Long-Term Management of Epileptic Patients
Acute Management Long-Term Psychological Management
1. Terminate seizure by IV 1. Behavioural analysis and
benzodiazepines or rectal diazepam conditioning procedures
2. Remove patients from potential 2. Biofeedback on arousal based on
sources of injury EEG rhythms
3. Check oxygen saturation to rule out 3. Self-control strategies
hypoxia 4. Individual psychotherapy
TABLE 31.21
Use of Psychotropic Drugs in Epilepsy
Antidepressants/Mood
Stabilizers Antipsychotic Drugs
Recommended • SSRIs • Haloperidol
psychotropic drugs • Moclobemide • Trifluoperazine
• ECT is indicated for severe • Sulpiride
depression and ECT has
anticonvulsant effects
Contraindicated • Amitriptyline (epileptogenic) • Chlorpromazine (epileptogenic)
psychotropic drugs • Lithium (epileptogenic when • Depot antipsychotics (complex mechanism)
patient takes an overdose) • Clozapine (very epileptogenic)
• Zotepine (epileptogenic)
Source: Taylor, D. et al., The Maudsley Prescribing Guidelines, Informa Healthcare, London, U.K., 2009.
31.14.1.2 Neuropsychiatric Sequelae of Head • Seizure occurs in 5% of head injury victims. If dura

Injury (Birds and Roger, 2007) mater is penetrated, the risk of epilepsy is 30%.
• Postconcussion syndrome (PCS): 50% after 2 • Dementia pugilistica (punch-drunk syndrome)
months, 12% after 1 year. is resulted from repeated head injury (e.g. boxer).
• Depression and anxiety are common. The underlying pathology is the neurofibrillary
• Secondary mania: 9%. tangle and plaque formation. Clinical features
• Schizophreniform disorder 2.5%. include ataxia, dysarthria, tremor, apathy, spas-
• Paranoid psychosis: 2%. ticity, morbid jealousy, irritability, disinhibition,
• Psychotic depression: 1%. and dementia (Table 31.22).
• Impulsive personality as a result of decreased
31.14.1.3 Aetiological Factors and
levels of 5-HIAA after head injury.
• Dementia is usually nonprogressive. Severity of Head Injury
• Memory deficit is the most frequent chronic 31.14.1.3.1 Biological Factors
cognitive disturbance. 1. Age at the time of injury
• Head injury in children is associated with restlessness, 2. The extent and location of brain injury
overactivity, disobedience, and temper tantrums. 3. Post-traumatic epilepsy
TABLE 31.22
Classification of Head Injury
Primary Head Injury Secondary Head Injury
Primary head injury is a result of either rotational or horizontal Secondary head injury is caused by
acceleration or deceleration.
Rotational acceleration or deceleration results in diffuse 1. Haemorrhage (subdural, extradural,
shearing of long central fibres and micro-haemorrhages in the and intracerebral).
corpus callosum and rostral brain stem. This will result in 2. Reactive brain swelling.
diffuse axonal injury. 3. Acute fluid collections.
The rotational acceleration or deceleration also causes 4. Raised in intracranial pressure.
centrifugal pressure waves to spread out so that the brain 5. Coning of brainstem.
undergo repeated buffeting against the skull and tentorium
where there are sharp bony edges or corners. The frontal poles,
orbitofrontal regions, temporal poles, and medial temporal
structures are particularly vulnerable.
31.14.1.3.2 Psychological Factors 31.14.2 Postconcussion Syndrome

1. Premorbid personality PCS occurs after minor head injury. PCS is associated
2. Premorbid intelligence with premorbid physical and social problems. It usu-
3. Psychological reactions to injury ally lasts from several weeks to 3 months and more
31.14.1.3.3 Social Factors likely to be persistent in women. Common physical
symptoms include headache, nausea, and sensitivity
1. Premorbid social functioning
to light and noise. Common psychological symptoms
2. Social support
include cognitive impairment, poor concentration, and
3. Mild head injury
irritability.
31.14.1.4 Mild Head Injury
Glasgow Coma Scale (GCS): 14–15 31.14.3 Posttraumatic Amnesia
Pay attention if the patient
Measure of diffuse axonal injury: length of post-trau-
1. Shows neurologic signs matic amnesia (PTA) is an index of severity:
2. Has haematoma
3. Has a history of coagulopathy, drug or alcohol • l–24 h of PTA: moderate (1 h = 1 month of absence
consumption, epilepsy, and past neurosurgery from work)
4. Is aged >60 years • 24 h of PTA: severe and associated with delir-
ium, permanent disability in cognition, depres-
31.14.1.5 Moderate Head Injury sion, and personality change
GCS: 9–13 • 1 week of PTA: invalidism for 1 year, severe
Outcomes psychiatric and intellectual disability in 5 year
follow-up
1. Mortality: <20%.
2. Morbidity: 50%. 31.14.3.1 Intracranial Pressure and Head Injury
3. Positive neuroimaging findings: 40%. The intracranial pressure (ICP) increases initially with
4. 8% require neurosurgery. rise in mean arterial pressure and cerebral blood flow and
then decreases (Figure 31.7).
31.14.1.6 Severe Head Injury
GCS <9 31.14.3.1.1 Interpretation of ICP
Outcomes • Normal ICP: <15 mmHg
• ICP >20–25 mmHg: associated with an increase
1. 10% of all head injury in morbidity, mortality, neurological deteriora-
2. Mortality: 40% tion, and unilateral dilation of pupil
80
Cerebral blood flow (mL/min/100 g)
50
ICP
20
20 80 100 140 180
Mean arterial pressure (mmHg)
FIGURE 31.7 The relationship between mean arterial blood pressure, cerebral blood flow, and ICP.
31.14.3.2 Imaging and Head Injury Fracture

MRI images of diffuse axonal injury: MRI is a better Epidural
option because CT scan may not show any lesion. MRI haematoma
scan often shows multiple and diffuse abnormalities in
the brain.
31.14.3.3 Neuropsychiatric Sequelae
of Frontal Lobe Injury Dura
mater
• Frontal polar damage leads to poor judgement
and insight, apathy, and impaired problem solv-
ing. There is often no understanding of the
impact of the disability on the others. Brain
• Orbitofrontal damage is associated with personal-
ity change, impaired social judgement, impulsiv-
ity, hyperactivity, disinhibition, lability of mood,
excitability, and childishness or moria (childlike
interest).
• Dorsolateral damage is associated with execu-
tive dysfunction, apathy, psychomotor retarda- FIGURE 31.8 Epidural haematoma.
tion, preservation, poor initiation of tasks, and
memory impairment.
• Dorsolateral damage is associated with akinetic
Dura mater
mutism.
• Left frontal lesion is associated with impair- Subdural haematoma
ment in verbal recall.
31.15 NEUROPSYCHIATRIC SEQUELAE
OF HAEMATOMA
Epidural haematoma occurs in 0.5% of patients after
head injuries. It results from blunt trauma to temporopa-
rietal region with subsequent arterial tears, resulting in
ongoing collection of blood between the dura mater and
the skull (Figure 31.8).
Patients may develop symptoms and signs of increased
Brain
ICP, ranging from headache to coma and death. A lucid
interval may be present before the symptoms occur.
Around 15%–20% of patients with epidural haematoma
die of head injury.
SDH is caused by sudden acceleration–deceleration FIGURE 31.9 Subdural haematoma.
injury with tearing of bridging veins. SDH is common
among old people and alcoholics and classified as acute,
subacute, or chronic (Figure 31.9). initial injury, in which 50% patients cannot recall the
Acute SDH carries the worst prognosis and details of head injury.
requires urgent surgical decompression. Chronic Symptoms mainly result from increase in ICP and
SDH develops over days to weeks after relatively depend on the extent and site of bleeding. Other symp-
minor head injury. The bleeding is slow and may not toms include loss of consciousness or fluctuating loss of
be discovered until months or even years after the consciousness, irritability, seizures, and ataxia.
TABLE 31.23
Summary of Rehabilitation Strategies in a Multidisciplinary Team
Professionals Rehabilitation Techniques
Psychiatrists 1. Avoid psychotropic medication if possible.
2. Carbamazepine or valproate is indicated for epilepsy and
episodic dyscontrol syndrome.
3. Treat depression by SSRI and psychosis by the second-
generation antipsychotics.
4. Methylphenidate may improve attention and concentration.
Neuropsychologist 1. Regular assessment of neuropsychological function.
2. Prepare report for medicolegal purposes.
Nurse or community 1. To build rapport and handle emotional aspects and adjustment
psychiatric nurse to head injury.
2. To assist family members to cope with behavioural problems.
Psychologist 1. Token economy or behavioural therapy to reinforce positive
behaviours.
Occupational therapist 1. ADL assessment and social skill training.
2. Memory aids and strategies.
Physiotherapist 1. To enhance motor function and improve physical disabilities.
31.15.1 Rehabilitation of Patients • Tumour in hypothalamus or third ventricle:

Suffering from Head Injury dementia and confabulation.
• Hypothalamic hamartoma is a benign
Rehabilitation is offered in a multidisciplinary team tumour. Patients may present with gelastic
(Table 31.23). epilepsy. Patients may present with aggres-
sive behaviour such as hypothalamic rage.
31.16 NEUROPSYCHIATRIC ASPECTS The onset occurs in the childhood. Patients
may develop learning disability and other
OF BRAIN TUMOUR
behaviour problems such as shoplifting.
1. The general effect of brain tumours is a result of • Thalamus: worsening intellectual deficit,
the rise in ICP that leads to headache, drowsi- hypersomnolence, and narcolepsy.
ness, confusion, and apathy. • Pituitary: mental slowing, apathy, emo-
2. The local effects of tumour depend on the speed tional lability, and paranoid ideation.
of growth. Rapid-growing tumour is associated
with mental disturbances and slow-growing 31.16.1 Multiple Sclerosis
tumour is associated with psychiatric symptoms
and personality change. 31.16.1.1 Epidemiology
3. Neuropsychiatric sequelae depend on neuroana- 1. Prevalence: 85,000 people suffering from mul-
tomical locations: tiple sclerosis (MS) in the United Kingdom
• Corpus callosum: severe cognitive 2. Lifetime risk 1:8000
deterioration. 3. Onset: 20–50 years
• Parietal lobe: disturbance of body image. 4. F:M = 2:1
• Temporal lobe: seizures, dysphasia, mem- 5. Geographical pattern: greater frequency as the
ory loss, affective disorder, and psychosis. distance from the equator increases
• Frontal lobe: 80% of patients have psychiat-
ric symptoms including irritability, atypical 31.16.1.2 Pathology
depression and apathy, cognitive slowing, MS is a relapsing and remitting autoimmune dis-
disinhibition, and childishness. order with diverse neurological signs as a result of
plaques of demyelination and degenerative axonal 5. Anxiety: SSRIs such as paroxetine or sertraline;
loss throughout the white matter except the periph- pregabalin (anticonvulsant that may control
eral nerves. MS also involves in focal blood–brain anxiety) and CBT.
barrier disruption. 6. Steroid-induced mania: reduction of steroid
dose and consider second-generation antipsy-
chotics (e.g. olanzapine or quetiapine to avoid
31.16.1.3 Clinical Features EPSE).
Symptoms and signs include hypoesthesia, muscle weak- 7. Pathological laughter or crying: TCAs (e.g.
ness, muscle spasms and difficulties in coordination and amitriptyline) or SSRI (e.g. fluoxetine, citalo-
balance, dysarthria, dysphagia, and visual disturbances. pram, and sertraline).
In advanced cases, patients may present with sphincter 8. Psychosis: second-generation antipsychotics
disturbance. Often, the initial attacks are transient, mild, (e.g. olanzapine, risperidone).
and self-limited. Bilateral internuclear ophthalmoplegia 9. Cognitive impairment: treat depression and sleep
is the pathognomonic eye sign. problems. Donepezil may be useful to treat mild
to moderate dementia. Modafinil may be useful
to treat cognitive fatigue. Methylphenidate may
31.16.1.4 Psychiatric Manifestations
improve poor attention.
1. Fatigue: 80%
2. Depression: 14%–27%; associated with inter-
feron treatment 31.17 NEUROPSYCHIATRIC ASPECTS
3. Anxiety: 14%–25% OF LYME DISEASE
4. Elation: 10%; associated with high dose of steroid
therapy or plagues in bilateral temporal horns Lyme disease is caused by spirochete Borrelia burgdor-
5. Mania or hypomania: 2% feri that is transmitted by Ixodes ticks. The nymph-stage
6. Pathological laughter and crying: 10% ticks feed on humans and transmit spirochetes.
7. Suicide: 7.5 times higher than general popula-
Lyme disease has three stages:
tion; 15% of mortality is related to suicide
8. Schizophreniform psychosis: 1%; related to tem- Stage 1: rash
poral lobe pathology and high-dose steroid therapy
Stage 2: early neurological signs including lympho-
cytic meningitis, radicular pains, facial palsy, transverse
31.16.1.5 Cognitive Impairments myelitis, and cranial and peripheral neuropathies
1. 30%–50% have cognitive symptoms and more
Stage 3 (occurs 7 years after the initial diagnosis): late
prominent in the later course of the illness.
neurological signs including Bell’s palsy, dementia,
Memory impairment is common and MS also
encephalomyelitis, hemianopsia, hemiplegia, radiculo-
affects problem solving, abstract reasoning,
neuropathy, and seizures
planning, and organizational skills.
2. The prevalence of dementia is 5%. Diagnosis
3. Subcortical pattern.
1. For a positive or equivocal enzyme-linked
31.16.1.6 Management of Neuropsychiatric immunosorbent assay (ELISA) finding, it must
Conditions Associated with be further verified by the Western blot. After
MS (Taylor et al., 2009) treatment, neither IgM nor IgG antibody titers
1. Depression: SSRIs CBT, combination of SSRI are evidence of recent infection, since antibod-
and CBT. Anergia and fatigue may favour more ies may persist after treatment.
stimulating antidepressants such as fluoxetine, 2. CSF examination reveals lymphocytosis, excess
bupropion, or stimulant. protein, IgG, and B. burgdorferi antibodies
2. Depression with pain: SNRIs. (specific Lyme disease antibodies).
3. Severe depression: ECT. 3. Magnetic resonance imaging studies show infarct
4. Fatigue: CBT, amantadine as second-line treatment. patterns, white matter disease, and hydrocephalus.
TABLE 31.24
Summary of Clinical Features and Development of Syphilis
Time after
Infection 3 Days 2–8 Weeks 1–10 Years 11–20 Years 21–30 Years
Primary syphilis Painless chancre regional
lymphadenopathy
Secondary syphilis Skin: maculopapular
rash
Genitalia: condylomata
lata Mouth: snail-track
ulcers CNS: headache,
meningism
Tertiary syphilis Skin: gumma Argyll Robertson
Cardiac: aortitis, pupil
aneurysm Tabes dorsalis
formation Charcot’s joints
Psychiatric
manifestations
Congenital Early signs: rash Anaemia Osteochondritis Late signs: saddle
syphilis Hepatosplenomegaly nose, frontal
bossing,
Hutchinson’s teeth
Treatment 3. The mean age of onset of OCD is 7.4 years.

4. The mean age of onset of tics is 6.3 years.
Early Lyme disease is treated by
5. Comorbidity such as hyperkinetic disorder,
oppositional defiant disorder, or major depres-
1. Doxycycline, 100 mg BD for 21–28 days
sion is common.
2. Amoxicillin, 500 mg TDS for 21–28 days
3. Cefuroxime, 500 mg BD for 21 days
31.18.2 Pathophysiology
Late Lyme disease is treated with intravenous 1. PANDAS is caused by the Group A beta-haemolytic
benzylpenicillin. streptococcus.
2. There is usually a 6–9 month delay between
31.17.1 Neurosyphilis the first infection and the presentation of the
PANDAS symptoms. Recurrences may have
(See Table 31.24)
shorter time lag, for example, days to weeks.
31.18 PAEDIATRIC AUTOIMMUNE 31.18.3 Clinical Features

NEUROPSYCHIATRIC
1. Tic disorder.
DISORDERS ASSOCIATED WITH 2. OCD.
STREPTOCOCCAL INFECTIONS 3. Symptoms first become evident between 3 years
of age and puberty.
31.18.1 Epidemiology (Swedo et al., 1998)
4. Neurological abnormalities such as motor
1. 80% of Pediatric Autoimmune Neuropsychiatric hyperactivity, tics, and choreiform movements
Disorders Associated with Streptococcal are common.
Infections (PANDAS) patients suffer from tics. 5. The course of illness is episodic with significant
2. 56% of PANDAS patients meet the DSM-IV cri- improvement and occasional resolution between
teria for OCD. episodes.
31.18.4 Investigations 31.18.5 Treatment
1. Children with an explosive OCD or tic exacer- Antibiotics should only be used to treat streptococcal
bation should have a throat culture. If symptoms infections after a positive throat culture or rapid strep-
are present for more than 1 week, serial anti- tococcus test.
streptococcal titers should be ordered.
Standard psychiatric treatments should be used:
2. Infection is confirmed by a positive throat
culture or elevated antistreptococcal anti-
body titers. In order to meet the diagnosis of 1. SSRIs and CBT for OCD.
PANDAS, the antistreptococcal antibody titers 2. Alpha agonists and antipsychotics for tics.
require at least two peak levels after the initial 3. Intravenous immunoglobulin (IVIG) and plasma-
infection. Anti-GAS antibody titers decline with pheresis are options for acutely, severely ill chil-
time subsequently. dren who meet the standard PANDAS criteria.
CASC STATION ON HEAD INJURY

Name: Mr. A
Age: 19
Occupation: student prior to head injury
You are interviewing the mother of Mr. A who has jumped into the river but he denies any suicidal inten-
tion. Mr. A suffered from a head injury following a pub fight 2 years ago. His mother reports that his per-
sonality has changed since the head injury. She has made this appointment to see you and discuss about
his problems.
Task: Elicit information about the psychiatric sequelae and complications of head injury.
CASC Grid
Empathetic statement: I was informed that Mr. A was assaulted 2 years ago and I am very sorry to hear about
this. I understand that this has been a difficult time for you since his injury.
(A3) Course of (A4) Other (A5) Current

(A) Cognitive (A2) Extent of Memory Neuropsychological Treatment and
Impairment (A1) Injury Injury Problem Changes Rehabilitation
‘Can you tell me what ‘Can you ‘Does he often ‘When you compare ‘How did Mr. A react
happened to Mr. A describe the make mistakes Mr. A before and to the assault?’
immediately after the extent of his after the head after the head ‘Did Mr. A go
injury?’ injury?’ injury?’ injury, are there any through a treatment
(explore duration of ‘Did he require ‘What does he do changes in his programme for
unconsciousness and an operation in if he cannot function and people suffering
duration of his head?’ remember or character?’ from head injury?’
confusion) ‘What did the recall? Does he (look for changes in ‘Was he given any
‘Did he lose his doctor say about make up the personality, medication by the
consciousness? If so, his outcome?’ answer?’ memory, capacity to doctor or GP? Does
how long did it last?’ ‘What happened handle finance, it help?’
‘For how long did Mr. in the first one ability to study/
A lose his memory?’ year after the work)
‘Did he develop fits head injury? Did ‘Can he look after
after the head he show any himself?’ (assess
injury?’ improvement?’ basic ADL)
(B) Impairment
of Function
Based on Specific
Neuroanatomical (B1) Frontal Lobe (B2) Parietal (B3) Temporal (B4) Occipital (B5) Postconcussion
Areas Symptoms Lobe Symptoms Lobe Symptoms Lobe Symptoms: Syndrome
‘How is his mood at this Explore features ‘How do you find ‘Does Mr. A have ‘Does he have
moment?’ of Gerstmann’s Mr. A’s any problems headaches?’
‘Can you tell me more syndrome that communication? with his vision?’ ‘Does he feel giddy?’
about his mood?’ (look involves Does he have ‘If so, is his ‘Is he fearful of light?’
for liability) dominant difficulty in visual field ‘How about nausea and
‘How about his temper?’ parietal lobe reading and defect vomiting?’
‘Does he make jokes very (e.g. finger writing?’ associated with ‘How do you find his
often?’ agnosia, ‘Does Mr. A hear headache?’ concentration?’
‘Is he motivated to do acalculia, and voices when no ‘Can he recognize ‘What is his
things?’ dysgraphia). one is around?’ people?’ understanding of the
‘Can he plan? Can he Explore ‘Has Mr. A ever current problem?’
prioritize tasks?’ nondominant mentioned that ‘Has he ever had fits?’
‘How does he interact with parietal lobe someone wanted ‘Do the aforementioned
women? Has he been symptoms: to harm him?’ symptoms improve in
overfamiliar?’ (look for apraxia. Explore other the first 6 months after
disinhibition) features such as the injury?’
‘Can you tell me more trancelike states,
about his judgement?’ hyposexuality,
‘Does he understand the hyperphagia,
impact of his behaviours and temporal
on other people?’ lobe epilepsy.
(C) Risk (C1) Danger to Other (C3) Safety at
Assessment People (C2) Self-Harm Home (C4) Capacity (C5) Driving
‘Has Mr. A been aggressive ‘Has Mr. A tried ‘Has there been ‘Can Mr. A ‘Does Mr. A drive after
to the others?’ to harm any accident at handle his the head injury?’
‘Has he been more violent himself?’ home?’ (such as finance?’
after the head injury?’ ‘Has he ever fire, fall)
‘Is he hyperactive and thought of
cannot sit still?’ ending his life?’
(D) Other
Psychiatric
Comorbidity and (D2) Past
Com\pensation Psychiatric (D3) PTSD (D4) Substance
Issues (D1) Compensation Issues History Symptoms Abuse (D5) Closing
‘Did he receive any ‘Did Mr. A consult ‘Is he disturbed by ‘Does Mr. A use Thanks for your
compensation after head a psychiatrist nightmare?’ any recreational information. I am sorry
injury? (e.g. insurance or before or after ‘Does he have drug? If yes, is it to hear the changes in
from third party)’ the head injury? flashback of the before the head Mr. A after his head
‘Is there any unsettled legal If yes, what was assault?’ injury or after the injury and the impact
matter?’ the reason?’ ‘Does he avoid to head injury?’ on the family. I would
go to pub or ‘Does he drink like to meet him and
other places very often prior assess him. Then I can
related to the to the head formulate a plan to
assault?’ injury?’ help Mr. A and his
family.
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32 Addiction and Psychoactive
Substance Use Disorders
32.1 CLASSIFICATION AND DEFINITIONS • Substance-induced psychotic disorder

• Substance-induced sleep–wake disorder
ICD-10 classification of mental and behavioural disor- • Substance-induced sexual dysfunction
ders caused by psychoactive substance use • Substance-induced neurocognitive disorder
F10 Mental and behavioural disorders caused by the use
of alcohol
F11 … … opioids 32.1.2 Acute Intoxication
F12 … … cannabinoids ICD-10: This is a transient condition following the use of
F13 … … sedatives or hypnotics a psychoactive substance, resulting in disturbance of one
F14 … … cocaine or more of the following:
F15 … … stimulants, including caffeine
F16 … … hallucinogens • Consciousness level
F17 … … tobacco • Cognition
F18 … … volatile solvents • Perception
F19 … … multiple drug use and use of other psycho- • Affect
active substances • Behaviour
Specific clinical conditions are additionally coded as
follows: Its intensity is closely related to dose and lessening with
time, and the effects disappear when following cessation
0 Acute intoxication of the intake of the psychoactive substance. Recovery is
1 Harmful use usually complete.
2 Dependence syndrome The DSM-5 criteria state the recent ingestion of
3 Withdrawal state substance. The ingestion leads to clinically significant
4 Withdrawal state with delirium behavioural or psychological changes such as inappro-
5 Psychotic disorder priate sexual or aggressive behaviour, mood lability,
6 Amnesic syndrome impaired judgement, and impaired social or occupational
7 Residual and late-onset psychotic disorder functioning. Each substance is associated with specific
8 Other mental and behavioural disorders intoxication symptoms.
9 Unspecified mental and behavioural disorder Pathological intoxication applies only to alcohol and
refers to sudden aggressive behaviour, out of character,
32.1.1 DSM-5 after drinking small amounts, which would not produce
intoxication in most people.
The DSM-5 proposes a number of conditions induced by
substances:
32.1.3 Harmful Use
• Substance-induced anxiety disorder
• Substance-induced bipolar disorder This is use that is causing damage to physical or
• Substance-induced depressive disorder mental health. It does not refer to adverse social
• Substance-induced delirium consequences.
• Substance-induced obsessive–compulsive or Use disorder: The DSM-5 proposes a problematic
related disorders pattern of substance use leading to clinically significant
507
impairment or distress within a 12-month period and • Progressive neglect of other activities with
requires at least two of the following criteria (APA, increasing time spent in acquiring, taking, or
2013): recovering from the effects of the substance
• Persisting with substance use despite evidence
1. The substance is often taken in large amounts of harmful consequences
over a long period of time.
2. There is a persistent failure and unsuccessful The DSM-5 does not propose a dependence syndrome.
effort to cut down the substance use. The dependence syndrome in DSM-IV-TR is replaced by
3. The patient spends a great of time to obtain the use disorder in DSM-5.
substance.
4. Recurrent substance use resulting in a failure to fulfil
major role obligations. 32.1.5 Withdrawal State
5. Continued substance use despite having per- ICD-10: Symptoms occur upon withdrawal or reduction
sistent or recurrent social or interpersonal of a substance after repeated, usually high dose, and pro-
problems. longed use. Onset and course are time limited and dose
6. Abandonment of important occupational, social related and differ according to the substance involved.
and recreational activities. Convulsions may complicate withdrawal.
7. Recurrent substance use in dangerous situations DSM-5: DSM-5 is similar to ICD-10 and it empha-
(e.g. driving). sizes on the significant distress or impairment in social,
8. Continued substance use despite harmful physi- occupational, or other important areas of functioning as
cal and psychological effects. a result of substance withdrawal.
9. Tolerance: As a result of diminished effect, there
is a need for increased amounts of substance to
achieve intoxication or desired effect. 32.1.6 Withdrawal State with Delirium
10. Withdrawal: Presence of characteristic with- ICD-10: This is where the withdrawal state is complicated
drawal syndrome and relief of withdrawal by the by delirium. Alcohol-induced delirium tremens is a short-
same substance. lived, sometimes life-threatening, toxic confusional state
11. Craving or strong urge to use the substance. precipitated by relative or absolute alcohol withdrawal in
severely dependent users. Classic symptoms include
The DSM-5 proposes the following specifier: early
remission (3 months < duration of use < 12 months),
• Clouding of consciousness
sustain remission (no substance use > 12 months), or
• Hallucinations and illusions
in a controlled environment where access to substance
• Marked tremor
is limited.
It involves prodromal symptoms of
32.1.4 Dependence Syndrome
This is diagnosed if three or more of the following • Insomnia
have been present together at some time in the previ- • Tremulousness
ous year: • Fearful affect
• Compulsion to take the substance It is usually accompanied by

• Difficulties in controlling substance-taking
behaviour: onset, termination, or levels of use • Delusions
• Characteristic physiological withdrawal state • Agitation
when substance reduced or withdrawn; use • Insomnia
of substance to avoid or relieve withdrawal • Autonomic overactivity
symptoms
• Increased tolerance, so larger doses are In addition, convulsions may occur.
required to achieve effect originally produced DSM-5: This condition is called substance-intoxication
by lower doses or withdrawal delirium, and it requires the evidence from
Addiction and Psychoactive Substance Use Disorders 509
history, physical examination, or laboratory findings that the Confabulation may be present but not invariably so.
aforementioned symptoms developed during or shortly after Korsakov’s psychosis is included here.
a withdrawal syndrome and not accounted by dementia. The DSM-5 proposes a similar condition called sub-
stance-induced neurocognitive disorder. The temporal
course of the neurocognitive deficits is consistent with the
32.1.7 Psychotic Disorder
aetiological relationship, and the cognitive domains involved
ICD-10: Psychotic symptoms occur during or immediately must be consistent with the particular substance misused.
after psychoactive substance use, in relatively clear sensorium
(some clouding of consciousness but not severe confusion). It
32.1.9 Residual and Late-Onset
is not a manifestation of drug withdrawal or a functional psy-
chosis. The characteristics of the psychosis vary according to Psychotic Disorder
the substance used, but the following are common: ICD-10: Alcohol- or psychoactive substance-induced
changes of cognition, affect, personality, or behaviour
• Vivid hallucinations in more than one modality persist beyond the period during which the substance
• Delusions might reasonably be assumed to be operating. The onset
• Psychomotor disturbances is directly related to substance use.
• Abnormal affect Residual and late-onset psychotic disorder is further
subdivided by ICD-10 into
Stimulant-induced psychotic disorders are generally
related to prolonged high-dose use. Typically, it resolves at • Flashbacks—episodic psychotic experiences that
least partially within 1 month and fully within 6 months. duplicate previous drug-related experiences and
In ICD-10, further subdivisions may be specified: are usually very short-lived (seconds or minutes)
• Personality or behaviour disorder
• Schizophrenia-like • Organic mood disorder
• Predominantly delusional • Dementia—may be reversible after an extended
• Predominantly hallucinatory (includes alcoholic period of abstinence
hallucinosis) • Other persisting cognitive impairments
• Predominantly polymorphic
• Predominantly depressive symptoms The DSM-5 has one disorder under this category, the hal-
• Predominantly manic symptoms lucinogen persisting perception disorder.
• Mixed
The DSM-5 proposes similar criteria as ICD-10 32.2 ALCOHOL: THE CHEMICAL AND
and specifies the onset that is during intoxication or PHARMACOLOGICAL PROPERTIES
withdrawal.
32.2.1 Unit of Alcohol
The concentration of alcohol in beverages is stated
32.1.8 Amnesic Syndrome
in terms of ‘proof’ scales. In the United States, one-
ICD-10: This is induced by alcohol or other psychoactive degree proof is equal to a concentration of 0.5% by
substances. Requirements for diagnosis include volume (v/v). In the United Kingdom, one-degree
proof is equal to 0.5715% by volume (v/v).
• Chronic prominent impairment of recent mem- One unit of alcohol in the United Kingdom is approxi-
ory; remote memory may be impaired; dif- mately 8–10 g of ethanol (C2H5OH) and is the amount
ficulty learning new material; disturbance of contained in (Figure 32.1)
time sense.
• Immediate recall preserved; other cognitive • A standard measure of spirits
functions are usually relatively preserved and • A standard glass of sherry or fortified wine
consciousness is clear. • A standard glass of table wine
• A history of chronic and usually high-dose use • One half-pint of beer or lager of standard
of alcohol or drugs. strength (3%–3.5% by volume)
3 9 2 3
units units units units
1 Single shot
12% Bottle Pint unit 25 mL
5% 5.2%
Wine Beer Spirit
(Number of pints) × (Number of %) × Volume (mL)

Units =
1000
FIGURE 32.1 Units of alcohol in different forms of beverages.
32.2.2 Levels of Consumption admitted to hospital for illnesses unrelated to alcohol are

drinking at potentially hazardous levels (Royal College
Up to 21 units of alcohol per week for men and up to of Physicians, 2001).
14 units of alcohol per week for women, not consumed Abstinence or minimal alcohol intake is recom-
in one go and not consumed every day, are considered mended in pregnancy, because of the risk of the develop-
to be low-risk levels of intake. Women are more sus- ment of fetal alcohol syndrome.
ceptible to the harmful effects of alcohol because their
lower lean body mass results in higher blood alcohol
levels per unit taken. 32.2.3 Mechanism of Action
Table 32.1 classifies the level of consumption based
GABAA, serotonin, nicotinic, dopamine, and opioid
on alcohol units. Hazardous drinking refers to the pat-
receptors are involved.
tern of alcohol consumption that increases a person’s risk
of harm in terms of physical, mental, and social conse- GABA receptors: The alcohol enhances neurotransmis-
quences (NICE, 2010). Harmful drinking is more serious sion, and the interaction between alcohol and the GABA A
than hazardous drinking and results in physical or mental receptors leads to decreased level of consciousness (stu-
damage. It is estimated that around 1/4 of adults drink por or coma if large amount is consumed), reduction of
in a hazardous or harmful way in the United Kingdom anxiety, disinhibition, and aggression (see Figure 32.2).
(the NHS Information Centre, 2009) and 1/5 of patients Its interaction with the GABA A receptor can lead to
TABLE 32.1
Summary of Safe, Hazardous, and Harmful Levels of Alcohol Consumption
and Recommendations from the U.K. Government on Sensible Drinking
Hazardous Dependent Sensible Against Heart
Safer Levels Levels Harmful Levels Levels Drinking Disease
Men 21 units per 21–35 units 35–50 units per >50 units per Max 3–4 units 2 units per day for
week per week week week per day men >40 years
Women 14 units per 14–21 units 21–35 units per >35 units per Max 2–3 units 2 units per day after
week per week week week per day menopause
Note: Abstinence or minimal alcohol intake is recommended in pregnancy, because of the risk of the development of
fetal alcohol syndrome.
GABAA receptor
Alcohol
binding site Cl– Cl–
Cl–
Cl– Cl– Cl– Cl
–
Alcohol GABA
Cl– Cl– Cl– Cl– Cl–
Gamma Alpha
subunit subunit Cl–
GABA
1 2 3
Cl–
Cl–
Cl–
FIGURE 32.2 The binding of alcohol to GABAA receptor and influx of chloride ions.
delay in reaction time. It also affects the GABA A trans- found to reduce drinking in early alcoholics and in com-
mission in cerebellum and results in unsteady gait and bination with naltrexone.
difficulty in standing. Alcohol withdrawal is associated Nicotinic receptors: Alcohol enhances the action of nico-
with reduction in GABA function. tinic receptors and increases the excitatory neurotrans-
Serotonin receptors: Alcohol enhances the action of sero- mission, resulting in aggression (Figure 32.4).
tonin at the 5-HT3 receptors (see Figure 32.3). Serotonin Dopamine receptors: Alcohol releases dopamine from
plays a role in control of impulse. The change in level of the ventral tegmental area and nucleus accumbens, lead-
serotonin will result in lability of mood and aggression. ing to euphoria and impaired attention and judgement.
Alcohol withdrawal is associated with reduction in 5-HT3 Dopamine is involved in reward or novelty seeking,
receptor function. Ondansetron, a 5-HT3 antagonist, was as well as other mesolimbic and cortical projections.
Nicotinic acetylcholine receptor
Na+
Na+ Na+
Alcohol Acetylcholine
Na+
Alcohol
Nucleus
accumbens 5-HT3
Alpha
subunits
5-HT
FIGURE 32.3 The binding of alcohol to 5-HT3 receptors and FIGURE 32.4 The binding of alcohol to nicotinic acetylcho-
release of serotonin. line receptors and influx of sodium ions.
Withdrawal of
alcohol Glutamate
G G
G
G G
G
Ca G Ca
Ca
Ca G Glycine
Ca
Mg2+
Ca2+
Alcohol
Opioid Opioid
receptor
Euphoria
FIGURE 32.6 Alcohol withdrawal and enhancement of glu-
tamate actions at the NMDA receptors.
FIGURE 32.5 The binding of alcohol to µ-opioid receptors
in mice prone to withdrawal convulsions. Chronic etha-
and subsequent release of opioid.
nol administration also causes an upregulation of NMDA
Alcohol withdrawal is associated with reduced dopa- receptors in mouse hippocampus, more evident in mice
minergic function. Prolonged heavy drinking decreases prone to withdrawal convulsions. Both of these receptor
the number of dopamine transporters, and this may changes promote central nervous system (CNS) excitabil-
sensitize people with alcohol dependence to dopamine ity and increase the likelihood of convulsions.
transmission and lead to early relapse after alcohol Although ethanol exposure is the cause of increased
withdrawal. numbers of NMDA receptors, its presence protects
against the neurotoxicity of glutamate overstimulation.
Opioid receptors: Alcohol consumption can stimulate the Ethanol withdrawal increases glutamate in the brain,
release of opioid in the mesolimbic forebrain and results which damages neurons. Repeated withdrawal causes
in euphoria, poor attention, and impaired judgement (see increased neuronal death.
Figure 32.5). On the other hand, the withdrawal of alcohol (see
NMDA receptors: Ethanol at low concentrations Figure 32.6) enhances the actions of glutamate at the
(5–10 mmol/L) inhibits the action of NMDA–glutamate NMDA receptors and the voltage-sensitive Ca2+ chan-
controlled ion channels and potentiates the actions of nels. This will attenuate the action of GABA at inhibitory
GABA type A controlled ion channels. These are the GABAA receptors, resulting in agitation during alcohol
main excitatory and inhibitory systems of the brain; the withdrawal. Intracellular mechanisms (e.g. Ca2+ chan-
overall effect of ethanol is therefore as a central nervous nels) play a role in tension relief reward conditioning with
depressant. At slightly higher ethanol concentrations, the reinstitution of alcohol.
actions of voltage-sensitive calcium channels and chan-
nels controlled by serotonin are affected. 32.2.4 Adverse Effects of Alcohol
Chronic administration of ethanol produces altera-
on Physical Health
tions in the GABA, NMDA, and voltage-sensitive cal-
cium channel systems. The reduction in the production Alcohol accounts for one-fifth to one-third of medical
of subunits of the GABA receptors is seen particularly admissions to hospital.
32.2.4.1 Nervous System • Oesophageal varices

Neurological disorders that are associated with excessive • Nausea and vomiting, particularly in the morn-
drinking include ing, prevented by drinking more alcohol
• Gastritis
• Convulsions occurring mainly secondary to alco- • Peptic ulcers
hol withdrawal, tonic–clonic in nature, within • Diarrhoea
the first 48 h (also secondary to brain damage or
hypoglycaemia), occurring in 10% of alcoholics.
• Marchiafava–Bignami disease is a rare fatal 32.2.4.4 Malnutrition
demyelinating disease characterized neuro- This may result from
pathologically by widespread demyelination
affecting the central corpus callosum and often • Poor intake
also the middle cerebellar peduncles, the white • Malabsorption
matter of the cerebral hemispheres, and the • Impaired metabolism
optic tracts. It presents clinically with emotional
disturbance and cognitive impairment followed Results of malnutrition may include
by epilepsy, delirium, paralysis, and coma.
• Cerebellar degeneration, affecting mainly the • Thiamine deficiency presenting with Wernicke’s
vermis, resulting in ataxia of gait and sen- encephalopathy acutely, leading in a high pro-
sory ataxia (failure in the heel–shin test) with portion of cases to Korsakov’s psychosis (may
depressed deep tendon reflex. also present with high output heart failure of
• Central pontine myelinolysis causing bulbar beriberi)
palsy dysarthria, locked-in syndrome, quadri- • Niacin deficiency (vitamin B3) presenting with
plegia, loss of pain sensations, and death. pellagra, causing confusion, diarrhoea, and
• Optic atrophy due to demyelination. light-sensitive rash
• Retrobulbar neuropathy resulting in loss of central • Vitamin C deficiency presenting with skin
vision and preventable with vitamin B replacement. haemorrhages and gingivitis
• Peripheral neuropathy resulting in numbness
and paraesthesias in glove and stocking distri-
bution, occurring in 45% of alcoholics. 32.2.4.5 Liver
• Coarse tremor (5–7 Hz). Hepatic damage is another important result of exces-
sive alcohol intake. Fatty infiltration leading to an acute
32.2.4.2 Cardiovascular System increase in the size of the liver occurs within a few
Cardiovascular system disorders include days of excessive intake; it may cause pain in the right
hypochondrium, nausea, and vomiting but is usually
• Hypertension, poorly responsive to conventional not detected. It is reversible with abstinence. Alcoholic
treatment but responsive to abstinence hepatitis (AST > ALT) may occur secondary to long-term
• Coronary artery disease heavy daily drinking.
• Cardiac arrhythmias particularly after binge Liver cell necrosis and inflammation occur, presenting
drinking (holiday heart syndrome) with right hypochondrial pain and jaundice, sometimes
• Cardiomyopathy, presenting with gradual onset accompanied by ascites and encephalopathy.
of heart failure (the prognosis is poor with con- Cirrhosis with permanent fibrotic changes occurs.
tinued drinking) This may present with signs of liver failure, including
• Haemorrhagic and thrombotic CVA, even in the
young • Ascites
• Encephalopathy
32.2.4.3 Gastrointestinal Disorders • Bleeding oesophageal varices
These include
However, cirrhosis may be symptomless initially. Short-
• Cancer of mouth and pharynx acting benzodiazepine such as oxazepam can bed in alco-
• Mallory–Weiss tears hol withdrawal.
32.2.4.7 Electrolyte Disturbance

BOX 32.1 NICE GUIDANCE ON ASSESSMENT Hyponatraemia, hypomagnesaemia, hypophosphatae-
AND MANAGEMENT OF ALCOHOL- mia, and hypercalcaemia can occur.
RELATED LIVER DISEASE (NICE, 2010)
32.2.4.8 Endocrine and Sexual Disorders
1. Exclude alternative causes in alcoholics
with abnormal liver function test results. Endocrine and sexual disorders can occur. There is
2. Refer the patients to hepatic specialists for gonadal atrophy that affects both sexes. Direct toxic
further assessment. effects upon the gonads result in reduced sex hormone
3. For patients with alcohol-related hepatitis, synthesis. Liver disease results in oestrogenization in
assess nutritional requirements and offer men resulting in gynaecomastia. Fertility may recover
nutritional support (e.g. NG tube feeding). with abstinence. Autonomic nervous system dysfunction
4. Use the discriminant function (DF) to may result in erectile impotence and central effects cause
determine treatment in people with alco- anorgasmia. There is an increased risk of miscarriage
hol-related hepatitis. and recurrent abortion in women.
5. If the score of DF is larger than 32, con- Alcoholic pseudo-Cushing’s syndrome may cause
sider liver biopsy to confirm diagnosis of • Obesity
alcohol-related hepatitis. • Hirsutism
6. Corticosteroid (e.g. prednisolone) is used • Hypertension
to treat severe alcohol-related hepatitis.
7. Consider liver transplantation in patients Skin, Muscle, and Skeleton
who have decompensated liver disease after
best management and 3 months’ abstinence Dermatological disorders that may occur include acne
from alcohol. and rhinophyma.
Musculoskeletal disorders that are associated with
excessive drinking include
32.2.4.6 Pancreas
• Myopathy, presenting acutely with pain and ten-
Acute and chronic pancreatitides lead to food malabsorp-
derness of swollen muscles (usually symmetri-
tion and diabetes in some cases.
cal; if severe, may cause renal failure due to
myoglobinuria)
• Proximal muscle weakness and wasting (com-
BOX 32.2 NICE GUIDANCE ON ASSESSMENT
mon in alcoholics)
AND MANAGEMENT OF ALCOHOL-
• Palmar erythema
RELATED PANCREATITIS (NICE, 2010)
• Osteoporosis
1. Diagnosis is established by clinical history, • Avascular necrosis
imaging to assess the pancreatic structure
(e.g. CT scan), and tests of pancreatic exo- 32.2.4.9 Blood
crine and endocrine function. Haematological changes may occur, since alcohol is a
2. Do not offer prophylactic antibiotics to bone marrow toxin, resulting in the following:
people with mild acute pancreatitis, unless
otherwise indicated. • Macrocytosis (positive predictive value of alco-
3. Offer pancreatic enzyme supplements to peo- hol misuse is 85%)
ple with steatorrhoea or poor nutritional status. • Folate deficiency
4. Offer enteral tube feeding rather than par- • Impaired clotting caused by vitamin K defi-
enteral nutritional support if possible. ciency and/or reduced platelet functioning
5. Offer endoscopy surgery to people with • Iron-deficiency anaemia, often as a result of gas-
obstructive chronic pancreatitis. trointestinal haemorrhage
6. Offer celiac axis block, splanchnicectomy, or
surgery to people with nonobstructive chronic 32.2.4.10 Infections
pancreatitis if pain is poorly controlled. There is an increased risk of infections such as tuberculo-
sis and pneumonia, particularly in the homeless.
32.2.4.11 Metabolism 32.2.4.15 Pregnancy

A variety of metabolic abnormalities may occur, including Excessive alcohol consumption in pregnancy can lead to
permanent fetal damage.
• Alcohol-induced lactic acidosis. Features of the resulting fetal alcohol syndrome include
• Alcoholic ketoacidosis.
• Hyperlipidaemia in one-third of alcohol-depen- • Cardiac abnormalities (e.g. atrial septal defect)
dent subjects (low levels of intake appear pro- • Low-set ears
tective, however). • Absent philtrum
• Hypoglycaemia: Alcohol-induced hypoglycae- • Long upper lip with narrow vermilion border
mia occurs in people who are dependent on • Depressed bridge of the nose
alcohol after a large drink. • Small nose
• Hyperuricaemia. • Ocular hypertelorism
• Haemochromatosis. • Microcephaly
• Porphyria cutanea tarda. • Strabismus
• Pectus excavatum
32.2.4.12 Neoplasms • Poor growth
There is an increased incidence of the following types of • Increased neonatal mortality
cancer:
The DSM-5 originally proposed the neurobehavioural
• Oropharyngeal disorder associated with prenatal alcohol exposure in
• Oesophageal its draft. Although this disorder does not appear in the
• Colorectal final version, readers may find the criteria useful in
• Pancreatic clinical practice.
• Hepatic Neurocognitive impairment, as evidenced by one (or
• Lung more) of the following:
32.2.4.13 Early Death
1. Global intellectual impairment (i.e. IQ of 70 or
The top four causes of early death among alcoholics below)
2. Impairment in executive functioning
• Heart disease 3. Impairment in learning (e.g. lower academic
• Cancer achievement)
• Accident 4. Impairment in memory
• Suicide 5. Impairment in visual–spatial reasoning (e.g.
disorganized or poorly planned drawings)
32.2.4.14 Trauma
Accidents and trauma may result from alcohol consump-
Impairment in self-regulation in one (or more) of the
tion. These include
following:
• Road accidents
• Assaults (including head injuries) 1. Impairment in mood or behavioural regulation
• Falls (including head injuries) 2. Attention deficit
• Drowning 3. Impairment in impulse control
• Burns
• Death by fire Deficits in adaptive functioning as manifested in two
(or more) of the following:
The most common traumatic injuries include
• Rib fractures 1. Communication deficit

• Head injuries 2. Social impairment
• Subdural/extradural haematomas 3. Impairment in daily living
• Long-bone fractures 4. Motor impairment
32.2.5 Adverse Effects of Alcohol 32.2.5.1.2 Delirium Tremens

on Mental Health In chronic heavy drinkers, a fall in the blood alcohol
concentration leads to withdrawal symptoms including
The major types of psychiatric morbidity that are associ-
delirium tremens. The peak onset is within 2 days of
ated with excessive alcohol intake are
abstinence, and it usually lasts for about 5 days.
• Organic brain syndromes There is a prodromal period with
• Alcoholic hallucinosis • Anxiety
• Pathological jealousy • Insomnia
• Mood disorders • Tachycardia
• Personality disorder • Tremor
• Neurotic disorders • Sweating
• Psychosexual disorders
The onset of delirium is marked by
Each of these is now considered in turn.
• Disorientation
32.2.5.1 Organic Brain Syndromes • Fluctuating level of consciousness
Organic brain syndromes that are associated with excessive • Intensely fearful affect
alcohol intake may be considered under the headings of • Hallucinations
• Misperceptions
• Acute/subacute syndromes • Tremor
• Alcoholic blackouts • Restlessness
• Delirium tremens • Autonomic overactivity
• Withdrawal fits
• Wernicke’s encephalopathy The hallucinations are often visual and are commonly
• Chronic syndromes Lilliputian in nature. Auditory and tactile hallucinations,
• Korsakov’s syndrome and secondary delusions, may also be present. There is a
• Alcoholic dementia mortality rate of about 5%, associated with cardiovascular
collapse or infection. The treatment of delirium tremens
Each of these is now described. is supportive with sedation, fluid and electrolyte replace-
ment, and high-potency vitamins (especially thiamine to
32.2.5.1.1 Alcoholic Blackouts prevent an unrecognized Wernicke’s encephalopathy pro-
Intoxication frequently leads to episodes of short-term gressing to Korsakov’s psychosis—see succeeding text).
amnesia or blackouts. These may occur after just one
bout of heavy drinking and are estimated to have been 32.2.5.1.3 Withdrawal Fits
experienced by 15%–20% of those who drink. Withdrawal fits may take place within 48 h of stopping
Three types of blackout are recognized, which, in drinking.
order of increasing severity, are as follows:
BOX 32.3 NICE GUIDANCE ON
1. State-dependent memory loss. Memory for
THE MANAGEMENT OF DELIRIUM
events occurring while intoxicated is lost when
TREMENS OR SEIZURES (NICE, 2010)
sober but returns when next intoxicated.
2. Fragmentary blackouts. There is no clear demar- 1. Oral lorazepam should be used as first-line
cation of memory loss, and islets of memory exist treatment for delirium tremens or seizures.
within the gap. Some recovery occurs with time. 2. If symptoms persist or encountering diffi-
3. En bloc blackouts. There is a clearly demarcated culty to administer oral lorazepam, consider
total memory loss, with no recovery of this lost a. Parenteral lorazepam.
memory over time. If this memory loss extends b. Parenteral haloperidol (caution in
for days, the subject experiences a fugue-like patients suffering from conditions pre-
state in which he or she may travel some dis- disposing to convulsions)
tance before coming around, with no memory of c. Parenteral olanzapine.
the events occurring during this time.
Wernicke’s encephalopathy is a medical emergency and

3. The aforementioned medications do not should be treated with intravenous thiamine plus other B
have U.K. marketing authorization for vitamins. Postmortem examination of the brains of those
treating delirium tremens or seizures. dying of Wernicke’s encephalopathy reveals petechial
Informed consent should be obtained and haemorrhages in the
documented if possible.
4. Do not use phenytoin to treat alcohol • Mammillary bodies (see Figure 32.7)
withdrawal seizures. • Walls of the third ventricle (less commonly than
in the mammillary bodies)
• Periaqueductal grey matter (less commonly
32.2.5.1.4 Wernicke’s Encephalopathy than in the mammillary bodies)
Wernicke’s encephalopathy is caused by severe deficiency • Floor of the fourth ventricle (less commonly
of thiamine (vitamin B1), which is usually caused by alco- than in the mammillary bodies)
hol abuse in Western countries. Other causes include • Inferior colliculi (less commonly than in the
mammillary bodies)
• Lesions of the stomach (e.g. carcinoma) causing
malabsorption Nicotinic acid depletion can sometimes give rise to pel-
• Lesions of the duodenum causing malabsorption lagra encephalopathy, a confusional state resembling
• Lesions of the jejunum causing malabsorption Wernicke’s encephalopathy.
• Hyperemesis
• Starvation 32.2.5.1.5 Korsakov’s Syndrome
Korsakov’s syndrome is an alcohol-induced amne-
Important clinical features of Wernicke’s encephalopa- sic syndrome that, as mentioned earlier, is frequently
thy include preceded by Wernicke’s encephalopathy. It has been
described as being ‘an abnormal state in which mem-
• Ophthalmoplegia ory and learning are affected out of all proportion to
• Nystagmus other cognitive functions in an otherwise alert and
• Ataxia responsive patient’ (Victor et al., 1971). Clinical fea-
• Clouding of consciousness tures include
Ten per cent of patients with Wernicke’s encephalopathy • Retrograde amnesia

have the classical triad including ataxia, ophthalmople- • Anterograde amnesia
gia, and memory disturbance. Peripheral neuropathy may • Sparing of immediate recall
also be present. • Disorientation in time
Wernicke’s encephalopathy and Korsakov’s psycho- • Inability to recall the temporal sequence of
sis (see the succeeding text) have overlapping pathology. events
Eighty per cent of untreated Wernicke’s encephalopa- • Confabulation
thy would convert to Korsakov’s psychosis if untreated. • Peripheral neuropathy
Fornix
Mammillary body
Amygdala
Hippocampus
FIGURE 32.7 Neuroanatomical areas involved in Wernicke’s encephalopathy.

Neuropathologically, there are scarring and atrophy improve with abstinence. If symptoms persist with absti-
of the mammillary bodies and anterior thalamus, with nence, antidepressants should be considered. The suicide
substantial frontal lobe dysfunction on neuroimaging. rate is at least 50 times greater in alcoholics than in the
Improvement may occur with abstinence and high-dose general population. Between one-quarter and one-third
thiamine and replacement of other B vitamins, which of completed suicides occur in alcoholics, and up to four-
should be continued for 6 months. fifths of those who kill themselves have been drinking.
32.2.5.1.6 Alcoholic Dementia 32.2.5.1.10 Personality Disorder

Those who have abused alcohol for some years com- Those with sociopathic personality disorder engage in
monly suffer mild to moderate cognitive impairment, excessive drinking, and those who drink heavily often
which may improve over a number of years of abstinence. engage in antisocial acts. If antisocial behaviour predates
Women, who are known to suffer physical complications alcoholism by several years, then the primary diagnosis
of alcohol abuse earlier than men, also develop cogni- is of personality disorder.
tive impairment earlier in their drinking histories. A CT Cloninger (1987) described two types of alcoholic:
or structural MRI scan of the brain in alcoholics com-
• Type 1 (milieu limited). This is the least severe,
monly shows ventricular enlargement and sulcal widen-
occurring in men and women and of adult onset
ing, which does not correlate with the degree of cognitive
(older than 25 years), in dependent, anxious,
impairment and largely reverses with abstinence.
rigid, less aggressive types, whose biological
Chronic alcoholics show a coarsening of personality,
father or mother may have a mild adult-onset
which appears to be related to frontal lobe atrophy.
alcohol problem. This type of drinkers has
greater ability to abstain from alcohol.
32.2.5.1.7 Alcoholic Hallucinosis • Type 2. This is severe and of early onset
A rare disorder caused by chronic alcohol intake is alco- (younger than 25 years), occurring in men who
holic hallucinosis, characterized by auditory hallucina- are socially detached and confident, whose bio-
tions in clear consciousness. It is distinguished from logical fathers (but not mothers) often have teen-
schizophrenia by the following features: age-onset alcoholism and criminality. This type
is thought by some to be alcoholism secondary
• Unpleasant sound or threatening voice to sociopathic personality disorder. Genetic pre-
• Association with alcohol abuse disposition has a powerful aetiological effect,
• Lack of family history with little contribution from the environment.
• Onset at an older age (40 or 50 years)
• More acute presentation with resolution com- There does not appear to be a relationship between
monly within a month (if abstinent) schizophrenia and alcoholism other than that occurring
• Absence of thought disorder by chance. Genetic studies find that people suffering
• More appropriate affect from alcoholism and schizophrenia have a predisposition
to each condition separately.
It may follow abstinence but can present or recur in those
who are still drinking. Alcohol hallucinosis carries good 32.2.5.1.11 Neurotic Disorders
prognosis and shows rapid response to antipsychotics. If Neurotic disorders may predispose to alcoholism in an
it persists for longer than 6 months, the likely diagnosis attempt by the patient to self-medicate. Generalized anxiety,
is schizophrenia. panic attacks, and phobic disorders, particularly agorapho-
bia and posttraumatic stress disorder, may precede alcohol-
32.2.5.1.8 Pathological Jealousy ism. The patient should be reassessed once abstinent, and
Pathological jealousy is a well-recognized association any underlying condition should be appropriately managed.
with alcoholism but may occur with other conditions
such as schizophrenia and depression.
32.2.5.1.12 Sleep Disturbance
32.2.5.1.9 Mood Disorder Alcohol decreases sleep latency and duration of REM
Chronic heavy drinking can itself produce severe, usu- sleep. It causes more fragmentation in sleep and longer
ally transient depressive symptoms, which generally episodes of awakening.
32.2.5.1.13 Psychosexual Disorders Major costs to the country associated with the use of
Psychosexual disorders are a common association with alcohol are incurred through
excessive alcohol intake. In men, intoxication leads to
erectile impotence and delayed ejaculation. Chronic • Lost productivity and unemployment
heavy drinking in men can cause • Damage
• Medical costs
• Loss of libido • Legal costs
• Reduction in the size of the testes • Social costs
• Reduction in the size of the penis
• Loss of body hair
32.3 ALCOHOL CONSUMPTION
• Gynaecomastia
AND MISUSE
In women, chronic heavy drinking can cause 32.3.1 Epidemiology of Alcohol
Consumption and Misuse
• Menstrual cycle abnormalities
• Loss of breast tissue There is a close association between liver cirrhosis mor-
• Vaginal dryness tality and the national consumption of alcohol. Mortality
figures are a useful index of national alcohol consumption.
Other indices include the number of arrests for drunken-
32.2.6 Adverse Effect of Alcohol ness, drunken driving, cases of assault and battery, and
on Social Functions deaths from alcohol poisoning. Ten per cent of the drink-
ing population drinks half of all the alcohol drunk.
Heavy drinking is often associated with gambling and Price greatly affects levels of drinking. Countries
the use of other psychoactive substances. The social with cheap alcohol consume more than countries with
costs of excessive alcohol consumption are high. They more expensive alcohol. As the prices of alcoholic bev-
include erages rise, the quantity drunk by even chronic depen-
dent drinkers falls, and the amount of alcohol-related
• Family breakdown morbidity falls.
• Crime It is estimated that of the 55 million U.K. popula-
• Road traffic accidents and trauma tion, 36 million are regular drinkers, 2 million are heavy
• Economic harm drinkers (>80 g alcohol daily for men and >40 g for
women), 700,000 are problem drinkers, and 200,000 are
One-third of problem drinkers cite marital discord as dependent drinkers.
one of their problems; one-third of divorce petitions Men outnumber women, but the sex ratio of alcohol-
cite alcohol as a contributory factor; three-quarters related problems is falling. About 15 years ago, alcoholic
of battered wives describe their husbands as fre- cirrhosis was five times as common in men as in women,
quently drunk or subject to heavy drinking. Children but the sex ratio has fallen to about 2:1.
of alcoholics often suffer neglect, poverty, or physical The age of first drinking has fallen to between 12 and
violence. 14 years in both sexes. The highest rates of heavy drink-
Alcohol misuse is strongly associated with crime, paring are seen between adolescence and the early twenties.
ticularly against the person and against property. Half
of those committing homicide have been drinking at the
time of the offence, and half of victims are intoxicated. 32.3.2 Aetiology of Alcohol
Half of rapists were drinking at the time of the offence. Consumption and Misuse
One- to two-thirds of burglaries are committed under the
influence of alcohol. 32.3.2.1 Genetic Factors
It is estimated that 1200 deaths each year, representing There is good evidence that heavy drinking runs in fami-
one-fifth of all deaths on the roads, result from drink- lies. The relatives of alcoholics have higher rates of alco-
driving. Alcohol is implicated in one-third of accidents holism than the relatives of controls.
at home and deaths by drowning and 40% of deaths by Twin studies indicate that monozygotic twins have a
fire and falling. higher concordance rate than dizygotic twins. In normal
• Withdrawal avoidance. Prolonged drug use

TABLE 32.2 results in tolerance, with CNS adaptation to
Comparison of Monozygotic and Dizygotic Ratio allow normal functioning despite the chronic
in Alcohol Abuse and Dependence between Men presence of the psychoactive drug. If the drug
and Women is suddenly withdrawn, this adaptation results
in drug-withdrawal symptoms, which are usu-
Monozygotic:Dizygotic Ratio
ally opposite to the effects of the drug. Thus,
Alcohol abuse in men 70%:45% in terms of this theory, the dependent person
Alcohol dependence in men 40%:15%
continues drug use in order to avoid the adverse
Alcohol abuse in women 50%:40%
effects of drug withdrawal.
Alcohol dependence in women 30%:25%
• Positive effects of the drug. According to this
Source: Caldwell, C.R. and Gottesman, I.I., Behav. Genet., 21, theory, the pleasant effects of the drug reinforce
563, 1991. drug-taking behaviour, despite adverse social
and physical consequences.
• Motivational distortion. According to this the-
twins, approximately one-third of the variance in drink- ory, the repetition of drug-taking behaviour, or
ing habits has been estimated to be genetic in origin the effects of the drugs themselves, changes the
(Table 32.2). motivational system supporting that behaviour.
Adoption studies support the hypothesis of the genetic Habit strength is a term describing the strength
transmission of alcoholism. The sons of alcoholic parents of the link between stimuli that cues a behav-
are three to four times more likely to become alcoholic iour. It is possible that it involves habituation at
than the sons of nonalcoholics, irrespective of the home the neuronal level.
environment. • Modelling and social learning from other peo-
Strains of rats have been bred, which voluntarily ple who misuse alcohol (e.g. parents, siblings,
consume large quantities of alcohol. These rats appear and peers).
to have abnormalities in brain levels of serotonin, nor-
adrenaline, and dopamine. Each of these theories accounts for some but not all
aspects of addiction.
32.3.2.2 Biological Factors 32.3.2.4 Psychiatric Illness
The EEG of sober, awake alcoholics shows an excess of This can predispose patients to harmful drinking, par-
fast activity and a deficiency of α, θ and δ activity. The ticularly anxiety disorders, phobic disorders, depression
sons of alcoholics also show an excess of fast activity and bereavement and mania in adulthood, hyperkinetic
when compared to controls, leading to speculation that disorder, conduct disorder, and being a victim of abuse
this may be a specific marker for alcoholism. in childhood.
Electrically evoked responses show reduced P3 volt-
age in both abstinent chronic alcoholics and in the young 32.3.2.5 Personality Factors
sons of alcoholics when compared to controls. It has been suggested that some problem drinkers are pre-
The metabolism of alcohol is genetically deter- disposed to harmful drinking by their personality; how-
mined and varies between individuals. Over half of ever, studies in this area give contradictory results. It is
Orientals develop an unpleasant flushing response known that those with sociopathic personality disorder
when alcohol is ingested, related to the accumulation have a high prevalence of heavy drinking and alcoholism.
of acetaldehyde, caused by the absence of the isoen- However, there is no typical pre-alcoholic personality.
zyme aldehyde dehydrogenase (ALDH2). It is thought
that this intolerance of alcohol protects them from 32.3.2.6 Social Factors
developing alcoholism, since it is much less prevalent This can predispose patients to harmful drinking, partic-
in those of Oriental heritage. ularly marital or relationship problems, migration, work-
related stress, poor income, low education, and social
32.3.2.3 Psychological Factors isolation. Certain occupational groups are at greater risk
There are three main components to psychological theo- of drinking problems. Those with jobs in the drink indus-
ries of dependence: try are at highest risk, including publicans, bartenders,
and brewers. Those whose jobs take them away from • Have you ever felt you should cut down on your
home, such as fishermen, armed service personnel, and drinking?
executives, and those with professional autonomy, such as • Have people ever annoyed you by criticizing
doctors, are also at higher risk. your drinking?
• Have you ever felt guilty about your drinking?
• Have you ever had a drink first thing in the
32.3.2.7 Cultural Factors
morning to steady your nerves or get over a
There are high rates of alcoholism in countries where hangover? (an eye-opener)
alcohol is drunk routinely with family meals and in
places where it is cheap.
For patients presenting with alcohol withdrawal, con-
sider using an assessment tool such as the Clinical
32.3.2.8 Religion Institute Withdrawal Assessment (CIWA) scale in addi-
There are low rates of alcoholism in certain religions tion to history taking. CIWA scale is a validated 10-item
such as conservative Protestantism, Jewish religion, scale to quantify the severity of the alcohol withdrawal
and Islam. syndrome and to monitor patients throughout detoxifi-
cation (Stuppaeck et al., 1994).
When alcohol dependence is suspected or diagnosed,
it is essential to carry out a full physical examination
32.3.3 Diagnosis of Alcohol Intoxication and
bearing in mind the multiple-organ systems damaged by
Dependence (Tables 32.3 and 32.4) this substance.
32.3.4 Management
32.3.4.1 Clinical Assessment 32.3.4.2 Investigations
For screening purposes, the CAGE questionnaire is • Blood investigations include alcohol levels
widely used. Positive answers to two or more of the four in the intoxicated (breathalyzers can be use-
questions are indicative of problem drinking. The CAGE ful to give an indication of levels of recent
questionnaire is as follows: drinking).
TABLE 32.3
Comparison between the ICD-10 and the DSM-5 Criteria Acute Intoxication of Alcohol
ICD-10 Criteria (WHO, 1992) DSM-5 Criteria (APA, 2013)
Dysfunctional behaviour At least one of the following The following changes developed during or
1. Disinhibition shortly after ingestion:
3. Aggression 1. Inappropriate sexual or aggressive behaviour
4. Lability of mood 2. Mood lability
5. Impaired attention 3. Impaired judgement
6. Impaired judgement 4. Impaired social or occupational functioning
7. Interference with personal functioning
Other signs At least one of the following must be present: One of the following signs after recent ingestion
1. Unsteady gait 1. Slurred speech
2. Difficulty in standing 2. Incoordination
3. Slurred speech 3. Unsteady gait
4. Nystagmus 4. Nystagmus
5. Decreases level of consciousness 5. Impaired in attention and memory
6. Flushed face 6. Stupor or coma
7. Conjunctive injection
Note: The DSM-5 does not propose criteria on alcohol dependence. It is called alcohol use disorder.
TABLE 32.4
Comparison between the ICD-10 and DSM-5 Criteria on Alcohol Dependence or Alcohol Use Disorder
Categories ICD-10 Criteria (WHO, 1992) DSM-5 Criteria for Alcohol Use Disorder (APA, 2013)
Number of criteria met Three or more of the following manifestations should At least two manifestations in a 1-year period
and duration have occurred together for at least 1 month. If the
manifestations persist for less than 1 month, they
should have occurred together repeatedly within a
1-year period
Compulsion A strong desire or sense of compulsion to consume A persistent desire to use alcohol
alcohol
Control Impaired capacity to control drinking in terms of its Unsuccessful effort to control and cut down
onset, termination, or levels of use. Alcohol is being
often taken in larger amounts or over a longer period
than intended. There is persistent desire to or
unsuccessful efforts to reduce or control alcohol use
Withdrawal Physiological withdrawal state: shaky, restless, or Characteristic withdrawal symptoms and the same
excessive perspiration substance is taken to avoid withdrawals
Tolerance There is a need for significantly increased amounts of Two components: need to increase the amount and
alcohol to achieve intoxication or the desired effect or diminished effect with continued use
a markedly diminished effect with continued use of
the same amount of alcohol
Preoccupation Important alternative pleasures or interests being given Important social, occupational, and recreational
up or reduced because of drinking or a great deal of activities are reduced
time being spent in activities necessary to obtain, take,
or recover from the effects of alcohol
Other criteria Persistent alcohol use despite clear evidence of harmful A great deal of time is spent in activities to obtain the
consequences even though the person is actually substance and continued consumption despite
aware of the nature and extent of harm knowledge
Course specifier • Currently abstinent (early, partial, and full • Early remission (3 months < duration of use
remission) <12 months)
• Currently abstinent but in a protected environment • Sustained remission (no substance use >12 months)
• Currently on a supervised maintenance or • Controlled environment where access to substance is
replacement regime limited
• Currently abstinent but receiving treatment with
aversive or blocking drugs
• Currently using the substance with or without
psychotic features
• Continuous use
• Episodic use
Note: The DSM-5 proposes the diagnostic criteria for alcohol withdrawal. The cessation of heavy and prolonged alcohol use leads to at least two
of the following: anxiety, autonomic hyperactivity hand tremor, insomnia, nausea or vomiting, transient hallucinations or illusions, gener-
alized seizure, and psychomotor agitation. Alcohol withdrawal causes clinically significant distress or impairment in social, occupational,
or other important areas of functioning. This withdrawal is not resulted from a general medical condition.
• Alcoholism is the most common cause of after continued abstinence. Raised g-gluta-
raised mean corpuscular volume (MCV), myl transferase may occur; this is good for
and it is raised in 60% of alcohol abusers. screening as an indication of recent alcohol
Since the life of a red blood cell is 120 days, use, but it can be raised after only one heavy
the MCV should return to normal 4 months drinking session.
• Liver function tests (e.g. aspartate transaminase)

may be abnormal, particularly during acute BOX 32.5 NICE GUIDANCE ON THE
alcoholic hepatitis, less so in fatty liver, and may TREATMENT FOR ACUTE ALCOHOL
be normal in cirrhosis. WITHDRAWAL (NICE, 2010)
1. Consider offering benzodiazepines: Both
diazepam and chlordiazepoxide have U.K.
32.3.5 Management on Withdrawal marketing authorization for the management
and Detoxification of acute alcohol withdrawal symptoms.
• Detoxification can usually be conducted as an 2. Alternatives to benzodiazepines
outpatient unless severe withdrawal effects a. Carbamazepine can be used in the
such as delirium tremens or convulsions are management of alcohol-related with-
likely to occur; the patient’s mental state drawal symptoms, but it does not have
causes concern, or there are severe social the U.K. marketing authorization for
problems, in which case inpatient care should this treatment purpose.
be organized. b. Clomethiazole can be used as in the man-
• The score of CIWA scale can be used as a ref- agement of alcohol-related withdrawal
erence to determine treatment setting. If the symptoms for patients who are deter-
score of CIWA scale is ≤10 (mild withdrawal), mined to discontinue drinking and in
the patient is suitable for home treatment. If the the inpatient setting as it can lead to fatal
CIWA score is >15 (moderate to severe with- respiratory depression when combined
drawal), the patient is suitable for community or with alcohol in patients with cirrhosis. It
hospital treatment. has the U.K. marketing authorization.
The dosage of chlordiazepoxide based on Maudsley’s

BOX 32.4 NICE GUIDANCE ON THE guideline recommendations
MANAGEMENT SETTING IN ACUTE
ALCOHOL WITHDRAWAL (NICE, 2010) • Mild dependence: Small dose is enough to treat
mild perceptual disturbance, and it is safe to be
Offer admission to hospital: used in pregnancy.
• Moderate dependence: Larger dose is required
1. Person at risk of alcohol withdrawal sei-
(e.g. 20 mg qid on day 1), and titrate over 5–7
zures or delirium tremens
days to 5 mg bid on day 5.
2. Young person under 16 years in acute
• Severe dependence: 40 mg (five times a day) on day
alcohol withdrawal
1, and titrate over 10 days to 10 mg nocte on day 10.
Consider admission to hospital: Attention should be paid to the state of hydration and
1. Vulnerable people who are frail and nutrition of the patient.
have cognitive impairments or multiple
comorbidities
BOX 32.6 NICE GUIDANCE ON
PREVENTION OF WERNICKE’S
Do not offer admission to hospital:
ENCEPHALOPATHY (NICE, 2010)
1. Person not at high risk of delirium tre- 1. Thiamine should always be given to peo-
mens or seizures ple at high risk of developing or with sus-
2. Person older than 16 years and not consid- pected Wernicke’s encephalopathy.
ered vulnerable 2. Indications for prophylactic oral thiamine
a. Malnourishment
b. Decompensated liver disease
Drug treatment for the symptoms of acute alcohol with- c. Acute withdrawal
drawal should be started.
patient’s readiness to change based on a model developed by

3. Indications for prophylactic parenteral Prochasaka and DiClemente (see Figure 32.8). If patient is at
thiamine the precontemplation stage, motivational interviewing can
a. Malnourishment or decompensated be offered to help the patient to move to contemplation stage.
liver disease
b. Attendance at emergency department 32.4 PHARMACOLOGICAL TREATMENTS
c. Admission to hospital with acute ill-
ness or injury Medication can be used to help maintain abstinence.
d. Suspected Wernicke’s encephalopathy
4. Parenteral thiamine should be given for a 32.4.1 Disulfiram
minimum of 5 days and followed by oral
Disulfiram is an aversive agent, and prescribing doctor
thiamine
should ensure that the person has not consumed any alco-
hol for at least 1 day before starting disulfiram. Patients
must be well motivated and aware of the risks of taking
Before thiamine treatment, a glucose load should be alcohol with these agents. Efficacy requires compliance
avoided as this can precipitate or exacerbate thiamine with taking the aversive agent; involving the spouse or
deficiency. The suicide risk should be assessed. partner in administration can improve the success rate.
32.4.1.1 Mechanism of Action

32.3.6 Maintenance of Abstinence
• Disulfiram inhibits ALDH2 (see Figure 32.9)
Before offering pharmacological and psychological treat- and leads to acetaldehyde accumulation after
ment to maintain abstinence, it is important to assess the drinking alcohol, resulting in unpleasant effects.
Pre-contemplation: The patient does not Motivational interviewing: Help the patient to analyse the
acknowledge or accept the diagnosis of pros and cons of continued drinking.
alcohol misuse and does not see the need
to change.
Contemplation: The patient acknowledges the alcohol misuse
and consider the pros and cons of drinking
Relapse: Restart of addictive pattern of
use after abstinence.
Decision: The patient has decided to

quit alcohol.
Maintenance: The changes has been
integrated into the patient’s life. He or
she has been abstinent from alcohol.
Action: The change has been integrated Action: The patient has made the change to quit
into the patient’s life. alcohol (e.g. join AA, takes acamprosate)
FIGURE 32.8 ‘Stages of change’ model developed by Prochaska and DiClemente.
Ethanol Acetaldehyde Acetate

Alcohol Aldehyde
dehydrogenase dehydrogenase
(Gene is on (Gene is on
chromosome 4) chromosome 12)
FIGURE 32.9 Metabolism of ethanol by alcohol dehydrogenase and ALDH2.
• Disulfiram blocks dopamine beta-hydroxylase 32.4.2.1 Mechanism of Action

and leads to dopamine accumulation in the CNS, • The withdrawal of alcohol (see Figure 32.10)
resulting in psychosis in people with underlying enhances the actions of glutamate at the
schizophrenia when talking disulfiram. NMDA receptors and the voltage-sensitive cal-
cium channels. This will attenuate the action of
32.4.1.2 Aversive Effects with Ingestion of Alcohol GABA at inhibitory GABA A receptors, result-
• Aversive effects include flushing, headache, ing in agitation and craving during alcohol
palpitations, tachycardia, nausea, and vomiting withdrawal.
with ingestion of small amounts of alcohol and • Acamprosate is a GABA agonist and gluta-
air hunger, arrhythmias, and severe hypotension mate antagonist. It inactivates the NMDA
with large amounts of alcohol. receptors and prevents the calcium influx.
• These effects occur 10–30 min after drinking This will reverse the GABA and gluta-
and are dose dependent. The reaction to alco- mate imbalance when abstaining from alco-
hol discourages the person from drinking and hol and reduce the long-lasting neuronal
reduces the number of days spent on drinking. hyperexcitability.
• Doctors need to inform patients that the aversive • Hence, acamprosate blocks increased glutamate
effects may last for 1 week, and alcohol should be in withdrawal and is neuroprotective.
avoided for 1 week after cessation of disulfiram.
32.4.1.3 Dosage 32.4.2.2 Dosage

Starting dose of disulfiram is 800 mg and then is reduced The starting dose is 666 mg three times a day and indi-
to 100–200 mg daily. cated for adult with body weight larger than or equal
to 60 kg.
32.4.1.4 Side Effects
• Halitosis (common side effect, bad breath from
oral cavity).
Withdrawal of
• Nausea. alcohol Glutamate
• Liver damage.
• Reduction in libido. G G
• Peripheral neuritis. G
G G
• Dangerous side effects include arrhythmia,
G
hypotension, and collapse. G
Ca Ca
Ca
32.4.1.5 Drug Interactions and Contraindication Ca G Glycine
Ca
• Disulfiram increases level of warfarin, diaz- Mg2+
epam, diazepam, and theophylline.
• Disulfiram is contraindicated in people with
cerebrovascular disease, epilepsy, cardiac fail-
ure, coronary artery disease, advanced liver dis-
Ca2+
eases, and pregnancy and breast-feeding.
Acamprosate
32.4.2 Acamprosate
Acamprosate, in combination with counselling, may
also be helpful in maintaining abstinence. It should be
initiated as soon as possible after the achievement of
abstinence. It should be maintained if a relapse occurs.
The patient is allowed to have only one relapse while
they are taking acamprosate. If there is more than one
relapse, the psychiatrist should advise the patient to FIGURE 32.10 Acamprosate inactivates the NMDA recep-
stop acamprosate. tors and prevents the calcium influx during alcohol withdrawal.
32.4.2.3 Side Effects 32.4.3.2 Mechanism of Action

• Diarrhoea Opioid receptors are responsible for reward, result-
• Nausea ing in craving. Naltrexone is an opioid antagonist (see
• Rash Figure 32.11). Alcohol becomes less rewarding when opi-
• Pruritus oid receptors are blocked, and the person does not experi-
• Bullous skin reactions ence euphoric effects.
• Fluctuation in libido
32.4.2.4 Drug Interactions and Contraindications 32.4.3.3 Dosage

• Acamprosate can be used in combination with The starting dose of naltrexone is 25 mg and then
disulfiram. increases to 50 mg per day on weekdays and 100 mg per
• Contraindications include severe renal or hepatic day on weekend.
impairment, pregnancy, and breast-feeding. The
use of acamprosate is not licensed for elderly.
32.5 PSYCHOLOGICAL TREATMENTS
32.4.3 Naltrexone
32.5.1 Alcoholics Anonymous
32.4.3.1 Medical Use
• It is not licensed to treat alcohol dependence in • Alcoholics anonymous (AA) is a self-help group,
the United Kingdom because of mortality after which some alcoholics find helpful.
overdose and potential withdrawal. • AA supports the families of alcoholics, and
• It is only used in people who are in abstinence Alateen the teenage children of alcoholics.
and highly motivated. • AA offers the 12-step approach, which empha-
• It is also used to treat violent behaviours among sizes that addiction damages the whole per-
people with learning disability. son and group therapy allows peer pressure
to overcome the denial and resistance com-
mon in people addicted to alcohol or other
substances.
• The AA group usually meets two to three times
per week.
• The strongest predictor of the AA group
attendance is the severity of alcohol-related
problems.
In brief, the 12 steps are summarized as follows:
1. Admission of being powerless over alcohol.

2. Belief that greater power can restore the person
Naltrexone back to sanity.
Alcohol 3. Seek help from God.
Opioid Opioid
receptor
4. Admit to God their wrongs.
5. Let God remove all the defects in character.
6. Ask God to remove their shortcomings.
7. Searching for moral inventory.
No euphoria 8. Make a list of the people who were harmed
(victims).
9. Direct amends to the victims.
10. Continue to take personal inventory.
11. Seek help through prayer and meditation.
FIGURE 32.11 The mechanism of action of naltrexone on 12. Finally, a spiritual awakening as the result of the
opioid receptors. earlier steps.
32.5.2 Other Psychological Treatments • Methodology: Seven treatment sites around

Birmingham, Cardiff, and Leeds were established
1. Brief intervention known as FRAMES (Miller and involved 742 clients with alcohol problems.
and Sanchez, 1993) Subjects were randomized into the social behav-
a. Feedback about drinking iour and network therapy group versus motivational
b. Responsibility enforcement enhancement therapy group. Outcome measures
c. Advice to change include alcohol consumption, alcohol dependence,
d. Menu of alternatives and alcohol-related problems and were compared
e. Empathetic style between the two groups over 12 months.
f. Self-efficacy • Conclusion: The novel social behaviour and net-
2. Cognitive behaviour models appear to be par- work therapy for alcohol problems did not differ
ticularly effective in relapse prevention. Such significantly in effectiveness from the estab-
therapies include cue exposure, relapse preven- lished motivational enhancement therapy.
tion strategies, contingency management, social
skills, and assertiveness training. 32.5.3.1 Prognosis
Good prognostic factors include
32.5.3 Clinical Trials • Good insight
There are two main trails on the efficacy of psychological • Strong motivation
treatments for people with alcohol dependence. • Good social and family support
Relapse can be precipitated by
• Project MATCH (Project MATCH research
group, 1993): It is a multicentre clinical trial com- • Emotional stress
paring cognitive behaviour coping skills, 12-step • Interpersonal conflict
facilitation therapy, and motivational enhance- • Social pressures
ment therapy. Long-term follow-up of alcoholics over a period of
• Conclusion: The 12-step facilitation therapy is 10 years finds that
more effective, and outcome is determined by • 25% continue troubled drinking.
readiness to change and self-efficacy. • 12% are abstinent.
U.K. Alcohol Treatment Trial (UKATT Research Team, The remainder follow a pattern of intermittent troubled
2005) drinking and abstinence.
CASC STATION ON ALCOHOL DEPENDENCE SYNDROME

A 28-year-old homeless man suffers from treatment-resistant schizophrenia and was admitted to the hospital due
to relapse of psychotic symptoms. Prior to admission, he was advised to consider clozapine, but he refused. Due
to his poor compliance and insight, he is given depot antipsychotic, intramuscular risperidone fortnightly. He is
noted to have binge drinking behaviour. His psychotic symptoms have subsided, and he is ready for discharge.
In the first station, take a history from the patient on the alcohol misuse and its relationship to schizophrenia. You
will speak to his father in the second station.
Approach to this station
People with schizophrenia are three times more likely than the general population to abuse alcohol and six times
more likely to abuse drugs (Ries, 2000):
1. Assess the alcohol dependence syndrome based on the Alcohol Use Disorders Identification Test
(AUDIT) (See Box 32.7) (Barbor, 2001).
2. The alcohol consumption history should include information about the evolution of the problem (drink-
ing career, drink-related problems, dependence) and typical recent drinking day (initial, then hourly
quantification of alcohol intake, waking nausea, tremor, nightmares, and night sweats).
(continued)
3. Explore the presence of first-rank symptoms of schizophrenia and its relationship with alcohol misuse
(e.g. self-medication, relief of anxiety or insomnia).
4. Explore the use of other drugs such as amphetamine, cocaine, cannabis, and hallucinogens and com-
mon reasons for misuse (e.g. to relieve dysphoria, depression, and negative symptoms).
5. Explore current living arrangement such as homelessness.
6. Explore the need for detoxification as this is a case of episodic binge drinking.
7. Explore patient’s knowledge on previous liver impairment, which may affect the metabolism of
antipsychotics
8. Explore the reasons of his refusal of clozapine (e.g. the inconvenience of weekly full blood counts) and
the effect on his alcohol consumption if he has taken clozapine for a brief period.
Explore complications associated with concomitant usage of intramuscular risperidone depot injection and
drinking (e.g. combination of extrapyramidal side effects and cerebellar signs).
In the second station, his father wants to meet you as he is upset with his son’s illness and the discharge plan.
Address his father’s concerns and explain the management plan. You have the permission from the patient
to speak to his father.
Approach to the second station
1. Address the disappointment from his father and explore the source of his anger (e.g. poor control of
schizophrenia symptoms, worsening alcohol misuse, poor anger control, and he feels that the addiction
service is not doing enough).
2. Explain discharge planning: It will be a planned discharge with the aim to integrate outpatient treat-
ment for both alcohol misuse and schizophrenia. There will be at least one to two contacts per week.
3. Refer the patient to the assertive community treatment (ACT) to increase medication compliance.
4. Refer to social worker for residential accommodation as housing instability is closely related in sub-
stance misuse and mental illnesses.
5. Reexplore the option of clozapine as it can reduce the rates of smoking and drinking.
6. Explain long-term treatment (e.g. social and vocational skills training).
BOX 32.7 QUESTIONS USED TO (to estimate the average number of

ASSESS ALCOHOL DEPENDENCE units of alcohol consumed weekly)
BASED ON THE AUDIT 3. Frequency of heavy drinking: ‘How often
do you have six or more drinks on one
Introduction: Now, I am going to ask you some occasion?’
questions about your use of alcoholic beverages
during this past year. Then, candidates need to Dependence symptoms
explain what is meant by ‘alcoholic beverages’ 4. Control over drinking: ‘How often have
by using local examples of beer, wine, and vodka. you found that you were not able to stop
drinking once you had started?’
Hazardous alcohol misuse 5. Increased salience of drinking: ‘How often
have you failed to do what was normally
1. Frequency of drinking: ‘How often do you expected from you because of drinking?’
have a drink containing alcohol?’ 6. Morning drinking: ‘How often have you
2. Average daily quantity: ‘How many needed a first drink in the morning to
drinks containing alcohol do you have on get yourself going after a heavy drinking
a typical day when you are drinking?’ session?’
Harmful alcohol use TABLE 32.5

Colloquial Names for Some Abused Drugs and
7. Guilt after drinking: ‘How often have you had
a feeling of guilt or remorse after drinking?’ Length of Time to Be Detected in Urine Drug Screen
8. Blackouts: ‘How often have you been unable Length of Time
to remember what happened the night before Drug Colloquial Name Detected in Urine
because you had been drinking?’ Amphetamines Speed, whizz 48 h
9. Alcohol-related injuries: ‘Have you or some- Barbiturates Downers 24 h (short acting),
one else been injured as a result of your 3 weeks (long acting)
drinking?’ Cannabinoids Grass, hash, ganja, pot 3 days to 4 weeks
10. Concerns from significant others: ‘Has a Cocaine Snow, coke, girl, lady 6–8 h (metabolites
relative or friend or a doctor or another 2–4 days)
health worker been concerned about your Heroin Smack 36–72 h
drinking or suggested you cutdown?’ LSD Acid 12–24 h
MDMA Ecstasy, XTC, Adam, E 48 h
A note on AUDIT scores and management PCP Angel dust, peace pill 8 days
(McCloud et al., 2007) Temazepam Jellies 6–48 h
AUDIT score: capsules
0–7: Alcohol education
8–15: Simple advice
16–19: Simple advice, brief counselling, and con- meprobamate, pentazocine, phentermine, and
tinued monitoring temazepam. They are subject to the special pre-
20–40: Referral to specialist for diagnostic evalua- scription requirements (except for phenobarbi-
tion and treatment tal and temazepam) but not to the safe custody
A high AUDIT score is strongly associated with requirements (except for buprenorphine, diethyl-
suicidality. propion, flunitrazepam, and temazepam) nor to the
need to keep registers (although there are require-
ments for the retention of invoices for 2 years).
32.6 NONALCOHOLIC PSYCHOACTIVE • Schedule 4 includes, in Part I, benzodiaz-
SUBSTANCES: LEGAL ASPECTS IN THE epines (except flunitrazepam and temazepam,
UNITED KINGDOM (TABLE 32.5) which are in schedule 3) and zolpidem, which
are subject to minimal control. Part II includes
32.6.1 Misuse of Drug Regulations 2001 androgenic and anabolic steroids, clenbuterol,
These regulations divide drugs into the following five sched- human chorionic gonadotropin (HCG), non-
ules, which specify the requirements that govern such issues HCG, somatotropin, somatrem, and somatropin.
as their supply, possession, prescription, and record keeping: Controlled drug prescription requirements do
not apply, and schedule 4 controlled drugs are
• Schedule 1 includes drugs such as cannabis not subject to safe custody requirements.
and lysergide, which are not used medicinally. • Schedule 5 includes those preparations that,
Possession and supply are prohibited except in because of their strength, are exempt from virtu-
accordance with the authority of the Home Office. ally all controlled drug requirements other than
• Schedule 2 includes drugs such as diamorphine retention of invoices for 2 years.
(heroin), morphine, remifentanil, pethidine,
secobarbital, glutethimide, amfetamine, and
cocaine and is subject to the full controlled drug 32.6.2 Misuse of Drugs Act 1971
requirements relating to prescriptions, safe cus- (Modification) Order 2003 and
tody (except for secobarbital), the need to keep
Misuse of Drugs Regulations 2003
registers, etc. (unless exempted in schedule 5).
• Schedule 3 includes the barbiturates (except Changes were made to the legislation on the misuse of
secobarbital, which is in schedule 2), buprenor- drugs by these regulations, which came into force on July 1,
phine, diethylpropion, flunitrazepam, mazindol, 2003. The following eight substances were brought under
the control of the Misuse of Drugs Act 1971 and its associ- Schedule 4 (Part II) now comprises 54 anabolic sub-
ated subordinate legislation for the first time: stances; examples are nandrolone and testosterone (and the 4
newly added anabolic substances: 4-androstene-3, 17-dione;
Remifentanil 4-Androstene-3, 17-dione 19-nor-4-androstene-3, 17-dione; 5-androstene-3, 17-diol; and
Dihydroetorphine 19-Nor-4-androstene-3, 17-dione 19-nor-5-androstene-3, 17-diol). Persons already authorized
Gamma-hydroxybutyrate (GHB) 5-Androstene-3, 17-diol by the 2001 Regulations (e.g. doctors and pharmacists) or by
Zolpidem 19-Nor-5-androstene-3, 17-diol a written Home Office authority to produce, supply, or pos-
sess schedule 4 (Part II) drugs are authorized in respect of the
Remifentanil and dihydroetorphine are controlled as class A four newly added drugs; in other cases, an appropriate writ-
drugs. Both are powerful opiates and have similar pharma- ten Home Office authority is required. (Note that possession
cological properties to existing class A drugs. Both are listed licences are not required if the substances are in medicinal
under schedule 2 of the Misuse of Drugs Regulations 2001. product form.) The Regulation 15 prescription requirements
4-Hydroxy-n-butyric acid or GHB and zolpidem are (including handwriting) do not apply to schedule 4 (Part II
controlled as class C drugs. Both are listed under schedule drugs). Regulations 22, 23 (keeping and preservation of
4 (Part I) of the 2001 Regulations. GHB has been used as records), 26 (furnishing of information), and 27 (destruc-
an anaesthetic and to treat alcohol and drug dependence tion—holders of written authorities to produce only) also
but has also been misused by clubbers. Zolpidem is a pre- apply to schedule 4 Part II drugs. Schedule 4 Part II drugs are
scription medicine (a nonbenzodiazepine hypnotic with a not subject to the statutory safe custody requirements.
short duration of action) and acts in a similar same way
as some sedatives such as benzodiazepines. 32.6.3 Prescribing Controlled Drugs
The following four anabolic substances are listed in The main regulations relating to prescriptions for con-
schedule 4 (Part II) of the 2001 Regulations: trolled drugs specified in schedules 2 and 3, under the
Misuse of Drugs Regulations 2001, are as follows.
4-Androstene-3, 17-dione 5-Androstene-3, 17-diol
Prescriptions ordering controlled drugs subject to pre-
19-Nor-4-androstene-3, 17-dione 19-Nor-5-androstene-3, 17-diol
scription requirements must be signed and dated by the
prescriber and specify the prescriber’s address. The pre-
They are now controlled as class C drugs.
scription must always state in the prescriber’s own hand-
Note that schedule 2 drugs are subject to the addi-
writing in ink or otherwise so as to be indelible:
tional prescription requirements of Regulation 15 (see
the following; among other things, prescriptions must be • The name and address of the patient
handwritten by doctors). Regulations 14 (documentation), • In the case of a preparation, the form and where
16 (supply on prescription), 18 (marking of containers), appropriate the strength of the preparation
19, 20, 21, 23 (keeping and preservation of registers), • The total quantity of the preparation, or the
26 (furnishing of information), and 27 (destruction) also number of dose units, in both words and figures
apply to schedule 2 drugs. Most schedule 2 drugs are also • The dose
subject to the statutory safe custody requirements. • The words ‘for dental treatment only’ if issued
Schedule 4 (Part I) includes benzodiazepines (e.g. diaze- by a dentist
pam, lorazepam, and nitrazepam). GHB and zolpidem have
A prescription may order a controlled drug to be dispensed
been added to the list of drugs in schedule 4 (Part I). Persons
by instalments. If so, the amount of the instalments and the
already authorized by the Regulations (e.g. doctors and
intervals to be observed must be specified. Prescriptions
pharmacists), or by a written Home Office authority to pro-
ordering ‘repeats’ on the same form are not permitted. A pre-
duce, supply, or possess schedule 4 (Part I) drugs, are auto-
scription is valid for 13 weeks from the date stated thereon.
matically so authorized in respect of GHB and zolpidem. In
It is an offence for a prescriber to issue an incomplete
other cases, an appropriate written Home Office authority
prescription, and a pharmacist is not allowed to dispense
is required. The Regulation 15 prescription requirements
a controlled drug unless all the information required by
(including handwriting) do not apply to schedule 4 (Part I)
law is given on the prescription.
drugs. Regulations 22, 23 (keeping and preservation of
records), 26 (furnishing of information), and 27 (destruc-
32.6.4 Opioids
tion—holders of written authorities to produce only) also
apply to schedule 4 (Part I) drugs. Schedule 4 (Part I) drugs Note: Drugs derived from opium poppies are known as opi-
are not subject to the safe custody requirements. ates. Synthetically derived opiates are known as opioids.
32.6.4.1 Heroin (Gear, Smack, Scag) The DSM-5 proposes the following opioid-induced
Heroin (3,6-diacetylmorphine) is produced from mor- disorders: major neurocognitive disorder, amnestic dis-
phine, which is derived from the sap of the opium poppy. order, psychotic disorder, depressive or bipolar disorder,
It may be smoked or chased by heating on tin foil and anxiety disorder, sexual dysfunction, or sleep disorder.
inhaling the sublimate. It is also injected intravenously
and much less commonly subcutaneously (skin-popping). 32.6.4.4 Effects of Opioid Withdrawal
Street heroin is usually 30%–60% pure, and 0.25–0.75 g During opioid withdrawal, there is an excessive release of
is a common daily consumption for addicts. noradrenaline and results in rhinorrhoea or sneezing, lacri-
mation, muscle cramps or aches, abdominal cramps, nau-
32.6.4.2 Epidemiology sea or vomiting, diarrhoea, pupillary dilatation (mydriasis),
The number of addicts notified to the Home Office has piloerection, recurrent chills, tachycardia, hypertension,
increased dramatically over the last 30 years. This is yawning, and restless sleep. The ICD-10 criteria (F11.3
thought to be related to the wider availability of cheap opioid withdrawal state) require the presence of any three
opiates imported from the Middle East. Youth culture has of the aforementioned symptoms. The DSM-5 criteria are
become much more accepting of drug use, and polydrug similar to the ICD-10 criteria. Opioid withdrawal is seldom
use is much more common than it used to be. The approx- associated with withdrawal fits (Figure 32.14).
imate numbers of notifications have been These begin within 4–12 h of last heroin use. Peak
intensity is at about 48 h, and the main symptoms dis-
1960 500 appear within a week of abstinence. Although it is
1980 5,000
unpleasant, opiate withdrawal is not generally dangerous
1990 15,000
(exceptions include pregnancy, when abortion may result
from precipitous withdrawal).
Most heroin users are aged between 20 and 30 years. The
steepest increase has occurred in those aged 16–24 years. 32.6.4.5 Harmful Effects
The male/female ratio is 2:1.
32.6.4.5.1 Effects of the Drug Itself
32.6.4.3 Drug Action Overdose can be caused by the uncertain concentration of
The stimulation of opiate receptors produces analgesia, street drugs or to reduced tolerance following a period of
euphoria, miosis, hypotension, bradycardia, and respira- abstinence (e.g. upon release from prison). The clinical fea-
tory depression. tures of opiate overdose include stupor or coma, pinpoint
Opioid receptors fall into different types, each of which pupils, pallor, severe respiratory depression, and pulmo-
has subtypes. The main types are μ, κ, and δ receptors. nary oedema. Supportive treatment and administration of
The μ receptor is essential for the development of opioid an opioid antagonist such as naloxone is indicated. The
dependence. The μ receptor is potassium channel linked half-life of opioid antagonists is less than that of most opi-
and inhibits adenylate cyclase. The binding of morphine ate drugs, so the patient must be observed for several hours
to the μ receptors inhibits the release of GABA from the to ensure that the underlying opiate overdose has passed.
nerve terminals, reducing the inhibitory effect of GABA
on the dopaminergic neurons. The increased activation of 32.6.4.5.2 Intoxication
dopaminergic neurons in the nucleus accumbens and the These include accidents.
ventral tegmental areas that are part of the brain’s ‘reward
pathway’ and the release of dopamine into the synaptic 32.6.4.5.3 Inhalation
result in sustained activation of the postsynaptic mem- The inhalation of heroin commonly exacerbates or causes
brane. Continued activation of the dopaminergic reward lung conditions such as asthma. There are increased rates of
pathway leads to the feelings of euphoria (Figure 32.12). pneumonia and tuberculosis in those who are HIV positive.
Euphoria is initially intense and is related in part to
the method of administration. Thus, methods delivering 32.6.4.5.4 Intravenous Use
a large bolus quickly to the CNS are associated with a The hazards of intravenous use are many and include
greater initial rush. Intravenous and inhalational tech- the transmission of infection through the use of shared
niques of heroin fulfil these conditions; oral and subcu- needles. HIV and hepatitis B, C, and D are commonly
taneous methods do not. Dependence may arise within transmitted through this route. Those who are HIV posi-
weeks of regular use (Figure 32.13 and Table 32.6). tive have a poorer outcome if they continue to inject.
Nerve terminal in
nucleus accumbens
Morphine binds
to μ receptor
Morphine
Dopamine Dopamine
receptor (DOPA)
Postsynaptic membrane
Opioid binding at the μ receptors stimulates release of dopamine into an area called
the nucleus accumbens.
This increased dopamine activity in the nucleus accumbens is associated with euphor
and other pleasurable sensations.
FIGURE 32.12 The mechanisms of actions of morphine and the µ receptor.
32.6.4.5.5 Bacterial Infection 32.6.4.5.8 Fungal Infection

Bacterial infection results from the lack of aseptic tech- Systemic fungal infections have been reported, which are
nique; the risk is not eliminated by using clean needles difficult to treat and result in death or blindness because
since the drug itself is not of pharmaceutical quality, has of ophthalmic involvement.
often been adulterated with other substances, and is often
not suitable for intravenous administration because of the 32.6.4.5.9 Vascular Complications
presence of nonsoluble components. Vascular complications include the obliteration of the
lung vascular bed with continued prolonged injection of
particulate matter. The same effect is seen in the lym-
32.6.4.5.6 Skin Infection phatic system, resulting in puffy hands. Deep vein throm-
Skin infection at injection sites leads to abscess forma- bosis may develop at the site of femoral administration.
tion and thrombophlebitis. Staphylococcus aureus and Arterial administration can result in occlusion caused by
Streptococcus pyogenes are often responsible. spasm or embolism. The loss of a limb may result.
32.6.4.5.10 Long-Term Physical Effects
32.6.4.5.7 Blood Infection Long-term users may develop membranous glomerulone-
Most injecting results in transient bacteraemia. This can phritis or amyloid disease.
result in septicaemia and/or bacterial endocarditis, even
in those with previously normal heart valves. Septic 32.6.4.5.11 Social Effects
emboli may be carried to distant sites. Septic embolism Because of the effects of tolerance and dependence, her-
can result in osteomyelitis. oin users usually escalate the dose of drug taken in an
Nerve terminals in
nucleus accumbens
δ or κ
Opiate receptor
GABA
Morphine serves as This inhibits release GABA

a weak agonist at the of GABA from the receptor
delta (δ) and kappa (κ) nerve terminals More dopamine is
opiate receptors
released to activate the
Dopamine postsynaptic membrane
Blood brain
barrier
Heroin Morphine
FIGURE 32.13 The mechanism of action of heroin and opioid receptors.
that this saves society over £30,000 per addict in drug-

TABLE 32.6 related crime. Relationships and family commitments
ICD-10 Criteria of Acute Intoxication due to Use usually come second to drug-related activities, and fam-
of Opioid (F.11) ily breakdown often results. It is difficult to continue in
employment when seriously addicted to heroin.
Dysfunctional Behaviour
(At Least One of the Signs (At Least One of the
Following) Following Must Be Present) 32.6.5 Codeine
1. Apathy and sedation 1. Drowsiness Misuse of codeine preparations is common. Preparations
2. Disinhibition 2. Slurred speech include DF118 (dihydrocodeine 30 mg) and codeine linc-
3. Psychomotor retardation 3. Pupillary constriction tus (codeine phosphate 15 mg/5 mL).
4. Impaired attention 4. Decreased level of consciousness
5. Impaired judgement 32.6.5.1 Management of Opiate/Opioid Dependence
6. Interference with personal
32.6.5.1.1 AIMS
functioning
The aims of management are to
Note: The DSM-5 only specifies pupillary constriction, drowsiness
or coma, slurred speech, and impairment in attention or • Help the person to deal with drug-related problems
memory for opioid intoxication. • Reduce damage occurring during drug use
• Reduce duration of episodes of drug use
• Reduce the chance of relapse
attempt to continue to achieve the euphoriant effects and • Help the person to remain healthy until he or she
to keep the unpleasant withdrawal effects of the drug at manages to attain a drug-free state
bay. The result is often that the addict turns to acquisitive
crime in order to fund the growing drug habit. It is esti- 32.6.5.1.2 History and Examination
mated that the stabilization of heroin addicts on to metha- Before any treatment is initiated, it is essential to estab-
done costs the NHS over £1,000 per year per addict but lish that the person is in fact drug dependent. A history
Nerve terminal in
nucleus accumbens
NA NA
NA
Lack of morphine NA
Dopamine NA
binding to μ receptor NA
(DOPA) NA NA
Dopamine NA
receptor NA
Repeated use of an opioid causes μ receptors to become tolerant—the first sign of physical
dependence and higher doses of the opioid are needed to produce the intended effect.
FIGURE 32.14 The development of tolerance and withdrawal with chronic opioid misuse.
of drug use, past and current; an account of withdrawal Patients should receive information about harm
symptoms experienced upon cessation of the drug; a minimization, and HIV and hepatitis testing should be
social history including sources of support, accommo- arranged after counselling and with the person’s consent.
dation, and employment; the funding of the drug habit; The ultimate aim of treatment is to achieve opi-
and a medical and psychiatric history are all considered ate abstinence. However, this is unacceptable to some
necessary. patients, in which case the aim is to minimize the harm
Physical examination should seek signs of current associated with opiate abuse (harm minimization).
drug use and of complications related to the route of
administration. It is essential to test urine for a drug 32.6.5.1.3 Harm Minimization
screen, to establish that on two separate occasions, The aims are to stop or reduce the use of contaminated
the person was taking the drugs claimed. Most drugs injecting equipment, to prevent the sharing of injecting
will show up on urine screens for at least 24 h after equipment, to stop or reduce drug use, to stop or reduce
ingestion. unsafe sexual practices, to encourage health conscious-
Once it is established that the person is opiate depen- ness and a more stable lifestyle, and to establish and
dent, it is necessary to assess his or her motivation for retain contact with the drug services.
treatment and to reach an agreement about the aims of To achieve these aims, education about the poten-
treatment. tial hazards is important. Sterile injecting equipment
The Home Office should be notified. The person and condoms should be provided, nonimmune indi-
should be informed that there is a legal obligation upon viduals should be offered hepatitis B vaccination, and
the doctor to do this but that the information will not be substitute oral opiates such as methadone should be
made available to the police. prescribed.
32.6.5.1.4 Detoxification 32.6.6 Methadone

Recommendations from the NICE guidelines on opioid
32.6.6.1 Indications
detoxification
1. Opioid drugs are taken on a regular basis.
1. Detoxification should be offered to people 2. There is convincing evidence of opioid
who are opioid dependent and have expressed dependence.
an informed choice to become abstinent after 3. There is an opportunity to supervise the daily
being counselled on the adverse effects of use of methadone for at least 3 months.
opioid misuse.
32.6.6.2 Contraindications
2. Methadone or buprenorphine should be offered
as the first-line treatment in opioid detoxification. 1. QTc prolongations (consider buprenorphine)
2. Refusal to be supervised
32.6.5.1.5 Substitute Prescribing 32.6.6.3 Properties of Methadone

32.6.5.1.5.1 Nonopiate Substitutes If dependence is • Methadone is a synthetic opiate (opioid) that can
not severe, reassurance, support, and symptomatic treat- be taken orally or intravenously.
ment with nonopiate drugs may suffice. The following • Methadone is a long-acting opioid agonist (t½ =
may be used: 24–36 h), allowing once-daily oral prescribing.
• Methadone produces cross-tolerance in opioid
1. Clonidine misusers because it also blocks μ receptors.
a. An α-adrenergic antagonist that inhibits • Methadone is excreted in the urine in a slower
noradrenergic overactivity by acting on the pace as compared to heroin.
presynaptic autoreceptors. • Methadone is rapidly absorbed, and the peak
b. Provide some symptomatic relief in opiate levels are achieved within 2–6 h after oral
withdrawal (hypotension can be a problem). administration.
2. Lofexidine
a. An α2 agonist, which acts centrally to reduce 32.6.6.4 Administration
sympathetic tone (reduction in blood pres- • Oral methadone mixture 1 mg/mL is the usual
sure is less marked than that produced by choice.
clonidine). • Any doctor can prescribe methadone to a drug
b. Pharmacodynamics: counteracts the adrener- misuser.
gic hyperactivity during opioid withdrawal. • Daily dispensing reduces the risk of overdose
c. Indications: (1) detoxification within short and abuse.
period of time (5–7 days) and (2) depen-
dence in young people. 32.6.6.5 Dose
d. Dosage: start with 800 mcg daily, increase • Methadone at 60–100 mg/day is more effective
to 2.4 mg in divided daily doses over 3 days, than lower dosages in reducing heroin misuse.
and then reduce in 4 days. • Methadone at 20–40 mg can attenuate with-
3. Propranolol—for somatic anxiety drawal symptoms.
4. Thioridazine—relieves anxiety in low doses • The starting dose of methadone is 10–30 mg per
5. Promethazine—a sedative antihistamine effec- day and increases by 5–10 mg per week to reach
tive for mild withdrawal therapeutic dose.
6. Benzodiazepines—for anxiety (do not give for
longer than 2 weeks) 32.6.6.6 Duration of Maintenance Treatment
• For maintenance, a substitute opiate is pre-
32.6.5.1.6 Substitute Opioids scribed indefinitely in an effort to stabilize the
32.6.5.1.6.1 Levo- α-Acetylmethadol Levo-α- addict’s life and reduce risks of intravenous use.
Acetylmethadol (LAAM) is a synthetic opioid that can • For long-term withdrawal, substitute pre-
block the effects of heroin for up to 72 h. The frequency scribing takes place over a period of months
of usage is three times a week because of its long duration to years with the long-term aim of opiate
of action. LAAM is associated with torsades de pointes. abstinence.
• For rapid withdrawal, withdrawal takes place 32.6.6.9 Cardiovascular Risks

over a period of weeks by the use of a substitute 1. Torsades de pointes
drug in decreasing doses. 2. QTc interval prolongation
• For gradual withdrawal, withdrawal takes place
over a period of months by the use of a substitute 32.6.6.10 Management of Pain
drug in decreasing doses.
1. Nonopioid analgesics such as NSAIDs are
preferred.
32.6.6.7 Treatment Setting 2. If opioid analgesics are required, titrate up the
• Treatment should be undertaken initially by the dose of methadone slowly (Table 32.7).
general practitioner (GP), possibly with help
from the local community drug team. If these
approaches fail, referral to the more specialized 32.6.7 Buprenorphine
drug dependency unit may be required.
32.6.7.1 Indications
• People who are dependent on more than one
drug, those with a history of several failed 32.6.7.1.1 Chemical Properties
attempts, those with coexisting mental or physi- • Buprenorphine is a partial μ-opioid agonist and
cal disease, those who are violent or highly κ-opioid antagonist.
manipulative, and those requiring injectable or
high doses of substitute drugs should be consid- 32.6.7.2 Pharmacodynamics (Figure 32.15)
ered for specialist referral. 32.6.7.3 Pharmacokinetics
• Buprenorphine is metabolized in the body by
32.6.6.8 Management of Methadone Overdose both N-dealkylation and conjugation by the
1. Administer intravenous naloxone (0.4–2 mg cytochrome P450 enzyme system and excreted
over 3 min to a maximum of 10 mg). principally in faeces and urine.
TABLE 32.7
Advantages and Disadvantages of Methadone Maintenance Programme
Advantages Disadvantages
1. The opportunity to escape from the subculture 1. The substitution of one addicting drug for another
2. Relief from the great expenditure of money and time necessary to 2. The need for the most careful structuring or the procedures
obtain illicit supplies at the dispensing centres to prevent diversion
3. The possibility of less criminal behaviour that would reflect both 3. The fact that polydrug use is common and the psychiatrist
upon the addict and the community is dealing with part of the problem
4. The avoidance of physical harm derived either from accidental 4. There are very large political difficulties in setting up such
overdose or infections a programme and having it accepted in the community
5. Methadone has longer half-life as compared with the usual agents of 5. It may cause major schisms in the public health authorities
addiction 6. There are problems about the safety of methadone itself, for
6. The possibility that continuing contact with the methadone example, children have died from taking their parent’s methadone
programme may permit the use of other forms of treatment 7. Methadone dispensing facilities become the centres of a social
network of addicts in which other drugs are traded and the
subculture is preserved or enhanced
8. Methadone can be used merely to tide addicts over the times when
illicit drugs are in short supply and reduce their motivation to quit
9. Addicts on programmes find it difficult to get to the appointed
places at the proper times particularly if they go to work or if they
live in the rural area
10. People who were addicted to nothing at all can get onto a
programme and become addicted to methadone
Nerve terminal in
nucleus accumbens
Suboxone binds
to μ receptor
Suboxone
(buprenorphine−naloxone) Dopamine Dopamine
(DOPA)
receptor
Suboxone binds to the μ receptors, reinitiating opioid activity in the brain. As a partial agonist,
buprenorphine produces less euphoria than a full opioid agonist but is sufficient to suppress
withdrawal and cravings.
Buprenorphine’s high affinity for the μ receptor keeps it from being displaced by other opioids.
Once maintenance dosing is established, most μ receptors remain filled and the patient’s
withdrawal and cravings are controlled.
FIGURE 32.15 The neurochemical effects of buprenorphine/naloxone.
• Peak plasma concentration occurs approximately • Hypersensitivity to buprenorphine is rare (fewer

3 h after dose administration. than 1% of patients).
• Buprenorphine has a terminal half-life of about
3–5 h. 32.6.7.6 Contraindications
• Absolute contraindication: hypersensitivity
32.6.7.4 Dosage • Relative contraindication: alcohol or benzodiaz-
• The titration dosing for induction starts with 2 epine dependence
or 4 mg on the first day.
• The dose can then be increased in 2–4 mg incre- 32.6.7.7 Withdrawal of Buprenorphine
ments to 12–16 mg on the second day. • Symptoms include yawning, rhinorrhoea,
• Most people can be stabilized on 8–32 mg/day. abdominal cramps, nausea, diarrhoea, lacrima-
tion, sweating, insomnia, and irritability.
32.6.7.5 Side Effects
• The primary side effects of buprenorphine are 32.6.7.8 Diversion
similar to those of other μ-opioid agonists: nau- • Intravenous misuse of buprenorphine occurs
sea, vomiting, and constipation. These side and leads to associated medical complications
effects may be less intense than those produced such as infective endocarditis and cutaneous
by full agonist opioids. complications.
• Combination buprenorphine/naloxone (suboxone) 32.6.7.13 Relapse Prevention

rather than buprenorphine alone can avoid diver- Described by Marlatt, this is a short-term intervention
sion because the effects of the opioid antagonist nal- with extensive follow-up and preparation of the patient to
oxone predominate when people inject suboxone. anticipate urges to return to the drug-taking behaviour for
a considerable period after abstinence has been achieved.
32.6.7.9 Antagonist Treatment People undergoing relapse prevention therapy are
Naltrexone, an opioid receptor antagonist, is indicated for peo- more likely to internally attribute change, and are more
ple who prefer abstinence programme and are fully informed likely to remain opiate-free during follow-up, or to con-
the risk of withdrawal. Naltrexone is most efficacious in tain a temporary relapse. The internal attribution of con-
middle-class adults who are highly motivated. Naltrexone has trol over drug use maximizes treatment effects.
longer half-life than naloxone. Naltrexone cannot be given Naltrexone is a long-acting opioid antagonist that pre-
until all opioids have been cleared from the body. The initial cipitates a withdrawal syndrome in the opiate-dependent
dose is 25 mg and then increases to maintenance dose of 50 person. It is used in the detoxified addict who requires
mg per day. It is particularly helpful if a partner administers it additional help to remain drug-free. The euphoriant
and if used in conjunction with cognitive behaviour therapy. effects of opiates are abolished, thus aiding abstinence.
Dihydrocodeine is a semisynthetic opioid analgesic. In the Group therapy and support groups, such as Narcotics
United Kingdom dihydrocodeine is a class B drug available Anonymous, often focus on discussions with other people
in 30 mg tablets. Among GPs in England and Wales, it is the misusing opioid and on sharing experiences and effective
second most commonly prescribed drug (after methadone) coping methods.
for opioid addiction. Dihydrocodeine is much shorter acting
than methadone because of its lower affinity of binding to 32.6.7.14 Prognosis
the µ-opioid receptor. Common side effects include constipa- • The mortality rate for intravenous drug abusers
tion, giddiness, hypersensitivity, itching, flushing, and other is 20 times that of their nondrug-using peers.
effects of blood vessel dilation. Tolerance and physical and • Since the 1980s, the prevalence of HIV infection
psychological dependence develop with repeated use. It is not among intravenous drug users has increased to
recommended by the NICE guidelines for routine usage. approximately 50%–60% in some groups (e.g.
New York, Edinburgh), and mortality among
32.6.7.10 Psychosocial Intervention this group has increased further.
The NICE guidelines recommend two types of psychoso-
cial interventions: 32.6.8 Cannabis (Grass, Hash, Ganja, Pot)
1. Contingency management (e.g. offering incen- The major active constituent in cannabis is 9-tetrahydro-
tives contingent on each drug-negative test such cannabinol. It is derived from cannabis salve, the Indian
as giving vouchers that can be exchanged for hemp plant; the dried leaves contain 1%–10% (mari-
goods or privileges that allow the person tak- juana); the resin contains 8%–15% (hashish). It is usually
ing methadone home) can be offered up to 3–6 smoked, but it can be eaten, and it is widely used. It is
months after opioid detoxification. highly lipophilic, so it can be detected in the blood 20 h
2. For people taking naltrexone: They have to following a single dose.
receive contingency management with behav-
ioural family intervention for the person and a
nondrug-misusing family member. 32.6.8.1 Mechanism of Actions (Figure 32.16)
32.6.8.2 Cannabinoid Receptors
32.6.7.11 Psychological Methods There are two subtypes of the cannabinoid receptor,
Therapeutic outcome is improved if substitute prescrib- CB1 and CB2 receptors. The CB1 receptors are highly
ing is combined with various forms of behaviour therapy. expressed in the hippocampus, cortex, basal ganglia, cer-
ebellum, and spinal cord, and this accounts for the effects
32.6.7.12 Motivational Interviewing of cannabis on memory, cognition, and movement. Both
Motivational interviewing is a cognitive behaviour CB1 and CB2 cannabinoid receptors are coupled to
approach that takes into account the patient’s stage of inhibitory G proteins.
preparedness for change and prompts the patient to con- Activation of the cannabinoid receptors causes inhibi-
sider the favourable reasons to change. tion of adenylate cyclase and a subsequent decrease in the
1
Tetrahydrocannabinol
of cannabis
2 Inhibits Na+
channel MAP Cannabinoid
kinase CB1 receptor
Inhibits N and P/Q type
3 voltage dependent γ
Ca2+ channel α
β
Adenylate
cyclase
Protein
kinase
4 Stimulates inwardly
rectifying K+ channel Inhibits A-type
K+ channel
FIGURE 32.16 Neurochemical effects of cannabis.
concentration of cAMP in the cell. This will ultimately

result in the inhibition of neurotransmission. TABLE 32.8
The active ingredient of cannabis is ∆9-tetrahydrocan- Summary of the ICD-10 Criteria of Acute
nabinol (∆9-THC), and it is thought to exert its effect by
Intoxication due to Use of Cannabinoids (F.12)
binding to CB1 receptors on presynaptic nerve terminals
in the brain. ∆9-THC binding to CB1 receptors activates Dysfunctional Behaviour (At Signs (At Least One of the
G proteins, which causes changes from 2 to 4 as stated in Least One of the Following) Following Must Be Present)
the earlier figure. The changes of these channels will lead 1. Anxiety or agitation (20% of 1. Conjunctival injection
to the euphoric feelings associated with cannabis use. patients) (reddening of eyes)
∆9-THC has anticholinergic effects, and its action 2. Auditory, visual, or tactile 2. Dry mouth
is particularly marked in the hippocampus. It thus has illusions 3. Increased appetite
adverse effects on memory, cognition, and other higher 3. Depersonalization or (cannabis is a well-known
serialization appetite suppressant)
mental functions. ∆9-THC inhibits luteinizing hormone,
4. Euphoria and disinhibition 4. Tachycardia
prolactin, and growth hormone production.
(e.g. giggles)
Carriers of the COMT valine (158) allele are most 5. Hallucinations with preserved
likely to exhibit psychotic symptoms and to develop orientation
schizophreniform disorder if they use cannabis (Caspi 6. Impaired judgement, attention,
et al., 2005). or reaction time
functioning
32.6.8.3 Clinical Features 8. Suspiciousness or paranoid
When a patient smokes cannabis, the peak effect occurs at ideation
about 30 min, and the effects last for 2–4 h. The motor and 9. Temporal slowing (a sense that
cognitive effects may last from 5 to 12 h. Cannabis can also time is passing very slowly or
be taken orally when it is mixed with food, but the oral route rapid flow of ideas)
is less effective as compared to inhalation (Table 32.8).
The DSM-5 criteria for cannabis intoxication are less specific
In high-dosage perceptual distortions, confusion, than ICD-10. The DSM-5 criteria state that the d ysfunctional
drowsiness, bradycardia, hypotension, hypothermia, behaviour and signs (conjunctival injection, increased appe-
bronchodilatation, and peripheral vasoconstriction can tite, dry mouth and tachycardia) occur within 2 h of
occur. An acute toxic psychosis that resolves with absti- cannabis use.
nence may occur.
32.6.8.4 Drug Withdrawal using opioids. Cocaine remains relatively expensive

In chronic users, cessation of cannabis is often fol- in the United Kingdom although its use is increas-
lowed by a withdrawal syndrome. The DSM-5 criteria ing. Amphetamines tend to be the preferred stimulant
state that the patient should have a least three of the of abuse in the United Kingdom. Fewer than 10% of
following symptoms within 1 week after withdrawal cocaine addicts are notified to the Home Office.
of cannabis: anxiety, aggression, depression, insom- Common psychiatric comorbidity of cocaine users
nia, irritability, poor appetite, and weight loss. The includes dissocial personality disorder (33%), alcoholism
patient should have at least one of the following physi- (28%), cyclothymia and dysthymia (20%), and schizo-
cal symptoms causing significant discomfort: stomach phrenia (20%).
pain, shakiness/tremors, sweating, fever, chills, or
headache. Craving and psychological dependence do 32.6.9.3 Drug Action
not occur. Cocaine blocks dopamine uptake at the dopamine reup-
take site. Extracellular levels of dopamine are mark-
32.6.8.5 Harmful Effects edly increased. Dopaminergic activity, particularly at
Chronic cannabis use can lead to a deterioration in the nucleus accumbens, has been found to have a major
personality (a motivational syndrome). An increase role in the pleasurable and reinforcing effects of cocaine,
in aggressiveness may also occur. Flashbacks, and amphetamine, phencyclidine, nicotine, and alcohol.
prolonged depersonalization and derealization, Genetic polymorphisms at the dopamine reuptake site
may occur. may contribute to an individual’s liability to become
Cognitive and psychomotor impairments resulting dependent (Figure 32.17).
from even small amounts of cannabis make the perfor- The half-life is 50 min. Acute effects last about 20 min
mance of skilled tasks (such as driving) hazardous. and include euphoria, reduced hunger, tirelessness, agita-
tion, tachycardia, raised blood pressure, sweating, nausea,
32.6.8.6 Treatment vomiting, dilated pupils, and impairment of judgement
The treatment is abstinence and support.
Nerve terminal in
32.6.9 Stimulants nucleus accumbens
Stimulants considered here are cocaine, amphetamines,
and caffeine.
MAO
32.6.9.1 Cocaine (Coke, Snow, Crack)

Cocaine is derived from the leaves of the coca shrub.
Coca leaves are chewed, and the paste derived from the
leaves is smoked.
Cocaine hydrochloride, a white powder usually Dopamine
re-uptake
snorted, may be injected. Crack cocaine (rock or stone) transporter
is produced by solvent extraction by using NH3 to sepa-
rate cocaine base from hydrochloride salt. Perforated
soft drink can, metal foil, and crack pipe are used for Cocaine inhibits the
Dopamine re-uptake of dopamine
consumption. This provides a powerful hit that produces receptor
strong psychological dependence.
It is a class A drug, requiring notification.
32.6.9.2 Epidemiology Postsynaptic membrane

There has been an epidemic of cocaine use in the United
States. Based on the World Health Organization, there
are 35 millions of people using amphetamine, 15 mil-
lions of people using cocaine, and 10 million of people FIGURE 32.17 The mechanism of action of cocaine.
and social functioning. High doses may lead to an acute 32.6.9.6 Cocaine Withdrawal
toxic psychosis with marked agitation, paranoia, and audi- Following the initial rush of well-being and confi-
tory, visual, and tactile hallucinations (cocaine bug). dence, when the effects of the drug wear off, there
Chronic use leads to tolerance, withdrawal symptoms, follows a rebound crash. The ICD-10 criteria include
and a chronically anxious state, possibly caused by dopa- lethargy, fatigue, psychomotor retardation or agita-
mine depletion. tion, craving for cocaine, increased appetite, insom-
nia or hypersomnia, and unpleasant dreams. The crash
32.6.9.4 Routes of Administration phase lasts 9 h to 4 days. The withdrawal phase of 1–10
• Cocaine can be administered by the intranasal weeks is the period of the greatest risk of relapse. The
and intravenous routes. final phase is of unlimited duration, when stimuli can
• Intranasal use results in earlier seeking behav- trigger craving.
iour (after 10–30 min) compared to intravenous
route (50 min).
32.6.9.7 Harmful Effects
• Injection causes a euphoric rush that lasts for
10–15 min. • General effects on the CNS: acute dystonia, tics,
migraine-like headaches. 2/3 acute toxic effects
occur within 1 h of intoxication.
• Stroke: Nonhaemorrhagic cerebral infarction, sub-
Cocaine produces a dose-related increase in arousal, arachnoid, intraparenchymal, and intraventricular
improved performance on tasks of vigilance and alertness, haemorrhages. Transient ischaemic attacks have
and a sense of self-confidence and well-being (Table 32.9). also been associated with cocaine use. The patho-
physiological mechanism is vasoconstriction.
• Seizures occur 3%–8% of cocaine users. At
TABLE 32.9 high doses, convulsions may occur. The risk of
Summary of the ICD-10 Criteria of Acute having cocaine-induced seizures is highest in
patients using crack cocaine.
Intoxication due to Use of Cocaine (F.14)
• Cardiovascular system: Myocardial infarctions,
or Other Stimulants Including Caffeine (F.15)
arrhythmias, and excessive use can also lead to
Dysfunctional Behaviour (At Least Signs (At Least One of the hypertension with cardiac failure.
One of the Following) Following Must Be Present) • Perforation of the nasal septum can follow long-
1. Abusiveness or aggression 1. Cardiac arrhythmias term administration by the nasal route because of
2. Argumentativeness 2. Chest pain the vasoconstriction caused by cocaine. Intravenous
3.Auditory, visual, or tactile illusions 3. Convulsions use carries with it the risks described earlier.
4. Euphoria and sensation of 4. Evidence of weight loss • Other life-threatening conditions: ischaemic colitis,
increased energy 5. Hypertension (sometimes rhabdomyolysis, hyperthermia, coma, and death.
5. Grandiose beliefs or actions hypotension) • Cocaine abusers often take sedatives, includ-
6. Hallucinations, usually with 6. Muscular weakness ing heroin, alcohol, and benzodiazepines. As
intact orientation 7. Nausea or vomiting well as taking the edge off the high produced
7. Hypervigilance 8. Pupillary dilatation by cocaine, some of the metabolites of the
8. Interference with personal 9. Psychomotor agitation cocaine–alcohol interaction have been found to
functioning (sometimes retardation) have a much longer half-life than cocaine alone.
9. Lability of mood 10. Sweating and chills It is possible that this prolongation of the effects
10. Paranoid ideation 11. Tachycardia (sometimes of cocaine contributes to its use with alcohol.
11. Repetitive stereotyped bradycardia) • Long-term stimulant abuse results in a ste-
behaviours reotyped compulsive repetitive pattern of
behaviour and paranoid psychosis resembling
Note: The DSM-5 criteria for stimulant intoxication are very similar to
the ICD-10 criteria. The DSM-5 proposes the following stimu-
schizophrenia.
lant-induced disorders, which include psychotic disorder, • Pregnant women who misuse cocaine often
depressive disorder, bipolar disorder, anxiety disorder, sexual have babies (crack babies) with low birth weight,
dysfunction, or sleep disorder. small head circumference, early gestational age,
and growth retardation.
32.6.9.8 Pharmacological Treatment 32.6.10.1 Amphetamines (Speed, Whizz, Sulphate)

32.6.9.8.1 Management of Cocaine Intoxication Amphetamine is in the form of powder, while methylam-
• Benzodiazepines: safest drug to be used. phetamine (street name: ‘ice’) is in the form of large clear
• Alpha-adrenergic blocker (e.g. phentolamine): crystal. It is a long-acting stimulant and the half life is 10
to treat hypertension. h. These stimulants are cheap and widely available in the
• Alpha- and beta-blocker (e.g. labetalol): to treat United Kingdom and the United States. The highest rate of
tachycardia. amphetamine used is between 18- and 25-year-olds, and
• Avoid pure beta-blocker (e.g. propranolol), amphetamine abuse occurs in all socioeconomic groups
which may lead to cardiac ischaemia. and increases among white professionals. They are used
clinically in the treatment of narcolepsy, as appetite sup-
32.6.9.8.2 Management of Cocaine Withdrawal pressants and selectively in the hyperkinesis of childhood.
• Severe withdrawal: amantadine
In contrast to cocaine,
32.6.9.8.3 Management of Cocaine Misuse
1. Abstinence • Amphetamine does not have local anaesthetic
a. Complete or partial hospitalization with fre- properties.
quent cocaine misuse • Amphetamine has a longer duration of action.
b. Behavioural contract or contingency man- • Amphetamine has more potent peripheral sym-
agement with positive reinforcement for pathomimetic effects.
negative urine drug screens
2. Medications for relapse prevention Routes of administration: Amphetamine is administered
a. Dopaminergic medications: amantadine orally and intravenously.
(causes dopamine release) and bromocrip- Mechanism of action: Amphetamines cause excessive
tine (dopamine agonist) release of dopamine. This leads to hyperexcitable state
b. Tricyclic antidepressants (e.g. desipramine has such as tachycardia, arrhythmia, hyperthermia, and irri-
been found to reduce the intensity of cocaine tability. It causes pupil dilation (Figure 32.18).
craving irrespective of other psychopathology)
c. SSRI 32.6.10.2 Clinical Features
d. Bupropion Psychotic-like state results from acute or chronic inges-
e. Modafinil: weak psychostimulant tion. It leads to paranoia, hallucination, and sometimes
f. Methylphenidate: cocaine misuse and ADHD a delirium-like state. The effect usually lasts for 3–4
days. In contrast to paranoid schizophrenia, amphet-
32.6.9.9 Prognosis amine-induced psychosis is associated with visual
Poor prognostic factors include hallucinations, appropriate affect, hyperactivity, hyper-
sexuality, and confusion. Thought disorder and alogia
• High frequency or intensity of use are not found in amphetamine-induced psychosis. It
• Severe withdrawal symptoms usually resolves with abstinence but may continue for
• Comorbid alcohol misuse some months.
• Comorbid psychiatric conditions (anxiety/ In the withdrawal state (aka crash), the person will
depression) develop fatigue, hypersomnia, hyperphagia, depression,
• Poor social support and nightmare.
• Forensic psychiatry Following chronic use, profound depression and
fatigue occur. Long-term use leads to CNS serotonergic
32.6.10 Course neuronal destruction.
• In the early course, the cocaine users experi-
ence intense euphoria, alertness, well-being, and 32.6.10.3 Treatment
self-confidence. 1. Abstinence: an inpatient setting and combina-
• Chronic use of cocaine is associated with dys- tion of psychotherapy techniques
phoria and increase in negative effects. 2. Amphetamine-induced psychosis: antipsychotics
• Repeated cocaine use is associated with psychotic 3. Agitation and hyperactivity: diazepam
symptoms similar to paranoid schizophrenia. 4. Depression: bupropion
MAO
AMP binds to MAO
prevents degradation
of DOPA
AMP binds DOPA

to AMP re-uptake
binding site transporter
AMP stimulates
Amphetamine the release of DOPA
(AMP) from synaptic vesicles AMP inhibits the
re-uptake of DOPA
Dopamine
(DOPA)
FIGURE 32.18 Mechanisms of actions of amphetamines.
32.6.11 3,4-Methylenedioxymethamphetamine 32.6.11.4 Clinical Effects

(MDMA, Ecstasy, XTC, E, Adam) • MDMA produces a combination of stimulants
and psychedelic effects. The stimulant effects
32.6.11.1 Background resemble those of amphetamine, and hallucino-
• MDMA is a hallucinogenic amphetamine and genic effects resemble those of LSD.
was developed by Merck in 1914. • MDMA causes a feeling of closeness to other
• MDMA is a designer drug and serotonin neuro- people, altered sensual and emotional over-
toxin. It possesses both stimulant and mild hal- tones, increase in empathy, and extroversion.
lucinogenic properties. People taking MDMA report accelerated think-
• This synthetic drug involves combination of ing, impaired decision-making, and memory
amphetamine, ephedrine, or pseudoephedrine impairment with chronic use.
with components of lithium batteries. Purity • Psychiatric conditions (psychosis, depression,
varies depending on the substitutes used, and it anxiety) in previously vulnerable individuals
is often impure. can occur following MDMA use.
• It is widely used at parties or raves by young • Acute effects include sweating, tachycardia, dry
people, particularly in the 1990s. mouth, jaw clenching, muscle aches, bruxism,
jaw clenching, and gait disturbances.
32.6.11.2 Chemical Properties • Physical dependence does not occur.
• MDMA causes potent release and reuptake
inhibition of serotonin and associated with sero-
toninergic neurotoxicity in humans. 32.6.11.5 Other Harmful Effects
• MDMA does not cause dependence. • Deaths have occurred in those with preexist-
ing cardiac disease caused by cardiac arrhyth-
32.6.11.3 Administration mias. In the fit user at normal doses, deaths have
• MDMA is taken orally or intranasally. occurred as a result of hyperpyrexia, resulting in
• Taken orally in tablet or capsule form, its effects disseminated intravascular coagulation, rhabdo-
last 4–6 h; multiple dosing is tried, but tolerance myolysis, and renal failure.
develops rapidly, and subsequent doses have less • Convulsions can also occur. Most deaths of this
potency. nature occur when the user has been dancing
vigorously for a considerable period, in high 32.6.12.3 Dose and Clinical Effects
ambient temperatures, with inadequate fluid • A dose of 80–200 mg produces mood elevation,
replacement. MDMA has a direct effect upon increased alertness and clarity of thought, increased
the thermoregulatory mechanisms that com- gastric secretion, tachycardia, raised blood pres-
pound these conditions. sure, diuresis, and increased productivity.
• Hypertensive crises may occur leading to CVA • In overdose (greater than 250 mg per day) caffein-
in some. ism occurs. This results in anxiety, restlessness, nau-
• Toxic hepatitis has been reported in MDMA sea, muscle twitching, and facial flushing. Patients
users possibly related to impurities in the may demonstrate rambling thought and speech.
preparation. The DSM-5 proposes that the minimum amount for
• Neurotoxicity is an established fact. Serotonergic caffeine intoxication is 250 mg per day or (e.g. more
nerve terminals are damaged by this drug, and than two to three cups of brewed coffee).
although rat studies indicate that this is reversible, • At levels of intake in excess of 600 mg per day,
primate studies indicate the opposite. The long- dysphoria replaces euphoria, anxiety and mood
term consequences of MDMA-induced serotoner- disturbances become prominent, and insomnia,
gic neurotoxicity in humans are not known. muscle-twitching, tachycardia, and sometimes
cardiac arrhythmias occur.
32.6.11.6 Management • The DSM-5 proposes two caffeine-induced dis-
Abrupt discontinuation is recommended, there being no orders (e.g. caffeine-induced anxiety disorder
advantage to gradual withdrawal. Psychiatric disturbance and or caffeine-induced sleep disorder).
should be treated accordingly.
32.6.12.4 Other Systemic Effects of Caffeine
1. CNS: migraine.
32.6.12 Caffeine
2. Gastrointestinal system: Caffeine relaxes the
32.6.12.1 Chemical Properties lower oesophageal sphincter and can predis-
• Caffeine is a methylxanthine (1,3, pose to gastro-oesophageal reflux disease. It
7-trimethylxanthine). also causes hypersecretion of gastric acid and
• Caffeine is widely available in coffee, tea, and increases the risk of gastric ulcer.
chocolate and is added to soft drinks and propri- 3. Renal system: Caffeine causes diuretic effect,
etary cold preparations. and people are advised to abstain from consum-
• Coffee contains about 80–150 mg of caffeine per ing caffeine in situations where dehydration may
cup depending upon the brewing method. Peak be significant.
blood levels occur 15–45 min following oral 4. Pregnancy: low birth weight and miscarriage.
administration; the half-life is 6 h. Metabolism Caffeine enters amniotic fluid and breast milk.
is increased by smoking and reduced by oral It affects infants because of slow metabolism of
contraceptives and pregnancy. Neonates cannot caffeine in fetus.
metabolize caffeine; therefore, there is a very
long half-life. 32.6.12.5 Dependence and Withdrawal
1. 10% of caffeine users experience withdrawal
32.6.12.2 Mechanisms of Actions of Caffeine effects (e.g. more than six cups per day). Withdrawal
starts at 1–2 h post ingestion and becomes worst at
• The main action of caffeine is the competitive
1–2 days and recede with a few days.
antagonism of adenosine A1 and A2 receptors,
2. Common withdrawal effects include headache,
which contribute to the neuropsychiatric effects
irritability, sleeplessness, anxiety, tremor, and
such as psychosis in caffeine intoxication as a
impairment of psychomotor performance.
result of the release of dopamine.
• Higher doses cause inhibition of phosphodi-
32.6.13 Hallucinogens
esterases, blockade of GABAA receptors, and
release of intracellular calcium. It reaches its Hallucinogens are substances that give rise to marked
peak blood levels after 1–2 h and reduces cere- perceptual disturbances when taken in relatively small
bral blood flow although it is a stimulant. quantities.
32.6.13.1 Epidemiology The DSM-5 proposes the following hallucinogen-

• The lifetime prevalence is 0.6%. induced disorders: psychotic disorder, bipolar disorder,
• Misuse of hallucinogen is common among depressive disorder, and anxiety disorder.
young white men.
• The peak of hallucinogen misuse was between 32.6.13.4 Treatment
1965 and 1969, and it was overtaken by 1. Severe psychosis: haloperidol and diazepam
stimulants. 2. Hallucinogen persisting perception disorder:
clonazepam, valproate, and carbamazepine
32.6.13.2 Route of Administration
• Most hallucinogens are well absorbed after oral 32.6.14 Lysergic Acid Diethylamide (LSD,
ingestion.
Trips, Acid, Microdots, Supermans)
• Tolerance for hallucinogens develops rapidly
and takes places after 3 or 4 days of continuous 32.6.14.1 Chemical Properties
use. Tolerance disappears rapidly, usually in 4–7 LSD is a 5-HT2A agonist and the most potent hallucino-
days after discontinuation of hallucinogen. gen. LSD suggests the role of serotonin in causing hal-
lucination in schizophrenia.
32.6.13.3 Clinical Effects (Table 32.10)
The DSM-5 has similar criteria for hallucinogen intoxi- 32.6.14.2 Route of Administration
cation. Additional criteria include synaesthesia shortly 1. LSD is available in tablets or absorbed onto paper.
after hallucinogen use. The DSM-5 has an additional cat- 2. LSD has been commonly distributed as ‘blot-
egory called hallucinogen persisting perception disorder, ter acid’, and these are sheets of paper that are
which involves reexperience of false fleeting perceptions soaked with LSD.
in the peripheral fields, flashes of colour, geometric pseu- 3. Then the sheet is dried and perforated into small
dohallucinations, positive afterimages, macropsia, and squares and each square containing 30–75 mg
micropsia after cessation of hallucinogen use. of LSD. Minute amounts (£100 μg) produce
marked psychoactive effects.
4. The onset of action of LSD occurs within an
hour, peaks in 2–4 h, and lasts 8–12 h.
TABLE 32.10 5. Intravenous use is not common because the
Summary of the ICD-10 Criteria of Acute onset of the trip is very rapid with oral ingestion
Intoxication due to Use of Hallucinogens (F.16) (15 min).
6. Tolerance develops rapidly; sensitivity to its
Dysfunctional Behaviour (At Signs (At Least One of the
effects returns rapidly with abstinence.
Least One of the Following) Following Must Be Present)
1. Anxiety and fearfulness 1. Tachycardia
32.6.14.3 Drug Action
2. Auditory, visual, or tactile 2. Palpitations
illusions or hallucinations 3. Sweating and chills The substance acts at multiple sites in the CNS, the
occurring in a state of full 4. Tremor effects being thought to be related to 5-HT antagonism.
wakefulness and alertness 5. Blurring of vision The effects are dose related.
(it may lead to accidents and 6. Pupillary dilatation Psychic effects include the heightening of perceptions,
hallucinations are recurrent) 7. Incoordination with perceptual distortion of shape; intensification of colour
3. Depersonalization and sound; apparent movement of stationary objects; and
4. Serialization changes in sense of time and place. Hallucinations may occur
5. Paranoid ideation but are relatively rare. The user usually retains insight into
6. Ideas of reference
the nature of the experiences. Delusions (e.g. belief in the
7. Lability of mood
ability to fly) may occur. Emotional lability, heightened self-
8. Hyperactivity
9. Impulsive acts
awareness, and ecstatic experiences can occur. Synesthaesias
10. Impaired attention in which a stimulus in one sensory modality is experienced
11. Interference with personal in another modality (e.g. hearing colours) are common.
functioning The physical effects are sympathomimetic, with tachy-
cardia, hypertension, and dilated pupils.
Flashback phenomena (posthallucinogen perception Drug interactions: Chlorpromazine may induce anticho-
disorder) occur, in which aspects of the LSD experience linergic crisis after LSD use.
occur spontaneously some time after LSD use. These are Treatment: The treatment of bad trip involves diaz-
usually fleeting. epam 20 mg. Antipsychotics may worsen the experience.
32.6.14.4 Drug Withdrawal

32.6.15 Hallucinogenic Mushrooms
Physical withdrawal symptoms do not occur following
the abrupt discontinuation of LSD or other hallucinogens. (Magic Mushrooms)
There are a number of fungi growing in the United Kingdom
32.6.14.5 Harmful Effects that contain psychoactive substances such as psilocybin and
Accidents may occur while under the influence of hal- psilocin. Liberty cap and fly agaric mushrooms are the ones
lucinogens, such as jumping from a height because of the most commonly used for their psychoactive effects. Ingestion
delusional belief that the user can fly. of these in the raw state is legal, but any attempt to process
Flashback phenomena occur many months after drug them, such as by cooking, drying, or freezing, is illegal.
elimination, giving rise to the possibility that these sub- Ingestion causes mild LSD-like effects, with marked
stances may cause permanent neurological changes. euphoria. At high doses, hallucinations, bad trips, and
acute psychoses can occur.
32.6.14.6 Clinical Effects
1. LSD produces psychedelic effects (such as 32.6.16 Mescaline
synesthaesia, stimulation of one sense stimu-
lates sensation in the other sense, e.g. intense Mescaline is the active component of the Mexican peyote
experience of hearing the colour) as little as cactus. Mescaline is similar to noradrenaline. It is hal-
25–50 μg. lucinogenic and is orally administered.
2. At 100 mcg, LSD produces perceptual distor- LSD is 200 times as potent as psilocybin, which is
tions, hallucinations, mood changes (elation or 30 times as potent as mescaline.
depression), paranoia, and panic.
3. Physical signs include pupillary dilation, 32.6.17 Phencyclidine (PCP, Angle Dust)
increased blood pressure and pulse, facial flush-
ing, salivation, lacrimation, and hyperreflexia. 32.6.17.1 Chemical Properties
LSD leads to persisting perception disorder • PCP is a dissociative anaesthetic agent as the per-
even the person is not using LSD. Physical with- son remains conscious during anaesthetized state.
drawal is not commonly seen. • PCP is an arylcyclohexylamine related to ketamine.
4. Death caused by cardiac or cerebrovascular It is taken by smoking, snorting, and injecting.
pathology related to hypertension or hyperther-
mia can occur with hallucinogenic use. 32.6.17.2 Neurochemical Effects
5. The flashbacks: It refers to the spontaneous occur- • PCP blocks NMDA glutamate receptors
rence of episodic visual disturbances, which resem- (Figure 32.19).
ble to prior LSD trips. Flashbacks may diminish in
intensity with time, and psychoeducation should 32.6.17.3 Clinical Effects
be offered on the nature of the flashbacks. 1. It produces stimulant, anaesthetic, analgesic,
6. The bad trip: Unpleasant experiences may and hallucinogenic effects. At low doses, it
occur, and these are more likely in the inex- induces euphoria and a feeling of weightless-
perienced or if the ambient mood is disturbed. ness. At high doses, visual hallucinations and
Users generally avoid being alone, in case of bad synesthaesias occur.
trips or dangerous behaviour, while under the 2. Psychosis, violence, paranoia, and depression
influence. The features of adverse experiences can occur following a single dose.
include anxiety, depression, dizziness and dis- 3. Physical effects include incoordination, slurred
orientation, and a short-lived psychotic episode speech, blurred vision, convulsions, coma, and
characterized by hallucinations and paranoid respiratory arrest.
delusions. With heavy use, an acute schizo- 4. Prolonged use can result in a withdrawal syn-
phreniform psychosis may persist. drome upon cessation.
The most common route of administration is oral, but

some abusers attempt to inject the contents of capsules or
Glutamate ground tablets intravenously.
G G
G 32.6.20.1 Epidemiology
G G
G Over 1 million of the UK population use benzodiazepines
Ca G Ca continuously for more than 1 year.
Ca
Ca G Glycine
Ca
Mg2+ 32.6.20.2 Drug Action
This group of sedatives potentiates the inhibitory actions
PCP of the GABAA receptor in the limbic areas of the brain.
They have anxiolytic, hypnotic, and anticonvulsant prop-
Ca2+
erties at normal doses (Table 32.11).
The DSM-5 has similar criteria for sedative/hypnotic
intoxication but has less signs and symptoms.
The DSM-5 proposes the following sedative-/hyp-
notic-induced disorders: major neurocognitive disorder,
persisting amnestic disorder, psychotic disorder, depres-
sive or bipolar disorder, anxiety disorder, sexual dysfunc-
tion, or sleep disorder.
FIGURE 32.19 The mechanism of action of phencyclidine.
32.6.20.3 Drug Withdrawal
32.6.18 Ketamine (K) Tolerance occurs rapidly. There is rebound anxiety after
• Ketamine is a shorter-acting derivative of PCP. 4 weeks of use; dependence is seen in 45% of users after
• Ketamine is in the form of tablets and it is 3 months.
snorted or injected. The onset and intensity of withdrawal symptoms are
• The action of ketamine is mediated by competi- related in part to the half-life of the drug used (shorter
tive inhibition from the NMDA receptor complex. half-lives lead to a more abrupt and intense withdrawal
• It leads to cramps, fatigue, depression, and irri- syndrome). The withdrawal syndrome is also related to
tability. It may lead to violent reactions (may
harm other people) and flashbacks.
TABLE 32.11
• Severe intoxication produces a state of virtual
Summary of the ICD-10 Criteria of Acute
helplessness and lack of coordination.
Intoxication due to Use of Benzodiazepine (F.13)
32.6.19 Sedatives Dysfunctional Behaviour (At Signs (At Least One of the
CNS sedatives depress CNS activity with little analgesic
effect. They include alcohol (see aforementioned), barbi- 1. Abusiveness or aggression 1. D
ecreased level of consciousness
turates, benzodiazepines, and carbamates. All the CNS 2. Apathy and sedation (e.g. stupor, coma)
depressants have abuse potential and cause both psycho- 3. Anterograde amnesia 2. Difficulty in standing
logical and physical dependence. Cross-tolerance between 4. Euphoria and disinhibition 3. Erythematous skin lesions or
groups occurs, and the withdrawal syndromes are similar. blisters
5. Impaired attention
When taken repeatedly in high doses, all these drugs pro- 4. Nystagmus
6. Impaired psychomotor
duce sadness/depression, a worsening of confusional states, performance 5. Slurred speech
and withdrawal syndromes in which anxiety is prominent. 6. Unsteady gait
functioning
32.6.20 Benzodiazepines 8. Lability of mood
Widely prescribed, these have widespread physical Note: The DSM-5 has similar criteria for sedative/hypnotic intoxica-
dependence among licit users and are very popular with tion but has less signs and symptoms.
illicit substance abusers.
the dose used. Onset is usually within 1–14 days after change, persistent intoxication, labile affect, poor concen-
drug reduction/cessation and may last for months. tration, impaired judgement, and incoordination.
Withdrawal symptoms include somatic effects such as
autonomic hyperactivity (tachycardia; sweating; anorexia; 32.6.21.2 Drug Withdrawal
weight loss; pyrexia; tremor of hands, tongue, and eyelids; This causes anxiety, tremor, sweating, insomnia with
GI disturbance; sleep disturbance with vivid dreams due marked REM rebound, irritability, agitation, twitching,
to REM rebound), malaise and weakness, tinnitus, and vomiting, nausea, tachycardia, orthostatic hypotension,
grand mal convulsions. delirium, and convulsions.
There are cognitive effects with impaired memory
and concentration. There are also perceptual effects with 32.6.21.3 Harmful Effects
hypersensitivity to sound, light, and touch; depersonal-
Barbiturates are dangerous in overdose. Their therapeutic
ization; and derealization. Delirium may develop within
index is low. Tolerance to psychotropic effects exceeds
a week of cessation, associated with visual, auditory, and
tolerance to respiratory depression.
tactile hallucinations and delusions.
Parenteral administration of oral preparations is
Affective effects such as irritability, anxiety, and pho-
attempted by some addicts, incurring all the risks described.
bic symptoms may also occur.
32.6.20.4 Harmful Effects 32.6.21.4 Management

In a high-dose abuser, severe withdrawal symptoms occur A gradual tapering of the dose is considered to be the most
if the person is unable to acquire the usual dose of drug. appropriate way to manage barbiturate dependence. Short-
As in these doses the drugs have usually been acquired acting compounds should first be substituted by long-acting
illicitly, supply cannot be guaranteed. compounds, diazepam being the most commonly used
Benzodiazepines are relatively safe in overdose but form for the purposes of withdrawal. After stabilizing on
are liable to produce respiratory depression, and in com- diazepam, dose reduction is commenced. At high doses,
bination with other drugs, they can be lethal. this can occur quite rapidly (e.g. at 5 mg per week) until the
The injection of street benzodiazepines incurs all the patient starts to complain of unpleasant effects, when the
dangers of injecting described earlier but is particularly rate of reduction can be reduced. If symptoms of depression
liable to cause limb ischaemia and gangrene, with result- are present, an antidepressant is indicated. Propranolol may
ing amputation. help with some of the somatic symptoms of anxiety.
Psychological support is very important, with weekly con-
32.6.20.5 Management tact initially. The family should be involved in the process.
The withdrawal of barbiturates similarly needs phased
Withdrawal from sedative drugs is potentially lethal and
withdrawal; inpatient admission is often necessary.
should usually be managed on a medical ward.
32.6.21 Barbiturates 32.6.22 Nicotine
Although the prescribing of barbiturates has largely 32.6.22.1 Epidemiology
been superseded by the safer benzodiazepines, they still • In the United Kingdom the prevalence of smok-
appear in the form of phenobarbitone, amylobarbitone, ing has reduced in the past three decades. Around
and quinalbarbitone (Tuinal) and are widely available. 20% of male adults are smokers. The highest
rates of smoking are people between 20- and
32.6.21.1 Drug Action 25-year-olds where 30% of these young adults
Barbiturates potentiate action at the GABAA receptor, thus are smokers.
increasing CNS depression. This is particularly marked in • For people older than 60 years, the prevalence of
the reticular activating system and cerebral cortex. smoking is around 10%.
Clinical effects include impaired concentration, • In the United Kingdom analyses of the interac-
reduced anxiety, and dysphoria. In increasing doses, dys- tions between smoking, drinking, and cannabis
arthria, ataxia, drowsiness, coma, respiratory depression, use indicated that the relationship between sub-
and death occur. stance use and psychiatric morbidity was pri-
Chronic use results in tolerance caused by hepatic marily explained by regular smoking and to a
enzyme induction, cross-tolerance with alcohol, personality lesser extent regular cannabis use.
TABLE 32.12
Summary of the ICD-10 Criteria of Acute
Intoxication due to Use of Tobacco (F.17)
Dysfunctional Behaviour (At Signs (At Least One of the
1. Bizarre dreams 1. Cardiac arrhythmias
2. Serialization 2. Nausea or vomiting
3. Insomnia 3. Sweating
4. Interference with personal 4. Tachycardia
functioning
5. Lability of mood
Note: The DSM-5 does not have tobacco intoxication disorder.

Nicotine
Dopamine
FIGURE 32.20 Mechanism of action of nicotine. 32.6.22.6 Pharmacological Treatment

32.6.22.6.1 Varenicline
32.6.22.2 Pharmacodynamics (Figure 32.20)
Varenicline has high affinity to α4β2 nicotine Ach recep-
• The nicotinic receptors are found on presynaptic
tors and prevents tobacco withdrawal syndrome.
dopaminergic neurons.
• Smoking of tobacco leads to release of dopamine. Dosage:
• Effects of nicotine include euphoria, enhancing
Day 1–3: 0.5 mg per day
motivation, and sustained vigilance.
Day 4–7: 0.5 mg bid
• Nicotine also suppresses the insulin production
Day 8: Day to quit alcohol
from the pancreas (slight hyperglycaemia).
Week 12: 1 mg bid
32.6.22.3 Pharmacokinetics Contraindication: age < 18 years, pregnancy, end-stage
• Nicotine influences the metabolism of drugs renal failure.
through cytochrome P450 mechanism. For
32.6.22.6.2 Bupropion
example, nicotine induces P450 1A2 system and
enhances metabolism of olanzapine. 1. Chemical properties: antidepressant with norad-
• There is a need to reduce the antipsychotic dos- renergic activity that reduces the effect of nico-
age after smoking cessation. tine withdrawal
• On the other hand, there are reduced smoking 2. Dosage: starting dose 150 mg/day and increase
rates in some patients after taking clozapine. to 150 mg bid
3. Side effects: epilepsy (1/1000)
32.6.22.4 Clinical Effects (Table 32.12) 4. Contraindications: history of epilepsy, eating
The proposed DSM-5 does not have tobacco intoxication disorders, CNS tumour, and bipolar disorder
disorder. 5. Side effects: headache (30%), insomnia, and
rash (0.1%)
32.6.22.5 Tobacco Withdrawal Syndrome
32.6.22.7 Nicotine Replacement Therapy
This syndrome may develop if a person stops smoking
1. Duration of treatment: 8–12 weeks.
after 3–10 weeks of tobacco consumption. The onset may
2. Route of administration: sublingual tablets,
be within an hour after the last cigarette. As a result of the
gum, patch, and nasal spray.
reduction in dopamine release, the person feels depressed
3. Side effects: local irritation, worsen glucose
(lasting for 1 month) and irritable. The DSM-5 proposes
control in diabetes.
other criteria including anxiety, poor concentration,
4. It is not recommended to administer bupropion and
increased appetite, weight again, restlessness, and insom-
Nicotine Replacement Therapy (NRT) together.
nia. The aforementioned symptoms cause the person to
crave for tobacco. Behavioural treatment is used in nicotine addiction.
32.6.22.8 Prognosis of death is during an episode of sniffing. Butane squirted

Among all substances, nicotine causes the highest num- directly into the mouth can cause cardiac arrest. Propellants
ber of death. squirted directly into the mouth are cooled to −20°C, which
can cause burns to the throat and lungs, and may freeze the
larynx, causing cardiac arrest through vagal nerve stimula-
32.6.23 Volatile Solvents
tion. Rebreathing from plastic bags can result in asphyxiation.
Volatile substances are inhaled (glue-sniffing) in order to There are approximately 100 deaths per annum in the
experience their psychoactive effects. Solvents from glue United Kingdom with 20% of these occurring in first-
(such as toluene), correction fluids (e.g. trichloroethane), time users and the majority in those aged under 20 years.
butane gas, and other aerosol propellants are popular. There are reports of long-term damage to the CNS,
Solvents have been tried by 3%–5% of 15-year-olds. heart, liver, and kidneys. Chronic use may cause a persis-
Often fumes are rebreathed from a plastic bag with content cerebellar syndrome and peripheral neuropathy.
centrated vapour, but sometimes an aerosol is sprayed
directly into the oropharynx (this is particularly dan- 32.6.23.4 Management
gerous). Rapidly absorbed, its effects last about 30 min. Abrupt discontinuation is recommended. Advice from
social services and/or a child psychiatrist may be needed.
32.6.23.1 Drug Action (Table 32.13)
The DSM-5 proposes the following inhalant-induced 32.6.23.5 Khat
disorders such as mild neurocognitive disorder, major • Khat is a form of fresh leaves that are chewed
neurocognitive disorder, psychotic disorder, depressive socially in Arabic and African countries.
disorder, or anxiety disorder. • The main constituent is cathinone that has
Chronic use causes Goodpasture’s syndrome, hypoka- amphetamine-like properties and induces psy-
laemia, and optic neuropathy. High doses cause stupor chosis and hypomania.
and death. Aspiration of vomit can occur at any time. • Adverse effects include paralytic ileus.
32.6.23.2 Drug Withdrawal 32.6.23.6 Anabolic Steroid

There is no physical withdrawal syndrome. • People misuse anabolic steroid to increase mus-
cle growth and body bulk.
32.6.23.3 Harmful Effects • It can be swallowed or injected.
• Adverse effects include gynaecomastia in men
Acute intoxication can lead to fatal accidents, particularly
and clitoral enlargement in women, bone hyper-
through falling or drowning. However, the greatest risk
tension, cardiac disorders, liver (e.g. drug-induced
hepatitis) and renal impairment, shrinking of tes-
ticles, and priapism. It also leads to aggression
TABLE 32.13
and irritability.
Summary of the ICD-10 Criteria of Acute • Death may occur as a result of overdose or
Intoxication due to Use of Solvent (F.18) severe infection as a result of repeated intramus-
Dysfunctional Behaviour (At Signs (At Least One of the cular injection.
1. Apathy and lethargy 1. Blurred vision or diplopia 32.7 ADDICTION WITHOUT SUBSTANCES
2. Argumentativeness 2. Decreased level of
3. Abusiveness or aggression consciousness 32.7.1 Pathological Gambling
4. Lability of mood 3. Difficulty in standing
5. Impaired judgement 4. Muscle weakness
6. Impaired attention and memory 5. Nystagmus Findings from the British Gambling Prevalence Survey
7. Psychomotor retardation 6. Slurred speech (2007)
8. Interference with personal 7. Unsteady gait
• 67.9% of 8968 respondents (65.2% of female
functioning
respondents and 70.7% of male respondents)
Note: The DSM-5 calls this inhalant intoxication, which shares in English, Scotland, and Wales participated
similar criteria as ICD-10. in any form of gambling in the past 12 months
before the survey.
• The prevalence of problem gambling for adults 5. Psychosocial risk factors

was around 0.8%. a. Learning theories: monetary gain and
• Internet gamblers were more likely to be young excitement acting as positive reinforcers.
men, single, well educated, and in professional b. Cognitive theories: cognitive distortions such
or managerial employment. as magnification of one’s gambling skills,
• The top five gambling methods in United superstitious beliefs, and interpretive biases.
Kingdom were the national lottery, scratch c. Non-Caucasian British men with smoking
cards, betting on horses, fruit/slot machines, history were all more likely to be preoccu-
and ‘other’ lotteries such as private betting, pied chasers or antisocial impulsivist gam-
bingo, and sport betting. blers, rather than nonproblematic gamblers.
• Men were more common than women to be d. Adolescents: male gender, parental gambling,
involved in all gambling activities except play- dominated school characteristics, Asian eth-
ing scratch cards, which has equal gender ratio. nicity, no sibling, and gambling as a source of
• It is important to note that the prevalence of income (Forrest and McHale, 2011).
problem gambling for adolescents was 1.9% and
the figure was higher than adults. 32.7.1.3 Clinical Features
The DSM-5 criteria state that there are at least four symp-
McBride et al. (2010) classified British gamblers into toms for 1-year period:
three types:
1. Tolerance: Patient needs to gamble with increas-
1. Nonproblematic gambler: 88.9% ing amounts of money in order to achieve the
2. Preoccupied chaser: 9.7% desired excitement.
3. Antisocial impulsivist gambler: 1.4% 2. Withdrawal: Patient is restless or irritable when
attempting to cut down or stop gambling.
32.7.1.2 Aetiology and Risk Factors 3. Repeated unsuccessful efforts to control, cut
32.7.1.2.1 Biological Risk Factors back, or stop gambling.
1. Genetics (Lodo and Kennedy, 2009) 4. Preoccupation with gambling (e.g. persistent
a. The heritability of pathological gambling thoughts of reliving past gambling experience).
is 55%. 5. Gambles often when feeling distressed (e.g. help-
b. Pathological gambling and subclinical path- less, guilty, anxious, depressed).
ological gambling are a continuum of the 6. Chasing the loss by gambling more after losing
same disorder. money in gambling.
c. Pathological gambling shares genetic vul- 7. Lying to conceal the extent of involvement with
nerability factors with antisocial behaviours, gambling.
alcohol dependence, and major depressive 8. Loss a significant relationship, job, or educational
disorder. or career opportunity because of gambling.
d. Genetic factors underlie the association 9. Relying on others to provide money for gam-
between exposure to traumatic life events bling as a result of financial problems.
and pathological gambling.
2. Neurochemistry (Potenza et al., 2011) Mania must be excluded, and course specifiers include
a. Serotonin, noradrenaline, and dopamine chronic, episodic, and in remission.
have been implicated in the aetiology of
32.7.1.4 Management
pathological gambling.
b. There is an increased level of 5-HT1B recep- 32.7.1.4.1 Pharmacological Treatment
tors in the brain of pathological gamblers. • Naltrexone, an opioid antagonist, may reduce
3. Imaging (van Holst et al., 2010) urges and thoughts in pathological gamblers.
Pathological gambling is consistently associ- • SSRIs such as fluvoxamine and paroxetine
ated with blunted mesolimbic–prefrontal cortex may reduce of gambling behaviour, urges, and
activation to nonspecific rewards and increased thoughts in pathological gamblers.
activation when exposed to gambling-related • Mood stabilizers such as lithium and valproate
stimuli in cue exposure paradigms. may be useful.
32.7.1.4.2 Psychological Treatment 32.8.3.1.2 Imaging

1. Financial counselling, limiting access to money, 1. Structural MRI showed that adolescents with
and restricting admission into gambling venues internet addiction had lower grey matter den-
are simple measures and can be applied to most sity in the left anterior cingulate cortex and left
pathological gamblers. posterior cingulate cortex compared to normal
2. Motivational enhancement therapy (face-to-face controls (Zhou et al., 2011).
or telephone counselling) and self-help work- 2. Functional MRI showed that the follow-
books are indicated for patients who are ambiva- ing areas are activated when patients with
lent about quitting gambling or entering treatment Internet addiction are playing online game
or who are not keen on long-term therapy. (Ko et al., 2009):
3. Cognitive behaviour therapy a. Right orbitofrontal cortex (compulsion)
a. Cognitive therapy aims at correcting gam- b. Right nucleus accumbens (motivation)
blers’ beliefs about randomness and chance c. Right dorsolateral prefrontal cortex (impulse
and the false notion that they can control control)
and predict outcome. d. Right caudate nucleus (compulsive behaviour)
b. Behaviour therapy involves imaginal desen-
sitization, imaginal relaxation, behavioural 32.8.3.2 Psychological Theories
monitoring, covert sensitization, and spou- • Learning theory emphasizes on the positive
sal contingency contracting. reinforcing effects of Internet use, which can
c. Relapse prevention follow-up further improves induce feelings of well-being and euphoria in
the outcome. the user. The other positive reinforcements
4. Gamblers Anonymous: 12-step recovery include social contact with no real social pres-
programme. ence, contact with relative strangers, and imme-
diate gratification.
• Deficient social skill theory: Internet is used by
32.8 INTERNET ADDICTION a shy or anxious individual to avoid anxiety-pro-
32.8.1 Historical Development voking situations such as face-to-face interac-
tion. This reinforces Internet use by avoidance
• Ivan Goldberg is the first person to use the term conditioning.
Internet addiction in 1995. • Internet use is linked to sensation-seeking
behaviour and impulsivity.
32.8.2 Epidemiology • Development theory: Erikson crisis that involves
identity versus intimacy in young adults.
• The global prevalence rate is between 1.5% and
8.2%.
• The heterogeneity in prevalence is a result of 32.8.4 Clinical Features
different age groups and different instruments
used in the study. 32.8.4.1 Young’s Definition
• The use of the Internet for more than 38 h per week
• Clinically significant impairment or distress
32.8.3 Aetiology and Risk Factors
32.8.4.2 Proposed Criteria
32.8.3.1 Biological Theories 1. Preoccupation with Internet gaming
32.8.3.1.1 Genetics 2. Withdrawal symptoms when the Internet is
• The SS genotype of the serotonin transporter taken away
gene (5HTTLPR) is associated with Internet 3. Tolerance: the need to spend increasing amounts
addiction in Asians (Lee et al., 2008). of time engaged in Internet gaming
• The nicotinic acetylcholine receptor subunit 4. Unsuccessful attempts to control Internet gam-
alpha 4 (CHRNA4) genotype: the CC genotype ing use
is associated with Internet addiction in German 5. Continued excessive Internet use despite knowl-
women (Montag et al., 2008). edge of negative psychosocial problems
6. Loss of interests, previous hobbies, and enter- • Reminder cards—negative consequences of

tainment as a result of excessive Internet use Internet use are written down on a reminder
7. Use of the Internet gaming to relieve dysphoria card and carried by the patient all the time.
8. Has deceived family members, therapists, or • Personal inventory—make a list of hobbies to
others regarding the amount of Internet use replace Internet use.
9. Has jeopardized or lost a significant relation-
ship, job, or educational or career opportunity 32.8.8.2 Pharmacological Treatment
because of excessive Internet use • Stimulants: Methylphenidate can be used to
treat attention deficit and hyperkinetic disorder
(ADHD) and reduce Internet addiction at the
32.8.5 Subtype of Internet Addiction
same time.
Young classifies Internet addiction into four subtypes: • Antidepressants: SSRIs (e.g. escitalopram) to
reduce obsessions and compulsions associated
• Net compulsions: online shopping and online with Internet use.
gambling addictions • Opioid antagonist: naltrexone.
• Online game playing addiction • Mood stabilizers: lithium and sodium valproate.
• Cybersexual addictions
• Cyber-relational addiction (chat rooms, social 32.8.8.3 Prognosis
networking, personal messaging, and email
One-year remission rate is 50%.
addiction)
Poor prognosis factors include
32.8.6 Psychiatric Comorbidity • High exploratory excitability
• Anxiety • Low reward dependence
• Depression • Low self-esteem
• ADHD • Low family function
• Alcohol misuse • Online game playing
• Fatigue
• Cognitive impairment in adolescents (Park Good prognostic factors include
et al., 2011)
• Low hostility
• Low interpersonal sensitivity
32.8.7 Medical Complications
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33 Disorders Specific to Women
and Perinatal Psychiatry
33.1 PREMENSTRUAL SYNDROME 33.1.2.2.2 Serotonin

Postsynaptic serotonergic responsivity is altered
33.1.1 Epidemiology of PMS during the late luteal phase of the menstrual cycle.
Forty per cent of women experience some cyclical pre- It is thought that gonadal hormones cause changes
menstrual symptoms; 2%–10% report severe symptoms. in the levels of activity of serotonergic systems.
There are associations with the following: Carbohydrate craving and depression are linked
to serotonergic brain changes, which are marked in
• There is a higher prevalence in those around 30 the late luteal phase.
years of age. Plasma taken from subjects suffering from PMS
• Prevalence increases with increasing parity. inhibits serotonin uptake in rat brain synaptosomes to a
• There is a higher prevalence in those women greater degree than serum taken from controls.
who have experienced natural menstrual cycles
(unmodified by oral contraceptives and uninter- 33.1.2.2.3 Noradrenaline
rupted by pregnancy) for longer periods of time. 3-Methoxy-4-hydroxyphenylglycol (MHPG, a metabo-
• Women using oral contraceptives, especially if lite of noradrenaline) in cerebrospinal fluid is elevated in
nulliparous, have reduced rates of premenstrual PMS subjects premenstrually.
syndrome (PMS).
• Prevalence is increased in those experiencing 33.1.2.2.4 Androgens
higher levels of psychosocial stress. Serum androgens are higher in women with premen-
strual irritability and dysphoria than in controls. Serum-
33.1.2 Aetiology of PMS free testosterone levels are significantly higher in PMS
subjects than in matched controls around ovulation, and
33.1.2.1 Genetic Factors
17-hydroxyprogesterone levels are higher in PMS women
Highly significant correlations between mother and in the luteal phase.
daughter have been reported on a variety of menstrual
variables including premenstrual tension. 33.1.2.2.5 Others
Condon (1993) reported concordances for global PMS Various hypotheses have been explored, particularly in
scores: relation to the balance between oestrogen and proges-
• 0.28 in dizygotic (DZ) twin pairs terone with a relative lack of progesterone and excessive
• 0.55 in monozygotic (MZ) twin pairs production of prolactin, aldosterone, or antidiuretic hor-
mone. None are conclusive.
Concordances for MZ twins exceeded those of DZ twins
on every subscale. The findings support the hypothesis 33.1.2.3 Neurophysiological Factors
that the familial aggregation of PMS symptoms is deter- The following have been reported:
mined largely by genetic factors.
• There are consistent cycle-dependent changes
33.1.2.2 Neuroendocrine Factors in electroencephalographic recordings, most
33.1.2.2.1 Beta-Endorphin prominent in the α range.
Anxiety, food cravings, and physical discomfort in PMS • There are alterations in response to dichotic
subjects are associated with a significant decline in auditory stimuli premenstrually in comparison
β-endorphin (these symptoms are also found in opiate with the follicular phase, most markedly in suf-
withdrawal). ferers of PMS.
557
• There are alterations in skin conductance in

response to auditory stimuli premenstrually in TABLE 33.1
comparison with the follicular phase, most mark- Common Symptoms Experienced
edly in sufferers of PMS. by Women Suffering PMS
Mood Symptoms Other Symptoms
33.1.2.4 Personality Factors
Irritability Bloated abdomen
Neuroticism may be an important determinant of wom-
Easily angry or upset without Tender breasts
en’s experiences and reports of their menstrual cycle good reason Carbohydrate craving
and is higher in those reporting PMS. Tension Disturbed sleep
Women with coronary-prone type A behaviour expe- Emotional lability Poor concentration
rience 50% more PMS symptoms than women with Depressed mood Clumsiness
noncoronary-prone type B behaviour. Violent feelings Headaches
Muscle and joint pain
Spots
33.1.2.5 Psychological Factors
Psychological views of PMS attribute it to an impover-
ishment of the ego in relation to feminine self-accep-
33.1.4.2 Pharmacological Treatment
tance and identification with the mother. It is suggested
that popular beliefs that derogate femininity are internal- No single medication has proven effective in the treat-
ized and form part of the socialization of women. ment of PMS.
Self-report of PMS is strongly related to psycho- 33.1.4.2.1 Antidepressants
social stress, particularly unusual stress and unhappy Favourable results are sometimes found particularly
relationships. when a serotonergic antidepressant is used. Psychic, but
not somatic, symptoms improve. A 70% reduction in
33.1.3 Symptoms of PMS premenstrual irritability and depressed mood is found
using clomipramine, compared to a 45% reduction with
PMS includes emotional and/or physical symptoms
placebo. Similar results have been obtained using fluox-
occurring premenstrually (late luteal phase) but remitting
etine, adding support to the hypothesis that a serotonergic
usually during the week before menstruation (follicular
imbalance is involved in premenstrual psychic symptoms.
phase).
More than 150 symptoms have been implicated in 33.1.4.2.2 Oral Contraceptive Pill
PMS. There are considerable differences in the patterns Somatic symptoms are improved but psychic symptoms
of symptoms, but there is strong support for cycle-related are not. Oestrogenic effects are thought to exacerbate
variability in most subjects. The existence of PMS as a premenstrual irritability, and progestogenic effects exac-
discrete entity has often been questioned; there is a lack erbate premenstrual depression.
of consensus about its definition. Oral contraceptive users report significantly less
The common symptoms experienced by those women menstrual pain and premenstrual breast tenderness than
suffering PMS are listed in Table 33.1. controls but also show significantly less improvement in
negative mood during the menstrual phase than nonusers.
33.1.4 Management of PMS 33.1.4.2.3 Gamma Linolenic Acid
Treatment should be supportive and directed towards Gamma linolenic acid (GLA), an n-6 essential fatty acid,
symptom relief, psychosocial support, stress reduction, has been reported to help with several PMS symptoms,
and dietary change. such as mastalgia. It is found in products such as evening
primrose oil.
33.1.4.1 Nonpharmacological Treatment
33.1.4.2.4 Other Treatments
• Special diets: increasing complex carbohydrates
Other treatments used for which there are conflicting
and dietary fibre to 20–40 g/day
reports of efficacy include
• Decrease intake of refined sugar and salt
• Cognitive therapy • Alprazolam—some reports of usefulness, but
• Exercise double-blind placebo-controlled trial showed
• Relaxation absence of any therapeutic benefit.
Disorders Specific to Women and Perinatal Psychiatry 559
• Hysterectomy—no change in cyclical mood fol- Animal evidence shows that stress leads to abortion
lowing hysterectomy. in a number of mammalian species including baboons.
• Vitamin B6—produces a reduction in prolactin O’Hare and Creed (1995) studied the relationship
synthesis; use advocated, but little evidence of between life events and miscarriage in 48 case–control
improvement in PMS symptoms pairs matched for known predictors of miscarriage. They
• Progesterones—use advocated, but little evi- found that the miscarriage group was more likely to have
dence of improvement in PMS symptoms. experienced
• Diuretics—produce some relief in symptoms
of bloatedness but no improvement in psychic • A severe life event in the 3 months preceding
symptoms. miscarriage
• Bromocriptine—effective only in the relief of • A major social difficulty
breast symptoms. • Life events of severe short-term threat in the
fortnight immediately beforehand
33.2 CYCLIC PSYCHOSIS Fifty-four per cent of the miscarriage group had experi-
A few reports of cyclic psychoses related to menstruation enced some psychosocial stress, compared to only 15%
exist in the literature. Psychotic symptoms appear suddenly a of controls.
few days before menstruation, resolve with the onset of men- Other factors significantly associated with miscar-
strual bleeding, and reappear with the next cycle. Between riage include
psychotic episodes, the woman appears largely asymptom-
atic. Most cases do not show familial psychiatric morbidity. • Childhood maternal separation
The first psychotic episode usually occurs at a young age. • Poor relationships with partners
The psychiatric picture is nonspecific and changes • Few social contacts
with every menstruation. Some common features include
psychomotor retardation, anxiety, perplexity, disorienta- Stress-induced abortion may involve increased cat-
tion, and amnestic features. Transitory EEG abnormali- echolamine levels and α-adrenergic stimulation of the
ties may occur, not amounting to epileptic activity. myometrium. Serotonin, implicated in stress responses,
It has been suggested that in some cases menstrual psy- promotes abortion. This may be mediated via reduced
choses should be regarded as a specific variant of PMS. gonadotropin output.
Recommended treatments for menstrual cyclic psy- In the management of recurrent miscarriage, a psy-
chosis include chosocial history should be taken in order to ascertain
any sources of stress amenable to social intervention.
• Bromocriptine that reduces prolactin
• Progesterone that inhibits ovulation 33.3.1.1 Consequences of Miscarriage
• Clomiphene citrate A high percentage of women experience profound loss
• Acetazolamide, a diuretic following miscarriage, reporting symptoms typical of
• Psychotropic medications (results inconclusive) the grief that follows bereavement. Friedman and Gath
(1989) found that at 4 weeks after miscarriage 48% of
The prognosis is good, and spontaneous remission is women were psychiatric cases as measured on the PSE,
usual. all suffering depressive disorders. Many of the women
were already recovering at this time.
Symptoms are increased in women who have experi-
33.3 PREGNANCY enced a previous miscarriage. Many women are fearful
of experiencing loss in a future pregnancy.
33.3.1 Miscarriage
Other factors increasing women’s vulnerability to
Miscarriage occurs in 12%–15% of clinically recognized developing depressive symptoms are lack of a supportive
pregnancies. About one-half are associated with chromo- partner, childlessness, neuroticism, and previous psychi-
somal abnormalities. Other recognized causes include atric consultation.
uterine malformation, cervical incompetence, trauma, Psychiatric morbidity can persist for several months.
infection, endocrine disorder, toxins, irradiation, and The duration of bereavement reaction is appreciably
immune dysfunction. shortened by support and counselling.
33.3.2 Termination of Pregnancy spontaneously by the second trimester, so reassur-

ance and psychological interventions are usually
Psychological disturbance occurring in association with most appropriate.
therapeutic abortion is severe or persistent in only a Benzodiazepines should be avoided particularly in the
minority, about 10% of women. Depression and anxiety first and third trimesters.
are most common with psychosis reported very uncom-
monly, in 0.003% of cases. Of the latter, most have a pre-
vious psychiatric history. 33.3.3.2 Major Mental Illness
Women at greater risk of adverse psychological It was previously believed that pregnancy offered protec-
sequelae include tion against mental illness. It is now known that this is
not the case. The prevalence of depression in pregnancy
• Those with a previous psychiatric history is high.
• Younger women It is always best to avoid drugs in pregnancy if pos-
• Those with poor social support sible. Stable patients may often be withdrawn from
• Those from cultural groups opposed to abortion medication before conception. In those with great risks
of relapse, a judgement has to be made about the rela-
About one-third of women experience feelings of loss, tive risk of relapse against the relative risk of taking
guilt, and self-reproach at 6 months after abortion, partic- medication.
ularly those ambivalent towards the termination of preg- If there is a need to prescribe psychotropic drug,
nancy. Those requiring therapeutic abortion because of the dose should be maintained at a minimum during
fetal abnormalities or medical complications have poorer the first and second trimesters. The dose needs to be
psychological outcomes. increased in the third trimester as a result of expansion
Gilchrist et al. (1995) studied psychiatric morbidity of blood volume. It is best to withdraw anticholinergics
following termination of pregnancy compared with other if possible since the risk of teratogenesis in humans is
outcomes of unplanned pregnancy in a large prospective inconclusive.
cohort study. They found The NICE guidelines and Maudsley’s guidelines
(2012) have made recommendations of psychotropic
• Rates of total psychiatric disorder were no medications for major psychiatric disorders. The recom-
higher after termination of pregnancy than after mendations are summarized as follows.
childbirth.
• Women with a previous psychiatric history were
most at risk of disorder after the end of their 33.3.3.2.1 Depressive Disorder and
pregnancy, whatever its outcome. Pregnancy (Table 33.2)
• Women without a past history of psychosis had The NICE and Maudsley’s guidelines recommend the
a lower risk of psychosis after termination than following:
after childbirth.
• In women without a past psychiatric history, 1. Consider cognitive behavioural therapy (CBT)
deliberate self-harm was more common in or interpersonal therapy (IPT) as first-line
those who were refused a termination (relative treatment.
risk = 2.9) or who had a termination (relative 2. Consider antidepressant if it is preferred by the
risk = 1.7). patient.
• There was no overall increase in psychiat- 3. Consider another monotherapy or electrocon-
ric morbidity in those having a termination of vulsive therapy (ECT) before combination of
pregnancy. antidepressants.
33.3.3 Mental Disorders in Pregnancy

33.3.3.2.2 Bipolar Disorder and
33.3.3.1 Minor Mental Illness Pregnancy (Table 33.3)
There is an increased risk of minor mental ill- The NICE and Maudsley’s guidelines recommend the
ness in the first trimester. This usually resolves following:
TABLE 33.2
Drug Choices for Depressive Disorder in Pregnancy
Effect on Fetus TCA SSRI Not Recommended
SSRI causes pulmonary
Amitriptyline and imipramine Fluoxetine has the most data Bupropion Mirtazapine
hypertension (after 20 weeks)
TCAs have been used for many on safety Moclobemide Reboxetine
in the newborn
years without causing Paroxetine is associated with Trazodone
The neonates may experience
teratogenic effects fetal heart defects in the first Venlafaxine (associated with
withdrawal (agitation and
The use of TCAs in the third trimester and is less safe as hypertension in high dose and
irritability) especially with
trimester may lead to withdrawal compared to other SSRIs. toxicity in overdose)
paroxetine and venlafaxine
effects and increase the risk of Sertraline may reduce the These drugs are not recommended
preterm delivery Apgar score because of the lack of safety data
SSRIs are associated with
reduction in the gestational
age, reduction in birth weight,
and spontaneous abortion
Source: Taylor, D. et al., The Maudsley Prescribing Guidelines, Wiley-Blackwell, West Sussex, U.K., 2012.
, recommended; , not recommended.
TABLE 33.3
Drug Choices for Bipolar Disorder in Pregnancy
Effect on Mother and Fetus Mania Bipolar Depression Not Recommended
The risk of relapse is high if
Mood stabilizing CBT for moderate bipolar Valproate is the most
medication is stopped abruptly
antipsychotics depression teratogenic mood stabilizer and
Lithium: Incidence of the Ebstein’s
• Haloperidol Fluoxetine has the most data on should not be combined with
anomaly is between 0.05% and
• Olanzapine (increase risk safety and indicated for severe other mood stabilizers
0.1% after maternal exposure to
of gestational diabetes) bipolar depression, especially Lamotrigine requires
lithium in the first trimester
ECT is indicated if for those patients with very few further evaluation because it is
Valproate: Incidence of fetal birth
antipsychotic fails previous manic episodes not routinely prescribed in
defect (mainly neural tube defect)
is 1 in 100 pregnancy. Lamotrigine
Carbamazepine: Incidence of fetal causes oral cleft (9 in 1000)
birth defect is 3 in 1000 and Stevens–Johnson
syndrome in infants
1. Treat with an antipsychotic if patient has an 5. The treatment of bipolar depression follows the
acute mania or if she is stable. recommendation of treatment for depression.
2. Consider ECT or mood stabilizer if the patient
33.3.3.2.3 Schizophrenia and Pregnancy
does not respond to an antipsychotic.
(Table 33.4)
3. If lithium is used, the woman should undergo level 2
ultrasound of the fetus at 6 and 18 weeks’ gestation. The NICE and Maudsley’s guidelines recommend the
following:
4. If carbamazepine is used, prophylactic vitamin
K should be administered to the mother and 1. Consider switching from an atypical antipsy-
neonate after delivery. chotic to a low-dose typical antipsychotic.
TABLE 33.4
Drug Choices for Psychosis or Schizophrenia in Pregnancy
Antipsychotics and Other
Effect on Mother and Fetus/Neonate Treatments Not Recommended
Prior to pregnancy, avoid drugs (e.g. risperidone and
Chlorpromazine Depot antipsychotics
sulpiride) that cause hyperprolactinaemia
Trifluoperazine Anticholinergic drugs
Low risk of relapse if antipsychotic is continued with
Haloperidol Clozapine (causing agranulocytosis in fetus)
good social support
Olanzapine (gestation DM
Antipsychotic discontinuation syndrome occurs in the
and weight gain)
neonate, and mixed breast-/bottle-feeding can minimize
Quetiapine
withdrawal
CASC STATION ON PREGNANCY AND USE OF LITHIUM

A 30-year-old lady wants to consult you on the management of bipolar disorder. She is 8-week pregnant. She has
history of bipolar disorder, and she takes lithium CR 800 mg every night.
Task: Discuss with the patient on the specific issues that arise in the use of lithium during pregnancy.
Approach to this CASC station
1. The use of psychotropic medication during pregnancy requires careful risk and benefit analysis espe-
cially in the first trimester when major organs are formed in the fetus. The psychotropic medication in
general plays a role as prophylactic or symptomatic treatment.
2. Candidates need to assess her current mood status (happy or depressed) and inquire whether her preg-
nancy is planned or unplanned. Past psychiatric history should be explored with special focus on
precipitants and severity of previous episodes, previous outcomes of reducing or stopping lithium, past
suicide attempts, previous pregnancies and complications, smoking habits, past or current substance
abuse, and current social and environmental factors, including support network.
3. There are generally six different approaches:
a. Continue lithium at current dose if there is high risk of relapse or at the lowest effect dose.
b. Switch to an antipsychotic gradually such as haloperidol and expose the fetus as few drugs as
possible.
c. Consider ECT if antipsychotics fail.
d. Stop lithium gradually in the first trimester and resume lithium in the second trimester.
e. Avoid all psychotropic drugs throughout the pregnancy if the patient is well and at low risk of
relapse.
f. If she is predominantly depressed rather than manic, consider CBT for moderate depression and
prescribing an SSRI for more severe depression. The candidate should inform the patient the pos-
sible risk to switch to mania. In this station, the candidate is expected to help the patient to make
an informed decision.
4. If the patient chooses to continue lithium, the candidate should inform the risk of fetal heart defects
(6 in 100) and Ebstein’s anomaly (1 in 2000). Stopping lithium at this stage does not remove the risk of
malformations.
5. The candidate needs to assess patient’s commitment to come back for regular follow-up and monitor-
ing. She needs to check serum levels every 4 weeks, then weekly from the 36th weeks, and within
1 day after childbirth. The regular blood monitoring is important because it will guide the psychiatrist
to adjust the dose of lithium and keep the serum lithium levels towards the lower end of the therapeutic
range. The candidate should advise the patient to maintain adequate fluid intake.
6. Explore her view on nonpharmacological interventions (e.g. CBT).
7. The candidate needs to find out the current antenatal care and liaise with the obstetrician to ensure
adequate fetal screening. The patient needs to undergo level 2 ultrasound of the fetus at 6 and 18
weeks’ gestation to screen for Ebstein’s anomaly. During delivery, the obstetrician needs to be
aware that fetal goitre may press on the fetal trachea and leads to a potential complication during
delivery. For patients prescribed with valproate or carbamazepine, they should receive prophylactic
folic acid. Prophylactic vitamin K is required to the mother and neonate if carbamazepine is used.
8. If the patient is prescribed with other psychotropic medications, the patient should be given adequate
information on the risks and benefits of the particular medication. The psychiatrist needs to obtain
an informed consent prior to prescription, and the patient must fully understand the options of other
treatments or no treatment. The dose of the medication may need to be increased in the third trimes-
ter. There is an increase in blood volume by 30% towards the end of pregnancy, which will affect the
distribution of medication. The CYP 1A2 and 2D6 activities increase by more than 50%, and this will
affect the metabolism of medication.
9. If lithium is continued or a new medication is started, the psychiatrist needs to monitor adherence
and look for factors that may affect adherence. The nurse educator should provide information on the
effects of medications on pregnancy, and midwife can help the patient to prepare for delivery.
10. If the patient chooses not to take any medication and she has high risk of relapse, inform her that risk
of relapse and potential harm is through poor self-care, poor judgement, and impulsive behaviour.
The relapse of mania may affect her fetus.
11. The candidate should advise the patient to quit smoking and drinking. She can switch to nicotine
replacement therapy.
12. The candidate should seek permission from the patient to get her partner involved and offer more sup-
port to the patient.
13. Reassure the patient that there will be planned intervention to monitor herself and the newborn.
During delivery, fluid balance and the risk of lithium toxicity will be monitored especially in
prolonged labour. The risk of relapse is 1 in 3 in the first 90 days following childbirth. Additional
measures such as augmentation with antipsychotic will be considered to prevent relapse in the post-
partum period. The candidate should explore the expectation of the patient on breast-feeding and
childcare after delivery.
CASC STATION ON PREGNANCY AND SUBSTANCE ABUSE

You are the psychiatrist working in a local addiction service. You are seeing a 25-year-old woman who is depen-
dent on heroin. She is currently 8-week pregnant.
Task: Take a history to assess the extent of her substance abuse and address her concerns.
You will speak to her husband in the next station.
Approach to this station

Substance abuse in pregnancy involves the excessive nontherapeutic use of recreational (e.g. alcohol, tobacco,
heroin, cannabis, amphetamine) or prescribed drugs (e.g. benzodiazepines and analgesics) resulting in adverse
effects on both the mother and her fetus. Such effects also depend on the trimester of pregnancy. Anticipated
postnatal problems need to be addressed during the antenatal period.
(continued)
(A2) Assess her Desire

to Continue
(A) Obtain Pregnancy and Assess (A4) Antenatal Care
Information about (A1) Planning of the her View on and Outcome of
Current Pregnancy Pregnancy Motherhood (A3) Current Antenatal Care Previous Pregnancies
‘Can you tell me how you ‘How do you feel of ‘Do you see a GP? Is your GP Explore previous fetal
got pregnant this time? being a mother? Are aware of this pregnancy? viability and
Was it planned or you looking forward Have you seen by any abnormality. Assess
unplanned?’ If it is to see your baby?’ obstetrician or midwife?’ her adherence in
unplanned, explore the previous antenatal
underlying reasons (e.g. visits
failure in contraceptives)
‘Who is the father of the
fetus? Can you tell me
more about him?’
(B2) Explore Previous
(B1) Explore the Types Dependence and (B4) Current usage of
(B) Substance of Substances Previously Withdrawal (B3) Previous Contact with Heroin and other Drugs
Abuse History Used Symptoms Local Drug Services and Assess Motivation
Including opiate and ‘In the past few years, ‘Have you undergone any ‘Can you tell me when
nonopiate (e.g. cannabis, is there any change treatment programme with was your last injection
amphetamine), in dosage or pattern local drug service? What is of heroin?’
prescribed medication of heroin usage?’ the outcome?’ (Explore ‘How often do you inject
such as benzodiazepine ‘What would happen treatment nihilism.) heroin nowadays?’
and analgesics, cough if you stop using the ‘Can you tell me the length of the ‘How much do you
medicine, smoking heroin? Do you longest period without using usually inject?’
habit, and alcohol experience teary heroin?’ (abstinence period) ‘Do you mix heroin with
misuse. eyes, runny nose, ‘What was the reason for other substances?’
yawning, or tummy relapse?’ ‘What is your view of
pain?’ ‘Have you heard about using heroin in
methadone? What is your pregnancy? Do you
experience with methadone?’ have any concern?’
‘If methadone is safe for ‘Do you want to replace
yourself and your fetus, are heroin with
you keen to try?’ methadone?’
(C) Complications
Associated with
Heroin Misuse
and Risk (C1) Physical (C2) Psychiatric (C3) Legal or Forensic
Assessment Complications Complications Complications (C4) Risk Assessment
Explore the status of Depression, suicide, Current housing situation ‘Have you ever harmed
blood-borne infections and psychotic Explore previous yourself? If so, how
such as HBV, HCV, and features imprisonment for drug- many times? What was
HIV and complications ‘Are you seeing a related offences and history the reason?’
associated with psychiatrist at this of abusing children ‘Do you still harbour
intravenous injection such moment?’ any suicidal thought?’
as DVT and endocarditis ‘Are you taking any ‘Has your partner been
Explore past medical psychotropic aggressive towards you?’
history and reasons for medication?’ ‘Did you hurt yourself
previous hospitalization after taking too much
drugs?’ (e.g. head
injury)
(D) Social
Assessment and (D1) Assess her Current
Address her Support System and her (D2) Financial (D4) Address her
Concerns Views about her Partner Situation (D3) Care of other Children Concern
‘Is your partner looking ‘Do you work at this ‘Do you have other children? ‘Thanks for talking to me.
forward to seeing your moment? How do Who is looking after them? May I know whether you
newborn?’ you get your How is your relationship have other concerns?’
‘Besides your partner, are income? Have you with your children?’ (e.g. concerns about drug
there other people worked as a use, her own health, and
supporting you?’ commercial sex issues related to the
worker in exchange fetus)
for money? If yes,
do you practise safe
sex? Are you
receiving allowance
from social
welfare?’
After you have spoken to the patient, her partner is very keen to meet you because he is very concerned about
her pregnancy.
Task: Explain the management plan to her partner assuming the patient has given you the consent to speak to him.
Approach to this CASC station
First, the candidate needs to seek the partner’s view on the pregnancy and his view on fatherhood.
The basic principle is to consider a substitute (e.g. methadone) to minimize harm and manage the patient in a
holistic care with the involvement of an addiction specialist, a neonatologist, and an obstetrician. This can take place
at any stage of pregnancy and carries a much lower risk than continuing usage of heroin that may lead to withdrawal
or overdose as a result of fluctuating opiate level (Table 33.5).
Reassure the partner that physical examination will be performed to assess her nutrition status and look for
tattoos, needle marks, and signs of anaemia. Investigations such as full blood count (FBC), liver function test
(LFT), renal function test (RFT), and urinary drug screen will be ordered. You will liaise with the obstetrician
to perform an ultrasound scan to ensure fetal viability.
Short-term management includes establishing therapeutic alliance and stabilization of heroin intake by referring
the patient to a methadone treatment programme. When the patient reaches the second trimester, the addiction spe-
cialist will withdraw the methadone over a period of 4 weeks. She will undergo regular monitoring by an obstetrician.
The drug prevention worker or counsellor will work with the patient in relapse prevention by motivational interview-
ing and compliance therapy. Social worker will enhance other supports, and psychologist will offer supportive psy-
chotherapy with focus on pregnancy issues. The psychiatrist will offer treatment for comorbid psychiatric disorders.
Education will be offered to her partner and prepare him for the upcoming fatherhood. Prior to discharge, the social
worker will be involved if the patient has difficulty to look after the newborn and other children. If there is history
of child abuse, it may be necessary to seek a court order to protect the existing children and newborn. The candidate
needs to stress to the partner that all decisions will be made in the best interest of the patient and the newborn.
Medium-term management includes establishing a delivery plan with input from all specialties. The psychia-
trist will educate the patient on neonatal abstinence syndrome (NAS). Both the patient and the newborn will be
transferred to the mother-and-baby unit after delivery. The psychiatrist will monitor her mood and look for signs
suggesting postnatal depression and puerperal psychosis. Postnatal education involves advice on breast-feeding.
Methadone is compatible with breast-feeding, and the dose should be less than 20 mg/day.
For long-term management, the psychiatrist will assess the patient after delivery and decide whether abso-
lute detoxification or harm minimization technique is appropriate. Her GP will be informed of the outcome of
delivery and ensure the well-being of the patient and her newborn in the community.
TABLE 33.5
Summary of the Maudsley’s Guideline Recommendation of Detoxification of Opiate during Antenatal
and Postpartum Period
First Trimester Second Trimester Third Trimester Delivery and Postpartum
Minimization of drugs If detoxification is Increase methadone dose Antenatal assessment by an

that are harmful in the first required, it is best done in the because the metabolism will anaesthetist is required to handle
trimester, for example, second trimester increase towards the end of potential risks. The anaesthetist needs
benzodiazepines, alcohol, Detoxification is safe and pregnancy. Patient should be to decide on the analgesic requirements
and heroin abstinence can be achieved in offered divided dose of based on dose of methadone given
Optimizing nutrition and stable cases methadone to prevent withdrawal Management of NAS Newborns who
supplementation with folate The use of methadone is The main objective during the are born with mother dependent on
and iron tablets recommended during the delivery is to minimize opiate may develop vomiting and
Detoxification in the first antenatal period withdrawal in the newborn and diarrhoea leading to dehydration and
trimester is not Buprenorphine needs more ensure assisted breathing for poor weight gain
recommended because data to support its safety in floppy and sedated newborn Other symptoms include
opiate withdrawal in the first pregnancy Detoxification is not • Excessive cry and sucking
trimester may lead to recommended after 32 weeks • Hyperreflexia
spontaneous abortion because it may lead to preterm • Increased in muscle tone
delivery and stillbirth • Fever
33.4 PUERPERAL DISORDERS 33.4.2.1 Epidemiology

It occurs in about 50% of women, peaking at the third to
33.4.1 General Issues fifth day postpartum.
There are associations between the puerperal mental con-
ditions. Severe postnatal blues can progress to postnatal 33.4.2.2 Aetiology
depression; there may also be an association between
There is some evidence of links with biological factors,
postnatal blues and puerperal psychosis, since there is an
including
excess of onset of the latter towards the end of the first
week postpartum.
• A history of premenstrual tension.
ICD-10 does not categorize puerperal mental disorders
• Serum calcium levels.
separately unless they do not meet criteria for disorders
• Monoamines, serum tryptophan, and platelet
classified elsewhere. Thus, under the F50-59 ‘Behavioural
a2-adrenoceptors.
syndromes associated with physiological disturbances
• Progesterone withdrawal postdelivery—women
and physical factors’ is a section (F53) ‘Mental and behav-
experiencing severe blues have higher antenatal
ioural disorders associated with the puerperium, not else-
progesterone levels, a steeper rise in the last 2
where classified’, which includes mild, severe, and other
weeks of pregnancy, a bigger decrement from
mental and behavioural disorders associated with the
antenatal levels to the day of peak blues score,
puerperium (WHO, 1992).
and lower progesterone levels on the day of
peak blues.
33.4.2 Postnatal Blues
Postnatal blues is a brief psychological disturbance, char- Postnatal blues have also been positively associated with
acterized by tearfulness, emotional lability, and confu-
sion in mothers occurring in the first few days after • Poor social adjustment
childbirth. • Poor marital relationship
• High scores on Eysenck Personality Inventory recent stressful life events. Younger age, poor marital rela-
(EPI) neuroticism scale tionships, and absent social supports were also notable.
• Fear of labour Early postpartum blues were associated with postnatal
• Anxious and depressed mood during pregnancy depression in the absence of life events, suggesting a small
subgroup of postnatal depression with a hormonal aetiol-
There is no association between the development of post- ogy. A past psychiatric history was a strong risk factor with
natal blues and life events and demographic and social or without life events.
factors or obstetric factors. Murray et al. (1995) found that postnatal depression,
Postnatal women differ significantly from women but not control depression, was associated with a poor
undergoing elective gynaecological surgery in the fre- relationship with the woman’s own mother.
quencies of different symptoms at different times, sug- Postnatal depression is more contingent upon the
gesting that postnatal mood swings are characteristic of acute biopsychosocial stresses caused by the arrival of a
the puerperium and are not simply nonspecific reactions child, whereas depression not associated with childbirth
to stress. is more closely related to longer-term social adversity and
deprivation.
Postnatal blue is associated with tearfulness, irritability, 33.4.3.2.2 Hormonal Factors
and anxiety. Despite the modest association between progesterone lev-
els and postpartum blues, no direct association has been
33.4.2.4 Management demonstrated between progesterone levels and postnatal
The woman should receive reassurance. No psychotropic depression.
medication is required and prognosis is good. Oestrogens affect dopaminergic transmission in the
CNS; their precipitate drop after delivery may be respon-
33.4.3 Postnatal Depression sible for psychosis and possibly also depression in predis-
posed women.
Postnatal depression is a depressive illness not qualita- Puerperal women, whether depressed or not, are non-
tively different from nonpsychotic depression in other suppressors in terms of the dexamethasone-suppression
settings. It is characterized by low mood; reduced self- test. However, no associations have been found between
esteem; tearfulness; anxiety, particularly about the baby’s postnatal depression and cortisol.
health; and an inability to cope. Mothers may experience Transient hypothyroidism, sometimes preceded by
reduced affection for their baby and may have difficulty hyperthyroidism, occurs in up to 5% of women in the
with breast-feeding. postpartum year, peaking at 4–5 months. Such postpar-
tum thyroid dysfunction is associated with depression. It
is estimated that 1% of postpartum women in the general
Postnatal depression occurs in 10%–15% of postpartum population will experience a depressive episode associ-
women usually within 3 months of childbirth. Those ated with thyroid dysfunction.
women who are emotionally unstable in the first week
after childbirth are at an increased risk of developing 33.4.3.3 Clinical Features
postnatal depression. Common symptoms seen in the mother
Postnatal depression is not associated with parity.
1. Irritability, tearfulness, poor sleep, and tiredness
33.4.3.2 Aetiology
2. Feeling inadequate as a mother
33.4.3.2.1 Environmental Factors 3. Loss of confidence in mothering
Of the puerperal psychiatric conditions, postnatal
depression has the least biological cause. Onset after Common symptoms related to the care and safety of the
childbirth is spread over a few months, and studies have baby
repeatedly indicated the importance of social stress in
its causation. 1. Anxieties about the baby’s health.
Paykel et al. (1980) found the strongest associated fac- 2. Expresses concerns that the baby is malformed
tor in mild postpartum depressives was the occurrence of and does not belong to her.
3. Reluctance to feed or handle the baby. Cooper and Murray (1995) distinguished between
4. Forty per cent of patients have thought of harm- those whose postnatal depression was a recurrence
ing the baby. of previous affective disturbance and those for whom
postnatal depression had arisen de novo. Those who
33.4.3.4 Management were suffering from a recurrence of depression were
The education of health visitors and midwives is nec- at raised risk of further non-postpartum episodes but
essary to identify cases early. The Edinburgh Postnatal not postpartum episodes. Those for whom the depres-
Depression Scale is a 10-item self-report questionnaire, sion had arisen de novo were at raised risk for further
used by health visitors to identify postnatal depression episodes of postnatal depression but not for non-post-
during the course of their normal contacts with new partum episodes.
mothers. The relapse rate for subsequent nonpsychotic depres-
Nondirective counselling by health visitors individu- sion is 1 in 6.
ally or in groups is effective in one-third of cases. Self-
help groups and mother-and-baby groups are useful to
33.4.4 Puerperal Psychosis
combat isolation.
In those with more severe symptomatology, or those The risk of developing a psychotic illness is increased
unresponsive to counselling, antidepressants are required. 20-fold in the first postpartum month. Certain symptoms
If depression is severe, admission, preferably with the that are distinctive are
baby to a mother-and-baby unit, may be required. Suicidal
mothers may have thoughts of taking their babies with • Abrupt onset, within the first 2 weeks after
them, so questions about the safety of the child should childbirth
form part of the normal assessment of mothers of young • Marked perplexity, but no detectable cognitive
children. ECT may be required, particularly if worthless- impairment
ness, hopelessness, and despair are present. • Rapid fluctuations in mental state, sometimes
Breast-feeding should not be routinely suspended. from hour to hour
Tricyclic antidepressants are transmitted in reduced quan- • Marked restlessness, fear, and insomnia
tities in breast milk. They are, however, safe. Lithium is • Delusions, hallucinations, and disturbed behav-
transmitted and should not be given to a breast-feeding iour, which develop rapidly
mother because of the risk of toxicity to the child.
33.4.3.5 Outcome 33.4.4.1 Epidemiology

If undetected, postnatal depression may last up to 2 years Kendell et al. (1987) linked psychiatric and obstetric reg-
with serious consequences for the marital relationship isters in Edinburgh and found the number of admissions
and the development of the child. There is good evidence for psychotic disorders to be substantially elevated in the
for a link between depressive disorders in mothers and puerperium. This is shown in Table 33.6.
emotional disturbance in their children.
The following are more frequent in the children of
mothers suffering postnatal depression: TABLE 33.6
Number of Admissions to Mental Hospitals
• Insecure attachment per Month in the Pre- and Postpartum Periods
• Behaviour problems Nonpsychotic Psychotic
• Difficulties in expressive language
Fifteen months preconception 8 2
• Fewer positive and more negative facial
During pregnancy 5 2
expressions
First postpartum month 17 51
• Mild cognitive abnormalities Second postpartum month 14 25
• Less affective sharing Third postpartum month 10 13
• Less initial sociability Fourth postpartum month 8 9
Fifth postpartum month 6 6
Social and marital difficulties are often associated with Mean for next 18 months 9 4
reduced quality of mother–child interactions.
Eighty per cent of puerperal psychoses are affective. as oestrogen occurring at the time of parturition plays
Schizophreniform psychoses often have manic features. an important role.
Those with a previous history of manic–depressive ill- In animals, the administration of oestrogen leads to
ness have a substantially higher risk than those with a increased striatal dopamine binding, and oestrogen with-
history of schizophrenia or depression. drawal leads to dopamine receptor supersensitivity.
The following factors are associated with women Wieck et al. (1991) have reported increased sensitiv-
developing puerperal psychoses: ity of dopamine receptors in the hypothalamus asso-
ciated with the onset of affective psychosis following
• Increased rate of Cesarean section childbirth. It is possible that these changes in sensitivity
• Higher social class are mediated by changes in circulating oestrogen levels.
• Older age at birth of first child Supersensitivity of dopamine receptors is then thought
• Primiparae to precipitate psychosis.
Common symptoms seen in the mother
Psychosis following childbirth is usually of an affective
type with a particularly high proportion of manic epi- 1. Sleep disturbance in early stage.
sodes within the first 2 weeks. 2. Mild confusion, disorientation, and perplexity
Puerperal psychoses follow 20%–30% of births in are common.
those with preexisting bipolar mood disorders. 3. Affective lability often present with marked agi-
tation and mania.
33.4.4.2 Aetiology 4. The clinical features may resemble affective dis-
33.4.4.2.1 Genetic Factors orders (70%), schizophreniform disorder (15%),
• Family studies of puerperal psychosis point to and organic illness (15%).
a familial aggregation of psychiatric disorder,
particularly affective illness. Common symptoms related to the care and safety of the
• Children of probands who have had puer- baby
peral psychosis have an increased psychiatric
morbidity. 1. Delusion may involve the baby and her family.
• Female relatives of puerperal probands have a 2. Suicidal and infanticidal thoughts may be present.
higher rate of puerperal illness than the general
population, but the majority of illness in the rel- 33.4.4.3 Management
atives of probands is nonpuerperal. The identification of high-risk patients during pregnancy
• The weight of evidence from clinical and fam- is important in the planning of postnatal management.
ily studies suggests that most cases of puerperal Admission to a psychiatric hospital is usually essential,
psychosis of early onset are closely related to and it is usually preferable to admit mothers with their
bipolar disorder. babies.
The following are some advantages of joint
33.4.4.2.2 Environmental Factors admission:
There is no evidence of any excess of life events in puer-
peral psychotics compared to matched normal puerperal • Most psychotic mothers are capable of looking
controls. The absence of social stress in this group con- after their babies with supervision and support.
trasts with the findings for postpartum depression and • There is evidence suggesting that joint admission
disorders with onset in pregnancy. These findings sug- may reduce the duration of illness and relapse rates.
gest that the aetiology of severe puerperal psychosis is
predominantly biological and interactive with previous The following are some disadvantages of joint
vulnerability. admission:
33.4.4.2.3 Hormonal Factors • There is a risk of nonaccidental injury to the child

The pathophysiology of puerperal psychosis is not well from the mother or fellow patients. A nurse should
understood, but it is likely that the precipitous fall in be dedicated to the care, and supervision of the
the levels of circulating sex steroid hormones such child and a lockable nursery should be provided.
• Joint admission needs higher staffing levels. In order to avoid breast-feeding during the peak drug
• The long-term effects of admission upon the levels in breast milk, psychotropic drugs should be taken
development of the child are not known. immediately after breast-feeding or before the infant’s
• The woman’s partner needs support and education. longest sleep period (Table 33.7).
33.4.4.3.1 Treatment
• Phenothiazines and lithium are effective in the TABLE 33.7
treatment of manic episodes. Control of lithium
Summary of the Maudsley’s Guideline
levels in the immediate postpartum period can
be difficult because of fluid and electrolyte Recommendation of Psychotropic
changes. Medications for Breast-Feeding
• ECT is particularly effective in the treatment of
Recommended Psychotropic
puerperal psychoses and accelerates recovery in
Psychotropic Medications That Are
all diagnostic categories. It is used generally if Medications Not Recommended
the drug treatment has failed.
• In breast-feeding mothers, lithium is contraindi- Bipolar disorder Bipolar disorder
cated because it is excreted into breast milk and Valproate can be used, Lithium
is toxic to the baby. but advise mother to (concentration in breast
ensure adequate milk is 50% of serum
• Neuroleptics can be administered to breast-feed-
contraception to prevent concentration). If
ing mothers, but high doses should be avoided,
pregnancy patient is taking lithium
and the baby should be observed for signs of during pregnancy, it
drowsiness, such as a failure to feed adequately. Depressive disorder
will be necessary to
• Neuroleptics should be maintained for at least Paroxetine and augment with an
3 months following recovery. If there are further sertraline antipsychotic during the
manic or depressive episodes, lithium should be TCA: Imipramine, postpartum period
considered. nortriptyline, and sertraline because the risk of
are present in breast milk relapse is high
33.4.4.4 Course at relatively low levels
Depressive disorder
Following discharge from hospital, the mother will Schizophrenia
Citalopram and
require close support and follow-up. An assessment of Sulpiride and fluoxetine are present in
the mother–baby interaction should be made prior to olanzapine breast milk at relatively
discharge. Anxiety and insomnia high levels
The initial prognosis is quite good. Cases often settle Mirtazapine,
Lorazepam for anxiety
within 6 weeks, and most are fully recovered by 6 months. venlafaxine
and zolpidem for
A few, however, have a protracted course. insomnia. Advise mother Schizophrenia
After one episode of puerperal psychosis, the risk of a not to sleep with her
further episode in each subsequent pregnancy is between Clozapine,
baby to avoid suffocation
aripiprazole, quetiapine,
one in three and one in five. For those with a previous psy- accident on the newborn
risperidone, and depot
chiatric history or a family history, the risk is higher; for
Substance abuse antipsychotic (infants
those whose puerperal episode was associated with life may show
events or Cesarean section, the subsequent risk is lower. Methadone is
compatible with extrapyramidal side
breast-feeding, but the effects [EPSE])
dose should be kept as
33.4.5 Breast-Feeding and Bulimia nervosa
minimum
Psychotropic Medication No breast-feeding if
patient is on high dose of
Premature infants, infants with renal, hepatic, cardiac, fluoxetine
and neurological impairments, are at a greater risk when
they are exposed to psychotropic drugs. Hence, the Source: Taylor, D. et al., The Maudsley Prescribing
Guidelines, Wiley-Blackwell, West Sussex,
lowest effective dose should be prescribed, and psychia-
U.K., 2012.
trist should avoid polypharmacy.
CASC STATION ON POSTPARTUM DEPRESSION AND PUERPERAL PSYCHOSIS

You are the psychiatric registrar working in liaison psychiatry. The gynaecologist referred a 30-year-old woman
who is a mother of two daughters (a 2-year-old child and 11-month-old baby). She is currently 9-week pregnant
and her partner is thrilled. The patient is not able to face another pregnancy, and she requests for an abortion.
She has had two previous episodes of severe postnatal depression and managed by her GP. She admits to feeling
tired, and the gynaecologist is concerned of her baby’s safety.
Task: Take a history from the patient to establish the diagnosis of postpartum psychiatric illness.
Perform a risk assessment.
Although this station states that the patient suffers from postpartum depression, candidates will fail this station if
they do not explore the symptoms of puerperal psychosis. Candidates are expected to listen in a warm and nonjudge-
mental manner to what the patient is presenting as the important issues for her. Her distress needs to be acknowledged.
(A) Explore the

Issues on
Abortion and (A3) Issues
Obtain More Related to
Information (A1) Clarify the (A2) Explore the Abortion and (A4) Risk Assessment (A5) Chronological
about Current Reason for Expectation from Current Related to her Intention History of Current
Pregnancy Abortion her Partner Pregnancy to abort the Fetus Pregnancy
‘I am sorry to hear that ‘You have told the ‘Can you tell me ‘Did you have abortion ‘Was the pregnancy
you have gone gynaecologist more about your before? If so, how many planned or
through two difficult that your partner background, such times? Was there any unplanned?’
periods after delivery is thrilled. Can as your religion complication? How did ‘How did you know
and current stress. you tell me more and culture? you feel afterwards?’ that you have
Can you elaborate about it? Is he Does abortion ‘If other people like the become pregnant
more on your hoping for a contradict your gynaecologist or your this time?’
intention to terminate boy? Is he religious and partner does not support ‘How did you feel
the current supporting you?’ cultural belief? If your request, will you do after knowing the
pregnancy? Why do ‘Does he know so, are you facing something harmful to the pregnancy test is
you want to go for an about your a lot of stress?’ fetus?’ positive? Do you
abortion?’ (Explore intention to go find yourself in a
transient stress, for an abortion?’ difficult situation?
chronic psychiatric If so, why?’
problem, or financial
problems.)
(B) Previous
Pregnancies
and (B2) Past
Postpartum (B1) Past Postnatal (B3) Postpartum (B5) Current
Illnesses Antenatal History History Depression (B4) Puerperal Psychosis Symptoms
‘Can you tell me ‘Can you tell me ‘How was your Delusions ‘Are you still
more about your more about the mood in the first ‘Have you ever worried that disturbed by the
experience during delivery of your 6 weeks after someone wants to harm symptoms that you
previous two children?’ delivery?’ yourself and your baby?’ have mentioned? Is
pregnancies?’ ‘How were they ‘Are you worried that there any change
‘Did you go for delivered?’ there is something wrong in the frequency
regular antenatal ‘Did they have with your baby? If yes, and severity?
checkups? If not, any complication which aspects?’ Which symptoms
what is the during delivery?’ are most
reason?’ troubling?’
(continued)
‘Did you suffer from ‘How did you feel ‘Did you feel ‘Have you done (Explore current
any complication after delivery?’ irritable? Did you something that may psychotic
such as high blood ‘Are you cry very often? be harmful to your symptoms,
pressure or diabetes breast-feeding How was your baby? If so, what have depressive
during pregnancy? your 11-month-old sleep and you done?’ ‘Have you symptoms, and
If so, were you baby at this appetite? Did you ever thought that you manic symptoms)
admitted to the moment?’ feel tired?’ are superior or special
hospital?’ ‘How do you see when compared to other
‘Did you take yourself as a people? If so, in what
medication during mother? ways?’
your previous Are you confident in Hallucinations
pregnancy?’ yourself? Does ‘Have you heard voices
‘Did you use any anyone offer help after delivery? If so, did
substance to look after your the voices give you any
including baby?’ instruction, such as
recreational drugs, ‘Were you admitted telling you to harm your
alcohol, or to the mother–baby baby?’
cigarettes?’ unit? If so, what ‘Have you suffered
was the reason and from any episode of
for how long? How confusion after
did you feel about delivery? How do you
the service?’ find your
concentration at this
moment?’
(C) Past
Psychiatric
History (C2) Treatment
and Risk (C1) Past of Previous (C5) Risk
Assessment Psychiatric History Episodes (C3) Insight (C4) Parenting Ability Assessment
Explore history of ‘Did the GP ‘What do you think ‘Do you feel confident ‘How is the health
mood disorder prescribe is the cause of the to look after your of your children?
(especially bipolar medication to treat earlier baby (e.g. feeding and Do they have any
disorder and the postnatal experiences? Do bathing the baby)?’ behavioural
use of depression?’ you think you will ‘Was there any episode problems?’
anticonvulsants). ‘Have you been be unwell again? when you left your ‘When you are
‘How do the others continuing those Do you find baby unattended? If stressed, do you hit
describe yourself medications?’ medication or yes, why did you do them? If yes, in
as a person?’ ‘Were you admitted talking therapy so?’ what ways? Were
(Explore to the psychiatric helpful?’ ‘Are you close to your they injured?’
personality.) ward before? If baby? Do you feel ‘Do you have
‘Do you know any so, why? Was the your baby attach to thought of harming
family member admission you?’ yourself at this
suffering from voluntary or moment, how
psychiatric illness. involuntary?’ about your
If so, what kind of children?’
illness?’
(D) Past
History and
Ending of (D1) Past Medical (D2) History of (D3) Social (D4) Developmental (D5) Ending of
Interview History Contraception History History Interview
‘Are you seeing ‘Do you or your ‘What is your ‘Can you tell me more ‘I can imagine that it
your GP? How partner use marital status? Can about your childhood may be a difficult
often do you see contraception? If you tell me more experience?’ period for you
your GP?’ (If so, why did it fail about the quality of ‘Can you tell me more because you need to
patient is not this time? Will your relationship about your parents? make a very major
seeing her GP, you use other with your partner?’ How do feel about decision. May I
explore the contraceptive ‘Do you hold a job them? Is such feeling suggest that we
underlying reason.) methods in the at this moment? affecting the way you shall invite your
‘May I have your future?’ Are you on sick treat your children?’ partner in the next
permission to leave?’ session? Would it be
speak to your GP?’ ‘How is your alright with you?’
financial status?’
33.5 MENOPAUSE 33.5.2 Clinical Features

33.5.1 Aetiology General population surveys indicate no major effect of the
menopause on a variety of common psychiatric symptoms.
33.5.1.1 Biological Factors If anything, women in the postmenopausal years show less
The biological changes during menopause are summa- evidence of psychiatric disturbance than younger women.
rized as follows: Hot flush (75%–85%) at night leads to sleep impair-
ment, fatigue, and irritability.
• Reduction in oestrogen production Urogenital atrophy is the second most common mani-
• Reduction of serotonin binding sites festation of oestrogen deficiency. The alkaline environ-
• Increase in D2 receptor sensitivity ment in vagina may lead to vaginitis. Atrophy of vagina
• Reduction in the activity of endogenous opioid also leads to psychosexual problem such as dyspareunia.
• Increase in noradrenaline activity (associated
with hot flushes)
33.5.3 Management
33.5.1.2 Psychological Factors Anxiety and depression in postmenopausal women do
• Negative self-image: dissatisfaction with self not respond to oestrogen therapy but may respond to anti-
• Premorbid personality: neurotic and dependent depressants such as SSRIs.
personality
• Psychological judgement: negative views towards
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34 Eating Disorders and
Metabolic Syndrome
34.1 ANOREXIA NERVOSA Twin studies have shown higher concordance rates
for monozygotic (MZ) than for dizygotic (DZ) twins.
34.1.1 Epidemiology Holland et al. (1988) found an MZ-to-DZ concordance
Incidence and prevalence estimates vary depending on ratio of 56:5. Fairburn and Harrison (2003) reported
the diagnostic criteria used and the population studied. that the concordance rates for MZ twins and DZ twins
However, the following can be stated: were 38%–55% and 0%–11%, respectively. Five per cent
of first-degree relatives are affected. This suggests that
• It is rare (prevalence about 1–2 per 1,000 genetic factors are significant in the aetiology. This study
women). The Epidemiological Catchment Area suggested that the heritability of AN is 80%. Linkage to
(ECA) study found only 11 cases in 20,000 per- genes controlling serotonin function on chromosome 1
sons studied. and AN has been found.
• The peak age of onset is 15–19 years. Data suggest a familial component to AN, but the very
• The incidence is 10 times higher in females low prevalence in the general population has prevented
compared to males. determination of whether this is genetic or environmen-
• There is a higher prevalence in higher socioeco- tal. There is a chance that genetic predisposition interacts
nomic classes and Western Caucasians and a with environmental factors and triggers the onset of AN.
significant association with greater parental educa- Relatives also have higher rates of obsessive–compul-
tion. Rates in private schools are 1%—much higher sive disorders, generalized anxiety disorder, panic disorder,
than in state schools (0.15%). Rates are much higher and substance misuse. There is an increased risk of mood
again in ballet or modelling schools (7%). disorders among first-degree biological relatives, particu-
• The clinical profile of eating disorders in Hong larly of those with binge-eating/purging type. The morbid
Kong has increasingly conformed to that of risk of affective disorder in families of the eating disor-
Western countries. Lee et al. (2010) studied eat- dered is similar to that of families of bipolar probands and
ing-disordered patients presented to a tertiary psy- is significantly greater than that in families of schizophren-
chiatry clinic between 1987 and 2007 and found ics or those with borderline personality disorder. This sup-
that patients were predominantly single (91.8%), ports growing evidence that AN and bulimia nervosa (BN)
female (99.0%), and in their early 20s. The num- (see following text) are closely related to affective disorder.
ber of patients increased twofold in 20 years.
Anorexia nervosa exhibited increasingly fat-pho- 34.1.2.2 Biological Factors
bic patterns, which resemble Western Caucasians. 34.1.2.2.1 Neurotransmitters
• The suggestion of increasing prevalence over Brain serotonin systems are implicated in the modulation
time is probably not supported, although greater of appetite, mood, personality variables, and neuroen-
numbers are coming to the attention of services. docrine function. An increase in intrasynaptic serotonin
reduces food consumption; a reduction in serotonin activ-
34.1.2 Aetiology ity increases food consumption and promotes weight gain.
Kaye et al. (1991) found increased cerebrospinal fluid
34.1.2.1 Genetic Factors (CSF) concentrations of major serotonin metabolite
Family studies show an increased incidence of eating dis- 5-HIAA in long-term weight-restored anorectics, which
orders among first- and second-degree relatives of those may indicate an increased serotonin activity contributing
suffering from anorexia nervosa (AN). to pathological feeding behaviour.
575
It has been suggested that amenorrhoea is caused by adolescence by repetitive reward-seeking behaviour.
primary hypothalamic dysfunction. This is supported by Gymnasts, wrestlers, and swimmers have higher risk to
the fact that a return to normal menstruation lags behind develop subclinical AN.
the return of body weight, and amenorrhoea sometimes Braun et al. (1994) found that 69% of eating-disordered
precedes weight loss. This, however, is not proven. patients had at least one personality disorder; these were
Amenorrhoea is caused by abnormally low levels of also more likely to have an affective disorder or substance
oestrogen, because of the diminished pituitary secre- dependence than those without personality disorder.
tion of follicle-stimulating hormone (FSH) and lutein- Anorexics are more likely to suffer from anxious–
izing hormone (LH). This is usually a consequence of avoidant personality disorders (cluster C), whereas dra-
weight loss, but, in a minority of individuals, it may actu- matic–erratic personality disorders (cluster B) are more
ally precede it. In prepubertal females, menarche may be common in bulimics.
delayed. Other psychological factors:
34.1.2.2.2 Other Biological Factors • Childhood obesity and teasing by classmates or

• Dopamine: A lower level of dopamine is released teachers
by striatum and leads to reduction in appetite. • Failure of identity formation and psychosexual
• Brain-derived neutropenic factors (BDNF): The development in adolescence
levels of BDNF are reduced in AN.
• Leptin: The levels of leptins are reduced in acute 34.1.2.4 Environmental Factors
AN and associated with poor appetite.
• Premature birth, small for gestational age, and 34.1.2.4.1 Family
cephalhaematoma are risk factors for AN. Minuchin et al. (1978) found that relationships in fami-
lies of anorexics are characterized by overprotection and
34.1.2.2.3 Physical Illness enmeshment. Kendler found that a typical anorexic came
from an inward, often overprotected, and highly con-
An excess of physical illnesses in childhood has been
trolled family. Young patients with AN may use the ill-
found in those with AN. Physical illness may be a risk
ness to gain control and overcome rigidity, enmeshment,
factor for the later development of AN, possibly by induc-
and overprotection in the family.
ing pathology in the family dynamics.
Higher rates of childhood sexual abuse are reported
Cases of AN have been reported with onset imme-
by eating-disordered patients than by controls. Childhood
diately related to a glandular fever-like illness. The dis-
sexual abuse appears to be a vulnerability factor for psy-
ruption of the central corticotropin-releasing hormone
chiatric disorder in general, not for eating disorders in
(CRH) regulation has been suggested as the mediator
particular.
of this.
34.1.2.4.2 Sociocultural Factors
34.1.2.3 Psychological Factors There is a cult of thinness. Anorexic and bulimic women
Psychodynamic theories include fantasies of oral impreg- viewing fashion images of women show a 25% increase
nation, dependent relationships with a passive father, and in their body size estimation afterward. The media pre-
guilt over aggression towards ambivalently regarded sentation of idealized women is likely to have some effect
mother. upon eating-disordered subjects.
Operant conditioning theories include phobic Among 15-year-old schoolgirls, the relative risk
avoidance of food resulting from sexual and social ten- of developing AN was eight times greater in those
sions generated by physical changes associated with who dieted compared to those who did not in a pro-
puberty. spective study.
Immigrants from low-prevalence to high-prevalence
34.1.2.3.1 Personality cultures may develop AN as thin-body ideals are assim-
Anorexics have a high prevalence of defined personal- ilated. Cultural factors influence the manifestation of
ity disorders and an excess of obsessive, inhibited, and the disorder: In some cultures, for example, body-image
impulsive traits. It is suggested that in an environment disturbance may not be prominent, and the expressed
that emphasizes thinness as a criterion for self-worth, motivation for food restriction may have a different con-
vulnerable individuals cope with the challenges of tent, such as epigastric discomfort or distaste for food.
Eating Disorders and Metabolic Syndrome 577
34.1.3 Classification Binge-eating or purging type: The patient has engaged

in recurrent episodes of binge-eating or purging behav-
34.1.3.1 ICD-10 (F50.0 Anorexia Nervosa) iour (i.e. self-induced vomiting or the misuse of laxatives,
This condition is characterized by deliberate weight loss diuretics, or enemas) during the last 3 months.
resulting in undernutrition with secondary endocrine and Restricting type: The patient has not engaged in recur-
metabolic disturbance. It requires the presence of all the rent episodes of binge-eating or purging behaviour dur-
following: ing the last 3 months.
1. Body weight maintained at 15% below

expected; Quetelet’s body mass index (BMI) 34.1.4 Differential Diagnosis of Anorexia
<17.5 kg/m2. (Quetelet’s BMI = mass/height2; Nervosa
age 16 or over.)
2. Weight loss self-induced by the avoidance of fat- Other causes of weight loss should be considered, espe-
tening foods and one or more of the following: cially when presenting features are atypical (e.g. an onset
self-induced vomiting, self-induced purging, of illness after 40 years of age).
excessive exercise, and the use of appetite sup- In medical conditions such as gastrointestinal dis-
pressants and/or diuretics. ease, brain tumours, occult malignancies, and acquired
3. Body-image distortion: a specific psychopathol- immunodeficiency syndrome (AIDS), serious weight
ogy comprising a dread of fatness that persists loss may occur. In these cases, the individuals do not
as an intrusive, overvalued idea; a low weight have a distorted body image or a desire for further
threshold is imposed on self. weight loss.
4. Amenorrhoea in women, loss of sexual inter- Superior mesenteric artery syndrome (postpran-
est and potency in men, endocrine disorder of dial vomiting is secondary to intermittent gastric outlet
hypothalamus–pituitary–gonadal axis (HPA), obstruction) should be distinguished from AN, although
elevated growth hormone and cortisol levels, it may develop in AN because of emaciation.
abnormal peripheral metabolism of thyroid hor- Depressives do not generally have a desire for exces-
mone, and abnormalities of insulin secretion. sive weight loss or a morbid fear of gaining weight.
5. If onset is prepubertal, the sequence of pubertal Schizophrenics may exhibit odd eating behaviours
events is delayed or arrested; puberty is often and occasionally weight loss. However, they rarely fear
completed with recovery, but menarche is late. weight gain or have body-image disturbance.
34.1.3.2 DSM-5 (Anorexia Nervosa) 34.1.5 Clinical Features

34.1.3.2.1 Diagnostic Features
34.1.5.1 Psychological Symptoms and Signs
1. Restriction of energy and food intake leading to a
The person may exhibit
significantly low body weight in the context of age,
sex, development, and health status. Significantly
• Morbid fear of fatness/excessive pursuit of
low weight is defined as a weight that is less than
thinness
minimally normal. DSM-5 does not specify the
• Denial of the problem
percentage of weight loss (i.e. more than 15%) as in
• Distorted body image
DSM-IV-TR.
• Fear of losing control of eating
2. Intense fear of weight gain or persistent behav-
• Problems with separation and independence
iour that interferes with weight gain, even
• Depressive feelings—insomnia, lack of concen-
though the weight is significantly low.
tration, and irritability
3. Body image disturbance as a result of repeti-
• Suicidal ideas
tive self-evaluation and poor insight of low body
• Obsessional thoughts and rituals that may
weight.
improve with weight gain
• Preoccupation with thoughts of food (enjoys
34.1.3.2.2 Subtypes cooking for others and does not like eating in
These are used to specify the presence or absence of reg- public)
ular binge eating or purging during the current episode. • Withdrawn
34.1.5.2 Physical Signs and Complications 34.1.5.2.7 Reproductive System

The person may exhibit the following: • Reduced growth, delayed puberty
• Amenorrhoea
34.1.5.2.1 General Appearance • Small ovaries and uterus
• Emaciation • Infertility
• Dehydration • Breast atrophy
• Hypothermia, cold intolerance
• Pallor (anaemia) 34.1.5.2.8 Musculoskeletal System
• Peripheral cyanosis • Osteoporosis from low calcium intake and
• Purpura secondary to reduced collagen in skin absorption, reduced oestrogen, and increased
and bone marrow suppression cortisol secretion
• Bone pain and deformity
34.1.5.2.2 Central Nervous System • Bone density reduction with increasing years of
• Seizures amenorrhoea
• Diffuse EEG abnormalities, reflecting meta- • Pathological fractures after about 10 years
bolic encephalopathy (may result from fluid and • Tetany
electrolyte disturbances) • Skeletal muscle wasting
• Increase in the ventricular/brain ratio secondary • Proximal myopathy
to starvation
34.1.5.2.9 Dermatological
• Impaired cognition
• Poor concentration • Lanugo hair
• Dry skin
34.1.5.2.3 Cardiovascular System • Brittle nail
• Bradycardia (30–40 beats/min) • Raynaud’s phenomenon: discolouration of fin-
• Hypotension (systolic BP <70 mmHg) gers and toes
• Prolonged corrected QT (QTc) Effects secondary to repeated self-induced vomiting:
• Cardiac arrhythmias and failure There may be
• Peripheral oedema
• Erosion of tooth enamel
• Mitral valve prolapse
• Dental caries
• Pericardial effusion
• Parotid gland enlargement
• Cardiomyopathy
• Russell’s sign (calloused skin over interphalan-
34.1.5.2.4 Gastrointestinal System geal joints)
• Delayed gastric emptying 34.1.6 Baseline Monitoring and Investigations
• Acute gastric dilatation
• Pancreatitis 34.1.6.1 Baseline Monitoring
• Degeneration of myenteric plexus of bowel • Blood pressure (BP) and pulse rate.
• Cathartic colon • BMI.
• Constipation and abdominal distension • Weight.
• Impaired liver function • Although the weight and BMI are important
indicators of severity of AN, the NICE guide-
34.1.5.2.5 Urinary System lines recommend that BMI and weight should
• Impaired renal function caused by chronic not be considered as sole indicators of physical
dehydration and hypokalaemia risk. The nature of the investigations should be
• Nocturia and renal stones adjusted based on the severity of AN.
34.1.5.2.6 Endocrine System 34.1.6.2 Full Blood Count

• Amenorrhoea/loss of libido • Anaemia: usually normochromic normocytic
• Reproductive system atrophy (shrunken uterus and anaemia.
ovaries with cystic multifollicular ovarian changes) • Microcytic (iron deficiency) or macrocytic (B12
• Hypoglycaemia deficiency) anaemia is possible.
• Leukopenia with relative lymphocytosis. 34.1.7 Management

• Reduced ESR.
• Thrombocytopenia. 34.1.7.1 Treatment Setting
Most people with AN should be treated on an out-
34.1.6.3 Electrolyte Disturbances patient basis before reaching severe emaciation. If a
• Hypokalaemia (cardiac arrhythmias, cardiac person is very emaciated, inpatient care may be neces-
arrest, renal damage) sary, and the NICE guidelines recommend the involve-
• Hypomagnesaemia ment of a physician or paediatrician with expertise in
• Hypozincaemia the treatment of medically at-risk patients with AN.
• Hypophosphataemia Other indications for inpatient treatment are listed
as follows:
34.1.6.4 Arterial Blood Gas
1. Persistent decline in oral intake or rapid decline
• Metabolic alkalosis (as a result of self-induced
in weight (e.g. >1 kg/week) in adults who are
vomiting)
already less than 80%–85% of their healthy
34.1.6.5 Renal Function Tests weights.
2. Vital sign abnormalities: heart rate <40 beats/
• Increase in urea as a result of dehydration
min and orthostatic hypotension (drop in BP of
• Renal failure
20 mmHg from supine to standing position).
34.1.6.6 Liver Function Tests 3. Low body temperature (less than 36°C).
4. Severe electrolyte imbalance: hyponatraemia or
• Reduced albumin
hypokalaemia.
• Raised serum amylase
5. Organ failure.
6. Poorly controlled diabetes.
34.1.6.7 Fasting Blood
7. Underlying psychiatric disorder (e.g. severe
• Hypercholesterolaemia as a result of low oestrogen depression and suicidal ideation).
• Hypoglycaemia 8. Failure of outpatient treatment.
9. Pregnancy: More intensive prenatal care is
34.1.6.8 Others required to ensure adequate prenatal nutrition
• Hypercarotenaemia and fetal development.
34.1.6.9 Hormones The NICE guidelines provide detailed recommendations

• Decrease in T3. on every aspect of management of AN, and the recom-
• Increase in CRH. mendations are summarized as follows:
• Increase in cortisol.
• Increase in growth hormone. 34.1.7.2 Weight Restoration
• Decrease in FSH. 1. An average weekly weight gain of 0.5–1 kg in
• Decrease in LH: The 24 h pattern of secretion of inpatient settings and 0.5 kg in outpatient set-
LH resembles that normally seen in the prepu- tings should be an aim of treatment. The weight
bertal individual. gain should not be more than 2 kg per week. This
• Decrease in oestrogen (in women) or decrease requires about 3500–7000 extra calories per week.
in testosterone (in men). 2. As a rule of thumb, the premorbid weight, or the
weight at which periods stopped plus 5 kg, is a
34.1.6.10 Imaging guide to a healthy weight.
• CT brain: brain pseudoatrophy 3. There may be reduced circulating oestrogens, a
• Bone scan: reduction in bone mineral density shrunken uterus, and small amorphous ovaries.
As weight is gained, the uterus increases in size,
In summary, most of the parameters are reduced and the ovaries become multifollicular. At nor-
except the following parameters are increased: amy- mal weight, the ovaries become follicular; this
lase, carotene, cholesterol, cortisol, CRH, and growth is detected by pelvic ultrasound and can be used
hormone. to indicate correct weight.
34.1.7.3 Feeding 2. The aims of psychotherapy should reduce risk,

1. A dietician should be consulted before the ini- enhance motivation, encourage healthy eating,
tiation of feeding. There is slowed gastric emp- and reduce other symptoms related to AN.
tying, so meals must be introduced slowly to 3. CBT targets at cognitive distortion and behav-
reduce the risks of gastric dilatation or rupture. iours related to body weight, body image, and
2. If the patient is very emaciated, liquid feeds eating.
may be better initially. Gradually build up from 4. The minimum duration for outpatient psycho-
1000–3500 kcal/day. logical treatment is 6 months.
3. A multivitamin/multimineral supplement in 5. If outpatient psychological treatment fails,
oral form is recommended for people with AN the psychiatrist can offer combined individual
during both inpatient and outpatient weight and family therapy and day-care or inpatient
restoration. treatment.
4. Total parenteral nutrition should not be used unless 6. Psychotherapy is difficult for patients with
there is significant gastrointestinal dysfunction. severe emaciation. Wait until the weight has
5. Feeding against the will of the patient should be increased and then offer a structured symptom-
the last resort option. This should only be done focused treatment regimen focusing on eating
in the context of the Mental Health Act (1983) or behaviour and attitude.
Children Act (1989). 7. Rigid inpatient behaviour modification pro-
gramme should not be used.
8. For inpatients, outpatient psychological treat-
34.1.7.4 Managing Risk
ment should be offered after discharge, and the
1. The frequency of the monitoring is determined duration is for at least 12 months.
by the severity of AN, and the doctor should 9. Family therapy is the treatment of choice, par-
inform the patient and their carers about the ticularly for children and adolescents with AN.
physical risk of AN. Individual appointments with a health-care pro-
2. Rapid feeding may lead to a life-threatening fessional should be offered and separate from
condition known as refeeding syndrome, which family members or carers.
usually occurs in the first 4 days of refeeding. 10. There are four types of family therapy:
As a result of prolonged starvation and mal- a. Strategic family therapy developed by Haley
nourishment, there is an intracellular loss of (1973) applies paradoxical interventions and
electrolytes such as phosphates. During feed- reduces family’s antagonistic views towards AN.
ing, there will be a sudden shift from lipid to b. Structural family therapy developed by
carbohydrate metabolism. The carbohydrate Minuchin (1978) focuses on hierarchy and
metabolism stimulates cellular uptake of phos- allows patient to have more autonomy in an
phate to generate adenosine-5′-triphosphate enmeshed, inflexible, and overprotective family.
(ATP). When phosphate is used up for ATP c. Systemic family therapy developed by Milan
production, this will lead to severe hypophos- (1974) views the family as a homeostatic system,
phataemia (<0.50 mmol/L) and lack of ATP and therapist acts as a neutral facilitator and helps
for cardiac muscles. The patient will develop family to solve their dilemmas towards AN.
cardiac failure, arrhythmias, and sudden death. d. Maudsley family therapy is the first-line treat-
Other features include rhabdomyolysis, leuko- ment for adolescents with AN. This therapy
cyte dysfunction, and seizure. Hence, refeeding was developed by Dale (1980) and involves
has to be gradual and should be determined by 15–20 sessions. Parents play an active role in
a dietician. helping the adolescent to recover, and their
participation is crucial for treatment success.
34.1.7.5 Psychotherapy The Maudsley’s therapy does not support the
1. For outpatients, cognitive analytic therapy (CAT), idea that family is pathological and causes
cognitive–behavioural therapy (CBT), interper- AN. Maudsley’s therapy is comprised of three
sonal therapy (IPT), focal dynamic therapy, and stages: stage 1: weight restoration, stage 2:
family interventions focused explicitly on eating develop control over eating, and stage 3: estab-
disorders are the treatment of choice. lish a healthy identity.
1. Medication should not be used as the sole or pri- TABLE 34.1
mary treatment for AN. Summary of Good and Poor Prognostic Factors
2. Be aware of cardiac side effects such as postural of AN
hypotension, prolonged QTc, arrhythmia, and Good Prognostic Factors Poor Prognostic Factors
hypothermia. Regular ECG monitoring should
• Onset <15 years of age • Onset at older age
be undertaken for drugs that can prolong QTc • Higher weight at onset and at • Lower weight at onset and at
(e.g. antipsychotics, tricyclic antidepressants). presentation presentation
3. Olanzapine is the most extensively studied anti- • Receive treatment within 3 • Very frequent vomiting and
psychotic in AN (Boachie et al., 2003; Bissada months after the onset of presence of bulimia
et al., 2008). It is associated with greater weight illness • Very severe weight loss
gain, reduction in obsessive symptoms, reduc- • Recovery within 2 years after • Long duration of AN
tion in anxiety, and increase in compliance. The initiation of treatment • Previous hospitalization
mean dose is around 6.6 mg. • Outpatient treatment • Extreme resistance to
4. Risperidone is associated with weight gain and • Supportive family treatment
• Good motivation to change • Continued family problems
reduction in anxiety when combined with an
• Good childhood social • Neurotic personality
antidepressant based on a case report (Newman-
adjustment • Male gender
Toker, 2000).
5. Quetiapine is associated with significant increase in
BMI and reduction in Eating Disorder Examination patterns of weight gain followed by a relapse. For adoles-
(EDE-12) restraint subscale scores over 8 weeks cents with AN, around 80% recover in 5 years and 20%
based on an open label study (Bosanac et al., 2007). may develop chronic AN. For adults with AN, 50% recover,
6. Fluoxetine failed to demonstrate any benefit 25% have intermediate outcome, and 25% have poor out-
in the treatment of patients with AN following come. 50% of restrictive AN may develop bulimia after 5
weight restoration based on a randomized con- years (Table 34.1).
trolled trail (Walsh et al., 2006). AN is a serious disorder with substantial mortality
7. Oestrogen administration should not be used (5%–20%). Sullivan (1995) found that the aggregate mor-
to treat bone density problems in children and tality rate for AN is 5.6% per decade. This is 12 times
adolescents because this may lead to premature the annual death rate due to all causes for females aged
fusion of the epiphyses. 15–24. The aggregate mortality rate for AN is substan-
tially greater than that reported for psychiatric inpatients
and the general population.
34.1.8 Prognosis
The causes of death were complications of eating dis-
The course and outcome are variable. Some patients order in 54% and suicide in 27%. Suicide rates are 200
recover fully after a single episode. Some exhibit fluctuating times greater than in the general population.
CASC STATION ON AN
You are the registrar working in an adolescent psychiatric service. You are seeing a 15-year-old secondary
school student with a 2-year history of AN. She is admitted to the hospital following a seizure after prolonged
fasting. On admission, her BMI is 10 and her heart rate is 35 beats/min. She has a younger sister aged 13 who
has developed AN recently. You are approached by her parents who beg you to save the patient, and they are also
very concerned about their younger daughter who is at home at this moment. The patient is not forthcoming, but
she has given the consent for you to speak to her mother.
Task:
1. Take a history from her mother to establish the aetiology, diagnosis, and course of AN for the 15-year-
old patient.
2. Assess the impact of AN of the two daughters.
(continued)
CASC Grid
(A3) Body-image (A4) Psychiatric (A5) Medical
(A) Course (A1) Longitudinal (A2) Methods to Distortion and Complications Complications
of AN Weight History Lose Weight Bingeing of AN of AN
‘I am sorry to hear that ‘What methods does ‘How does your elder ‘How do you find ‘How do you find
you have two your elder daughter daughter feel about your elder your elder
daughters suffering use to lose weight?’ her body? Does she daughter’s mental daughter’s physical
from eating disorders. ‘Does she avoid food? think that she is too health after health after
Can you tell me your If yes, how?’ fat?’ developing eating developing eating
views about their ‘Does she do ‘Have you ever disorder?’ disorder?’
conditions?’ excessive exercise? questioned why she ‘How do you find her ‘How is her menses?
‘Are they sick at this If yes, what kind of feels that she is too concentration?’ Do her menses
moment?’ exercise does she fat?’ ‘Does she follow your come regularly? If
‘Can you tell me more do?’ ‘How about her advice?’ not, how long have
about your elder ‘Does she induce sister? Does she ‘Is she very rigid and the menses been
daughter’s eating vomiting? If yes, share similar stubborn at this absent?’
disorder?’ how does she do it?’ belief?’ moment?’ ‘Has she ever fainted
‘What is her average ‘Does she use ‘Do they compare ‘How is her mood?’ or had a blackout?’
weight?’ laxatives or with each other in ‘Is she nervous?’ ‘Did she have a fit
‘What is her lowest diuretics to lose their body image?’ before?’
weight or highest weight?’ ‘Do they binge? If ‘Does she look pale?’
weight in the past two ‘What method does yes, do they feel ‘Does she feel weak
years?’ your younger guilty? If yes, what most of the time?’
‘How about her daughter use? Do would they do?’
younger sister? What they share the same (Look for self-
is her lowest weight?’ method?’ induced vomiting.)
(B2) Common
Precipitating
(B) Aetiology (B1) Predisposing Factors—Sibling (B3) Maintaining (B5) School and
of AN Factors in Family Rivalry Factors (B4) Development Peers
‘Can you tell me more ‘How is the ‘How do their ‘Can you tell me ‘Do your daughters
about your family?’ relationship illnesses affect the more about them play any sport? How
‘Are the family between the two family?’ when they were about ballet dancing
members close to daughters?’ ‘Do they get more young?’ or modelling?’
each other? Do you ‘How does your attention from you ‘Did they stay with you ‘How are their
think that you have elder child react to and your partner and your partner all academic
been too close to each her sister’s eating when they suffer the time?’ performances? Are
other?’ (Look for disorder?’ from eating ‘Was there any they very serious
enmeshment.) ‘Are they competing disorder?’ unhappy event about their
‘How do you nurture with each other?’ ‘How do you and during their academic
your children? Are ‘Was your elder your partner react childhood? If yes, performances? Do
you strict in daughter being when they develop what kind of event? they often compare
discipline? Could it be neglected when her eating disorder?’ Were they being with each other?’
too strict?’ younger sister ‘What is the family’s abused before?’ ‘Is your elder
‘How is your develops eating view on food and ‘Does your elder daughter in a
relationship with your disorder?’ body image? Are daughter encounter relationship at this
partner? Was there ‘What is your you very conscious any problem as a moment?’
any marital conflict?’ younger daughter’s about weight?’ teenager?’ (e.g. ‘Was she bullied in
‘Did eating disorder reaction towards identity problem) the school? If yes,
run in your family? her elder sister’s why? Was she obese
How about your eating disorder?’ in the past?’
partner’s family?’
(C) Course of
Illness, (C2) Outcomes
Comorbidity, (C1) Previous of Previous (C4) Explore (C5) Risk
and Risk Treatment Treatments (C3) Assess Insight Comorbidity Assessment
‘Did your elder ‘What was the ‘Does your elder ‘Does your elder ‘Has your elder
daughter receive any outcome of the daughter believe that daughter suffer other daughter ever
treatment before? If treatment?’ If it she is ill?’ psychiatric harmed herself? If
yes, what kind of fails, please ‘Does she see her problems? For yes, how did she do
treatment was explore the younger sister example, does she it?’
offered?’ underlying reason. suffering from check things ‘Did she tell you why
‘How about your ‘How does your eating disorder?’ repetitively or is she she wanted to harm
younger daughter? elder daughter feel If patient does not depressed?’ herself?’
What kind of about the treatment believe that she has ‘How do you describe ‘Have she ever
treatment did she for her sister?’ eating disorder, your elder daughter thought of harming
receive?’ explore with the as a person? Is she her younger sister?’
‘How did your elder mother the perfectionistic?’ ‘Did her younger
daughter feel when underlying reason ‘Does she use sister harm herself
your younger and how the elder recreational drugs?’ before?’
daughter received daughter sees ‘Does your younger
treatment?’ herself different daughter suffer
from her younger from other
sister. psychiatric
illness?’
(D) Explore the
Impact and (D5) Explore Her
Dynamics of Expectation on the
Having Two (D1) Explore Her (D2) Comparison (D4) Explore the Overlap Between
Daughters with Views on the of Her Daughters’ (D3) Assess Family’s Expectation Two Daughters’
AN Current Situation Eating Disorder Coping Strategies on the Management Treatment
‘Thanks for sharing ‘How do you feel ‘How do you and ‘What is your ‘Where does your
with me, and we have about their eating your partner cope expectation on the younger daughter
gone through a lot of disorders? Are they with their eating treatment of your receiving her
details about your similar? If yes, in disorders?’ elder daughter?’ treatment? Is she in
daughters’ eating what ways? ‘Do you get help ‘She has to be the same service?’
disorder. What is your Are they different? from other people?’ admitted to the ‘Do you want a
view on the cause of How are they ‘Do you have hospital. How do family therapist to
eating disorder in different?’ someone to turn to you feel about it?’ help the family to
them?’ when you undergo a ‘The treatment overcome the eating
lot of stress?’ mainly involves disorder?’
psychological
treatment aiming at
weight restoration
and family therapy.
How do you feel
about that?’
34.2 BULIMIA NERVOSA Beta-endorphin concentration in CSF of bulimics is

significantly reduced, possibly related to chronic activa-
34.2.1 Epidemiology tion of the HPA axis secondary to dieting.
• The prevalence among adolescent and young Cholecystokinin-8 (CCK-8) is involved in regulating
adult females is approximately 1%–3%. satiety and anxiety. It is dependent upon an intact 5HT
• The lifetime prevalence for strictly defined bulimia function. Bulimics have lower CSF CCK-8 concentra-
nervosa (BN) is 1.1% in females and 0.1% in males. tions than controls. A central, but not peripheral, CCK
• Kendler et al. (1991) estimate a heritability of dysfunction is implicated in BN.
liability to BN of 50%. Arginine–vasopressin (AVP) CSF concentrations are
• The social class distribution is more even than high in bulimics. An increased central AVP may be related
for AN (see preceding text). to obsessive preoccupation with the aversive consequences
• The average age of onset is 18 years, slightly of eating and weight gain. It also interacts with 5-HT.
older than in anorectics. There is a general reduction of sympathetic responsiv-
• The female-to-male ratio is 10:1. ity and activation of HPA activity in BN, probably as a
• It is reported more frequently in Caucasians result of long-term neuroendocrine adaptation to caloric
in Western Europe, North America, and restriction.
Australasia.
• There are reports of increasing prevalence with 34.2.2.3 Psychological Factors
time. Lee et al. (2010) reported that BN became 34.2.2.3.1 Personality
more common in Hong Kong. • Personality disturbance is more common in
• The DSM-IV-TR and DSM-5 have a category patients with eating disorders than in the gen-
known as binge-eating disorder, which has a eral population. On the Eysenck Personality
prevalence of 1%–2%. Onset is 40 years of age. Inventory, bulimics score higher for psychoti-
Twenty-five per cent of patients are men. cism and neuroticism than do anorexics and
controls. On the MMPI, bulimics have elevated
scores for psychopathic deviance.
34.2.2 Aetiology of Bulimia Nervosa
34.2.2.1 Genetic Factors 34.2.2.3.2 Other Psychological Factors
• In twins, the MZ–DZ concordance rate for nar- • Low self-esteem, low paternal care, external
rowly defined BN is 23:9. locus of control, and high neuroticism scores are
• Fairburn and Harrison (2003) reported that risk factors for bulimia.
the concordance rates were 35% (MZ) versus • Bulimics are more likely than anorexics to
30% (DZ). abuse substances (20%). Lifetime rates of alco-
hol dependence are high.
34.2.2.2 Biological Factors • The prevalence of social phobia in eating-
34.2.2.2.1 Neurotransmitters disordered subjects, especially in bulimics, far
Many abnormalities in eating disorders are secondary to exceeds that in the general population.
dieting, weight loss, and binge/purge behaviour. • Bulimics have high rates (40%) of major depres-
Serotonin is involved in the mediation of satiety sion. There is significant comorbidity between
responses to feeding as well as the regulation of mood, anorexia and bulimia.
anxiety, and impulsive behaviour. There is evidence in
normal-weight bulimics of altered postsynaptic 5-HT1c 34.2.2.4 Environmental Factors
receptor sensitivity and depression associated with dys- Prior to illness onset, bulimics are more likely to be over-
regulation of presynaptic 5-HT function. weight than their peers.
There is further support for the 5-HT dysregulation Rigid dieting is the most common precipitant of
hypothesis from findings that CSF concentrations of the binge eating. Gross bingeing is the most common pre-
serotonin metabolite 5HIAA and dopamine metabolite cipitant for self-induced vomiting. Dieting may affect
HVA are inversely correlated with a frequency of binge appetite and satiety mechanisms. Second World War
eating in the month prior to admission. veterans who had been prisoners of war and suffered
weight loss report more binge eating afterward than medications; fasting; or excessive exercise) to
veterans who had not been prisoners. Data are support- prevent weight gain.
ive of an aetiological role for eating restraint in promo- 4. Frequency of binge-eating and compensatory
tion of bingeing. behaviours: at least 1 per week for 3 months.
Many normal-weight bulimics are the eldest or only 5. Repetitive self-evaluation as a result of undue
daughters. Lacey et al. (1991) postulate that at times of influence by distorted body image.
parental marital discord, the mother can use her daughter 6. The disturbance does not occur exclusively dur-
as an easily available therapist, burdening the child at an ing episodes of AN.
age when she cannot deal with the expressed emotions.
Bulimics report more sexual abuse in childhood than
34.2.3.3 DSM-5 (Binge-Eating Disorder)
controls.
In this variation, there are recurrent episodes of
binge eating in the absence of the regular use of inap-
34.2.3 Classification propriate compensatory behaviours characteristic of
BN. The other criteria listed in BN apply. Furthermore,
34.2.3.1 ICD-10 (F50.2 Bulimia Nervosa)
the DSM-5 requires three of the following criteria: eat-
BN is characterized by repeated bouts of overeating and ing much more rapidly than normal, eating until feel-
excessive preoccupation with the control of body weight, ing uncomfortably full, eating large amounts of food
leading to extreme measures to mitigate against the fat- when not feeling physically hungry, eating alone to
tening effects of food. It shares the same specific psycho- avoid embarrassment, feeling disgusted with oneself
pathology of fear of fatness as AN. or very guilty after overeating, and marked distress
A diagnosis under ICD-10 requires all of the over binge eating.
following:
1. Persistent preoccupation with eating and an irre- 34.2.4 Differential Diagnosis

sistible craving for food; episodes of overeating
of Bulimia Nervosa
in which large amounts of food are consumed in
short periods of time. In certain medical conditions, such as the Kleine–Levin
2. Attempts to counteract the fattening effects syndrome, there is disturbed eating behaviour, but char-
of food by one or more of the following: self- acteristic psychological features of BN such as overcon-
induced vomiting, purgative abuse, alternating cern with body shape and weight are not present.
periods of starvation, and use of drugs (appe- Overeating is common in atypical depression, but
tite suppressants, thyroid preparations, diuret- sufferers do not engage in inappropriate compensatory
ics). Diabetic bulimics may neglect insulin behaviour or exhibit overconcern with body shape and
treatment. weight.
3. Morbid dread of fatness. Patient sets weight Binge eating is included in the impulsive behaviour
threshold well below healthy weight. Often criterion that is part of the DSM-5 definition of borderline
there is a history previously of AN. personality disorder. If full criteria for both disorders are
met, both diagnoses are given.
34.2.3.2 DSM-5 (Bulimia Nervosa)
34.2.3.2.1 Diagnostic Features 34.2.5 Clinical Features of Bulimia Nervosa
An episode of binge eating is characterized by both of
the following: 34.2.5.1 Psychological Symptoms and Signs
The person may exhibit
1. Recurrent binge eating of large amount of food
within short period of time (e.g. 2 h) • Morbid fear of fatness
2. Lack of self-control over recurrent binge eating. • Distorted body image—overconcern with shape
3. Recurrent inappropriate compensatory behav- and weight
iours after binge eating (e.g. self-induced vom- • An overwhelming urge to overeat, with subse-
iting; misuse of laxatives, diuretics, or other quent guilt and disgust
• Self-induced vomiting (90%), using fingers and, 34.2.5.2.1 Common Biochemical Abnormalities
later, reflex vomiting, which results in relief The NICE guidelines recommend that patients with BN who
from physical discomfort and reduction of fear are vomiting frequently or taking large quantities of laxa-
of gaining weight tives should have the following investigations performed:
• Laxative abuse (30%), excessive exercise, and
food restriction • Hypokalaemic alkalosis (caused by repeated
• Depression, irritability, poor concentration, and vomiting).
suicidal ideas • Metabolic acidosis with reduced serum bicar-
• Older than the anorectic, more socially compe- bonate in those abusing laxatives.
tent, and sexually experienced • Raised serum bicarbonate.
• Possibly normal weight or just slightly under- • Hypokalaemia—direct potassium loss from
weight or overweight vomiting and indirect renal loss in response
• Menstrual abnormalities (<50%) to raised aldosterone secondary to volume
• More insight than in AN, often eager for help depletion.
• Depressive symptoms (in the majority), anxi- • Hypochloraemia.
ety, impulsive and compulsive behaviours, and • Hypomagnesaemia.
problems with interpersonal relationships • Raised serum amylase (salivary isoenzyme)—
• Stealing and dependence upon substances monitoring serum amylase can be used to moni-
tor vomiting behaviour.
There is also a high prevalence of depression, self-
mutilation, attempted suicide, substance abuse, and low
34.2.6 Management
self-esteem.
Most patients with BN are treated in an outpatient setting.
For patients who are at risk of suicide or several medical
34.2.5.2 Physical Signs and Complications complications, inpatient treatment is recommended.
1. Related to vomiting:
a. Dental erosion and toothache 34.2.6.1 Psychotherapy
b. Parotid gland enlargement Freeman et al. (1988) conducted a controlled trial of
c. Callouses on backs of hands: Russell’s sign psychotherapy. The controls were left significantly
d. Oedema worse than all treatment groups at the end of the trial.
e. Conjunctival haemorrhages caused by Behavioural, cognitive–behavioural, and group therapies
raised intrathoracic pressure were all effective; 77% stopped bingeing. Improvements
f. Oesophageal tears were maintained at 1 year. Behavioural therapy was the
g. Ipecacuanha intoxication causing cardiomy- most effective, with the lowest dropout rate and earlier
opathy and cardiac failure, usually fatal onset of improvement. There seemed to be no advantage
2. Related to purgative abuse: in adding a cognitive element. Psychotherapy produces
a. Rectal prolapse a wider range of changes with more stable maintenance
b. Constipation than does drug therapy.
c. Diarrhoea The NICE guidelines provide detailed recommenda-
d. Cathartic colon, damaged myenteric plexus tions on every aspect of management of BN, and the rec-
3. Related to binges: ommendations are summarized as follows:
a. Acute dilatation of stomach (medical
emergency) 34.2.6.2 Cognitive–Behavioural Therapy for BN
b. Hypercarotenaemia: yellowish skin in palm This includes psychoeducation, self-monitoring, and cog-
and feet (binge on juices) nitive restructuring. Eating regular meals is very impor-
4. Other complications: tant. The course of treatment should be aimed at 16–20
a. Epilepsy sessions over 4–5 months.
b. Arrhythmia (caused by electrolyte disturbances) The aims of behavioural therapy are to stop binge-
c. Tetany ing and purging by restricting exposure cues that trigger
d. Muscle weakness (caused by electrolyte binge/purge behaviour, developing alternative behav-
disturbances) iours, and delaying vomiting.
34.2.6.3 Interpersonal Therapy • Wannamethee (2008) studied a total of 5128

If CBT fails, interpersonal therapy (IPT) should be con- British men aged 40–59 years and monitored
sidered, and the duration is between 8 and 12 months. them for 20 years. The MetS is associated
with a significant increase in risk of total
coronary heart disease (CHD) (myocardial
infarction, angina, or CHD death), stroke, and
1. Selective serotonin reuptake inhibitors (SSRIs) type 2 diabetes.
(specifically fluoxetine) are the drugs of first
choice for the treatment of BN in terms of accept-
ability, tolerability, and reduction of symptoms. 34.3.2 Psychiatric Diseases and MetS
2. The effective dose of fluoxetine is 60 mg per day.
3. Other psychotropic drugs are not recommended 34.3.2.1 Schizophrenia
for the treatment of BN. Mitchell et al. (2011) conducted a meta-analysis and
reported that the prevalence of MetS was 32.5% in
schizophrenia patients.
34.2.7 Prognosis
Findings from the Clinical Antipsychotic Trials in
The outcome for BN improves with time and generally Intervention Effectiveness (CATIE) study (Meyer et al.,
better than AN. The majority of patients make a full 2008)
recovery or suffer only moderate abnormalities in eating
attitudes after 10 years. • The prevalence of MetS was increased for olan-
There is comorbidity with depression, and promi- zapine (from 34.8% to 43.9%) but decreased for
nent anorectic features increase the likelihood of a poor ziprasidone (from 37.7% to 29.9%).
response. • At 3 months, olanzapine and quetiapine had
In a 10-year follow-up of treated bulimics, 52% recov- the largest mean increase in waist circum-
ered fully, 39% continued to suffer some symptoms, and ference (0.7 in. for both) followed by ris-
9% continued to suffer the full syndrome. peridone (0.4 in.) compared to no change for
In terms of prognostic factors, there is evidence from ziprasidone.
a number of studies that the following factors may be • Olanzapine demonstrated significantly different
associated with poor outcome (Keel and Michell, 1997; changes in fasting triglycerides at 3 months as
Quadflieg and Fichter, 2003): compared to ziprasidone.
• Depression
34.3.2.2 Depressive Disorder
• Personality disturbance
• Greater severity of symptoms Kahl et al. (2012) studied 230 patients with major depres-
• Longer duration of symptoms sive disorder in Germany and found that the age-stan-
• Low self-esteem dardized prevalence of MetS was 2.4 times higher than
• Substance abuse controls (41.0% vs. 17.0%).
• Childhood obesity Pyykkönen et al. (2012) reported that depressive
symptoms were related with the MetS and the individual
Bulimics with multi-impulsive personality disorder do components of MetS. Such associations were not driven
less well than those with bulimia alone. by the use of antidepressant medication.
34.3.2.3 Bipolar Disorder

34.3 METABOLIC SYNDROME The prevalence of MetS was between 22.4% and
26.5% in European patients with bipolar disorder
34.3.1 Epidemiology
(Garcia-Portilla et al., 2008; Salvi et al., 2011). Young
• In the United Kingdom one in four people are male patients and lack of exercise are important risk
affected by metabolic syndrome (MetS). MetS factors.
is more common in certain ethnic groups (such Elmslie et al. (2009) found that the frequency of MetS
as Asian and Afro-Caribbean people) and was 50% in bipolar disorder patients treated with sodium
among women with polycystic ovary syndrome. valproate. Dyslipidaemia is a major concern.
34.3.3 Classification
TABLE 34.2
The U.S. National Cholesterol Education Program Adult Summary of Recommendations from the NICE
Treatment Panel III (ATP-III) (2001) requires at least
Guidelines and Maudsley’s Guidelines (2012) on
three of the following:
the Management of MetS in Schizophrenia
• Dyslipidaemia: triglycerides (TG) ≥150 mg/dL Impaired • Monitoring: oral glucose tolerance test
(1.7 mmol/L) glucose (OGTT) or fasting glucose at baseline,
• BP: ≥130/85 mmHg control 1 month and 6 months for patients taking
• Fasting plasma glucose: ≥110 mg/dL (6.1 mmol/L) clozapine and olanzapine. Urine glucose or
• Central obesity: waist circumference ≥102 cm rapid blood glucose at baseline and annually
(male), ≥88 cm (female) for other antipsychotics
• Dyslipidaemia: high-density lipoprotein choles- • Aripiprazole, amisulpride, asenapine, and
terol (HDL-C) <40 mg/dL (male), <50 mg/dL ziprasidone
(female)
• Clozapine and olanzapine
• Prevention: lifestyle interventions aimed at
The World Health Organization criteria (1999) require
changing an individual’s diet (starchy foods
the presence of any two of diabetes mellitus, impaired or fibre-rich foods) and increasing the amount
glucose tolerance, impaired fasting glucose or insulin of physical activity (at least 30 min of
resistance, and one of the following: physical activities for 5 days per week) may
prevent impaired glucose tolerance to type 2
• BP: ≥140/90 mmHg from developing into diabetes.
• Dyslipidaemia: TG: ≥1.695 mmol/L and HDL-C Dyslipidaemia • Monitoring: fasting lipids at baseline, at
≤0.9 mmol/L (male), ≤1.0 mmol/L (female) 3 months and annually
• Central obesity: waist/hip ratio >0.90 (male),
• Haloperidol and risperidone
>0.85 (female), or BMI >30 kg/m2
• Microalbuminuria: urinary albumin excretion ratio • Clozapine and olanzapine
≥20 μg/min or albumin/creatinine ratio ≥30 mg/g • Prevention: cardioprotective diet (total fat
intake is ≤30% of total energy intake,
The International Diabetes Federation criteria (2006) saturated fats are ≤10% of total energy intake,
require the presence of central obesity (defined as waist or dietary cholesterol is less than 300 mg/day),
regular exercise, weight management,
circumference with ethnicity-specific values) and any
reduction of alcohol consumption, and
two of the following:
smoking cessation
• Offer 40 mg simvastatin for patients who are
• Raised TG: >150 mg/dL (1.7 mmol/L) or spe-
older than 40 years and have history of CHD,
cific treatment for this lipid abnormality
angina, stroke, peripheral vascular disease,
• Reduced HDL-C: <40 mg/dL (1.03 mmol/L) in diabetes, and dyslipidaemia.
males, <50 mg/dL (1.29 mmol/L) in females, or Weight gain • Measurement of BMI and waist circumference
specific treatment for this lipid abnormality at baseline and each outpatient visit
• Raised BP: systolic BP >130 or diastolic BP >85
• Aripiprazole, amisulpride, asenapine,
mmHg or treatment of previously diagnosed
haloperidol, sulpiride, and ziprasidone
hypertension
• Raised fasting plasma glucose: >100 mg/dL • Clozapine and olanzapine
(5.6 mmol/L) or previously diagnosed type 2 • Bupropion, metformin, and topiramate may
diabetes reduce body weight.
• If BMI is >30 kg/m2, central obesity can be • Refer patient to the weight management
programme. The patient should aim to lose
assumed and waist circumference does not need
5%–10% of original weight with maximum
to be measured
weekly weight loss of 0.5–1 kg.
34.3.4 Management
recommended; not recommended.
See Table 34.2.
34.4 DSM-5 Fairburn CG. 1993: Eating disorders. In Kendell RE and Zealley
AK (eds.), Companion to Psychiatric Studies. Edinburgh,
Feeding and eating disorders (APA, 2013): Scotland: Churchill Livingstone.
307.53 Rumination disorder: repeated regurgitation of Fairburn CG and Harrison PJ. 2003: Eating disorders. Lancet
food for at least 1 month. 361(9355):407–416.
307.59 Avoidant or Restrictive Food Intake Disorder: Fombonne E. 1995: Anorexia nervosa: No evidence of an
increase. British Journal of Psychiatry 166:462–471.
lack of interest in food and results in significant weight
Freeman CPL, Barry F, Dunkeld-Turnbull J, and Henderson A.
loss and nutritional deficiency. 1988: Controlled trial of psychotherapy for bulimia ner-
307.59 Atypical anorexia nervosa: no significant vosa. British Medical Journal 296:521–525.
weight loss but other criteria are met. Garcia-Portilla MP, Saiz PA, Benabarre A et al. (2008) The prev-
307.59 Bulimia nervosa (of low frequency or limited alence of metabolic syndrome in patients with bipolar dis-
duration): no or infrequent binge eating but other criteria order. Journal of Affective Disorders 106(1–2):197–201.
are met. Garfinkel PE, Lin E, Goering P et al. 1995: Bulimia nervosa
307.59 Purging disorder: recurrent purging. in a Canadian community sample: Prevalence and com-
parison of subgroups. American Journal of Psychiatry
307.59 Night eating syndrome: recurrent episodes of 152:1052–1058.
night eating. Gillies CL, Abrams KR, Lambert PC et al. 2007:
Pharmacological and lifestyle interventions to prevent
or delay type 2 diabetes in people with impaired glucose
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35 Sexual Disorders
35.1 HISTORY • The proportion occurring before age 16 has

increased over time. Fewer than 1% of women
• In 1910, Havelock Ellis, a British pioneer, was aged 55 or over report heterosexual intercourse
the first to subject normal as well as pathological before the age of 16, compared to 20% of those
sexuality to scientific investigation (Ellis, 2010). in their teens.
• Starting in 1948, Kinsey and associates con- • People today are more likely to use contraception
ducted landmark research into human sexual (usually condoms) than those of a previous genera-
experience in thousands of men and women. tion. However, the earlier first intercourse occurs,
A wide range of human sexual expression was the less likely it is that contraception is used.
noted. Methodological problems included non- • It is very rare for men’s first sexual intercourse
random sampling. Volunteers were recruited to be with a prostitute.
from a variety of sources, with a nonrepresen-
tative excess of college-educated people, crimi-
nals, and sex offenders (Kinsey et al., 1953). 35.1.3 Heterosexual Partnerships
• In 1957, William H. Masters and Virginia E. • Age and marital status are associated with mul-
Johnson studied human sexual response cycle in tiple partnerships. The young and those previ-
the United States and established the principles of ously married or single (including cohabitees)
sensate-focus therapy (Masters and Johnson, 1966). are most likely to report high partner numbers.
• In 1981, acquired immune deficiency syndrome • There is increasing partner change with increas-
(AIDS) was first described in the United States. ing social class.
It was initially believed to be confined to a • For young heterosexual British men, the main
small group of promiscuous homosexual men. predictor of the number of sexual partners in the
Subsequently, a primarily heterosexual world- last 5 years was the time since the first sexual
wide epidemic of major proportions has devel- intercourse.
oped and the awareness of safe sex was raised • Serial monogamy is more common in those
globally (Sepkowitz, 2001). aged 16–24. Concurrent partnerships are more
common in those over the age of 35.
• Raised odds of ever using a prostitute are asso-
35.1.1 British Sexual Behaviour and Attitudes
ciated with age, previous marriage or current
A major survey of British sexual attitudes and lifestyle cohabitation, working away from home, and a
(Johnson et al., 1994) has provided the most comprehen- history of having a homosexual partner.
sive evaluation of sexual behaviour in the British pub-
lic in the 1980s and 1990s. The survey involved 18,876
35.1.4 Heterosexual Practices
British men and women in a random population sample
aged 16–59. The following statistics were among many • Frequency of heterosexual sex (oral, vaginal, or
that emerged. Kupek (2001) studied the sexual attitudes anal intercourse) shows wide variability, with a
of 550 young heterosexual British men. small proportion of the population reporting a
very high frequency of sexual contact.
• Age is closely related to the number of acts, fre-
35.1.2 First Heterosexual Intercourse
quency peaking in mid-twenties, then gradually
• Age at occurrence is decreasing over time. In declining.
the past four decades, the median age of first • Frequency is affected by partner availability,
heterosexual intercourse has fallen from 21 to being highest in married and cohabiting groups
17 for women and from 20 to 17 for men. of all ages.
591
• There is a strong association in all age groups • Sex is not considered the most important part of a
between length of relationship and frequency of relationship; a monogamous relationship is consid-
sex: a much lower frequency in longer relationships. ered more likely to lead to greater sexual satisfaction.
• Vaginal intercourse predominates. Seventy-five
per cent have experience of nonpenetrative sex
35.1.7 Physical Health
and 70% have some experience of oral sex. Any
experience of anal intercourse is reported by • Multiple sexual partnerships are significantly
14% of men and 13% of women. associated with smoking and increasing levels
• Those not married have a wider repertoire of of alcohol consumption.
sexual practice. Prevalence of oral, anal, and • Attendance at a clinic for sexually transmitted
nonpenetrative sex increases with increasing diseases (STDs) is strongly associated with the
numbers of partners. number of heterosexual partners and a history of
homosexual partnerships.
• The likelihood of termination of pregnancy
35.1.5 Sexual Diversity and
increases markedly with the numbers of hetero-
Homosexual Behaviour sexual partners.
• No sexual attraction or experience of any kind
is reported by 0.4% of men and 0.5% of women. 35.1.8 Perceived Risk
• Some form of homosexual experience is reported
by 6% of men and 3% of women. • The use of oral contraception declines steeply
• Lifetime experience of homosexual orientation with age; condom use is most prevalent in the
is higher in higher social classes. young; sterilization increases with age.
• Recent homosexual experience is strongly asso- • The message to use condoms to prevent the risks
ciated with region. Greater London has more of STD has been more acceptable than the mes-
than twice the proportion of men reporting sage to restrict numbers of partners.
homosexual experience and current practice • The perceived risk of HIV infection is higher
than anywhere else in Britain. among those reporting higher risk behaviours.
• Those who had a boarding-school education are
more likely to report any homosexual contact; 35.2 SEXUAL RESPONSE CYCLE
this has little or no effect on homosexual prac-
tice in later life. The normal sexual response cycle consists of desire;
• Exclusively homosexual behaviour is rare. The arousal, mediated by the parasympathetic nervous sys-
majority of those with homosexual experience tem; plateau; orgasm, mediated by the sympathetic and
have had sex with both men and women. Ninety central nervous system; and resolution (longer in males
per cent of men and 95% of women reporting and increases with age):
same-gender sexual partners in their lifetime
have also had an opposite-gender partner. 1. Sexual desire is determined by cognitive pro-
• Men reporting anal sex do so usually (60%) as cess, mood, neurophysiological mechanisms
both the receptive and insertive partner. (e.g. hormones), personal preferences, and cul-
• Highest levels of homosexual activity are tural practices. There is a spontaneous occur-
reported by 25–34 year olds, nearly a decade rence of sexual thoughts and awareness of an
later than heterosexual partnerships, consistent interest in initiating sexual activity.
with later age at first experience. 2. Sexual excitement is signified by erection in
men and vaginal lubrication in women. Genital
response is caused by vasocongestion in both
35.1.6 Sexual Attitudes
men and women. Peripheral responses include
• Acceptance of premarital sex is now nearly uni- raised blood pressure, altered heart rate, skin
versal, as is its practice. temperature, and skin colour changes.
• Disapproval of infidelity extends to all age 3. Plateau is the maintenance of sexual arousal state.
groups, the young being marginally more toler- 4. Orgasm is the peak of sexual arousal with explosive
ant than older people. discharge of physical, emotional, and psychological
Sexual Disorders 593
Orgasm • Sexual aversion: Sexual interaction is associ-

ated with strong negative feelings of sufficient
Plateau
intensity that sexual activity is avoided.
• Lack of sexual enjoyment: Sexual responses
and orgasm occur normally but there is a lack
Excitement Resolution of pleasure. This is much more common in
women.
• Failure of genital response: In men, this is pri-
Desire marily erectile dysfunction (ED). In women, it is
primarily due to vaginal dryness.
• Orgasmic dysfunction: Orgasm does not occur
or is delayed. It is more common in women than
FIGURE 35.1 Sexual response cycle. men.
• Premature ejaculation: This is the inability to
buildup. In men, there is an ejaculatory inevitabil- control ejaculation sufficiently for both partners
ity and ejaculation follows within 1–3 s. In woman, to enjoy the sex act.
orgasm usually include vaginal contractions, height- • Nonorganic vaginismus: This is occlusion of
ened feeling of excitement, or somatic sensations. the vaginal opening caused by spasm of the sur-
Small proportions of women produce fluid from the rounding muscles. Penile entry is either impos-
glandular structures along the urethra. The rhyth- sible or painful.
mic muscle contractions may lead to ejaculation of • Nonorganic dyspareunia: Pain during inter-
fluid observed in some women. course may occur in both sexes. The term
5. Resolution refers to the return to an unarousal is used only if an organic cause is not pres-
state. In men, there is a refractory period that ent and if there is no other primary sexual
may last from minutes to hours when the person dysfunction.
remains unresponsive to further sexual stimuli. • Excessive sexual drive: This usually occurs
This helps men to replenish the sperm number. In in men or women during late teenage or early
contrast, women are able to experience repeated adult years. If it is secondary to mental ill-
multiple orgasms in a short period (Figure 35.1). ness (e.g. mania), the underlying disorder is
coded.
35.3 SEXUAL DYSFUNCTION
35.3.2 DSM-5 Classification
With sexual dysfunctioning the individual is unable to
participate in a sexual relationship as he or she would 302.72 Erectile disorder
wish. Both psychological and somatic processes are 302.73 Female orgasmic disorder
usually involved in the causation of sexual dysfunction. 302.74 Delayed ejaculation
Women present more commonly with complaints about 302.75 Early ejaculation
the subjective quality of sexual experience; men present 302.73 Female orgasmic disorder
with a failure of specific sexual response. 302.72 Female sexual interest/arousal disorder
302.71 Male hypoactive sexual desire disorder
302.76 Genito-pelvic pain/penetration disorder
35.3.1 ICD-10 Classification (WHO, 1992)
Substance/medication-induced sexual dysfunction
ICD-10 categorizes Sexual dysfunction not caused by 302.80 Sexual dysfunction not elsewhere classified
organic disorder or disease under ‘Behavioural syn-
dromes associated with physiological disturbances and
35.3.3 Sensate-Focus Therapy
physical factors’, as follows:
Masters and Johnson (1970) described behavioural psy-
• Lack or loss of sexual desire: This is not sec- chotherapy involving a couple in graded assignments
ondary to other sexual difficulties. It does not that may be modified according to the particular problem
preclude sexual enjoyment or arousal, but makes presenting. The process is used extensively in the treat-
initiation of sexual activity less likely. ment of sexual disorders affecting both men and women.
It consists of a combination of specified homework tasks 35.4.3 Aetiology of Erectile Dysfunction

together with setting specific limits to the extent of sexual
contact allowed: The aetiology can be organic (in about 50%), psychologi-
cal, or a combination.
• Stage 1: Touching partner without genital con- 35.4.3.1 Organic Causes
tact for subject’s own pleasure.
• Stage 2: Touching partner without genital con- 35.4.3.1.1 Local Organic Causes
tact for subject’s and partner’s pleasure. • Peyronie’s disease: There is progressive fibro-
• Stage 3: Touching partner with genital contact, sis in the tunica albuginea and sometimes also
but intercourse not permitted. in the cavernosa, resulting in curvature of the
• Stage 4: Simultaneous touching of partner and penis on erection. The cause is unknown.
being touched by partner with genital contact, • Congenital deformities: Examples are hypospa-
but intercourse not permitted. dias and epispadias, or the absence of suspen-
• Stage 5: If both feel ready, the female invites the sory ligaments.
male to put his penis into her vagina. Female in the • Priapism: Although rare, priapism may result in
top position heightens female control and allows the impotence if not treated adequately within 24 h.
male to relax. No thrusting is allowed. Initial con-
tainment is brief, being lengthened with each session. 35.4.3.1.2 Endocrine Causes
• Stage 6: Vaginal containment with movement • Diabetes causes a combination of arteriopathy
is allowed. Different positions are encouraged. and neuropathy. Two-thirds of diabetic males
This does not inevitably lead to climax. The have ED. Of these, it is complete in two-thirds
couple should practice stopping before climax. and partial in the remaining third. A few also
Provided physical contact is pleasurable, orgasm complain of other difficulties such as premature
is not necessary. ejaculation. Onset is insidious, the course pro-
gressive with marked decline in sexual activity
and desire.
35.4 ERECTILE DYSFUNCTION • Nocturnal erections are androgen dependent.
35.4.1 Normal Physiology Studies are conflicting on the role of androgens
in ED. Effects are probably mediated through
Erection is a neurovascular phenomenon requiring an lowered sexual interest.
intact arterial supply and intact venous valves, allowing • Hyperprolactinaemia may be secondary to hypo-
cavernosal pressures to rise to those approaching systolic thalamic/pituitary disease. It occurs in those on
blood pressures. Vascular changes are brought about by phenothiazines, and sometimes in alcoholics.
the parasympathetic autonomic nervous system (S2, 3, 4) • Naltrexone (endorphin) therapy significantly
influenced by tactile stimuli and central limbic and cog- improves ED in males with an apparent non-
nitive mechanisms. Psychic erections are mediated by organic cause. Alteration in central opioid tone
thoracic sympathetic outflow, whereas reflex erections may be responsible.
result from sacral parasympathetic outflow. Androgens
also influence erection, particularly those occurring in 35.4.3.1.3 Neurological Causes
sleep, via the limbic system. • There may be peripheral or autonomic neuropa-
thy (e.g. in diabetes, alcoholism).
• Radical pelvic surgery may cause autonomic
35.4.2 Epidemiology of Erectile Dysfunction
neurological disruption.
• In the United Kingdom, Dunn et al. (1998) • There may be a spinal cord lesion (e.g. transec-
reported that men aged 18–75 showed a rate of tion, multiple sclerosis).
26% and 39% for current and lifetime preva-
lence of ED, respectively.
• ED comprises about 50% of male cases present- 35.4.3.1.4 Vascular Causes
ing to a psychosexual disorder service. • Arterial disease can interfere with the blood
• The incidence rises with age, from about 1.3% at supply to pelvic organs.
35 years to 55% at 75 years. • Venous valves may be incompetent.
35.4.3.2 Pharmacological Factors • Distaste for female genitalia

Alcohol has complex effects, including neuropathy and indi- • Placing the partner on a pedestal
rect effects on sex steroids and gonadotropins. Oestrogen • Nonsexual stress
levels are raised causing gynaecomastia and testicular atro- • Unsympathetic or angry partner
phy in advanced liver disease. Raised blood alcohol levels • Trying too hard
inhibit sexual responses through central inhibitory effects.
Psychosocial factors are also prominent in these patients. 35.4.4 Assessment of Erectile Dysfunction
Ganglion blockers (antihypertensives) interfere with
both sympathetic and parasympathetic postganglionic The assessment of ED includes the following:
transmission and cause both ED and ejaculatory failure.
Propranolol crosses the blood–brain barrier and may exert • A full history is needed, including the nature
its effect centrally. Alpha-adrenergic blockers are not asso- of the current ED and previous erectile capac-
ciated with erectile failure, but cause ejaculatory failure. ity, detailed sexual history, history of physical
trauma to genitalia or spine, medical and psy-
35.4.3.3 Psychological Factors chiatric histories, medication and substance use,
past investigation, and treatment.
The classical history of ED that is suggestive of a psycho-
• Assessment of the couple’s relationship is
logical cause comprises lack of sexual interest but contin-
essential. Difficulties such as hostility, lack of
ued morning erections.
communication, and unresponsive or unerotic
partner may be important.
35.4.3.3.1 Psychoanalytic Concepts
• Identify predisposing factors such as poor past
Sexual physiological changes result from the interplay sexual experience, religious or cultural beliefs,
between conscious and unconscious thoughts and feel- restrictive upbringing, unclear sexual prefer-
ings and interpersonal relationships. Anxiety and fear, ence, and previous sexual abuse.
whether conscious or unconscious, can interfere with • Identify precipitating factors such as family
vascular changes required for erection. Arousal phase pressures, partner menopause, and acute physi-
disorders of ED in men are common. Interference with cal or mental problems.
abandonment to erotic feelings can impair arousal in men • Identify maintaining factors such as relationship
and lead to difficulties with erection. problems and ongoing physical or mental illnesses.
Psychoanalytic formulations of ED recognize anxi- • Physical examination includes the assessment of
ety about the persecutory object and unresolved Oedipal testes or penis; laboratory investigations includ-
conflicts. Deep ambivalence about intimate involvement ing blood glucose and tests of renal and hepatic
leading to fear of sexual failure is common. function.
In younger men with primary ED, Oedipal conflicts • The use of International Index of Erectile Function
are said to predominate, whereas in secondary impotence, (IIEF) is helpful to assess severity of ED.
neurotic partnership conflicts at a pre-Oedipal level, and
narcissistic crises in middle age are said to predominate.
35.4.5 Diagnostic Criteria
35.4.3.3.2 Cognitive Concepts ICD-10 classifies ED under the F52.2 Failure of genital
ED is considered to be a sign of negative self-image response. ED is defined as erection insufficient for inter-
within a depressive view of the relationship and is linked course when intercourse is attempted. There are four
to abandonment fear. types of ED:
Subjects with psychogenic ED have a situational sex-
ual disorder in which sexual anxiety plays an important 1. Full erection occurs during the early stages of
role. Compared to those with organic impotence or to sexual activity but disappears or declines before
controls, they view themselves as more insecure and tend ejaculation.
to overidealize their partners and their mothers. 2. Erection does occur, but only at times when
Consideration should also be given to the following: intercourse is not being considered.
3. Partial erection, insufficient for intercourse,
• Fear of hurting the female occurs, but not full erection.
• Fear of pregnancy 4. No penile tumescence occurs at all.
35.4.5.1 DSM-5 Criteria: 302.72 NPTR is a noninvasive investigation but requires

Erectile Disorder overnight measurement in hospital.
35.4.5.1.1 General Criteria (Apply to • Intracorporeal injection of a prostaglandin E
Most Sexual Dysfunctions) inhibitor (papaverine or phentolamine) can be
diagnostic to establish the capacity for erection
• The sexual dysfunction must have been present
and hence reduce the likelihood of a primarily
for at least 6 months and occur for at least for
arterial cause.
75% of sexual activity.
• Duplex ultrasound of penile arteries is a radio-
• The sexual dysfunction causes clinically signifi-
logical investigation that measures blood flow.
cant distress or impairment.
This investigation provides an excellent assess-
• The sexual dysfunction is not attributable to a
ment of penile vasculature in response to an
primary nonsexual psychiatric disorder, by the
injection of a prostaglandin E inhibitor.
effects of a substance/medication, by an under-
• Arteriography is a highly specialized procedure
lying medical condition, and by partner violence
and only be performed when an arterial lesion has
or other significant stressors.
been found on Duplex ultrasound investigation.
• Subtype includes acquired or lifelong type.
• Dynamic cavernosometry, in which normal
• Specifier include situational versus generalized,
saline is infused into the corpus cavernosum,
partner’s factors, relationship factors, individual
may detect venous incompetence.
vulnerability, cultural/religious factors, and
medical factors.
35.4.7 Management of Erectile Dysfunction
35.4.5.1.2 Specific Criteria 35.4.7.1 Objectives
• ED is defined as marked difficulty in obtaining The primary goals of management include
and maintaining erection during sexual activity.
• There is marked decrease in erectile rigidity that 1. Identify and treat reversible causes of ED (e.g.
interferes with sexual activity. testosterone for hypogonadism, treatment of
hyperthyroidism)
2. Initiate lifestyle change (e.g. regular exercise)
35.4.6 Investigations and risk factor modification
3. Provide psychoeducation to patient and his partner
The doctor needs to consider the background history in
deciding the choice of investigations:
The British Society for Sexual Medicine classifies ED
treatment as follows:
• As metabolic syndrome is a risk factor for ED,
fasting lipids and glucose should be measured in
35.4.7.2 First-Line Treatment
most patients.
• Thyroid function tests and prolactin levels can rule 35.4.7.2.1 Phosphodiesterase Type 5
out hyperthyroidism and hyperprolactinaemia, (PDE 5) Inhibitors
respectively. Orally administered phosphodiesterase type 5 inhibitors
• If a man is suspected to have hypogonadism, that are licenced for treatment of ED include sildenafil,
serum testosterone should be measured between tadalafil, and vardenafil.
8:00 to 11:00 a.m.
• A penile–brachial artery pressure index of less 35.4.7.2.2 Pharmacodynamics
than 0.6 is indicative of arterial disease to the 1. The mechanism of erection of the penis involves
penis. Angiography may be necessary, espe- release of nitric oxide (NO) in the corpus cav-
cially in younger patients. ernosum during sexual stimulation. NO then
• Nocturnal penile tumescence and rigidity activates the enzyme guanylate cyclase, which
(NPTR) can be used to measure circumference results in increased levels of cyclic guanosine
change in REM sleep erections. This can help monophosphate (cGMP), producing smooth
distinguish organic from psychogenic; if the muscle relaxation in the corpus cavernosum that
cause is organic, erections at night are abolished. allows the blood inflow.
No release during
sexual stimulation
Corpus
cavernosum
Cell
membrane
Enzyme guanylate
cyclase activated
GTP Increased levels Smooth musical relaxation

GMP of cGMP in corpus cavernosum
Phosphodiesterase
type 5
Increased blood flow
Sildenafil
Maintain erection
FIGURE 35.2 Pharmacodynamics of sildenafil.
2. Sildenafil citrate is ingested orally prior to sex- 35.4.7.2.4 Side Effects

ual intercourse and enhances the effect of NO The side effects of these drugs include dyspepsia, vom-
by inhibiting phosphodiesterase type 5 (PDE5), iting, headache, flushing, dizziness, visual disturbances,
which is responsible for degradation of cGMP in raised intraocular pressure, and nasal congestion.
the corpus cavernosum. Hypersensitivity reactions (including rash), priapism, and
3. The increase in cGMP resulting in smooth mus- painful red eyes have also been reported.
cle relaxation and inflow of blood to the corpus
cavernosum (Figure 35.2). 35.4.7.2.5 Nonresponders to PDE5 Inhibitors
• Approximately 25% of ED patients do not
The drugs are contraindicated in patients:
respond to PED5 inhibitors.
• Re-counsel on proper use and reevaluate for
• Receiving nitrates
new risk factors.
• In whom vasodilation is inadvisable
• Treat concurrent hypogonadism by apomor-
• In whom sexual activity is inadvisable
phine or testosterone.
• With hypotension
• With a history of recent stroke
• With unstable angina 35.4.7.2.6 Apomorphine
• With myocardial infarction Apomorphine hydrochloride is administered sublingually
and stimulates dopamine receptors in the hypothalamus
and midbrain regions. Once the sexual stimulation has
35.4.7.2.3 Drug Interactions occurred, apomorphine hydrochloride enhances the
These drugs should not be administered with other phar- excitatory signal that is transmitted via the spinal cord
macological treatments for ED. They should be used with to stimulate the parasympathetic activity in the pelvic
caution in cardiovascular disease, anatomical deforma- region (Figure 35.3).
tion of the penis (e.g. angulation, cavernosal fibrosis, Although apomorphine is licenced for the treatment
Peyronie’s disease), and in those with a predisposition to of ED, it is more effective in patients with sexual desire
prolonged erection (e.g. in sickle-cell anaemia, multiple disorder rather than ED. Vasovagal symptoms (including
myeloma, or leukaemia). sweating and syncope) can occur infrequently.
1. Sexual stimulus
Cerebral cortex
imagination, visual, olfactory,
neural afferents
2. Paraventricular Apomorphine hydrochloride

nucleus in
hypothalamus
D1, D2
receptors Sexual desire
Spinal cord
Erection
FIGURE 35.3 Pharmacodynamics of apomorphine.
35.4.7.2.7 Psychotherapy • These devices provide a safe method of obtain-

Psychotherapy can be combined with medication. ing an erection adequate for penetration in up to
Cognitive behavioural methods report success rates of 90% of patients.
70% for erectile impotence. Couple therapy appears to • Many couples derive substantial benefit from
be superior to surrogate or individual therapies. Factors their use, but the disadvantages of a not fully
associated with successful outcome include the state of rigid erection, lack of spontaneity, decreased
the marriage, better pretreatment communication, bet- sensation, and delayed or absent ejaculation in
ter general sexual adjustment, female partner’s interest some limit their acceptability.
and enjoyment of sex, absence of psychiatric history in • Adverse effects include bruising, local pain, and
the female partner, and early engagement in homework feeling cold in penis.
assignments.
Sensate focus therapy may need to be combined with
35.4.7.3 Second-Line Treatment
other methods, such as improvement in communication
skills. Once erections are starting to occur, a form of 35.4.7.3.1 Intracavernosal Injection
‘paradoxical intent’ may be used, in which the couple is of Vasoactive Drugs
instructed to get rid of the erection as soon as it occurs, and Papaverine is commonly used to treat impotence. Self-
then to resume touching. The purpose is to demonstrate injected, it gives an erection lasting about an hour and
that erections do not need to be used as soon as they arise. may be used up to twice a week. Half those presenting
Psychodynamic therapists challenge disturbing fanta- to a sexual dysfunction clinic benefit from intracorpo-
sies and prevent their reenactment. The patient is offered real papaverine. Many decline the treatment because of
a psychotherapeutic ‘holding’ to counteract the unsafe the perception that injection is cumbersome and inter-
internal world. Gradually he becomes freed from his rupts sexual foreplay or because of objection to the use
sexually disempowering psychic reality to respond to the of needles. Intracorporeal pharmacotherapy provides
external reality of erotic stimulation. Behavioural inter- a useful treatment option in the management of impo-
ventions may also be incorporated into the treatment. tence but it is limited by the method of administration.
Complications include priapism that should be treated
35.4.7.2.8 Vacuum Suction Devices promptly by the withdrawal of 20–60 mL of blood and
• Vacuum tumescence constriction therapy is effi- injection of an α-adrenergic agent such as phenyleph-
cacious and useful in those with organic as well rine 1–5 mg, or metaraminol 2 mg. Fibrosis is associated
as psychogenic impotence. with prolonged use and rises in proportion to the total
numbers of injections given. Hematomas and bruising are 35.6 LACK OF SEXUAL DRIVE OR
relatively common but of little significance. SEXUAL ENJOYMENT
35.4.7.3.2 Intraurethral Alprostadil 35.6.1 Aetiology and Risk Factors
Alprostadil (prostaglandin E1) is administered by intra-
• Ageing
cavernosal injection or intraurethral application for the
• Anticonvulsant
management of ED (after exclusion of treatable medical
• Depression
causes); it is also used as a diagnostic test.
• Hyperprolactinaemia
35.4.7.3.3 Alpha-Adrenergic Blocking Agents • Multiple sclerosis
• Malignancy
Phenoxybenzamine or phentolamine may also be used to
• Relationship problem
give more prolonged erection.
• Restrictive upbringing on the issues of sex
35.4.7.4 Third-Line Treatment
35.4.7.4.1 Penile Prosthetic Implants 35.6.2 Diagnostic Criteria
Surgically implanted penile prostheses are inserted into
the corpus cavernosa. Three types are available: mal- 35.6.2.1 ICD-10 Criteria (WHO, 1992)
leable, constructed of silastic with a malleable metal core 35.6.2.1.1 F52.0 Lack or Loss of Sexual Desire
giving permanent rigidity; self-contained inflatable; and 1. Lack or loss of sexual desire as manifested by
multipart inflatable prostheses. diminution of seeking out sexual cues and of
The psychological outcome of penile prosthesis thinking about sex or of sexual fantasies.
implantation appears to be mediated by the nature of the 2. Lack of interest in initiating sexual activity
marital relationship. Follow-up of recipients of penile either with a partner or during masturbation.
implants 2.5 years following surgery found that those Sexual activities become less frequent com-
with organogenic impotence had no adverse sequelae, but pared to the norms or previous level.
some of those with psychogenic impotence had an exac-
erbation of preexisting relationship difficulties. Ideally 35.6.2.1.2 F52.10/F52.11 Sexual Aversion
couple therapy should be offered as well as mechanical and Lack of Sexual Enjoyment
treatments, especially in those with a psychogenic cause. 1. The sexual interaction with a partner produces
sufficient aversion or anxiety. As a result, sexual
35.4.7.4.2 Vascular Surgery
activity is avoided. It is also associated with
Correction of venous leak may be successful if a specific strong negative feelings and an inability to expe-
leak is detected. Arterial surgery is less successful. Large rience any pleasure.
vessel reconstruction for proximal arterial obstruction 2. Genital response (e.g. orgasm or ejaculation)
generally gives poor results, as most patients also have may occur but is not accompanied by any plea-
distal arterial disease. surable sensations or feelings of excitement.
35.5 FAILURE OF GENITAL 35.6.2.2 DSM-5 Criteria (APA, 2013)

RESPONSES FOR WOMEN 35.6.2.2.1 302.72 Female Sexual Interest/
Arousal Disorder
The ICD-10 defines that there is a failure of genital response,
experienced as failure of vaginal lubrication and inadequate 1. The general criteria (6-month duration, fre-
tumescence of the labia. There are three different types: quency of 75%, subtype, specifier, and func-
tional impairment) for sexual dysfunctions
1. General: lubrication fails in all relevant apply.
circumstances. 2. Absence or reduced frequency in at least three
2. Lubrication may occur initially but fails to persist of the following criteria: interest in sexual activ-
for long enough to allow comfortable penile entry. ity, sexual/erotic thoughts or fantasies, initia-
3. Situational: lubrication occurs only in some sit- tion of sexual activity, sexual excitement/sexual
uations (e.g. with one partner but not another, or pleasure, and sexual interest/arousal in response
during masturbation). to any internal or external sexual/erotic cues.
35.6.2.2.2 302.71 Male Hypoactive 35.7.3 Aetiology of Premature Ejaculation

Sexual Desire Disorder
35.7.3.1 Nonphysical Factors
1. The general criteria (6-month duration, fre-
• Anxiety promotes emission but inhibits orgasm and
quency of 75%, subtype, specifier, and functional
thus plays a crucial role in premature ejaculation.
impairment) for sexual dysfunctions apply.
• Primary premature ejaculation is always pres-
2. Persistently or recurrently deficient (or absent) sex-
ent. Secondary premature ejaculation develops
ual/erotic thoughts or fantasies and desire for sex-
after a period of satisfactory sexual functioning.
ual activity. The judgement of deficiency is made
• Those with primary premature ejaculation are
by the doctor taking into account of background
more impaired in sexual functioning and are
factors such as age or sociocultural background.
more anxious. Those with secondary premature
ejaculation are more likely to have coexisting
35.6.3 Treatment erectile disorder, a reduction in sex drive, and a
reduction in arousal.
1. Treat the underlying psychiatric or medical
• In psychological terms, whereas erectile disorder
disorders.
seems to belong to a depressive organization, pre-
2. Couple therapy, cognitive therapy, or counsel-
mature ejaculation belongs to a phobic one.
ling may be useful.
• A variety of psychological factors may interfere
3. Apomorphine hydrochloride may improve sex-
with the learning process, impairing the ability
ual desire.
to identify the point of impending ejaculation.
35.7 PREMATURE EJACULATION 35.7.3.2 Physical Factors

There are few physical causes. Drugs do not cause pre-
35.7.1 Normal Physiology mature ejaculation. It is possible that the autonomic con-
Orgasm, seminal emission, and ejaculation are physio- trol of ejaculation is very sensitive and therefore more
logically distinct processes and are potentially separable. difficult to control in some individuals.
Ejaculation is the forceful expulsion of semen from Those with premature ejaculation do not have penile
the urethra. If semen is released from the urethra with- hypersensitivity compared to controls.
out force, it is emission. Before orgasm the male becomes No differences in the pituitary gonadal system are
aware that ejaculation is imminent and it follows within found between those with erectile impotence, premature
1–3 s—‘ejaculatory inevitability’. Ejaculation and emis- ejaculation, and normal controls.
sion are mediated by the α-adrenergic sympathetic ner-
vous system. Androgens have a role, since the first sexual 35.7.4 Diagnostic Criteria
consequence of castration is the inability to ejaculate,
which is rapidly restored with androgen replacement. 35.7.4.1 ICD-10 Criteria: F52.4 (WHO, 1992)
In severe premature ejaculation, emission alone may Premature Ejaculation
occur with no ejaculatory component, minimal or absent There is an inability to delay ejaculation sufficiently to
orgasm, and a long refractory period. enjoy sexual intercourse. Ejaculation occurs very soon
In youth, males have a tendency to ejaculate quickly. after the beginning of intercourse (before or within 15 s).
This usually diminishes with increasing age because of Ejaculation may occur in the absence of sufficient erec-
increasing control with experience, an ability to recog- tion to make intercourse possible.
nize the approach of ejaculatory inevitability, the damp-
ening in responsiveness with age, and the lessening of 35.7.4.2 DSM-5 Criteria: 302.75
novelty that arises in a stable relationship. Early Ejaculation
The general criteria (6-month duration, frequency of
75%, subtype, specifier, and functional impairment) for
35.7.2 Epidemiology of Premature Ejaculation
sexual dysfunctions apply.
Studies with community samples indicate the prevalence Persistent or recurrent pattern of ejaculation occur-
of 36%–38% for premature ejaculation. Thirteen per cent ring during individual or partnered sexual activity (vagi-
of attendees at a sexual disorders clinic present primarily nal or nonvaginal) within approximately 1 min from the
with this problem. beginning.
35.7.5 Management of Premature Ejaculation 35.8.3.1 Physical Factors

Education in ejaculatory control using the ‘pause’ tech- • In primary complete anorgasmia in both sexes,
nique is the treatment of choice. During sensate-focus the bulbocavernosus reflex has been reported to
exercises, the male, when he predicts that he will ejacu- be absent in a proportion; this is strongly cor-
late shortly, asks his partner to stop, allow his arousal related with the failure of treatment.
level to subside slightly, and then return to being caressed, • Sometimes local pain, possibly secondary to
repeating the process again when arousal increases. muscle spasm, or in local viscera (uterus, rec-
If difficulty is experienced using this method, then tum), can create fear of orgasm.
the ‘squeeze technique’ is used. Just before ejaculation • Opiates appear to have a direct inhibitory effect,
becomes inevitable, stimulation is stopped and the tip of and antiserotonergic drugs inhibit orgasm.
the penis is grasped firmly for about 10 s, reducing the • Female anorgasmia has been reported in asso-
reflex ejaculatory response. ciation with tricyclic, MAOI, and SSRI antide-
At therapeutic doses, some antidepressants (e.g. fluoxetine) pressants and neuroleptic drugs.
have a beneficial effect in men with premature ejaculation.
35.8.3.2 Psychological Factors
The aetiology of anorgasmia is usually psychologi-
35.8 ANORGASMIA cal. Anxiety inhibits orgasm in women but can hasten
35.8.1 Normal Physiology emission in men. Sex may be viewed as bad, disgust-
ing, or threatening the need to remain in control at all
The final stage of sexual excitement may be orgasm. In times. There may be a fear of pregnancy or venereal
both sexes, if no orgasm occurs, there is a slow resolu- disease.
tion of physical and psychological changes associated
with sexual excitement. Apart from ejaculation for which
there is no female counterpart, the correlates of orgasm 35.8.4 Diagnostic Criteria
are similar in the sexes. Heart rate and blood pressure
increase, there is a sudden increase in skeletal muscle 35.8.4.1 ICD-10 Criteria: F52.3 (WHO, 1992)
activity involving almost all parts of the body. Rhythmic Orgasmic Dysfunction
muscle contractions in the male genital tract expel semen; There is orgasmic dysfunction that involves either
in females, there is transient rhythmical contraction of absence or delay of orgasm. There are three forms:
the uterus and vagina. Psychologically there is an instant
sense of relief; at its most extreme, there can be a virtual 1. Orgasm has never been experienced in any
loss of consciousness, and relaxation ensues. situation.
The exact mechanism of orgasm is not known. In 2. Orgasmic dysfunction occurs in all situations
addition to local spinal mechanisms, the central nervous and with any partner.
activity is also involved. EEG recordings during intense 3. Orgasmic dysfunction is situational.
orgasm show changes that have been likened to those
occurring during epileptic fits. For women: Orgasm may occur in certain situations (e.g.
when masturbating or with certain partners).
For men: Orgasm may only occur during sleep and
35.8.2 Epidemiology of Anorgasmia never during waking state.
The prevalence in community samples is around 5%–10%
for inhibited female orgasm, and 4%–10% for inhibited 35.8.4.2 DSM-5 Criteria (APA, 2013)
male orgasm. Among attendees at a sexual disorders The general criteria (6-month duration, frequency of
clinic, 5% of males and 7% of females present primarily 75%, subtype, specifier, and functional impairment) for
with orgasmic dysfunction. In females, the prevalence of sexual dysfunctions apply.
anorgasmia reduces with increasing age. 302.73 Female orgasmic disorder: Marked delay in
orgasm, marked infrequency, or absence of orgasm and
markedly reduced intensity of orgasmic sensation.
35.8.3 Aetiology of Anorgasmia
302.74 Delayed ejaculation: Marked delay in ejacula-
Little is known. tion or marked infrequency or absence of ejaculation.
35.8.5 Management of Anorgasmia 35.9.4 Diagnostic Criteria

Sociocultural expectations and deficits in skills and sex- 35.9.4.1 ICD-10 Criteria (WHO, 1992)
ual techniques are the two most important factors present 35.9.4.1.1 F52.5 Nonorganic Vaginismus
in most cases. Direct masturbation training is the treat-
There is a spasm of the perivaginal muscles preventing
ment of choice.
entry of penis into vagina or make intercourse uncom-
Treatment may take place in individual, couple, or
fortable. There are two types:
group settings. Tasks include relaxation, fantasizing, and
masturbation. Treatment is often successful, but the gen-
1. Primary vaginismus: the patient has never been
eralization of orgasm induced by masturbation to that
experienced normal response.
induced by intercourse does not always occur.
2. Secondary vaginismus: the patient develops
For men with delayed ejaculation, yohimbine may
vaginismus after a period of relatively normal
assist ejaculation. Side effects include anxiety, agitation,
response. The patient may either have a nor-
diarrhoea, and flu-like symptoms.
mal sexual response when vaginal entry is not
attempted or any attempt at sexual contact can
lead to generalized fear and efforts be made to
35.9 VAGINISMUS AND DYSPAREUNIA avoid vaginal entry.
35.9.1 Normal Physiology
When sexually aroused, the upper two-thirds of the 35.9.4.1.2 F52.6 Nonorganic Dyspareunia
vagina are lax and capacious, whereas the lower third is For women:
closely invested by the surrounding musculature of the
pelvic floor. The strongest of these muscles is the leva- 1. Pain is experienced at the entry of the vagina,
tor ani that forms a U-shaped sling around the posterior either throughout sexual intercourse or only
and lateral vaginal wall. Intense spasm in a nullipa- when deep thrusting of the penis occurs.
rous woman can virtually occlude the vagina. If these 2. This disorder is either a result of vaginismus or
muscles are too tense, vaginal entry is impaired and failure of lubrication.
painful—a condition known as vaginismus. A vicious
circle ensues; pain or anticipation of pain causes further For men:
muscle contraction thereby increasing the likelihood of
experiencing pain. 1. Pain or discomfort is experienced during sexual
response. The timing of pain and the exact loca-
tion should be carefully recorded.
35.9.2 Epidemiology of Vaginismus 2. The discomfort is not the result of local physical
Ten per cent of women presenting to a sexual disorders factors or organic causes.
clinic have a primary presentation of vaginismus.
35.9.4.1.3 DSM-5 Criteria: 302.76 Genito-Pelvic
Pain or Penetration Disorder (APA, 2013)
35.9.3 Aetiology of Vaginismus
The general criteria (6-month duration, frequency of
The majority of cases are primary. The problem was 75%, subtype, specifier, and functional impairment) for
evident at first attempt at intercourse, and usually the sexual dysfunctions apply.
woman has been reluctant to introduce anything to her Persistent or recurrent difficulties with one or more of
vagina previously. the following during vaginal intercourse or penetration:
Occasionally onset can be related to a traumatic epi-
sode such as a painful vaginal examination or rape. 1. Marked vulvovaginal or pelvic pain
Sometimes vaginismus results from ambivalence 2. Marked fear or anxiety about vulvovaginal or
about the relationship, or it may be secondary to reluc- pelvic pain
tance to assume the mature adult’s role. Irrational fears 3. Marked tensing or tightening of the pelvic floor
may also underlie the condition. muscles
35.9.5 Management of Vaginismus 35.10.2 Diagnostic Criteria

Emphasis is upon helping the woman to gain comfort 35.10.2.1 ICD-10 (WHO, 1992)
in exploring her own genitalia and inserting her finger. 35.10.2.1.1 F64.2 Gender Identity
Finger insertion may be all that is required, combined Disorder of Childhood
with sensate-focus techniques. Additional dilatation may
For girls:
be required using graded dilators. Initially carried out on
her own, the partner is included when her confidence has 1. The child shows persistent and intense distress
increased. about being a girl and has a stated desire to be a boy.
2. Either of the following must be present:
a. Persistent marked aversion to feminine
35.10 DISORDERS OF GENDER IDENTITY clothing and insistence on wearing stereo-
35.10.1 Classification typical masculine clothing, for example,
boys’ underwear and other accessories.
The ICD-10 classification codes Gender identity disor- b. Persistent rejection of female anatomical
ders under ‘Disorders of adult personality and behaviour’. structures, as evidenced an assertion that (i)
she wants to have a penis, (ii) refuse to urinate
35.10.1.1 Transsexualism in a sitting position, and (iii) assertion that she
There is the desire to live as a member of the opposite does not want to grow breasts or have menses.
sex, discomfort with anatomic sex, and a wish to change 3. The girl has not yet reached puberty.
body into that of the preferred sex. 4. Duration of symptoms: at least 6 months.
It must have been persistently present for 2 years; it
For boys, the symptoms are very similar to girls. The pre-
must not be a symptom of another mental disorder such
pubertal child shows persistent and intense distress about
as schizophrenia, or be associated with an intersex,
being a boy and has a desire to be a girl. The child prefers
genetic, or sex-chromosomal abnormality.
female activities and clothing and rejects male anatomi-
cal structure.
35.10.1.2 Dual-Role Transvestism
This includes the wearing of clothes of the opposite sex 35.10.2.1.2 F64.0 Transsexualism
for part of the time to enjoy the temporary experience
The individual desires to live and be accepted as a mem-
of membership of the opposite sex, without the desire
ber of the opposite sex, usually accompanied by the wish
for a more permanent sex change. No sexual excitement
to make his or her body as congruent as possible with the
accompanies this cross-dressing, distinguishing it from
preferred sex through surgery and hormonal treatment.
fetishistic transvestism.
Duration required for persistent transsexual identity for
at least 2 years.
35.10.1.3 Gender Identity Disorder of Childhood
This is persistent, intense distress about assigned sex, 35.10.2.1.3 DSM-5 (APA, 2013)
together with desire to be of the other sex, usually mani-
302.6 Gender dysphoria (in children): The proposed
fest during early childhood, and always before puberty. It
DSM-5 criteria are very similar to the ICD-10 criteria
is relatively uncommon. There is a profound disturbance
with additional characteristics such as a strong preference
of the sense of maleness or femaleness.
for playmates of the other gender and functional impair-
Between one- and two-thirds of boys with gender
ment. The DSM-5 further classifies this condition as with
identity disorder of childhood show homosexual orien-
or without a disorder of sex development.
tation during and after adolescence. However, very few
exhibit transsexualism in later life, although most adults 302.85 Gender dysphoria (in adolescents or adults):
with transsexualism report having had a gender identity Marked incongruence between one’s gender and primary
problem in childhood. Some girls retain male gender and/or secondary sex characteristics, a strong desire to
identification in adolescence and some go on to homo- be rid of one’s primary and/or secondary sex characteris-
sexual orientation. Most, however, do not. tics, a stronger desire to be of and be treated as the other
It is more common in boys than girls in clinic samples. gender, displaying the typical feelings and reactions of
the other gender, and functional impairment for at least Course and prognosis: Onset is often during adolescence.
6 months. The DSM-5 further classifies this condition as Most fetishism diminishes after developing a satisfying
with or without a disorder of sex development. heterosexual relationship. The prognosis is worse in sin-
gle man or those with forensic history related to fetishism.
35.10.3 Treatment of Disorders
of Gender Identity 35.11.1.2 ICD-10 F65.1 Fetishistic Transvestism/
DSM-5 302.3 Transvestic Disorder
Sex-reassignment treatment for transsexuals is a pro-
Definition: Fetishistic transvestism is the wearing of
cess of active rehabilitation into the new gender role,
clothes of the opposite sex to obtain sexual excitement.
the provision and monitoring of opposite-sex hormones,
More than a single item is worn, often an entire outfit.
and after a reasonable period of successful cross-gen-
It is clearly associated with sexual arousal; there is no
der living, sex-reassignment surgery is performed. The
wish to continue cross-dressing once orgasm occurs, dis-
majority of transsexuals do experience a successful
tinguishing this from dual-role transvestism.
outcome in terms of subjective well-being and personal
happiness. Epidemiology: Fetishistic transvestism is more common
in men and most patients are heterosexual.
35.11 SEXUAL DEVIATION Aetiology: Fetishistic transvestism is caused by classi-

cal conditioning between the clothes and sexual arousal
35.11.1 Classification during masturbation. It is associated with temporal lobe
dysfunction.
The ICD-10 classification codes sexual deviation as
Disorders of sexual preference under ‘Disorders of adult
personality and behaviour’. The proposed DSM-5 classi-
fies these disorders as paraphilic disorders. 35.11.1.3 F64.1 Dual-Role Transvestism
1. The individual wears clothes of the opposite sex
35.11.1.1 ICD-10 F 65.0 Fetishism/DSM-5 in order to experience temporarily membership
302.81 Fetishistic Disorder of the opposite sex. There is no sexual motiva-
tion for the cross-dressing.
Definition: Fetishism is the reliance on some nonliving
2. The individual has no desire for a permanent
object as a stimulus for sexual arousal and gratification. It
change of gender.
is often an extension of the human body such as clothing
3. Age of onset: puberty and the behaviour is con-
or footwear. It is often characterized by texture such as
cealed without guilt.
plastic, rubber, or leather.
Epidemiology: Fetishism is more common in men and The DSM-5 specify minimum 6 month duration and fur-
20% are homosexuals. ther classify transvestic disorder into three types:
Aetiology: Fetishism is caused by classical condi-
1. With fetishism (sexually aroused by fabrics,
tioning between an object and sexual arousal dur-
materials, or garments)
ing masturbation. It is associated with temporal lobe
2. With autogynephilia (sexually aroused by
dysfunction.
thought or image of self as a woman)
Clinical features: Fetishism is diagnosed only if the
fetish is the most important source of sexual stimula- Treatment: No specific treatment is required for dual-role
tion. Fantasies are common but do not amount to disor- transvestism but allowing the person to ventilate their
der unless they are so compelling that they interfere with feelings may help to reduce the frequency of cross-dress-
sexual intercourse and lead to distress. ing. For fetishistic transvestism, behavioural therapy
The DSM-5 criteria specify minimum 6 month duration focusing masturbatory reconditioning and response pre-
and further classify fetishistic disorder as body part, non- vention may reduce.
living part, in a controlled environment or in remission.
Prognosis: The condition becomes less severe as sexual
Treatment: Behavioural therapy focusing masturbatory drive declines. Some patients with dual-role transvestism
reconditioning and response prevention. convert to fetishistic transvestism.
35.11.1.4 ICD-10 F65.2 Exhibitionism/DSM-5 heterosexual. Fifty per cent of paedophiles consumed

302.4 Exhibitionistic Disorder alcohol at the time of the offence.
Definition: Exhibitionism is the recurrent or persistent Clinical features: Included in this diagnosis are those
tendency to expose the genitalia to strangers or people men who retain a preference for adult sex partners, but
(usually of the opposite sex) in public places. There is when frustrated in their efforts turn to children as substi-
usually sexual excitement at the time, often followed by tutes. Paedophiles may have previously committed exhi-
masturbation. The tendency may only manifest at times bitionism and voyeurism. They have low self-esteem and
of emotional stress or crisis, without such behaviour feel more accepted by young children. The ICD-10 speci-
between. fies that the individual is at least 16 years old and at least
Clinical features: It is almost entirely limited to hetero- 5 years older than the child victim.
sexual males, exhibiting to adult or adolescent females, The DSM-5 criteria specify minimum 6 month dura-
usually from a safe distance in a public place. For some, it tion and the individual is at least 18 years old and at least
is their only sexual outlet; for others, they may also con- 5 years older than the child victim. The DSM-5 further
tinue a normal sex life. A reaction in the victim heightens specifies if the patient is sexually attracted to boys, girls
the excitement in the perpetrator and the patient usu- or both. Other classification include:
ally has no intention to have sexual intercourse with the
victim. 1. Classic type—sexually attracted to prepubes-
The DSM-5 criteria specify minimum 6 month dura- cent children (Tanner stage 1)
tion and further classify exhibitionistic disorder into 2. Hebephilic type—sexually attracted to early
three types: pubescent children (Tanner stages 2–3)
3. Paedohebephilic type—sexually attracted to
1. Sexually attracted to exposing genitals to pubes- both groups of young people
cent or prepubescent persons younger than
15 years of age 35.11.1.7 ICD-10 F65.5 Sadomasochism/DSM-5
2. Sexually attracted to exposing genitals to physi- 302.83 Sexual Masochism Disorder
cally mature older than 15 years of age and 302.84 Sexual Sadism Disorder
3. Equally sexually attracted to exposing genitals Definition: Sadomasochism is the preference for sexual
to both age groups activity that involves the infliction of pain or humiliation.
It is diagnosed only if this is the most important source of
35.11.1.5 ICD-10 F65.3 Voyeurism/DSM-5 sexual stimulation. The sadomasochistic activity involves
302.82 Voyeuristic Disorder a recipient (masochist) and a provider (sadist).
Definition: Voyeurism is the persistent tendency to look The DSM-5 criteria specify minimum 6 month dura-
at people engaging in sexual behaviour or undressing. It tion and specify a subtype of asphyxiophilia (i.e. sexually
usually leads to sexual excitement and masturbation. The aroused by asphyxiation).
victim is usually unaware. The voyeur has no intention of
35.11.1.8 DSM-5 302.89 Frotteuristic Disorder
sexual involvement with the person observed.
Froutteuristic disorder involves recurrent and intense sexual
Clinical features: The voyeur is usually a man who is shy, arousal from touching or rubbing against a nonconsenting
socially awkward with girls, and has difficulty with nor- person, as manifested by fantasies, urges, or behaviours.
mal sexual expression.
35.11.2 Multiple Disorders of Sexual Preference
35.11.1.6 ICD-10 F65.4 Paedophilia/DSM-5
302.2 Paedophilic Disorder This is when more than one disorder of sexual preference
occurs in one person and none is predominant.
Definition: Paedophilia is the sexual preference for chil-
dren, usually prepubertal or pubertal. Some are attracted
to either one or both sexes. 35.11.3 Other Disorders of Sexual Preference
Epidemiology: The overall prevalence is less than This includes obscene telephone calls (telephone scatologia),
3%. More than 90% of paedophiles are men and it is sexual activity with animals (bestiality), the use of anoxia to
rare in women. Ninety-five per cent of paedophiles are heighten sexual pleasure (anoxophilia), and necrophilia.
35.12 SEXUAL ORIENTATION immediate gratification and little regard to the

consequences. Threats of violence are common.
Sexual disorientation alone is no longer classed as a dis- • Sexually inadequate rapist. These are shy,
order. ICD-10 allows for variations of sexual development timid, and insecure, lacking social skills. They
or orientation that are problematic for the individual: often plan a rape against an attractive or sexu-
ally threatening woman.
• Heterosexual • Sadistic rapist. These have a deep-rooted hatred
• Homosexual of women arising from early relationships. The
• Bisexual object of the rape is the infliction of humiliation
• Other, including prepubertal and suffering; intercourse may be trivial in com-
parison to humiliating acts and the serious inju-
Evidence suggestive of a genetic basis to sexual orienta- ries inflicted. The rape is often carefully planned;
tion is provided in twin studies with 52% MZ to 22% DZ precautions are taken to avoid detection.
concordance in homosexual males, and 48% MZ to 16% • Psychotic rapist. These constitute a very small
DZ concordance in female homosexuals. Hamer et al. proportion of rapists. The rape is often bizarre,
(1993) carried out a family pedigree study in which the violent, and terrifying for the victim.
distribution of homosexuality in the male relatives sug-
gested a sex-linked inheritance. They found convincing 35.13.1.2 Paedophilia
evidence in this family of a correlation between homo- Paedophilia is the sexual attraction and preference for part-
sexual orientation and the inheritance of polymorphous ners who are physically immature. Offenders are mostly
markers at the Xq28 region of the X chromosome. men. Some prefer child victims of the opposite sex, some of
the same sex. About 10% are bisexual in their preference.
35.13 ANTISOCIAL SEXUAL BEHAVIOUR Adolescent offenders have a better prognosis than
older offenders.
The acceptability of sexual behaviour is determined by The mentally immature offender with poor social skills
society and is incorporated into the law. What constitutes may prefer child sexual partners because they are the only
unacceptable behaviour varies largely between cultures people with whom the person can relate at a general level.
and within the same culture over time. The persistent middle-aged offender often has evi-
Antisocial sexual behaviours can be divided into two dence of personality problems with poor relationships
groups: and unstable work patterns. These offenders usually have
low rather than high sex drives. There is often an emo-
1. ‘Normal’ activities carried out inappropriately, tional bond between them and their child victims.
without consent or with the wrong age group Some paedophiles are more dangerous than those
2. Sexual activity that is morally perverse described earlier. This offender has evidence of a serious
personality disturbance affecting more aspects of his or
35.13.1 Specific Antisocial Sexual Behaviours her life than choice of sexual outlet.
Killing a child as part of a sexual offence is rare. It
35.13.1.1 Rape usually results from a state of panic or from a desire to
Rape is unlawful sexual intercourse with a person by dispose of the evidence.
force or against the person’s will. Rapists are not a homo-
geneous group. 35.13.1.3 Incest
Classification of Rapists (Trick and Tennant, 1981) Incest is generally forbidden across cultures. In law it is an
offence for a man to have sexual intercourse with a woman
• Situational stress rapist. Otherwise sexually he knows to be his daughter, granddaughter, mother, sis-
normal, these individuals commit rape when ter, or half-sister and for a woman over 16 to allow a man
under extreme situational stress. There is much whom she knows to be her son, father, grandfather, brother,
guilt and remorse afterwards. or half-brother to have sexual intercourse with her.
• Sociopathic rapist. These have poor social Sibling incest relationships are the most common, but
adjustment with criminality, a poor work record, father–daughter relationships are most commonly seen in
involve substance abuse, and have unstable court. They often reflect some breakdown in the marital
relationships. Rape is often impulsive, with relationship.
Incestuous families are characterized by alienation, • Transvestites may be charged with behaviour
disorganization, and disintegration. They are rarely likely to cause a breach of the peace if they
reported to the police. cross-dress in public.
Sibling incest is often the result of experimentation. • Frotteurism is the practice of rubbing the penis
It is more likely if there is a lack of parental control. against another person in a clandestine way in
Youngest sisters are the most vulnerable. a public place. It is liable to charges of either
indecent assault or offence against public order.
35.13.1.4 Indecent Exposure
Indecent exposure is an offence under the 1824 Vagrancy 35.13.2 Treatment of Antisocial
Act: ‘openly, lewdly and obscenely exposing his person
Sexual Behaviour
with intent to insult any female’ (British Government,
1824). It is one of the most common sexual offences. In a critical review of the literature, Marshall et al.
Exhibitionism, the exposing of genitals to the opposite (1991) concluded that some treatment programmes have
sex, is categorized into the following two main groups: been effective with paedophiles and exhibitionists but
not with rapists. In examining the value of the various
• Type I—Inhibited young men of relatively nor- treatment approaches, they concluded that comprehen-
mal personality and good character who struggle sive cognitive behavioural therapy (CBT) were most
against the impulse but find it irresistible. They likely to be effective with paedophiles and exhibition-
expose with a flaccid penis and do not masturbate. ists. There was also a clear value in the use of antiandro-
They expose to individuals, not seeking a particu- gens in those offenders who engage in excessively high
lar response. The frequency of exposure is often rates of sexual activity.
related to other sexual stresses and anxieties, such
as marital conflict or pregnancy in the spouse.
• Type II—Less inhibited, more sociopathic men. 35.14 SEX OFFENDER TREATMENT
Individuals expose with erect penis in a state PROGRAMME
of excitement and may masturbate. Pleasure is • The Sex Offender Treatment Programme (SOTP)
obtained and little guilt is shown. The person aims at increasing the responsibility and motiva-
is more likely to expose to a group of women tion of the sexual offender to change.
or girls and may return repeatedly to the same • SOTP involves anger management, CBT, rela-
place. The person seeks a response from the tionship skill training, relapse prevention, sex
victim, either shock or disgust. There are fewer education, social skill training, stress manage-
attempts to resist the urge to expose. The behav- ment, and thinking skill programme.
iour is associated with other psychosexual disor- • Sex offenders are encouraged to develop victim
ders and other types of offences. This may lead empathy by understanding the consequences of
on to more serious sexual offences. their actions and minimize denial.
Eighty per cent do not reoffend if they are charged with a • Behaviour treatments include aversion, sensiti-
first offence. The chances of reconviction rise dramatically zation, and biofeedback with penile plethysmog-
with the second offence. There is a small group of recidi- raphy that measures the penile blood flow with
vists who persist, but these tend to reduce in their forties. thoughts of illegal sexual practices.
It is generally a harmless nonviolent offence, except in a
minority who may progress to more violent offences. 35.15 PHARMACOLOGICAL TREATMENT
There is a good prognosis associated with being mar-
ried, good social relationships, and work record. • The aim of the pharmacological treatment is to
reduce sexual drives and prevent future sexual
35.13.1.5 Others offences especially in sex offenders who fail to
response to SOTP.
• Fetishism may come to the attention of the police if
articles used are stolen (e.g. women’s underwear). Baseline investigations:
• Sadomasochism may result in conviction for • Blood investigations: FBC, LFT, RFT, and glucose
assault if extreme injury results, even if both • Hormonal investigations: LH, FSH, and serum
parties consent. testosterone
• ECG and bone scan Medroxyprogesterone provides negative feed-

• Baseline weight and blood pressure backs to the production of FSH and LH and reduce
testosterone production. The range of dose is between
Subsequent monitoring after initiation of treatment: 100 and 600 mg/day (oral) or 100 and 700 mg/week
(intramuscular). Medroxyprogesterone is contraindi-
• Weight and blood pressure during each visit cated in patients suffering from chronic liver diseases
• Monthly testosterone for the first 4 months and and thromboembolic disorders. Side effects include anx-
every 6 months afterwards iety, depression, excessive sweating, fatigue, hyperten-
• LFT, RFT, and prolactin levels every 6 months sion, insomnia, oedema, and weight gain.
• Bone scan for patients being prescribed with Leuprolide is a GnRH analogue that controls the
leuprolide release of LH and FSH and subsequently reduces the
testosterone production. The intramuscular dose is
SSRI: Commonly prescribed with less side effects; no con- between 3.75 and 7.5 mg/month IM or 11.5 and 22.5
sent is required but consent is required for following drugs. mg every 3 months. Leuprolide is contraindicated in
Cyproterone is a testosterone antagonist. The range patients suffering from osteopenia. Side effects include
dose is between 100 and 500 mg/day (oral) or 100 and excessive sweating, hot flushes, myalgia, oedema, and
600 mg/week (intramuscular injection). Cyproterone is osteopenia.
contraindicated in patients with chronic liver diseases and Finasteride is a 5α-reductase inhibitor and reduces
thromboembolic diseases. Side effects include depres- sexual drive by inhibiting the peripheral conversion of
sion, fatigue, gynaecomastia (15%), and weight gain. testosterone to dihydrotestosterone.
CASC STATION ON EXHIBITIONISM

You are a registrar receiving forensic psychiatry training and are asked to carry out a risk assessment on a 30-year-
old man, Mr. C. He has an 8-year history of multiple instances of flashing his genitalia to women in the park. He
has been referred to your outpatient clinic by his GP. He appears very anxious about being caught by the police.
Tasks:
1. Perform an assessment of exhibitionism and related psychopathology.

2. Perform a risk assessment.
CASC Grid
Seek permission and opening statement: ‘Hello Mr. C, I am Dr. Lucas. I am trying to understand what has hap-
pened to you. I need to ask you some questions. They may involve sensitive issues. Is it alright with you? I was
informed that you have exposed your genitals to ladies recently. Can you tell me more about your behaviour?’
(A) Index Offence: (A1) Onset of the (A3) Details of (A4) Previous (A5) Impact of
Exposure Problem (A2) Precipitants the Exposure Exposure Exposure
‘How old were you ‘What is your view ‘Did you plan ‘How many times ‘How is your mood?’
when it started?’ on the causes of beforehand?’ did you flash your ‘Do you feel
‘Can you tell me your behaviour?’ ‘Where did you penis?’ depressed?’
what happened at (explore attribution do it?’ ‘How did you ‘Do you feel guilty
that time?’ by patient) ‘What kind of manage to escape?’ over your act?’
‘What kind of people ‘What makes you people (gender, ‘Have the police or ‘How do you feel
do you choose to do it?’ age) were you legal system ever about the victims?
expose to? May I ‘Do you have a looking for? Did been involved?’ Do you feel sorry for
know why? Do you strong urge or you know them?’ If yes, were you sent them?’ (explore
feel an emotional mounting tension?’ ‘Did you do it to prison? If so, victim empathy)
attachment to ‘Was it part of your alone?’ (look for how many times?
them?’ fantasy?’ organized crime)
(A) Index Offence: (A1) Onset of the (A3) Details of (A4) Previous (A5) Impact of
Exposure Problem (A2) Precipitants the Exposure Exposure Exposure
Explore emotional ‘Do you use ‘Did you carry If patient does not feel
congruence with pornography?’ If any weapon with guilty, then ask him,
victims so, what kind you?’ ‘Do you feel excited
(especially (related to ‘Was your penis by exposing your
children) as paedophilia) and hard or soft genitals? Are you
patient may be what form when you concerned about the
fixated at the (Internet or book) flashed to them?’ fact that more
child’s level of ‘What did you do women will face
emotional next after sexual assault?’
development and flashing your
relate better to the genitalia? Did
young victims. you masturbate?’
‘Can you control
your urge to
expose?’
‘What is the worst
thing that might
happen?’
(B4) Acute and
(B1) Other Chronic
(B) Risk Avenues for (B2) Other Sexual (B3) Assessment Dynamic Risk (B5) Self-harm and
Assessment Exhibitionism Offences of Denial Factors Other Harms
‘Are you working ‘Do you make ‘Do you Acute risk factors: ‘Have you ever
at present? What obscene phone acknowledge isolation, thought of harming
do you do for a calls? If so, do you that your unemployment, yourself?’
living?’ (e.g. masturbate at the behaviour, like chaotic life style, ‘How about harming
postman or same time?’ flashing your relapse of the others?’
teacher who may ‘Have you ever genitalia, is an depression, ‘Have you ever been
expose to children touched other offence?’ intoxicated by violent to others?’
in the ladies?’ ‘Do you think the substances ‘Have you ever
neighbourhood or ‘Have you ever tried problem is Chronic risk factors: damaged any
school) to impose sex on serious?’ low self-esteem, property?’
‘Do you have someone?’ ‘Do you feel that poor impulse
contact with ‘Were you ever sent you need control, substance
young children in to prison for other treatment at this abuse
your daily life?’ sexual offences? If moment?’
yes, after you were Assess levels of
released from denial and
prison, did you classify in the
reoffend again?’ following: (1)
absolute denial,
(2) denial of
seriousness, (3)
denial of the
need for
treatment.
(continued)
(C1) Other
(C) Other Psychosexual (C2) Delusions or (C3) Psychotic (C5) Drug and
Comorbidity Disorders? Abnormal Beliefs Experience (C4) Personality Substance Abuse
‘Do you have other ‘How do you ‘Do you hear ‘Can you describe ‘Have you consumed
sexual preferences compare yourself voices talking to your personality?’ any alcohol or drug
(explore with the others?’ you when nobody ‘How do you feel prior to exposing
paraphilia, (explore is around?’ about authoritative yourself?’
voyeurism)?’ grandiosity) ‘If yes, what do figures?’ (look for
‘What is your ‘Have you ever they say?’ (look resentment)
sexual thought that you for command Look for sociopathic
orientation?’ are entitled to hallucinations) trait (impulsiveness,
‘Do you have any expose yourself to Assess threat/ hatred, not caring
sexual problem the ladies? If so, control and safety of others),
such as erectile what is your overcome (TCO) and social
dysfunction?’ rationale?’ ‘Do you feel incompetence.
Threatened by Look for avoidant
the voices?’ personality.
‘Can you exercise
Control over the
voices?’
‘Are you
Overcome by the
voices?’
(D) Family,
Personal and (D4) Relationship
Psychosexual (D2) Psychosexual (D3) Learning and Marital (D5) Social
History (D1) Family Development Disability History Adequacy
‘Can you tell me ‘How old were you ‘What is your If the patient is ‘Can you tell me
about your when you first highest level of single, ask, ‘How is about your
family?’ learn about sex?’ education?’ your dating relationship with
‘How do you feel ‘Have you ever ‘Have you experience?’ other people?’
about your encountered encountered If patient is married, ‘Can you comment on
parents? Did you difficulty with learning ask, ‘How’s your your self-esteem?’
separate from intimacy?’ difficulty? Were relationship with
them when you ‘Do you feel that you in a special your spouse or
were young? Do you need to school? Do you partner?’
you feel angry suppress sexual have any ‘Can you tell me
about them?’ feelings?’ difficulty to more about your
‘How did they treat understand the sexual life with
you? Have you other people?’ her?’
ever experienced ‘Does she know about
any abuse?’ your behaviour?’
(sexual, physical,
and emotional)
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36 Sleep Disorders
36.1 CLASSIFICATION 36.2.1.3 Clinical Features

The ICD-10 classification of nonorganic sleep disor- • The patient has history of being a ‘light’ sleeper
ders is with easily disturbed sleep.
F51.0 Nonorganic insomnia • The patient usually concerns about sleep dura-
F51.1 Nonorganic hypersomnia tion and quality. This often leads to increased
F51.2 Nonorganic disorder of the sleep–wake schedule cognitive, physiological, and emotional arousal
F51.3 Sleepwalking prior to sleep. Their over-concerns and poor
F51.4 Sleep terrors sleep often form a viscous cycle.
F51.5 Nightmares • The main result of insomnia is daytime tired-
ness or napping, low mood, decreased attention
The DSM-5 classifies sleep–wake disorders as follows: and concentration, low energy level, and fatigue.
780.52 Insomnia disorder
780.54 Hypersomnolence disorders
347.00 Narcolepsy/hypocretin deficiency 36.2.1.4 Diagnostic Criteria
327.23 Obstructive sleep apnoea hypopnoea syndrome 36.2.1.4.1 Nonorganic Insomnia (ICD-10)
Central sleep apnoea • The sleep disturbance occurs nearly every day
Sleep-related hypoventilation for at least 1 month and causes marked distress
Circadian rhythm sleep-wake disorder or interference with personal functioning in
307.46 Sleepwalking disorder daily living.
307.46 Sleep terror disorder • A complaint of excessive daytime sleepiness or
307.47 Nightmare disorder prolonged transition to the fully aroused state
327.42 Rapid eye movement sleep behaviour disorder upon awakening (sleep drunkenness).
333.94 Restless legs syndrome • Absence of narcolepsy or sleep apnoea (noctur-
Substance-induced sleep disorder nal breath cessation).
• Absence of any organic factor, psychoactive
36.2 DYSSOMNIAS substance use disorder, or effect of medication.
36.2.1 Insomnia 36.2.1.4.2 Insomnia Disorder (DSM-5)

Insomnia is the disturbance of normal sleep pattern and • The sleep difficulty occurs at least three nights
characterized by an insufficient quantity or quality of per week and is present for at least 3 months.
sleep. The sleep difficulty occurs despite adequate
opportunity for sleep.
36.2.1.1 Epidemiology • Specific insomnia symptoms such as difficulty
• The prevalence of insomnia is between 1% and initiating and maintaining sleep, early-morning
10% in general population. awakening with inability to return to sleep, and
• The estimated 1-year prevalence in adults ranges nonrestorative sleep.
from 15% to over 40%. • Significant distress and impairments such as
• Prevalence is particularly high in the elderly (up fatigue, cognitive impairment, mood distur-
to 25%). bance, behavioural problems, and impaired
• Gender ratio: F > M. functioning.
• For children, insomnia can be manifested as
36.2.1.2 Aetiology prolonged resistance to going to bed and/or bed-
Table 36.1 gives the main causes of insomnia. time struggles.
613
schedule and regular daytime exercise; limit

TABLE 36.1 time in bed; and remove clock from bedroom to
Causes of Insomnia avoid excessive monitoring.
Environmental Poor Sleep Hygiene 2. Sleep restriction therapy: the patient should keep
a sleep log that records the total sleep duration,
Change in time zone
bedtime, and wake-up time. The time allowed
Change in sleeping habits
Shiftwork
in bed is reduced to the total sleep duration and
Physiological Natural short sleeper
the patient is advised to increase the time in bed
Pregnancy by 15 min on a weekly basis by adjusting the
Middle age bedtime.
Life stress Bereavement 3. Stimulus control therapy: arise at the same
Exams time every morning, avoid daytime napping,
House move, etc. go to bed only when sleepy, use the bed only
Psychiatric Acute anxiety for sleep, leave the bed when unable to sleep,
Depression and reduce lighting and level of noise in
Mania bedroom.
Organic brain syndrome 4. Cognitive therapy aims at correcting cognitive
Physical Pain distortions (e.g. being catastrophic after insom-
Cardiorespiratory distress nia) and unrealistic expectations (e.g. must have
Arthritis
10 h uninterrupted sleep).
Nocturia
5. Behaviour therapy: progressive muscle relax-
GI disorders
Thyrotoxicosis
ation techniques for any associated anxiety.
Pharmacological Caffeine
36.2.1.6.2 Pharmacological Treatment
Alcohol
Stimulants 1. The NICE guidelines recommend that doctors
Chronic hypnotic use should consider offering nonpharmacological
Parasomnias Sleep apnoea treatments first. If they think that pharma-
Sleep myoclonus cological treatment is the appropriate way to
Primary sleep disorders treat severe insomnia that is interfering with
normal functioning, they should prescribe
Source: Reproduced from Puri, B.K. et al., Textbook of
one hypnotic agent for only short periods of
Psychiatry, 2nd edn., Churchill Livingstone,
time and strictly according to the licence for
Edinburgh, Scotland, 2002. With permission.
the drug.
2. Doctors are advised to consider nonbenzodiaz-
epine hypnotic agents such as
36.2.1.5 Differential Diagnosis a. Antihistamines: hydroxyzine.
Important disorders that may cause insomnia, and that b. Melatonin receptor agonists: agomelatine
should therefore be excluded, include and ramelton.
c. Sedating antidepressants: amitriptyline,
• Depressive disorders mirtazapine, and trazodone.
• Mania d. Antipsychotics: low-dose quetiapine.
• Anxiety disorders e. Melatonin: the Maudsley guidelines recom-
• Substance misuse and dependence mend the use of melatonin for the treatment
• Organic disorders (see Table 36.1) of insomnia in children and adolescents.
3. Benzodiazepines are only indicated for short-
36.2.1.6 Management term use (<4 weeks). Benzodiazepine hypnotic
36.2.1.6.1 Nonpharmacological Treatment agents include
1. Sleep hygiene education: a moderate intake of a. Benzodiazepines: temazepam, oxazepam,
easily digested warm food; a comfortable bed; lorazepam, and diazepam
avoid caffeine, nicotine, alcohol, and excessive b. Benzodiazepine receptor agonists: zaleplon,
fluid intake in the evening; keep a regular sleep zolpidem, and zopiclone
Sleep Disorders 615
4. Treatment should only be changed from one of • No symptoms of narcolepsy and evidence for
these hypnotics to another if side effects occur sleep apnoea.
that are directly related to the medicine. If treat- • No other causative factors.
ment with one of the benzodiazepines or ben-
zodiazepine receptor agonist does not work, the 36.2.2.4.2 Hypersomnolence Disorder (DSM-5)
doctor should not prescribe one of the others. • Frequency and duration: hypersomnolence
occurs at least three times per week and for at
36.2.1.7 Course and Prognosis least 3 months. The patient has a main sleep
• Insomnia typically occurs in young or middle period lasting at least 7 h per day.
adulthood. Chronic insomnia may last through • Symptoms of excessive sleepiness such as recur-
to old age. rent periods of sleep and naps within the same
• Previous insomnia is the most significant pre- day, a prolonged and nonrestorative main sleep
dictor for future insomnia. episode (>9 h), and sleep inertia with difficulty
• 50%–75% of patients have insomnia that lasts in waking up.
for more than 1 year. • The hypersomnolence causes significant impair-
• Insomnia caused by life event or stressor usually ments in functioning and is not accounted for by
has a limited course to a period of less than 1 year. another sleep disorder.
• Specify if:
36.2.2 Hypersomnia • With mental disorder/medical condition
• Acute/subacute/persistent
36.2.2.1 Epidemiology • Mild/moderate/severe
• Daytime drowsiness occurs in 0.3%–4% of the
population. 36.2.2.5 Differential Diagnosis
• Incidence over 5-year period: 8%. Important differential diagnoses include
• Lifetime prevalence: 15%.
• Narcolepsy
36.2.2.2 Aetiology • Sleep apnoea
The common causes of hypersomnia are • Organic disorders
• Fatigue states
• Family history of hypersomnia and association • Kleine–Levin syndrome (M/F = 3:1, begins in
with autonomic dysfunction adolescence and resolves by middle age, recur-
• As an early symptom of depressive disorder rent sleepiness, indiscriminate hypersexuality,
• Unknown cause: idiopathic compulsive overeating, and weight gain)
36.2.2.3 Clinical Features 36.2.2.6 Assessment and Investigations
• Long duration of major sleep episode (8–12 h) • Epworth Sleepiness Scale: cutoff score for men
with rapid onset of sleep and good sleep >11 and cutoff score for women >9.
efficiency • Multiple Sleep Latency Test (MSLT) involves
• Excessive daytime sleepiness and unrefreshing asking the patient to nap for 20 min and then
naps during normal waking hours causing a dis- being awaken. EEG, heart rates, and other
turbance of social or occupational functioning physiological parameters are recorded. The
• Sleep drunkenness with prolonged impairment MSLT measures sleep latency, which is the time
of alertness at sleep–wake transition and results elapsed from the start of the nap to the first signs
in difficulty waking in the morning of sleep (sleep latency = 0–5 min [severe sleepi-
ness], 5–10 min [troublesome sleepiness],
36.2.2.4 Diagnostic Criteria 10–15 min [manageable sleepiness], 15–20 min
36.2.2.4.1 Nonorganic Hypersomnia (ICD-10) [mild sleepiness]). The naps are repeated for four
• Excessive daytime sleepiness, sleep attacks, and to five times.
sleep drunkenness. • Polysomnography is an overnight procedure
• Frequency and duration: sleep disturbance that records the cardiac rhythm (ECG), brain
occurs nearly every day for at least 1 month. activity (EEG), muscular activity (EMG), eye
movement (EOG), and oxygen saturation (pulse • Sleep attacks: two to five episodes of sleep
oximetry) during sleep. Polysomnography pro- attacks per day. Sleep attacks are irresistible and
vides information on sleep onset latency, the last for 10–20 min with dreaming. The attacks
proportion of REM and non-REM sleep. Such cause functional impairments.
information allows specialists to establish the • Cataplexy (70%): sudden loss of muscle tone
diagnosis of breathing-related sleep disor- with consciousness lasting for a few seconds
ders, narcolepsy, and periodic limb movement to minutes. The hypotonia causes spontane-
disorder. ous grimaces and jaw opening with tongue
thrusting. Eye and respiratory muscles are
36.2.2.7 Management spared. Cataplexy can be precipitated by
• Treat any identified underlying cause. laughter. Cataplexy increases the risk of fall
• In idiopathic hypersomnia, stimulants are occa- and accident.
sionally used. • Hypnagogic hallucinations (20%–40%): usu-
• Methylphenidate has potential for misuse ally visual hallucinations or dreamlike imagery.
and associated with excessive sweating and Hypnopompic hallucinations are less common
insomnia. than hypnagogic hallucinations.
• Modafinil is a stimulant with less potential for • Sleep paralysis: mainly affecting ability to
misuse and less peripheral sympathomimetic speak and movement of four limbs. Diaphragm
effects. is spared in sleep paralysis.
• Common psychiatric comorbidity: depression,
36.2.2.8 Course and Prognosis anxiety, substance misuse, and parasomnia.
• The onset is usually gradual.
• The course is that of the underlying disorder and 36.2.3.3.1 DSM-5 Criteria (APA, 2013)
often chronic but stable. • Hypersomnia and recurrent sleep attacks have
• Idiopathic hypersomnia typically begins been occurring at least three times per week
between the age of 15 and 30 years and may over the last 3 months.
improve with age. • Cataplexy occurs at least a few times per month.
• Evidence of hypocretin deficiency, as measured
using cerebrospinal fluid hypocretin-1 immu-
36.2.3 Narcolepsy (Hypocretin Deficiency)
noreactivity measurements (<1/3 of values
36.2.3.1 Epidemiology obtained in healthy subjects tested during the
• Prevalence: 3–6/100,000. same assay, or ≤110 pg/mL). Low cerebrospinal
• Gender ratio: M = F. fluid hypocretin-1 must not be observed in the
context of acute brain injury, inflammation, or
36.2.3.2 Aetiology infection.
• Genetics: The genotype HLA-DQB1*0602 is • Nocturnal sleep polysomnography showing
present in nearly 99% of patients suffering from rapid eye movement (REM) sleep latency less
narcolepsy with cataplexy and 40% of patients than or equal to 15 min.
suffering from narcolepsy without cataplexy. • MSLT showing a mean sleep latency less than
Around 5%–15% of first degree relatives of pro- or equal to 8 min and two or more sleep onset
bands develop narcolepsy. REM periods.
• Loss of hypocretin cells in hypothalamus.
Hypocretin (aka orexin) is a neurotransmitter Investigation: The diagnosis is confirmed with overnight
regulating arousal and wakefulness. polysomnography.
36.2.3.3 Clinical Features 36.2.3.4 Management

• Onset: first symptom is almost always daytime 36.2.3.4.1 Nonpharmacological Treatment
sleepiness and occurs during adolescence. • Lifestyle adjustment
• Hypersomnia: sleepiness in between sleep attacks. • Scheduled napping
Sleep Disorders 617
36.2.3.4.2 Pharmacological Treatment Investigation: The diagnosis is confirmed with overnight

• Stimulants such as methylphenidate and modafinil polysomnography.
can reduce daytime sleepiness.
• REM suppressants such as SSRIs can treat hyp- 36.3.1.4 Management
nagogic hallucinations, cataplexy, and sleep • Psychiatrists or GPs should avoid prescribing
paralysis. benzodiazepines or sedative drugs.
• Refer patient to a weight management programme
36.2.3.5 Course to lose weight.
• Hypersomnia and cataplexy have stable course • Refer patient to see a sleep specialist, respira-
over time. tory specialist, or otolaryngologist for nasal
continuous positive airway pressure (CPAP),
nasal surgery, and uvulopalatoplasty.
36.3 BREATHING-RELATED SLEEP DISORDER
• Advise patient not to sleep supine.
36.3.1 Obstructive Sleep Apnoea • Advise patient to avoid alcohol.
• Obstructive sleep apnoea (OSA) is the most 36.3.2 Central Sleep Apnoea
common breathing-related sleep disorder. 36.3.2.1 Epidemiology
• Prevalence: 1%–10% of adult population.
• Prevalence: 0.1%–1% of adult population
• Higher prevalence of OSA is found in older
people. 36.3.2.2 Risk Factors
36.3.1.2 Risk Factors • Old age
• Cardiac diseases: congestive heart failure
• Obesity
• Neurological diseases: Parkinson’s disease, stroke,
• Increase in neck size (>43 cm in men and >41 cm
brainstem lesion, and encephalitis
in women)
• Skeletal diseases: cervical spine degeneration
• Structural abnormality such as adenotonsillar
enlargement and nasal airway obstruction
36.3.2.2.1 DSM-5 Criteria (APA, 2013)
The following criteria must be present:
36.3.1.2.1 DSM-5 Criteria (APA, 2013)
The following criteria must be present: • At least five central apnoeas per hour of sleep
during polysomnography
• Nocturnal breathing disturbances (e.g. snoring, • No other sleep disorders
breathing pauses)
• Daytime sleepiness and fatigue 36.3.2.3 Other Clinical Features
• At least five obstructive apnoeas or hypopnoeas • There is no evidence of airway obstruction
per hour of sleep during polysomnography • Less likely to be overweight
• No other sleep disorders
Investigation: The diagnosis is confirmed with overnight
36.3.1.3 Other Clinical Features polysomnography.
• Daytime naps are unrefreshing.
• Patients may complain of dull headache upon 36.3.2.4 Management
awakening, low mood, poor concentration, and • Treat underlying medical conditions.
memory disturbance. • Psychiatrists or GPs should avoid prescribing
• For children, they usually present with irritabil- benzodiazepines or sedative drugs.
ity, behavioural problems, and chest retractions • Refer to a respiratory specialist for CPAP or
during sleep. The number of apnoeas/hypop- bilevel positive airway pressure (BiPAP).
noeas supportive is expected to be lower (<5). • Advise patient to avoid alcohol.
36.3.3 Disorders of the Sleep–Wake Cycle • Irregular or non-24-h sleep–wake type (entrain-

ment failure): if entrainment failure is second-
Disorders of the sleep–wake cycle are characterized by ary to a lack of sleep–wake cues in a modality
sleep occurring out of phase with environmental and such as vision (because of poor vision, say), then
social cues (zeitgebers). cues from other modalities and a careful routine
36.3.3.1 Epidemiology may be employed.
• Shift work type: advise patient to take a nap
• The prevalence of delayed sleep phase type is
before work, schedule a nap on break, avoid light
between 0.1% and 4% in the general population.
during the day, and receive bright light at night.
• The prevalence of shift work type can be as high
as 50% among night shift workers.
36.3.3.2 Aetiology • Delayed sleep phase: onset is between adoles-
• Genetics: 40% of delayed sleep phase type have cence and early adulthood. The course may last
a family history. for years if without treatment.
• Shift work type: reversal of pattern in 2 weeks
36.3.3.3 Diagnostic Criteria after termination of shift work.
The circadian rhythm sleep–wake disorder (DSM-5
criteria): 36.3.4 Restless Leg Syndrome
• A persistent or recurrent pattern of sleep disrup- 36.3.4.1 Epidemiology
tion leading to excessive sleepiness, insomnia,
• The prevalence is between 2% and 10% of the
or both. This is caused by a change in the circa-
general population and up to 30% in people with
dian system, leading to a misalignment between
chronic medical illness.
the endogenous circadian rhythm and the sleep–
• The prevalence increases with age.
wake schedule required by the patient.
• Gender ratio: M = F.
• The sleep disturbance causes clinically signifi-
cant distress or impairment in functioning.
36.3.4.2 Aetiology
• There are five subtypes:
1. Advanced sleep phase: advanced sleep onset Restless leg syndrome is associated with the following
and awakening times as compared to the norms medical conditions:
2. Delayed sleep phase: delayed sleep onset and
awakening times as compared to the norms • Autoimmune thyroid disorders
3. Irregular sleep–wake type: a temporally • Iron deficiency or microcytic anaemia
disorganized and various sleep and wake • Diabetes mellitus
patterns in 24 h • Pregnancy
4. Non-24-h sleep–wake type: a pattern of • Renal failure
sleep and wake cycles that is not synchro- • Rheumatoid arthritis
nized to the 24-h environment, with a
delayed sleep phase 36.3.4.3 DSM-5 Criteria (APA, 2013)
5. Shift work type: insomnia during the major The DSM-5 criteria have two components:
sleep period and/or excessive sleepiness during
the major awake period as a result of shift work • Compulsory criteria include an urge to move the
legs as a result of unpleasant sensations, worsen-
36.3.3.4 Management ing of symptoms during periods of rest and at
• Treat any primary disorder. night, and no relief of symptoms by movement.
• Advanced sleep phase: bright light therapy in • Sequelae include clinical sleep disturbance, cog-
the morning. nitive impairments, daytime sleepiness, fatigue,
• Delayed sleep phase: advancing sleep in small hyperactivity, impulsivity, mood disturbance,
increments may help in cases of delayed sleep and impaired in functioning.
phase syndrome; offer bright light and melato- • The minimum duration of restless leg syndrome
nin in the morning. is 3 months.
Sleep Disorders 619
36.3.4.4 Other Clinical Features 36.4 NON-REM PARASOMNIAS

• Patients have a frequent desire to move arms and
legs to relieve uncomfortable sensations such as
36.4.1 Somnambulism (Sleepwalking)
burning, crawling, and tingling sensations. In this disorder, there occurs a state of altered conscious-
• Uncomfortable sensations and desires to move ness in which, while asleep, the individual arises and walks.
are getting worse in the evening.
• Restless leg syndrome is associated with delayed 36.4.1.1 Epidemiology
sleep phase, nocturnal awakenings, and daytime • Sleepwalking occurs at least once in 15% of
fatigue. children aged 5–12 years and in 0.5% of adults.
• Women are more affected than men (sex ratio
36.3.4.5 Management [F/M] = 4:3).
36.3.4.5.1 Nonpharmacological Treatment
36.4.1.2 Aetiology and Risk Factors
• Apply hot compresses to legs
• Somnambulism is familial in up to 20% of cases.
• Encourage sleep hygiene
• If both parents suffer from somnambulism, the
• Reduce alcohol, caffeine, and nicotine consumption
risk for somnambulism is 60%.
36.3.4.5.2 Pharmacological Treatment • There are no characteristic EEG changes.
• Sleep laboratory studies do not lend credence to
• Treat any primary disorder, for example, iron
the view that somnambulism represents the act-
deficiency.
ing out of dreams.
• Psychopharmacological treatment is indicated
• Risk factors include alcohol misuse, benzodiaz-
if symptoms impairing sleep for more than
epine use, fever, and sleep deprivation.
two nights per week. For example, benzodi-
azepine such as clonazepam, anticonvulsants 36.4.1.3 ICD-10 Criteria
such as gabapentin, and dopamine agonists • Repeated (two or more) episodes of arising from
such as levodopa. bed during the first third of nocturnal sleep and
walking for several minutes to 30 min.
36.3.5 Parasomnias • During the sleepwalking, the person exhibits a
blank staring face, unresponsive to others, and
Parasomnias are phenomena occurring as part of or can be awaken only with considerable difficulty.
alongside sleep; they are shown in Table 36.2. • The person has amnesia after sleepwalking.
• No impairment of mental activity or behaviour
after awakening.
TABLE 36.2
• No evidence of organic mental disorder.
Parasomnias
Sleepwalking (somnambulism) 36.4.1.4 DSM-5 Criteria (APA, 2013)
Night terrors (pavor nocturnus) • Sleepwalking is listed under non-rapid eye
Nightmares or dream anxiety movement sleep arousal disorder. The criteria
Bruxism (teeth grinding) are similar to ICD-10 with emphasis on impair-
Nocturnal enuresis ment in functioning.
Headbanging (jactatio capitis nocturna)
Sleep paralysis 36.4.1.5 Other Clinical Features
Nocturnal painful erections • Majority of episodes begin with first few hours
Cluster headache of sleep, during NREM stage 3 or 4 sleep.
Physical symptomatology occurring at night,
• The sufferer is difficult to awaken during an epi-
e.g. paroxysmal nocturnal dyspnoea, sleep epilepsy
sode and may suffer injury if sleeping in an unfa-
Sleep myoclonus
miliar setting.
Source: Reproduced from Puri, B.K. et al., Textbook of • Somnambulism in adults may be associated with
Psychiatry, 2nd edn., Churchill Livingstone, anxiety disorder, depressive disorder, and per-
Edinburgh, Scotland. With permission. sonality disorder. Somnambulism in children is
not associated with other psychiatric disorders.
• Although complex behaviours, including 36.4.2.4 DSM-5 Criteria (APA, 2013)

attempted homicide, have been described as • Sleep terrors are listed under non-rapid eye
occurring during somnambulism, in general, movement sleep arousal disorder. The criteria
this is not common. are similar to ICD-10 with emphasis on impair-
ment in functioning.
Important differential diagnoses include 36.4.2.5 Other Clinical Features
• Psychomotor epilepsy during sleep • Sleep terrors occur during sleep stages 3–4 and
• Fugue states therefore usually 1–2 h after sleep starts.
• Sleep drunkenness • Enuresis may occur during an episode.
• In children, there is no increase in rate of psy-
36.4.1.7 Management chopathology of mental disorders.
• The person’s nighttime surroundings should be • In adults, sleep terrors are associated with gen-
made safe in order to reduce the risk of injury eralized anxiety disorder, post-traumatic stress
during episodes. disorder, and personality disorders.
• Reassurance, anxiety-reduction techniques, and
offering psychoeducation to patient and family. 36.4.2.6 Differential Diagnosis
• Small doses of benzodiazepines, tricyclic anti- • The main differential diagnosis is nightmares.
depressants, and SSRIs may help in severe cases.
36.4.2.7 Management
36.4.2 Sleep Terrors (Night Terrors) Methods that may be tried include
• Reassurance—of the child and the parents
36.4.2.1 Epidemiology • Changing the settling routine
• In children, night terrors are common and occur • Keeping a diary and then waking the child just
on a frequent basis in 1%–4%. M > F. before each episode is expected
• They are far less common in adulthood (<1%). • Small doses of benzodiazepines, tricyclic anti-
M = F. depressants, and SSRIs may help in severe cases
36.4.2.2 Aetiology
Aetiological factors that have been suggested include
• The onset is usually between 4 and 12 years
• Stress and sleep terrors often resolve spontaneously by
• Previous loss of sleep adolescence.
• Familial: 10-fold increase in prevalence in first • Frequency of sleep terrors can range from every
degree relatives night to once per few weeks.
• Induction by benzodiazepine antagonists (hence • Adulthood sleep terrors often run a chronic
the theories about benzodiazepine receptor course.
changes or endogenous substances acting on
benzodiazepine receptors)
• Upper airway obstruction in children 36.5 REM PARASOMNIAS
36.5.1 Nightmares
36.4.2.3 ICD-10 Criteria
• Repeated (two or more) episodes of arising from Nightmares are ‘bad’ (i.e. frightening) dreams. They
bed during the first third of nocturnal sleep and occur universally.
presents with panicky scream, intense anxiety,
body mobility, and autonomic hyperactivity. 36.5.1.1 Epidemiology
• The duration of the episode is less than 10 min. • Young children (3–5 years old): 10%–50% have
• There is a lack of response followed by disorien- nightmares.
tation and preservative movements. • Adults: 3% report frequent nightmares and 50%
• The individual has limited recall for the event. report occasional nightmares.
• There is no known causative factor. • F/M = 2–4:1.
Sleep Disorders 621
36.5.1.2 Aetiology • Pharmacological treatment is indicated for

Aetiological factors that have been suggested include severe cases. REM suppressants such as SSRIs
are indicated.
• Negative dreams associated with • Prazosin, a sympatholytic agent, can treat
• Daytime depression PTSD-associated nightmares.
• Daytime anxiety
• Daytime stress
• Hypnotic withdrawal 36.5.2 REM Sleep Behaviour Disorder
• Alcohol withdrawal
• Medications: 36.5.2.1 Epidemiology
• β-adrenoceptor antagonists • REM sleep behaviour disorder is more common
• Reserpine in old men.
36.5.1.3 ICD-10 Criteria 36.5.2.2 Aetiology

• Awakenings during the second half of sleep and Aetiological factors that have been suggested include
patient presents with detailed and vivid recall of • Alcohol withdrawal
intensely frightening dreams, involving threats • Early signs of Parkinson’s disease, Lewy body
to survival, security, or self-esteem. dementia, and multisystem atrophy
• The person is orientated and alert after awaken- • Precipitation by antidepressants and beta-blockers
ing from a frightening dream.
• The dream experience cause marked distress to 36.5.2.3 DSM-5 Criteria (APA, 2013)
the individual.
• Behaviours include repeated episodes of arousal
• There is no known causative organic factor or
during sleep associated with vocalization and
substance misuse.
complex motor behaviours that may cause injury
36.5.1.4 DSM-5 Criteria (APA, 2013) to bed partner or self.
• The diagnostic criteria for nightmare disorder • The vocalization and complex behaviours
listed in DSM-5 are very similar to ICD-10 with correlated with dream mentation simultane-
the emphasis on impairment in functioning. ously and is often described as acting out of
dreams.
36.5.1.5 Other Clinical Features • The duration of behavioural disturbance is lon-
• Nightmares tend to occur during middle and ger than 90 min after sleep onset with more
late sleep; they usually occur during REM sleep frequent episodes during the later part of the
but occasionally during stages 1–2. nocturnal sleep.
• The dream is remembered and patients may • The person is orientated and alert after
have difficulties falling asleep again as a result awakening.
of anxiety. • Loss of REM atonia.
• Nightmares are not associated with violent body • Polysomnographic evidence of abnormal REM
movements and vocalization because of low behaviours or an established synucleinopathy
muscle tone in REM sleep. diagnosis if polysomnographic evidence is absent.
• Depression and anxiety symptoms are common in • Significant functional and occupational
people with frequent nightmares since childhood. impairment.
• No organic causative factor or substance abuse.
The main differential diagnosis is sleep terrors. Investigation: The diagnosis is confirmed with overnight
36.5.1.7 Management polysomnography.
• Any underlying disorder (e.g. PTSD) may
require treatment. 36.5.2.4 Management
• Nonpharmacological treatment: reassurance, • Ensure safety of patient and his or her bed
conflict resolution, image rehearsal therapy, and partner.
progressive muscle relaxation therapy. • Prescribe clonazepam in severe case.
REFERENCES NICE. NICE Guidelines on Zaleplon, Zolpidem and Zopiclone

for Insomnia. http:/www.nice.org.uk/nicemedia/pdf/
American Psychiatric Association. 2013: Desk Reference to TA077publicinfoenglish.pdf (accessed on 17 July 2012).
the Diagnostic Criteria from DSM-5. Washington, DC: Parkes JD. 1985: Sleep and Its Disorders. London, U.K.:
American Psychiatric Association Press. WB Saunders.
Avidan AY. 2009: Parasomnias and movement disorders of Sadock BJ and Sadock VA. 2007: Kaplan & Sadock’s Synopsis
sleep. Seminars in Neurology 29(4):372–392. of Psychiatry. Behavioral Sciences/Clinical Psychiatry,
Barion A and Zee PC. 2007: A clinical approach to circadian 10th edn. Philadelphia, PA: Lippincott Williams &
rhythm sleep disorders. Sleep Medicine 8(8):566–577. Wilkins.
DeMartinis NA and Winokur A. 2007: Effects of psychiat- Taylor D, Paton C, and Kapur S. 2012: The Maudsley Prescribing
ric medications on sleep and sleep disorders. CNS and Guidelines in Psychiatry, 11th edn. West Sussex, U.K.:
Neurological Disorders–Drug Targets 6:17–29. Wiley-Blackwell.
Edinger JD and Means MK. 2005: Cognitive behavioral ther- Thorpy MJ, Westbrook P, Ferber R, Fredrickson P, Mahowald M,
apy for primary insomnia. Clinical Psychology Review Perez-Guerra F, Reite M, and Smith P. 1992: The clinical
25:539–558. use of the multiple sleep latency test. Sleep 15:268–276.
Ekbom K and Ulfberg J. 2009: Restless legs syndrome. Journal Wise MS, Arand DL, Auger RR, Brooks SN, and Watson NF.
of Internal Medicine 266:419–431. 2007: Treatment of narcolepsy and other hypersomnias of
Golbin AZ, Kravitz HM, and Keith LG. 2004: Sleep Psychiatry. central origin. Sleep 30(12):1712–1717.
London, U.K.: Taylor & Francis Group. World Health Organization. 1992: ICD-10: The ICD-10
Laking PJ. 2002: Sleep disorders. In Puri BK, Laking PJ, and Classification of Mental and Behavioural Disorders:
Treasaden IH (eds.) Textbook of Psychiatry, 2nd edn, Clinical Descriptions and Diagnostic Guidelines.
pp. 844–853. Edinburgh, U.K.: Churchill Livingstone. Geneva, Switzerland: World Health Organization.
37 Child and Adolescent Psychiatry
37.1 EPIDEMIOLOGY 37.2 ASSESSMENT

37.1.1 Preschool The information to be obtained in a child psychiatric
interview is shown in Table 37.1.
The main epidemiological study is the Waltham Forest
Study (Richman et al., 1982) in the early 1970s of 3-year-
37.3 PERVASIVE DEVELOPMENTAL
olds, carried out in the London borough of that name.
The Vineyard study (Martha) essentially confirmed its DISORDERS
findings. The main findings included 37.3.1 Childhood Autism (ICD-10 F84.0)/
Autistic Disorder (DSM-5 299.0)
1. 7% prevalence of moderate to severe behavioural
and emotional problems, slightly greater in boys 37.3.1.1 Historical Development
than girls • The term ‘autism’ was coined by Leo Kanner
2. 15% prevalence of mild behavioural and emo- in 1943. Childhood autism is also known as
tional problems Kanner’s syndrome.
3. Strong associations found with
a. Maternal depression 37.3.1.2 Epidemiology
b. Poor parental marriage • Prevalence: 7−28/10,000.
c. Delayed development of language • Male/female ratio = 4:1.
4. Strong continuities of behaviour and language • Autism accounts for 25%–60% of all autistic
disorders over the early school years disorders.
• No epidemiological studies have demonstrated
an association between autistic disorder and any
socioeconomic status.
37.1.2 Middle Childhood
The main epidemiological studies are the Isle of Wight 37.3.1.3 Aetiology
and inner London borough studies (by Rutter and col- 1. Genetic causes:
leagues) in the 1960s, of 10- and 11-year-olds. Recent a. Heritability is over 90%.
studies in Norway and Puerto Rico essentially confirmed b. Monozygotic twins/dizygotic twins: 36%:0%.
the findings. The main findings included c. The recurrence rate in siblings is roughly
3% for narrowly defined autism but is about
• 6.8% overall point prevalence of child psychiat- 10%–20% for milder variants.
ric disorder in the Isle of Wight d. The loci may involve chromosome 2q and 7q.
• 4% prevalence of conduct disorder e. Family history of schizophrenia-like psy-
• 2.5% prevalence of emotional disorder chosis or affective disorder.
• Male to female sex ratio of 1.9:1 2. Neurodevelopmental theory:
• An overall point prevalence of child psychiatric a. Perinatal injuries (e.g. maternal bleeding
disorder in inner London twice that in the Isle after the first trimester or meconium in the
of Wight amniotic fluid).
b. Antenatal infections (e.g. congenital rubella,
cytomegalovirus).
c. Maternal use of sodium valproate in pregnancy.
37.1.3 Adolescence
d. Gestational age less than 35 weeks.
• 10%–20% prevalence of psychiatric disorder e. Birth defects associated with central nervous
• A male to female sex ratio of approximately 1:1.5 system malformation (e.g. cerebral palsy).
623
f. Presence of minor congenital abnormalities

TABLE 37.1 (e.g. ear abnormalities, dermatoglyphics)
Information to Be Assessed in a Child as a result of abnormal neuroectodermal
Psychiatric Interview development within the first trimester of
Source and nature of referral pregnancy.
Who made referral? g. Hypoplasia of cerebellar vermal lobules and
Who initiated referral? cortical abnormalities particularly polymi-
Family attitudes to referral crogyria that reflect abnormal cell migra-
Description of presenting complaints tions in the first 6 months of gestation.
Onset, frequency, intensity, duration, location (home, school, etc.) h. Immunological incompatibility (e.g. mater-
Antecedents and consequences nal antibodies directed at the fetus) may
Ameliorating and exacerbating factors contribute to autistic disorder.
Specific examples i. Respiratory distress syndrome, anaemia,
Parental and family beliefs about causation encephalopathy in neonatal period.
Past attempts to solve problem j. Exaggerated growth of the brain in the first
Description of child’s current general functioning 2 years of life and 20% of patients have head
School circumference above 97th percentile.
Behaviour and emotions
3. Association with learning disability.
Academic performance
4. Fragile X syndrome.
Peer and staff relationships
5. Tuberous sclerosis.
Peer relationships generally
6. Phenylketonuria.
Family relationships
Personal/developmental history
7. Neurofibromatosis.
Pregnancy, labour, delivery
8. Infantile spasms are recognized causes.
Early developmental milestones
37.3.1.4 Pathogenesis and Neurobiology
Separations/disruptions
Physical illnesses and their meaning for parents • High serotonin and 5-HIAA levels
Reactions to school • Hypodopaminergic activity
Puberty • Hypoplasia of cerebellar vermis
Temperamental style • Underactivation of fusiform gyrus
Family history • Abnormality in the medial temporal lobe
Personal and social histories of both parents, especially
History of mental illness 37.3.1.5 Theory of Mind
Their experience of being parented • This refers to the capacity to attribute independent
History of family development mental states to oneself and to others, thereby
How parents came together allowing one to predict and explain actions.
History of pregnancies • People with autism have an impaired ability to
Separations and effects on children understand other people’s thought process, moti-
Who lives at home currently vations, intentions, and feelings and to make infer-
Strengths/weaknesses of all at home ences about the thoughts of others. As a result, they
Current social stresses and supports
have impaired empathy and social reciprocation.
Information from observation of family interaction
Structure, organization, communication, sensitivity 37.3.1.6 ICD-10 Diagnostic Criteria and
Information from observation of child at interview
Clinical Characteristics
Motor, sensory, speech, language, social relating skills
Mental state, concerns, and spontaneous account if age appropriate
1. The presence of abnormal development that is
Results of physical examination
manifested before the age of 3 years including
Plan for future investigation and management abnormal receptive or expressive language,
abnormal selective or reciprocal social inter-
Source: Reproduced from Puri, B.K. and Treasaden, I.H., Textbook of action, and abnormal functional or symbolic
Psychiatry, 3rd edn., Churchill Livingstone, Edinburgh, U.K., play. Children with autism are often attached to
2011. With permission. odd objects and have relative lack of creativity
and fantasy in thoughts.
Child and Adolescent Psychiatry 625
2. Abnormal reciprocal social interactions include 5. DSM-5 has other specifiers: with intellectual
failure in eye gaze and body language, failure in impairment, known medical or genetic condi-
development of peer relationship, lack of socio- tion, catatonia and associated with another neu-
emotional reciprocity, and lack of spontaneous rodevelopmental disorder.
sharing with other people.
3. Abnormal communication include lack of devel- 37.3.2 NICE Guidelines
opment of spoken language, lack of social imitative
The NICE guidelines summarize the signs and symp-
play, failure to initiate or sustain conversational
toms of possible autism in preschool children, primary
interchange, and stereotyped and repetitive use of
school children, and secondary school adolescents.
language. Their languages are frequently associ-
ated with pronoun reversals. A child with child Consider the possibility of autism
autism may say, ‘You want the pencil’ when he
The NICE guidelines advise psychiatrists to not rule out
means he wants it. Echolalia (repetition of spoken
autism because of
words by others) and palilalia (repetitions of one’s
spoken words) are common. • Good eye contact, smiling, and showing affec-
4. Restricted, stereotyped, and repetitive behav- tion to family members
iour include preoccupation with stereotyped • Reported pretend play or normal language
interest, compulsive adherence to rituals, motor milestones
mannerisms, and preoccupation with part- • Difficulties appearing to resolve after an
objects or nonfunctional elements of play mate- intervention
rials. Some children with autism enjoy vestibular • A previous assessment that concluded that there
stimulations such as spinning and swinging. was no autism especially when new information
5. Other nonspecific problems include phobias, becomes available
sleeping and eating disturbances, temper tan-
trums, self-directed aggression, and self-injury Differential diagnosis
(e.g. wrist biting).
The NICE guidelines recommend that psychiatrists
6. There should be an absence of other causes of per-
should consider the following differential diagnoses.
vasive developmental disorders, socio-emotional
problems, and schizophrenia-like symptoms. 37.3.2.1 Neurodevelopmental Disorders
• Atypical autism (onset after 3 years without
37.3.1.7 Differences between the ICD-
full-blown symptoms)
10 and DSM-5 Criteria
• Asperger’s syndrome (no impairment in verbal
1. The DSM-5 criteria on autism spectrum disorder communication and higher verbal IQ than non-
emphasize two main symptom clusters: verbal IQ)
a. Persistent deficits in social communication, • Rett’s disorder (predominantly in girls, micro-
social interaction across contexts and main- cephaly, loss of previously acquired abilities
tain relationships after 6 months of normal development and ear-
b. Restricted, repetitive patterns of behaviour, lier onset of seizure)
interests, or activities • Childhood disintegrative disorder (a developmen-
2. There are no major differences between ICD-10 tal regression that follows at least 2 years of normal
and DSM-IV-TR in diagnostic criteria for development and better language development)
autism. A total of five symptoms are required • Epileptic encephalopathy
(At least three symptoms from the social domain
and the communication domain and one symp- 37.3.2.2 Mental and Behavioural Disorders
tom from the repetitive behaviour domain.). Children with the following disorders show normal com-
3. In ICD-10, atypical autism is a stand-alone dis- munication and social interaction:
order under pervasive developmental disorder.
4. ICD-10 also specifies that atypical autism dif- • Attention-deficit hyperactivity disorder (ADHD)
fers from autism in either the age of onset (after • Mood disorder
3 years) or not meeting all the diagnostic criteria • Anxiety disorder
for autism. • Attachment disorder
• Oppositional defiant disorder to identify autism. It has 57 questions divided into

• Conduct disorder five categories: (1) sensory functions, (2) relation-
• Obsessive–compulsive disorder ship, (3) use of body parts and objects, (4) lan-
• Childhood-onset schizophrenia (later age of guage, and (5) social function and self-help (Krug
onset, equal gender ratio, family history of schizo- et al., 1980).
phrenia, normal intelligence, and presence of psy- • Social Communication Questionnaire (SCQ):
chotic features) A questionnaire completed by parents with 40
‘yes-or-no’ items.
37.3.2.3 Other Conditions • Social Responsiveness Questionnaire (SRQ): A
• Selective mutism: lack of communication is not 15 min questionnaire that measures the severity of
consistent autistic social impairment across the entire range
• Deafness: usually respond to loud noises and of the autism spectrum, from nonexistent to severe.
abnormal audiogram • Pervasive Developmental Disorder Behaviour
• Severe visual impairment Inventory (PDDBI): PDDBI is used to evalu-
• Maltreatment ate children with the age range from 6 months to
• Schizotypal disorder (more social awareness 12 years who have been diagnosed with a pervasive
and emotional reciprocity but less stereotyped developmental disorder as defined by the DSM-IV.
behaviours and interests) Rating forms completed by parents and teachers
yield age-standardized scores that are helpful in
37.3.2.4 Physical Examination planning treatment, monitoring progress, assess-
The NICE guidelines recommend that the psychiatrist ing outcome, and making placement decisions.
should perform a general physical examination and look
specifically for Multidisciplinary assessment
• Microcephaly or macrocephaly • Audiological examination to differentiate

• Dysmorphic features (genetic evaluation may be autism from deafness.
necessary) • Speech therapist assessment.
• Skin stigmata of neurofibromatosis or tuberous • IQ test: children with autistic disorder are more
sclerosis using a Wood’s light skilled in visual–spatial tasks than in tasks
• Signs of injury, for example, self-harm or child requiring skill in verbal reasoning.
maltreatment • A Developmental NEuroPSYchological Assess
• Congenital anomalies and dysmorphic features ment (NEPSY) is a neurological test for children
including macrocephaly or microcephaly aged 3–16 years, and assessment is classified into
six domains: executive functions, language, senso-
37.3.2.5 Investigations rimotor functions, visuospatial functions, memory,
Instruments that require training and social perception. Other standardized neu-
ropsychological tests including Halstead–Reitan
• Autism Diagnostic Observation Schedule (ADOS) Battery and Luria–Nebraska Battery.
is a semi-structured instrument that aims to assess • EEG: 30% have nonspecific EEG abnormali-
patients aged from toddlers to adults. ties. EEG is indicated if there is history of clini-
• Autism Diagnostic Interview (ADI) is a semi- cal seizures, subclinical seizures (e.g. staring
structured instrument and assesses caregivers. spells), and developmental regression.
• Childhood Autism Rating Scale (CARS) is a • MRI is not routinely recommended. Ventricular
scale that differentiates children with autism enlargement is found in 20%–25% of people
from other pervasive developmental disorders. with autism.
(Schopler et al., 1980) • Metabolic testing: phenylketonuria.
Instruments that do not require training 37.3.2.6 Comorbidity

Medical comorbidity
• Autism Behaviour Checklist (ABC): This ques-
tionnaire was developed with behaviours selected • Epilepsy (30%)
from a variety of checklists and instruments used • Motor coordination problems
• Visual or hearing impairment • Naltrexone: reduce self-injurious behaviour

• Respiratory infections • Atomoxetine: reduce inattention, hyperactivity,
• Feeding problems: including restricted diets and aggression
• Constipation, altered bowel habit, faecal incon-
tinence, or encopresis Multidisciplinary treatment
• Loose bowel movements
• Urinary incontinence or enuresis The NICE guidelines recommend patients with autism to
be treated by a multidisciplinary team that include paedi-
Psychiatric comorbidity atrician and/or child and adolescent psychiatrist, speech
therapist, clinical and/or educational psychologist, and
• Learning disability: 70% of children with occupational therapist.
autism have mental retardation, mild to moder-
ate mental retardation (30%), and severe to pro- • Education programme: Autistic children often
found mental retardation (50%). do well in a well-structured educational set-
• Academic learning problems in literacy or ting with experienced teachers and educational
numeracy. psychologists.
• ADHD (50%). • Behaviour therapy establishes underlying rea-
• Obsessive–compulsive disorder (10%). sons for disruptive behaviour and provides
• Tics or Tourette’s syndrome. alternative and more socially acceptable ways
• Anxiety disorders. of indicating needs. Behaviour therapy also
• Depression: irritability and social withdrawal. aims at reducing behavioural problems such as
• Temper tantrums. temper tantrums, feeding and toilet problems,
• Oppositional defiant disorder. aggression, rituals, and obsessions.
• Self-injurious behaviour. • Social skill training helps the child to under-
stand beliefs and emotions of the others based
37.3.2.7 Treatment on the theory of mind. Teaching a child to ‘mind
Psychological treatment read’ by first helping a child understand his own
thoughts or feelings and thus eventually be able
• Applied behaviour analysis (ABA): operant con- to deduce actions from other people.
ditioning helps to develop specific social, com- • Speech therapy: Speech therapist can help the
munication and behavioural skills by reinforcing child to facilitate communication and the par-
positive behaviour. The triggers for problematic ents to understand echolalic speech and con-
behaviour are analysed. sider alternative mode of communication.
• Intensive behavioural intervention (IBI): the • Occupational therapy: Occupational therapist
design, implementation, and evaluation of envi- can assess a child’s behaviour from the sensory
ronmental modifications that aim to produce processing and self-regulation perspectives and
socially meaningful changes in behaviour. help the child to develop more adaptive ways to
• Sensory integration therapy: for example, self-regulate.
brushing of the skin or swinging to stimulate • Parent education and support is provided for
vestibular responses that will help to reduce the parents and family members about childhood
hypersensitivity to stimuli. autism and refer them to community resources
• Facilitated communication: training on reading for further support (e.g. autism advocacy and
and writing. support organizations).
Pharmacological treatment Alternative treatment
• Risperidone: reduce repetition and aggression • Casein- and gluten-free diet: requires further study
and improve behaviour • Highly unsaturated fatty acid supplements:
• Fluoxetine: reduce the levels of ritualistic behav- some success
iours and improved mood and anxiety • Secretin: no improvement in language
• Anticonvulsants: reduce self-injurious behaviour • Vitamins A and C
37.3.2.8 Course of Illness (e.g. trains, weather, and dinosaurs) or interest

• In the first 3 years of life, 70% of children with in other fields such as arts and music.
autism do not achieve normal development. • Impairment in social interactions:
• Peak age of seizure is between 11 and 14 years old. • Marked impairment in the use of multiple non-
• Inappropriate sexual behaviour may emerge in verbal behaviours (eye gaze, facial expression)
adolescence and early adulthood. • Failure to develop peer relationship
• Most children with autism show improvement • Lack of spontaneous seeking to share enjoy-
in social relation and communication but not in ment, interests, achievements
rituals or repetitive behaviour. • Lack of social or emotional reciprocity
• Childhood autism often causes lifelong disability. • Restricted repetitive and stereotyped patterns of
10% of people with autism will ultimately lose behaviour:
language skills with intellectual deterioration. • Inflexible adherence to routines and rituals
• Stereotyped and repetitive mannerism (e.g.
37.3.2.9 Prognosis hand or finger flapping)
• Persistent preoccupation with parts of objects
• The most important predictor is childhood IQ
and presence of speech by 5 years.
• Nonverbal IQ < 60 is associated with severe 37.4.4 Differences between Childhood Autism
social impairment and lack of independent and Asperger’s Syndrome (Table 37.2)
living.
37.4.5 Comorbidity
• 50% do not develop useful speech.
• Only 10% are able to work. • ADHD (most common comorbidity in children).
• Depression (most common comorbidity in adults).
• Anxiety.
37.4 ASPERGER’S SYNDROME (ICD-10 F84.5) • Obsessive–compulsive disorder.
• Possible development of schizophrenia.
• Criminal offending is related to lack of concern
• Asperger’s syndrome was coined by Hans of outcome, impulsivity, social naivety, overrid-
Asperger in 1944 and reappraised by Wing in ing compulsion to steal, and misinterpretation of
1981. actions from others.
37.4.2 Epidemiology 37.4.6 Treatment
• 3–4 per 1000 children • Psychoeducation should be offered to parents
• Male to female ratio is 9:1 to enhance acceptance and maintain routines at
home and school.
37.4.3 Clinical Features • As the child gets older, he will be helped by ver-
bally mediated treatment, supportive counsel-
• The DSM-5 criteria suggest merging Asperger’s ling, and self-sufficiency training.
syndrome into autistic spectrum disorder. • He will be encouraged to obtain employment
• People with Asperger’s syndrome usually do in jobs with regular routines. Sheltered employ-
not have delay in language development (e.g. ment and sheltered residence are reserved for
be able to speak single words by age of 2 years severe cases.
and communicate by age of 3 years) and cog-
nitive development. Speech is characterized
37.4.7 Prognosis
by poor prosody (stress, rhythm, intonation
of speech), unusual rate, poorly modulated • Good prognostic features include normal intel-
volume, tangentiality, circumstantiality, and ligence and high level of social skills.
verbosity. • There is a strong tendency for the abnormalities
• People usually have intense circumscribed inter- to persist into adolescence and adult life.
ests and this may develop into isolated special • Psychotic episodes occasionally occur in early
skills. Classic interests include scientific fields adult life.
TABLE 37.2
Compare and Contrast Autism and Asperger’s Syndrome
Autism Asperger’s Syndrome
Gender ratio Male to female ratio is 3:1 Male to female ratio is 9:1
Neuropathology Lesions in amygdala, corpus Right hemisphere lesions
callosum, and cerebellum Association with aminoacidurias
Development Abnormal early development Relatively normal early development
Onset is younger than 3 years The child is noted to have lack of warmth and
There is a delay in language interest in social relationships around the
development third year of life
Language development is not delayed and
single word should have developed by age of
2 and communicate phrases by age of 3
Motor milestones are delayed
Salient clinical Restricted, stereotyped, and Preoccupation with restricted, stereotyped,
features repetitive behaviours such as motor and repetitive interests. Extensive
mannerisms are more common than information is often acquired in a mechanical
Asperger’s syndrome fashion
Preoccupation with part-objects or Patients are good with logics, rules, and
nonfunctional elements of play routines. They tend to see the details and
materials is more common than argue over minor details without seeing the
Asperger’s syndrome whole picture
Intelligence Performance IQ is higher than Reasonably preserved IQ
quotient (IQ) verbal IQ Verbal IQ is higher than performance IQ
Speech Severe expressive speech disorder Fluent but monotonous, staccato, and pedantic
speech
37.5 RETT’S SYNDROME (ICD-10 F84.2) 37.5.4 Clinical Features and Course of Illness
37.5.1 Historical Development 1. Age: 0–6 months:
a. Normal prenatal and perinatal development
• Rett’s syndrome was coined by Andreas Rett in b. Normal head circumference at birth
1966. c. Normal psychomotor development in the
first 5 months of life
37.5.2 Epidemiology d. Plateau in social skill development by 6 months
• Prevalence rate is between 1 in 15,000 and 1 in 2. 7–24 months:
22,000 females. a. Deceleration in head growth.
• The incidence of sudden and unexpected death b. Loss of speech.
is around 2%. c. Loss of skills in locomotion.
• It is predominantly a female disorder but men d. Loss of purposive hand movements and
with clinical features similar to Rett’s syndrome replaced by hand-wringing stereotypies.
have been described. e. Hyperventilation.
f. Social and play development are arrested by
24 months.
37.5.3 Inheritance
g. Severe impairment in expressive and recep-
• Mutation in the transcription regulatory gene tive language.
MECP2 at chromosome Xq28 3. 4 years:
• X-linked dominant mutation with lethality in a. Trunk ataxia and apraxia: poorly coordi-
hemizygous males nated trunk movements.
b. Development of choreoathetoid movements: 37.6.4 Course of Illness

poorly coordinated gait.
c. Breathing dysfunction: irregular respiration, • Three-fourths of patients do not have further
episodes of hyperventilation, and apnoea. deterioration in behaviour and reach stabiliza-
d. Seizures (75%). tion. Life expectancy is normal.
e. Scoliosis. • Some children show recovery of previous devel-
f. Spasticity. opmental skills and few children have very good
g. Growth retardation. recovery.
h. Hypotrophic small feet are supportive diag- • Progressive deterioration occurs in one-fourth
nostic criteria. of children, especially in those associated with
i. Profound mental retardation: mental dete- a progressive neuropathological process and
rioration precedes motor deterioration. death may result.
j. Patients are usually in wheelchairs by their • Most patients suffer from moderate mental
late teens and die before the age of 30. retardation.
37.7 HYPERKINETIC DISORDER (ICD-10 F90)

37.5.5 Treatment
• Anticonvulsant treatment: seizure control 37.7.1 Attention Deficit and Hyperactivity
• Behaviour therapy: control self-injurious behaviour Disorder (DSM-5 314)
• Physiotherapy: prevent muscular dysfunction 37.7.1.1 Terminology
and regulate breathing
• ADHD is an American term. In the United
Kingdom, it is often known as ‘hyperkinetic
37.6 CHILDHOOD DISINTEGRATIVE disorder’.
DISORDER (ICD-10 F84.3)
37.6.1 Epidemiology • In the United Kingdom, 1.7% of school-aged
• Prevalence: 1.7 per 10,000 children suffer from hyperkinetic disorder
• Age of onset: 3–4 years old based on ICD-10 criteria and are more stringent
• Male predominance and require both hyperactivity and inattention to
be present.
• In the United States, 3%–10% of school-aged chil-
37.6.2 Clinical Features dren suffer from ADHD. Increased prevalence in
• Normal development for at least 2 years after birth the United States is a result of better recognition,
• Loss of previously acquired skills before age of 10 psychosocial adversity, and the change of DSM-
in the following areas: language, social skills, bowel III–DSM-IV criteria that classifies ADHD into
control, bladder control, motor skills, and play three subtypes. The DSM-5 requires either hyper-
• Qualitative impairments in social interactions activity or inattention to be present.
involving nonverbal behaviour, communications • Male to female gender ratio: 3:1.
involving spoken language, and stereotyped • Peak age of onset: 3–8 years.
behaviour (e.g. stereotypies or mannerism)
37.7.1.3 Aetiology
37.7.1.4 Genetics
37.6.3 Comorbidity
• ADHD is a heritable disorder. Siblings of
• Seizure disorders: 50% have EEG abnormalities ADHD children have twice the risk of ADHD
• Tuberous sclerosis when compared to the general population.
• Metachromatic leukodystrophy • Biological parents of children with the disorder
• Schilder’s leukoencephalopathy have a higher risk for ADHD than adoptive par-
• Landau–Kleffner syndrome (acquired aphasia ents. The parents of children with ADHD show an
with epilepsy): preserved social interest and increased incidence of hyperkinesis, sociopathy,
nonverbal communicative skills alcohol use disorders, and conversion disorder.
• Genes related to dopaminergic function are f. Other features: careless mistakes and for-
implicated (e.g. dopamine receptor D4 gene, getfulness in daily activities.
dopamine transporter (DAT1) gene, alpha 2A 4. Symptoms of hyperactivity and impulsivity
gene, norepinephrine transporter gene, cate- include (Mnemonic: WORST FAIL)
chol-O-methyltransferase (COMT) gene). a. Waiting for in lines or await turns in game
• First-degree biological relatives of ADHD cause frustration (impulsivity).
children are at high risk to develop ADHD and b. On the move most of the time such as run-
other disorders such as disruptive behaviour ning and climbing (hyperactivity).
disorders, anxiety disorders, and depressive c. Restlessness and jitteriness (hyperactivity).
disorders. d. Squirms on seat (hyperactivity).
e. Talk excessively without appropriate
response to social constraints (impulsivity).
37.7.1.5 Neurodevelopment
f. Fidgets with hands and feet (hyperactivity).
• September is the peak month for births of chil- g. Answers are blurted out before questions
dren with ADHD with and without comorbid (impulsivity).
learning disorders. h. Interruption of other people’s conversations
• Early infection, inflammation, toxins, and trauma (impulsivity).
cause circulatory, metabolic, and physical brain i. Loud noise in playing (hyperactivity).
damage and lead to ADHD in adulthood. 5. The DSM-5 classifies ADHD into three
• Psychosocial adversity (e.g. maternal psycho- subtypes:
pathology, large family size, parental conflict, a. Inattentive type: at least six symptoms of
and emotional deprivation) is associated with inattention but not hyperactivity and impul-
ADHD in childhood. sivity symptoms for 6 months.
b. Hyperactivity type: at least six symptoms of
37.7.1.6 Neurochemistry
hyperactivity and impulsivity but no symp-
• Noradrenaline: A dysfunction in peripheral toms of inattention for 6 months.
noradrenaline leads to negative feedback to the c. Combined type: at least six symptoms from
locus coeruleus and results in reduction of nor- both inattention and hyperactivity/impulsiv-
adrenaline in the central nervous system. ity for 6 months.
• Evidence: Stimulants and tricyclic antidepres- 6. The DSM-5 has raised the upper limit of age of
sants increase catecholamine concentrations onset to 12 year olds (previously 7 year olds).
by promoting their release and blocking their 7. The ICD-10 criteria require at least six symp-
uptake. Clonidine, a noradrenaline agonist, may toms of inattention, three symptoms of hyper-
reduce hyperactivity in ADHD. activity, and one symptom of inattention for
duration of 6 months. ICD-10 criteria do not
37.7.1.7 Clinical Features classify ADHD into three subtypes.
1. Persistent pattern of inattention, hyperactivity, 8. Adult ADHD: the symptoms of ADHD focus
and impulsivity across two different settings more on inattentive symptoms. Symptoms of
and result in significant functional impairments. hyperactivity tend to improve with time. The
The behaviours are maladaptive and inconsis- following are symptoms of adult ADHD:
tent with developmental level. a. Irritability
2. The onset is before the age of 7 years. b. Impatience
3. Symptoms of inattention include (Mnemonic: c. Forgetfulness
SOLID) d. Inattention
a. Starts tasks or activities but not able to fol- e. Impulsivity
low through and finish. f. Disorganization
b. Organization of tasks or activities is impaired. g. Distractibility
c. Loses things necessary for tasks and activi- h. Chronic procrastination with many projects
ties such as school assignments or stationary. underway simultaneously and trouble in
d. Instructions are not followed. completing them
e. Distraction by external stimuli. i. Difficulty in tolerating boredom
9. Mental state examination may reveal hyperac- disorder. About 75% of children with ADHD show
tivity, anxiety, distractibility, perservation, and behavioural symptoms of aggression)
concrete thinking. • Conduct disorder (30%–50%)
10. Neurological examination may reveal visual, audi- • Anxiety disorders (25%)
tory, motor impairments, and reflex asymmetries. • Tics (11%)
11. Cognitive assessment may reveal difficulty in • Substance abuse (e.g. cannabis, alcohol, nico-
copying age-appropriate figures and perform- tine, and cocaine)
ing rapidly alternative movements and left–right
differentiation. 37.7.1.12 Treatment
37.7.1.8 Rating Scales and Cognitive Assessment
• Connors’ rating scale: Connors’ rating scale is 1. Prior to initiation of medication, the psychiatrist
a diagnostic scale for ADHD using the DSM-IV is advised to
criteria. This scale includes measures of behaviour a. Look for exercise syncope, undue breath-
described by parents and teachers. The behaviour lessness, and other cardiovascular symp-
scale includes the following: (1) ADHD symptoms, toms in the history
(2) anxiety, (3) cognitive problems, (4) oppositional b. Perform physical examination including
behaviour, (5) perfectionism, and (6) social prob- measurement of heart rate and blood pres-
lems (Gladman and Lancaster, 2003). sure and examination of the cardiovascular
• Child Global Assessment Scale (CGAS): a score system
60/100 is the cutoff that requires treatment. c. Measure baseline height and weight
• Swanson, Nolan, and Pelham (SNAP) d. Order an electrocardiogram (ECG) if his-
Questionnaire: this teacher and parent rating tory of cardiac disease is present
scale is composed of 18 items and determines if
symptoms of ADHD are present. Stimulants
• Arrange direct school observation by a member
of Child and Adolescent Mental Health Service • Examples of stimulants include methylpheni-
(CAMHS). date and dexamfetamine.
• Psychometric testing such as IQ assessment • The stimulant inhibits dopamine reuptake and
or academic assessment if there is evidence of causes direct release of dopamine.
learning disability. • Stimulant is indicated for ADHD without comor-
bidity or ADHD with comorbid conduct disorder.
37.7.1.9 Further Investigations • Beneficial effects of methylphenidate: improve
1. EEG: increased beta waves and decreased delta attention span and hyperactivity for a certain
waves are associated with arousal and hyperactivity. number of hours while in the school setting.
2. MRI brain: • Dosing: Regular Ritalin requires 5–10 mg TID.
a. Reduction in size in corpus callosum and Consider modified release preparations (e.g.
cerebellum long acting Ritalin or Concerta XL) that allows
b. Decreased activities in the anterior cingulated single-day dosage and promotes adherence.
gyrus Starting dose is 18 mg OM and slowly titrates
c. Decreased activities in the thalamus, hippo- up to 54 mg/day.
campus, globus pallidus, and caudate • Common side effects include reduction in appe-
tite, gastric discomfort, insomnia, headache,
37.7.1.10 Differential diagnosis elevation of blood pressure, tics, dysphoria, and
• Early-onset bipolar disorder: mania is more irritability.
goal-orientated and episodic. • Serious and rare side effects include liver impair-
ment, leukopenia, and sudden cardiac death.
37.7.1.11 Comorbidity • Continuous monitoring for height and weight
• Speech or language impairment: 50% (every 6 months), cardiovascular status (every 3
• Oppositional defiant disorder (40% of children months), seizure, tics, psychotic symptoms, anx-
meet the diagnostic criteria of oppositional defiant iety symptoms, and drug diversion is required.
• There is a risk of misuse in patients with history 4. Nortriptyline or imipramine:

of stimulant misuse. a. Tricyclic antidepressants have weaker evi-
• Dexamfetamine is not the first-line stimulant dence in treating ADHD.
because it is associated with higher risk of b. Beware of anticholinergic side effects.
side effects in comparison to methylphenidate. c. Effects of imipramine tend to wear off and
Begin with low doses and offer divided doses cause dysrhythmias.
up to 20 mg/day. Children from age 6–18 years d. It is not advisable to combine methylpheni-
require up to 40 mg/day. Side effect profile is date and imipramine because of cardiovas-
similar to methylphenidate. cular stimulation.
• Continue treatment for as long as it is effective 5. Clonidine:
with regular review of clinical need, benefits, a. Clonidine is a centrally acting α-2 agonist.
and side effects. b. Indications:
i. More effective in controlling the aggres-
Nonstimulants sion or hyperarousal
ii. Less effective for inattention
1. Examples of nonstimulants include: iii. Comorbidity of ADHD and Tourette’s
a. Atomoxetine (a noradrenaline reuptake syndrome
inhibitor) iv. Dose of clonidine: 0.2–0.6 mg/day in
b. Imipramine or nortriptyline (a tricyclic divided doses
antidepressant) v. Monitor for hypotension
c. Bupropion (a dopamine–noradrenaline c. Common side effects include hypotension,
reuptake inhibitor) sedation, tachycardia, constipation, dizzi-
d. Clonidine: (an alpha adrenergic agonist) ness, dry mouth, weakness, loss of libido,
2. Indications for nonstimulants: agitation, and depression.
a. Inability to tolerate side effects (e.g. high d. Dangerous side effects associated with high
blood pressure) associated with stimulant doses include sinus bradycardia and atrio-
b. Unsatisfactory treatment response to two ventricular block.
types of stimulant 6. Omega-3 fatty acids and diet:
c. History of stimulant misuse a. Except in situations when dietary deficiency is
d. Comorbid condition (e.g. childhood-onset known, NICE guidelines do not recommend
schizophrenia, Tourette’s syndrome) any particular dietary supplements (such as
that makes the prescription of stimulant omega-3 fatty acids) in the treatment of ADHD.
contraindicated b. NICE guidelines do not recommend elimi-
e. Comorbid condition (e.g. depression or nation of artificial colouring and additives
anxiety) that requires tricyclic antidepres- from the diet but advise parents to keep a
sant and avoid polypharmacy in a child diary if there are foods or drinks that appear
3. Atomoxetine: to affect behaviour.
a. The starting dose of atomoxetine is
0.5 mg/kg/day and increase the dose to 37.7.1.13 Psychosocial Treatment
1.2 mg/kg/day. 1. Parent-training/education programmes
b. Common side effects include agitation, a. Offer referral to educational programmes to
irritability, appetite suppression, gastroin- learn about ADHD, the management, and
testinal discomfort, suicidal thinking, self- coping strategies.
harming behaviour, and unusual changes in b. Individual or group-based parent-training
behaviour such as psychosis or mania. or education programmes for parents.
c. Rare side effect: liver damage, abdominal c. Individual-based or group CBT or social
pain, unexplained nausea, malaise, and skill training for children and adolescents
darkening of the urine or jaundice. suffering from ADHD.
d. Monitoring on height, weight, cardiac func- d. Training for applying behavioural interven-
tion, blood pressure, seizure, and self-harm tions for teachers.
is required on a regular basis. e. Academic remediation.
2. Behaviour therapy b. The CAMHS team can provide support to

a. Positive reinforcement (e.g. reward sys- parents and teachers.
tem and praises to promote positive c. Consider referral to a special school if
behaviour). the child has low IQ or learning disability
b. Time-out skills include planned ignoring to (Table 37.3).
reduce negative behaviour.
c. Environmental modifications (e.g. plac-
ing the child in the front row in class may
37.7.2 Multimodal Treatment Study
reduce distractions). 1. In the Multimodal Treatment Study, 485 chil-
d. Combination of behaviour therapy and med- dren took part in a 3-year follow-up study. Their
ication is better than medication alone. mean age was 12 years. The primary outcome
3. Social interventions measures were severity of ADHD and opposi-
a. Working closely with school and parents in tional defiant disorder, reading scores, social
monitoring the child’s behaviour. skills, level of impairment, and diagnosis. At the
TABLE 37.3
Summary of Treatment Recommendations for ADHD from the NICE Guidelines
School-Age Children and School-Age Children and
Young People with Young People with Severe
Interventions Preschool Children Moderate ADHD ADHD Adults with ADHD
Pharmacological Pharmacological Pharmacological treatment is Offer drug treatment as Methylphenidate is
treatment treatment is not not indicated as first-line first-line treatment and part first-line treatment
recommended treatment of comprehensive treatment Dose: 5 mg TID and
Reserve drug treatment to programme increase to a maximum
children If patient and parents do not of 100 mg/day. Target
• With moderate accept pharmacological dosage is usually
impairment treatment, provide 1mg/kg/daily
• Non-pharmacological information about the Consider atomoxetine if
interventions have been benefits and superiority of drug diversion is a
refused pharmacological treatment problem. Maintenance
• Persistence of significant If patient and parents are still dose is 80–100 mg/day
impairment after not keen, offer a group Maximum dose of
psychosocial treatment parent-training or education dexamfetamine is up to
programme 60 mg/day
Parent-training Offer parents or carers Offer parents or carers Offer the parents a group- Not applicable
and education referral to a parent- referral to a parent-training based parent-training or
programme training or education or education programme as education programme with
programme as first-line treatment medication
first-line treatment
Interventions for Before discharge from Offer group CBT or social If psychological intervention Offer a comprehensive
the patient and secondary care, review skill training for the child is ineffective, discuss the treatment programme
family the child with their and young person possibility of (group or individual
parents and siblings Offer individual CBT or pharmacological treatment CBT) addressing
for residual coexisting social skill training for and highlight the benefits and psychological,
conditions older adolescents superiority of behavioural, and
Monitor for recurrence If the child has learning pharmacological treatment in occupational needs
of ADHD symptoms disability, refer to either severe ADHD
and associated individual or group setting
impairment after the based on preference of the
child returns to school child
end of the first year, the research protocol was 5. 20% of children with ADHD develop antisocial
dropped and allowed for more naturalistic and personality disorder in adulthood. 15% develop
personalized treatment. substance misuse in adulthood.
2. The Multimodal Treatment Study is composed
of four treatment groups:
a. Medication only 37.8 CONDUCT DISORDER (ICD-10
b. Psychoeducation
F91.0-F91.2/DSM-5 312) AND
c. Combined medication and psychosocial
treatment OPPOSITIONAL DEFIANT DISORDER
d. Community control group (ICD-10 F91.3/DSM-5 313)
3. The four treatment groups demonstrated
37.8.1 Epidemiology
reduction in ADHD symptoms. The combined
medication and psychosocial treatment group • Conduct disorder was diagnosed in 4% of children
demonstrated significant improvement. At 24 in the Isle of Wight study. The prevalence of oppo-
and 36 months, the magnitude of differences sitional defiant disorder is between 6% and 16%.
among the four groups reduced but the com- • The prevalence is higher in socially deprived
bination group still demonstrated superior inner city areas and large families.
outcomes. • The male to female gender ratio for conduct
4. Good prognostic factors include strong response disorder is 3:1. The male to female gender ratio
to initial treatment, high IQ, and strong social for oppositional defiant disorder is 3:1 before
network. puberty but approaching 1:1 after puberty.
5. This study shows that children with ADHD • The age of onset of conduct disorder begins earlier
continue to show higher than normal rates in boys (10–12 years) as compared to girls (14–16
of delinquency (4 times) and substance use years). The comorbidity of ADHD and aggressive
(2 times). behaviour is associated with early onset of conduct
disorder. The age of onset of oppositional defiant
disorder is before the age of 8 years.
• In the United Kingdom, the peak age of offend-
37.7.2.1 Prognosis
ing is between 14 and 17 years and the age of
1. ADHD symptoms persist at the age of 30 in criminal responsibility is 10 years.
one-quarter of ADHD children. Most patients • 5%–10% of children suffer from problems with
do not require medications when they get older. a mixture of oppositional defiant disorder and
Nevertheless, it is appropriate to continue treat- conduct disorder symptoms.
ment in adults whose ADHD symptoms remain
disabling.
37.8.2 Aetiology
2. Although symptoms of hyperactivity often
improve as the child grows older, inattention is 1. Genetic factors: conduct disorder is associated
likely to persist. with inheritance of antisocial trait from parents
3. Remission is unlikely before the age of 12 years. who demonstrate criminal behaviours.
When remission does occur, it usually takes 2. Biological factors:
place between the ages from 12 to 20 years. a. Low plasma serotonin level.
Overactivity is usually the first symptom b. Low plasma dopamine level.
to remit. Distractibility is the last symptom to c. Low cholesterol.
remit. d. Low skin tolerance.
4. Predictors for persistence of ADHD symptoms e. Excess testosterone excess.
into adulthood: f. Greater right frontal EEG activity.
a. Family history of ADHD g. Abnormal prefrontal cortex.
b. Psychosocial adversity h. History of head injury.
c. Comorbid conduct disorder i. Neurological impairment.
d. Comorbid depressive disorder j. Maternal alcohol and smoking during
e. Comorbid anxiety disorder pregnancy.
3. Psychological factors: 6. Protective factors:

a. Fearlessness theory states that children a. Economics stability in family.
with conduct disorder exhibit a lack of b. Family commitment to normal social
anxiety and fear. values.
b. Stimulation-seeking theory states that c. Female gender.
children with conduct disorder often have d. Good coping strategies.
low arousal level and need to engage in e. High IQ.
antisocial behaviour to increase arousal f. Positive social interaction.
levels. g. Prepubertal anxiety such as separation anxiety.
c. Difficult temperament and a poor fit between h. Resilience.
temperament and emotional needs. i. Stable social organization in the community.
d. Impulsivity. j. Warm supportive family.
e. Poor social skills.
f. Failure to take responsibility for actions.
g. Education retardation: for example, reading 37.8.3 Clinical Features
problems.
See Table 37.4.
h. Low IQ.
i. Substance misuse before the age of 12 years.
4. Parental factors:
37.8.4 DSM-5 Criteria (APA, 2013)
a. Failure to set rules and monitor.
b. Inconsistency. 1. The DSM-5 criteria suggest three symptom
c. Negativism. clusters for oppositional defiant disorder:
d. Harsh, punitive parenting with severe physi- a. Angry or irritable mood.
cal and verbal aggression. b. Defiant or headstrong behaviour.
e. Hostility, resentment, and bitterness between c. Vindictiveness.
parents with marital discord. 2. Conduct disorder involves repetitive and per-
f. Parental psychopathology (associated with sistent pattern of behaviours in which the basic
early-onset conduct disorder). rights of others or major age-appropriate soci-
g. Father with antisocial personality disorder etal norms or rules are violated, as manifested
and alcohol dependence. by the presence of three or more of the follow-
h. Maternal depression. ing symptoms (aggression, destruction, deceit-
i. Parental criminality. fulness, serious violation of rules) in the past
j. Repeated physical and sexual abuse. 12 months, with at least one criterion present in
k. Rejection from parents. the past 6 months.
l. Low income (associated with early-onset 3. Oppositional defiant disorder is defined as a
conduct disorder). recurrent pattern of negativistic, hostile, and
m. Unemployment. disobedient behaviour towards authority fig-
n. Single parent and death of parent of the ures for 6 months. The child should have at
same gender. least four symptoms: losing temper, arguing
o. Attention seeking from parents by inducing with adults, refusing to comply with adult’s
antisocial behaviour. requests, annoying the others, being angry,
5. Social factors: actively defiant, blaming the others for per-
a. Family dysfunction (associated with early- sonal mistakes, and showing spiteful behav-
onset conduct disorder). iour. In contrast to ICD-10 criteria, the child
b. Lack of supportive social network. should not meet the general diagnostic criteria
c. Lack of participation in community for conduct disorder.
activities. 4. The DSM-5 further divides conduct disor-
d. Uncaring and hostile school environment. der into two subtypes: childhood-onset and
e. Gang involvement and aberrant peer group. adolescent-onset. Childhood-onset conduct
f. Overcrowding environment with more than disorder carries a poor prognosis if left
4 children. untreated.
TABLE 37.4
Compare and Contrast the Conduct Disorder and Opposition Defiant Disorder
Conduct Disorder Oppositional Defiant Disorder
General criteria According to the ICD-10, there is a repetitive and According to the ICD-10, the general criteria for
persistent pattern of behaviour in which either the basic conduct disorder are met.
rights of the others or major age-appropriate societal
rules are violated. The minimum duration of symptoms
last for at least 6 months.
Individual symptoms The child often displays severe temper tantrums, being At least four symptoms from conduct disorder and
angry and spiteful, often telling lies, and breaking must have been present for 6 months.
promises. Children with oppositional defiant disorder tend to
To adults: frequent argument, refusing adults’ requests have temper tantrums, being angry and spiteful,
or defying rules, and staying out after dark against argument with adults, defying rules, and blaming the
parental prohibition (onset earlier than age 13 years). others.
To other people: annoying other people deliberately, Children with oppositional defiant disorder should not
blaming them for his mistakes, initiating fights with the have more than two symptoms related to physical
others, using weapons to harm the others, exhibiting assault, damage of property, and running away from
physical cruelty (also to animals), confronting victims school and home.
during a crime, forcing another person into sexual
activity, and frequently bullying the others.
To objects or properties: deliberately destroying
properties, setting fire, stealing objects of value within
home or outside, and breaking into someone’s house.
Running away from school (truancy occurs at the age
younger than 13 years) or from parental surrogate
home (at least twice).
Type of conduct disorder The ICD-10 criteria classify conduct disorder into mild, No sub-category.
moderate, and severe. The ICD-10 criteria recommend Although the ICD-10 criteria do not specific the age,
specifying the age of onset as childhood-onset children with oppositional defiant disorder are
(younger than 10 years) and adolescent-onset (older usually younger than 10 years old with onset at age
than 10 years). Substance abuse is not a diagnostic 3–8 years. The minimum duration of oppositional
criterion for conduct disorder. defiant disorder is 6 months. Defiant behaviours
F90.0: Conduct disorder confined to the family context. usually occur at home with familiar people.
F91.1: Unsocialized conduct disorder: poor relationships
with the individual’s peer group, as evidenced by
isolation, rejection, unpopularity, and lack of lasting
reciprocal relationship.
F91.2: Socialized conduct disorder: normal peer relationship
F92.0: Depressive conduct disorder: both criteria of CD
and mood disorders are met.
F92.8: Other mixed disorders of conduct and emotions.
Criteria of conduct disorder and one of the neurotic,
stress-related, somatoform disorders or childhood
emotional disorders are met.
F93: Mixed disorders and emotions, unspecified
5. In the DSM-5, the ICD-10 category ‘mixed dis- (2) Callous–lack of empathy, (3) unconcerned
orders of conduct and emotion’ does not exist about performance, and (4) shallow or deficient
(APA, 2013). affect).
6. The DSM-5 proposed a new specifier, the lim- 7. 90% of patient fulfil the DSM-IV-TR criteria
ited prosocial emotions for conduct disorder that conduct disorder also meet the diagnostic crite-
has four components ((1) lack of remorse/guilt, ria of oppositional defiant disorder.
37.8.5 Sex Differences • Anxiety disorders (30% of children with anxi-

ety disorders also suffer from conduct disorder)
• Girls with conduct disorder are more likely to
engage in covert behaviours and prostitution. Comorbidities for oppositional defiant disorder
Boys are more concrete and egocentric.
• Girls with conduct disorder are more verbal and • Anxiety disorders (14% of children with anxiety dis-
use indirect and relational aggression. Boys use order also suffer from oppositional defiant disorder).
physical aggression. • ADHD (5%–10% of preschoolers with oppo-
• Girls with conduct disorder are more likely to sitional defiant disorder will end up with
develop depression, anxiety, and somatization. ADHD).
• Both boys and girls with conduct disorder dem- • Depressive disorder (9%).
onstrate low empathy and ability to identify • Learning disabilities and language disorders are
interpersonal issues. common.
37.8.6 Differential Diagnosis
37.8.8 Management of Conduct Disorder
Differential diagnosis for conduct disorder
• Oppositional defiant disorder
• ADHD (more inattention and hyperactivity) • Aggression and acute behavioural problems:
• Mild mental retardation Antipsychotics such as risperidone, olanzapine,
• Pervasive developmental disorder and haloperidol reduce physical aggression and
• Mental retardation assault. Side effects include sedation and extra-
• Intermittent explosive disorder pyramidal side effects (e.g. acute dystonia or
• Childhood-onset bipolar disorder pseudoparkinsonism).
• Somatization disorder • Depression and impulsivity: SSRIs such as
• Borderline personality trait in adolescence fluoxetine, sertraline, paroxetine, and citalopram
• Substance misuse reduce impulsivity, irritability, and depression.
• Childhood-onset schizophrenia • Conduct disorder and ADHD: Stimulants
• Organic brain disorder reduce behavioural problems associated with
hyperactivity and improve attention.
Differential diagnosis for oppositional defiant disorder
Multimodal treatment
• Transient oppositional behaviours often occur
during the preschool and adolescent years.
1. Multimodal and multidisciplinary treatment.
• Conduct disorder.
2. Parent management training:
• ADHD (more inattention and hyperactivity).
a. The NICE guidelines recommend group-
• Mild mental retardation.
based parent-training and education
• Anxiety disorders (e.g. post-traumatic stress
programmes.
disorder, separation anxiety, and panic disorder.
b. When there are particular difficulties in engag-
Behavioural problems often limited to situations
ing with the parents or family’s needs are too
in which fear occur).
complex, individual-based parent-training or
• Depressive disorder.
education programmes are recommended.
• Bipolar disorder.
c. Training should be structured and have a
• Dissociative disorder.
curriculum informed by principles of social
learning theory.
37.8.7 Comorbidities
d. Include relationship-enhancing strategies
Comorbidities for conduct disorder and role-playing sessions.
e. Enable parents to identify their own parent-
• ADHD: 50% of children with conduct disorder ing objectives.
• Mood disorders (e.g. depressive/bipolar disor- f. 8–12 sessions to maximize the possible ben-
der): 5%–31% of patients efits for participants.
3. Family therapy. • Being argumentative, noncompliant, rule break-

4. Individual psychotherapy: ing, and demonstrating spiteful hurtful behav-
a. Problem solving iour predict aggressive conduct disorder.
b. Impulse control • Children with oppositional defiant disorder have
c. Anger management higher chance of developing mood disorders,
d. Social skill training anxiety disorders, impulse control disorders,
5. Environmental interventions: consistent and and substance abuse disorders in adolescence
structured environment (e.g. boy’s home). and adulthood.
37.8.9 Management of Oppositional 37.9 ELECTIVE MUTISM (ICD-10 F94.0)

Defiant Disorder
37.9.1 Epidemiology
• Behaviour therapy: discourage oppositional
Elective mutism usually manifests in early childhood
defiant behaviour and encourage appropriate
(peak age 6–10 years), and boys and girls are equally rep-
and adaptive behaviour. Parents can couch them
resented. The prevalence is below 0.8 per 1000 children.
to develop adaptive responses.
• Individual psychotherapy: restoration of self-
esteem may lead to positive responses to exter- 37.9.2 Aetiology
nal control.
• Overprotective mother
• Parental training: eliminating harsh and puni-
• Distant father
tive parenting; increasing positive parent–child
• Trauma
interactions.
• No association with social adversity
37.8.10 Prognosis 37.9.3 Diagnosis
Conduct disorder According to ICD-10, elective mutism is character-
ized by a marked, emotionally determined selectivity
• 40% of young people with conduct disorder in speaking, such that the child demonstrates language
develop dissocial personality disorder in adult- competence in some situations but fails to speak in other
hood. Borderline IQ, mental retardation, and (definable) ones. The mutism lasts at least for 4 weeks.
family history of dissocial personality disorder
are predictive factors.
• 35%–75% of patients have comorbid ADHD and 37.9.4 Clinical Features
the presence of ADHD predicts worse outcome In addition to the features given earlier, elective mutism
for boys with conduct disorder. tends to be associated with personality features such as
• Callous unemotional trait predict a more severe
and persistent course of conduct disorder. • Social anxiety
• Adolescent-onset conduct disorder carries a bet- • Withdrawal
ter diagnosis and those with adolescent-onset • Sensitivity
are less likely to show antisocial behaviour and • Resistance
commit a crime.
37.9.5 Management
Oppositional defiant disorder
Management approaches include
• Two-thirds of children with oppositional defiant
disorder no longer meet the diagnostic criteria • Excluding any speech abnormalities
after 3 years. One-third of children will develop • Behavioural approaches
conduct disorder. • Use of tape recordings or the telephone
• Children with early onset, more severe symptoms, • Play therapy
and comorbidity of ADHD are three times more • Art therapy
likely to progress to a diagnosis of conduct disorder. • Family therapy
37.9.6 Course and Prognosis 37.10.4 Pathophysiology

In general, in the long term, the prognosis is good 1. Neurotransmitter dysregulation:
unless other disorders are also present. Poor prognosis a. Increase in D2 receptor sensitivity
is associated with duration of elective mutism longer b. Reduction in noradrenaline
than 12 months. c. Reduction in choline in the left putamen
d. Abnormalities in the basal ganglia and cau-
date nucleus
37.10 TIC DISORDERS AND GILLES
37.10.5 Clinical Features
DE LA TOURETTE’S SYNDROME
(ICD-10F 95.2; DSM-5 A11) • Onset is before 18 years of age.
• Tics are sudden, rapid, and involuntary move-
37.10.1 Epidemiology ments of circumscribed muscles without any
purpose.
Between 10% and 24% of children manifest tics during
• Presence of multiple motor tics and at least one
development. Tourette’s syndrome (combined vocal and
vocal tic.
multiple motor tic disorder) is rare, with a prevalence rate
• Eye blinking is the most common initial pre-
of about 4.5 per 10,000 among 16 and 17 year olds, with
senting sign and tics occur in a downward pro-
a male to female ratio of about 2:1.
gression along the human body.
• Tics occur many times per day, most days for over
12 months without remission period being longer
37.10.2 Age of Onset than 2 months based on the ICD-10 criteria.
• The average age of onset is 7 years (range 2–15
years). Common simple motor tics include (ICD-10)
• Mean age of onset of motor tics is 7 years.
• Mean age of onset of vocal tics is 11 years. • Eye blinking
• Shoulder shrugging
• Neck jerking
37.10.3 Aetiology (Table 37.5) • Facial grimacing
TABLE 37.5
Aetiology of Tics
Family Individual
Family clusters reported, especially Tourette’s No gross neurological abnormalities
Prevalence of multiple tics in 14%–24% of Increased incidence of ‘soft’ neurological signs and
first-degree relatives of patients with Tourette’s ‘nonspecific’ EEG changes
Increased family psychopathology in families of Some verbal–performance discrepancies in functioning
ticqueurs, although may be cause or effect Some neuroleptic medications effective in controlling tics
Monozygotic/dizygotic ratio: 50%:10% Tics exacerbated by dopamine agonists or stimulants
The mode of inheritance varies from autosomal Wide range of psychological mechanisms proposed for
dominance to an intermediate of autosomal tic disorders, from the psychoanalytic to the classically
dominance and autosomal recessive behavioural
Tic movement have been shown to mimic involuntary
startle responses to sudden stimulus
Paediatric Autoimmune Neuropsychiatric Disorders
Associated with Streptococcal infections (PANDAS)
Source: Reproduced from Puri, B.K. and Treasaden, I.H., Textbook of Psychiatry, 3rd edn., Churchill
Livingstone, Edinburgh, U.K., 2011. With permission.
Common simple vocal tics include (ICD-10) 37.10.8 Comorbidity
• Throat-clearing • ADHD: up to 50% of children with Tourette’s

• Sniffing syndrome
• Barking • OCD: up 40% of children with Tourette’s syndrome
• Hissing • Depression
• Disruptive behaviour
Common complex motor tics include (ICD-10)
37.10.9 Management
• Hitting oneself Transient tics resolve spontaneously and thus require no
• Hopping further treatment.
• Jumping
Pharmacological treatment for Tourette’s syndrome
Common complex vocal tics include (ICD-10)
1. Indications for pharmacological treatment:
• Coprolalia. a. Disruptive behaviour at school or at home
• Repeating certain words. b. Very poor academic performance
• Palilalia. c. Rejection by peers
• DSM-IV-TR requires the tic-free period to be 2. Haloperidol (0.5–5 mg/day): up to 80% with
less than 3 consecutive months. satisfactory response. Haloperidol is associated
• The DSM-5 requires that the tics may wax and with extrapyramidal side effects.
wane in frequency but have persisted for more 3. Risperidone (1–4 mg/day) and sulpiride (100–
than 1 year since first tic onset. 400 mg/day) are effective and better tolerated
• Associated features include obsessions, compul- than haloperidol.
sions, learning difficulties, impulsivity, inatten- 4. Pimozide (1–2 mg/day): the child requires ECG
tion, and emotional disturbance. monitoring. There is little experience in chil-
dren younger than 12 years.
5. Clonidine (0.05 mg TDS) improves attention.
37.10.6 Investigations 40%–70% of patients benefit from clonidine.
• Two-thirds of children with Tourette’s syndrome Antipsychotics may be more effective than
demonstrate EEG abnormalities. clonidine.
6. Tricyclic antidepressant such as imipramine
may decrease disruptive behaviour.
37.10.7 Differential Diagnosis 7. 20%–30% of patients may require long-term
• Transient tic disorder (ICD-10 F95.0) affects 10%– pharmacological therapy.
20% of children. The age of onset is less than 18
years. Tics involving blinks, frowns, grimaces, Psychological treatment for Tourette’s syndrome
head flicks, grunts, throat clearing, and sniffing
from 4 weeks to 1 year. Prognosis is good. • Habit reversal involves performing simultaneous
• Chronic motor or vocal tic disorder (ICD-10 incompatible movements to reduce unwanted
F95.1) is rare and does not require the presence movements.
of both motor and vocal tics. The age of onset is • Behaviour therapy targets at replacing the tic
less than 18 years. The duration is longer than behaviour by a desired behaviour in premoni-
1 year with remission of less than 2 months. tory urge.
• Movement disorders: athetoid, choreiform, dys- • Massed practise involves repeating tics for many
tonia hemibalismic movements, mannerisms, times as an attempt to reduce the frequency of tics.
myoclonia, and stereotypic movements. • Other behaviour therapies include self-
• Neurological disorders include Huntington’s monitoring, incompatible response training, and
disease, Parkinson’s disease, Sydenham’s cho- removal of positive reinforcement.
rea, and Wilson’s disease. • Self-esteem building and social skill training
• Obsessive–compulsive disorder. may be helpful.
37.10.10 Course of Illness • Social communication disorder

• Speech sound disorder
• Transient tic disorder is not chronic or recurs • Childhood-onset fluency disorder
during periods of stress. There may be a pro- • Voice disorder
gression from simple tics to Tourette’s syndrome
in a minority of cases.
• Tourette’s syndrome is a chronic disease with 37.15 NONORGANIC ENURESIS (ICD-
remissions and exacerbations.
10 F98.0; DSM-5 307.6)
• People with severe syndrome may develop
severe depressive episode and suicide attempt. 37.15.1 Definition
• Chronic motor or vocal tic disorder usually lasts
for 4–6 years and stops in early adolescence. According to ICD-10, nonorganic enuresis is character-
ized by the involuntary voiding of urine, by day and/or
by night, which is abnormal in relation to the individual’s
37.11 PICA (ICD-10 F98.3) mental age and which is not a consequence of a lack of
bladder control resulting from any neurological disorder,
• Persistent eating of nonnutritive substances for epilepsy, or a structural urinary tract abnormality. The
at least twice per week for duration of 1 month. minimum duration of enuresis is 3 months. It is gener-
• Chronological and mental age is above the age ally not diagnosed before the age of 5 years and may be
of 2 years. subdivided into
• Associated with learning disability, psychosis,
and social deprivation. • Primary: urinary continence never achieved.
• Secondary: urinary continence has been
37.12 STAMMERING (ICD-10 F98.5) achieved in the past.
• A disturbance of rhythm and fluency of speech The DSM-5 criteria are similar to ICD 10 and further
by frequent repetition or prolongation of sounds subdivide enuresis into
or syllables, leading to hesitation.
• The duration of stammering is longer than 3 • Nocturnal only: passage of urine only during
months. nighttime sleep
• Affecting 1% of children at school entry. • Diurnal only: passage of urine during waking
• The peak age of onset is 5 years. hours
• Treatment: speech therapy. • Nocturnal and diurnal: a combination of the two
• Prognosis: 50%–80% of children recover from aforementioned subtypes
stammering.
37.13 CLUTTERING (ICD-10 F98.6) 1. Prevalence. The prevalence at different ages has
• A rapid rate of speech with breakdown in fluency been found to be
• No repetitions or hesitations a. 7 years—6.7% in boys and 3.3% in girls
• Reduction in speech intelligibility b. 9–10 years—2.9% in boys and 2.2% in girls
c. 14 years—1.1% in boys and 0.5% in girls
2. Sex ratio:
37.14 COMMUNICATION a. Male to female = 1:1 at the age of 5 years;
DISORDERS (DSM-5) approximately 2:1 in adolescence.
b. Secondary enuresis is more common in boys.
The DSM-5 includes the following seven communication
disorders:
• Language impairment Nonorganic enuresis may be associated with emotional
• Late language emergence problems, although it should be noted that the latter may
• Specific language impairment be secondary to the enuresis itself.
37.15.4 Aetiology 37.16 NONORGANIC ENCOPRESIS

Possible causes that have been proposed include (ICD-10 F98.1) (DSM 5 307.7)
37.16.1 Definition
• Genetic—70% have a first-degree relative with
late attainment of continence. According to ICD-10, nonorganic encopresis is the
• Stressful life events—a doubling of frequency. repeated voluntary or involuntary passage of faeces,
• Delayed toilet training. usually of normal or near-normal consistency, in places
• Developmental delay—twice as common in not appropriate for that purpose in the individual’s own
enuretic children as in controls. sociocultural setting. It is generally not diagnosed before
• Bladder structure—enuretic children are more the age of 4 years and there should be at least one episode
likely than non-enuretics to have a different per month for 6 months. It may be subdivided into
shape of bladder baseplate and to have a reduced
functional bladder volume. 1. Continuous encopresis: bowel control has never
been achieved.
2. Discontinuous encopresis: there has been a
period of normal bowel control in the past.
37.15.5 Management
Points in the management include DSM-5 criteria are similar to the ICD-10 except the mini-
mum duration is 3 months.
1. A full assessment including a physical assess-
ment to exclude a physical cause; look for evi-
dence of:
a. Urinary frequency • Prevalence. At the age of 5 years, the prevalence
b. Haematuria is 1.5%. In 12 year olds, the Isle of Wight study
c. Dysuria found a prevalence of 1.3% in boys and 0.3% in
d. Urgency girls.
2. Urinary microscopy and microbiological • The male to female sex ratio is between 3:1 and 4:1.
analysis
3. Urodynamic study if the patient is older than 15
years 37.16.3 Clinical Features
4. Observation period
The presentation of this disorder is summarized in
5. Fluid restriction at night
Table 37.6.
6. Star chart—relapse rate of approximately 40%
7. Pad and buzzer or, in older children, a pants
alarm—relapse rate of approximately 40% 37.16.4 Aetiology
8. Low-dose tricyclic antidepressants—but there
are side effects and there is a high rate of relapse Causes of nonorganic encopresis are shown in Table 37.7.
on discontinuation—can be useful for short
time periods (e.g. school trips)
9. Nasal desmopressin—should not be continued 37.16.5 Management
for more than 3 months without stopping for a Points in the management include
week for full reassessment
10. Exercises to increase the functional capacity of • A full assessment, but take care in carrying out
the bladder an anal and rectal examination as informed con-
11. Habit training sent is required from the child who may have
been sexually abused (if there is evidence of
sexual abuse, the appropriate procedures should
be brought into play)
37.15.6 Course and Prognosis
• Assessment of family relationships and the
In general, the prognosis is very good. home circumstances
TABLE 37.6
Presentation of Faecal Soiling (Encopresis)
Consistency of
Faeces Normal, Loose, or Constipated
Place deposited In pants, hidden, or in ‘significant’ places (e.g. in a particular person’s
cupboard)
Development Never continent (continuous), after period of continence (discontinuous),
or regression (in various contexts—see succeeding text)
Activity Smearing, anal fingering, or masturbation
Context Power battle, upsetting life events (e.g. sexual abuse, divorce), and/or
other psychiatric disorder
Physical With soreness, anal fissures, etc., or with normal anus
Source: Reproduced from Puri, B.K. and Treasaden, I.H., Textbook of Psychiatry, 3rd edn.,
Churchill Livingstone, Edinburgh, U.K., 2011. With permission.
TABLE 37.7
Causes of Encopresis
Constitutional Variability Can Include
Congenital Bowel Control
Individual Developmental delay
Physical trigger—anal fissure—constipation
(low-roughage diet)
Other bowel disorders
Chronic constipation
Hirschsprung’s disease
Anxiety (fear of soiling)
Parent–child Coercive toilet training
Emotional abuse or neglect
‘Battleground’ for relationship problems
Anger (protect against parents)
Wider environment Sexual abuse
Family disharmony
Source: Reproduced from Puri, B.K. and Treasaden, I.H., Textbook

of Psychiatry, 3rd edn., Churchill Livingstone, Edinburgh,
U.K., 2011. With permission.
• Investigations: thyroid function test, barium If the aforementioned procedures fail, an intense
enema if suspected obstructive lesions in bowels behavioural programme in hospital may be required
• Education of the carers with respect to the
mechanics of defaecation 37.16.6 Course and Prognosis
• Improving the child’s self-esteem
In general, the prognosis is very good.
• Individual therapy
• Family therapy
37.17 SCHOOL REFUSAL
• Pharmacotherapy to soften the stools or to pro-
mote gastrointestinal motility School refusal is refusal to attend or stay at school because
• Behaviour therapy, for example, star chart of anxiety and in spite of parental or other pressure.
37.17.1 Epidemiology 37.17.3 Management
Boys and girls are equally represented. There are three The mechanisms underlying the school refusal should
main incidence peak ages: be identified. If the condition is acute, a return to school
should be arranged as soon as possible (the Kennedy
1. Separation anxiety at age of 5 years approach), whereas if the condition is chronic, a graded
2. At age of 11 years, which may be precipitated by return to school should be arranged. Any specific prob-
the change from junior to secondary schooling lems (e.g. social phobia) should be addressed. If the indi-
3. At age of 14–16 years, which may be a symptom vidual does not return to school, then inpatient treatment
of a psychiatric disorder: may be necessary.
a. Depressive disorder
b. A phobia (e.g. social phobia)
The most common presentation is the one at 11 years. 37.17.4 Course and Prognosis
Younger children have a better prognosis. Most children
37.17.2 Differences from Truancy
and adolescents do return to school, but approximately
Truancy is an important differential diagnosis. Truancy one-third of older patients seen in clinics develop neu-
differs from school refusal in the following aspects rotic difficulties or social impairment or social with-
(Table 37.8): drawal in adulthood.
TABLE 37.8
Compare and Contrast School Refusal and Truancy
School Refusal Truancy
Ego Ego-dystonic Ego-syntonic and intended
Family history of Anxiety disorders and failure of parents Antisocial personality disorder
psychiatric disorders to separate from own families of origin or forensic history
Family size Small family and the patient is the Large family size
youngest child
Parenting style Overprotective parenting or unassertive Inconsistent discipline
parents (ineffective father, overanxious
mother)
Age of child and Three peaks: More common in adolescents
aetiology Age 5 years: manifestation of separation than younger children
anxiety at school entry
Age 11 years: triggering by transfer to
secondary school or avoidance
character
Age 14–16 years: manifestation of
depression or phobia such as
agoraphobia or social phobia
Symptoms Overt anxiety at the time of going to Not associated with psychiatric
school with ‘somatic disguise’ such as symptoms but wilful intention
abdominal pain (aka Masquerade to skip classes
syndrome)
Location when absent Usually at home with parental Usually outside home, engage
from school permission. Parents are aware of their in alternative activities
whereabouts without parental permission
and awareness
Academic performance Satisfactory academic performance Poor academic performance
37.17.5 Disorders in Scholastic Skills 37.19 SUBSTANCE MISUSE IN ADOLESCENCE

See Table 37.9. 37.19.1 Type of Substance Misuse
37.18 OTHER PSYCHIATRIC DISORDERS • Experimental use (e.g. initial use as a result of
IN CHILDHOOD (0–11 YEARS) AND curiosity)
• Recreational use (e.g. under peer pressure)
ADOLESCENCE (12–17 YEARS) • Dependent (e.g. strong compulsion to take illicit
See Tables 37.10 through 37.17. drugs)
TABLE 37.9
Summary of the ICD-10 Classifications
ICD-10 Classification ICD-10 Criteria
Common exclusion criteria include sensory impairment, IQ < 70, and extreme
inadequacies in education.
F80.0 Specific speech articulation Articulation skills are 2 standard deviation (SD) below the lower limit of child’s
disorder age and 1 SD below the nonverbal IQ. Language expression and comprehension
are within expected limit of child’s age.
F80.1 Expressive language disorder Expressive language skills are 2 SD below the lower limit of child’s age and 1 SD
below the nonverbal IQ. Receptive language skills, nonverbal communication,
and imaginative language functions are within expected limit of child’s age.
F80.2 Receptive language disorder Language comprehension are 2 SD below the lower limit of child’s age and
receptive language skills are 1 SD below the nonverbal IQ.
F80.3 Acquired aphasia with epilepsy Severe loss of expressive and receptive language skills occur over a period of time
(Landau–Kleffner Syndrome) not exceeding 6 months. Language development was normal before the loss.
Paroxysmal EEG abnormalities affecting one or both temporal lobes become
apparent within a time span within 2 years after the initial loss of language.
Hearing and nonverbal intelligence are within normal range.
F81.0 Specific reading disorder Prevalence is 4% among 9–10 year olds.
Male to female ratio is 3:1.
A score on reading and/or under comprehension that is 2 SE below the level
expected on the basis of the children’s chronological age and intelligence.
A history of serious reading difficulty at earlier age, spelling test score being at
least 2 SE below expected level, and the reading impairment significantly
interferes with academic achievement or ADL.
F81.1 Specific spelling disorder The score on a standardized test is at least 2 SE below the expected level but
scores on reading accuracy and comprehension are within normal range.
In spelling disorder, arithmetical skill is normal and vice versa.
F81.2 Specific disorder of arithmetical The difficulties have been present from the early stages of learning and lead to
skills significant interferences of academic achievement and activities of daily living
(ADL).
Epidemiological studies show that this disorder is more common in females.
F82 Specific developmental disorder The score on a standardized test of motor function is at least 2 SE below the
of motor function expected level with no diagnosable neurological disorder. Common exclusion
criteria: IQ is less than 70.
Other disorders F81.3 Mixed disorder of scholastic skills (combination of arithmetical, reading,
and spelling disorders).
F81.8 Other developmental disorders of scholastic skills.
F81.9 Developmental disorder of scholastic skills, unspecified.
Source: WHO, ICD-10: The ICD-10 Classification of Mental and Behavioural Disorders: Clinical Descriptions and
Diagnostic Guidelines, World Health Organization, Geneva, Switzerland, 1992.
TABLE 37.10
Compare and Contrast Childhood- and Adolescence-Onset Schizophrenia
Childhood-Onset Schizophrenia Adolescence-Onset Schizophrenia
Epidemiology Epidemiology
Psychosis is extremely rare before 13 years of age. • Prevalence is 2–3/1000.
• The prevalence of very early-onset schizophrenia (age 13 years) is
around 1/100,000.
• The prevalence of early-onset schizophrenia (age 18 years) is 18/100,000.
• Slight excess in boys.
Aetiology Aetiology
Strong family history of schizophrenia. • Genetic predisposition.
• Neurodevelopmental hypothesis with reduction in cortical volumes and
increase in ventricular size.
• Drug-induced psychosis.
• Organic causes (e.g. central nervous system infection).
• Tuberous sclerosis.
• Partial complex seizures.
• Leukodystrophies.
Clinical features Clinical features
• Uneven development with delay in language and social • Deterioration in scholastic ability and self-care may be the first sign.
behaviour. • Visual hallucinations and anxiety symptoms are common.
• Cognitive impairment and behavioural abnormalities in • Mood disturbance.
childhood. • Persecutory ideation.
• Gradual onset. • Abnormal perceptual experience.
• Common features include visual hallucinations ideas of • Cognitive and social impairment.
reference and negative symptoms. • Negative symptoms, passivity, well-formed delusions, thought disorders,
• Paranoid symptoms are less frequent compared to adults. and first rank symptoms are not common.
Differential diagnosis Differential diagnosis
• Disintegrative disorder in childhood. • Conduct disorder
• Obsessive–compulsive disorder. • Severe emotional disorder
• Subacute sclerosing panencephalitis
Treatment Treatment
• Risperidone is effective. • Similar to the treatment used in childhood schizophrenia.
• Children are more prone to the metabolic side effects • Lorazepam assists stabilization of acutely disturbed patients.
and weight gain associated with olanzapine. • Clozapine can be used in adolescents with treatment resistant schizophrenia.
• Avoid first-generation antipsychotic that associate with • Close liaison with paediatrician is necessary if the psychosis is a result of
high rate of extrapyramidal side effects. organic causes.
Prognosis Prognosis
• Childhood psychosis carries the worst prognosis among • 80% of adolescent diagnosed with schizophrenia still suffer from
all psychiatric disorders in childhood. schizophrenia in early adulthood.
37.19.2 Aetiology • Individual risk factors include low self-esteem,

high sensation seeking, and self-destruction.
• Community factors include widespread drug
availability, high crime rate, poverty, and cul-
tural acceptance of drugs.
• School factors include peer rejection, lack of 37.19.3 Smoking
interest in studies, and academic failures.
• Family factors include parental substance abuse • Two-thirds of 15- and 16-year-old adolescents
and family conflict. smoke cigarettes.
TABLE 37.11
Compare and Contrast Childhood- and Adolescence-Onset Depressive Disorder
Childhood-Onset Depressive Disorder Adolescent-Onset Depressive Disorder
• Prevalence is 1% (rare). • 6.6% at 15 years and 22.1% at 18 years.
• Boys and girls have equal frequency until the age • Similar to adult depression with female dominance (35% for girls,
of 14 years. 19% for boys).
• Childhood depression is less common than • Mean duration of illness is 7–9 months.
childhood dysthymia.
Aetiology Aetiology
• Genetic causes (50%). • 60–70% of patients are caused by adverse life events.
• Adverse parenting and maltreatment. • Arguments with parents.
• Conduct disorders in childhood carry an increased • Multiple family disadvantages.
risk for depressive symptoms in early adult life. • Positive family history of depression is common.
• Impair neurogenesis in hippocampus. Clinical features
Clinical features • Symptoms similar to adult with a minimum of 2 week period if
• Boredom. sadness, irritability, loss of interest, and loss of pleasure.
• Growth impairment. • Impairment in social and role functions.
• Low motivation to play. • Promiscuity may be the presenting feature.
• Poor academic performance. • Anxiety symptoms and conduct disorders are most commonly
• Poor feeding. associated disorders.
• Somatic complaints. • Less likely to have psychomotor retardation in comparison to
• Mood symptoms are similar to adults and severe adults.
cases may present with mood congruent psychotic
features.
• More anxiety and anger but fewer vegetative
symptoms when compared with adults.
Diagnostic instrument Diagnostic interview K-SADS-PL
• Children Depression Inventory (CDI). • Kiddie-Sads-Present and Lifetime Version (K-SADS-PL).
Treatment Treatment (NICE guidelines)
• Psychotherapy (e.g. CBT, family therapies) is the • Mild depression.
first-line treatment. • Watchful waiting for 2 weeks.
• For children at age 5–11 years, cautiously consider • Offer supportive psychotherapy, group-based CBT or guided
the addition of fluoxetine if psychotherapy fails self-help for 2–3 months.
after 3 months. There is no doubt that • No antidepressant is required.
antidepressants increase the risk of suicidal Moderate to severe depression (including psychotic depression)
behaviours in children. • Individual CBT, IPT, and short-term family therapy may be helpful.
• TCA is not effective in prepubertal children. • If the adolescent does not respond, consider alternative
• ECT is not recommended in children at age psychotherapy or augment with fluoxetine after multidisciplinary
between 5 and 11 years. review.
• If patient is unresponsive after combination treatment, arrange
another multidisciplinary review and consider either systemic
family therapy (at least 15 fortnightly sessions) or individual child
psychotherapy (30 weekly sessions).
Use of antidepressants
• Fluoxetine 10 mg/day is the first-line treatment for those who need
antidepressant.
• Citalopram and sertraline can be used if there is clear evidence after
a trial of fluoxetine and psychotherapy.
• Antidepressants should be discontinued slowly over 6–12 weeks to
reduce discontinuation symptoms.
• Avoid TCA, paroxetine, venlafaxine, and St John’s wort.

Compare and Contrast Childhood- and Adolescence-Onset Depressive Disorder
Childhood-Onset Depressive Disorder Adolescent-Onset Depressive Disorder
Prognosis Prognosis
• Most children have good prognosis. • High remission rate: 90% by 2 years.
• Very early-onset depression is associated with • High recurrence rate: 40% by 2 years.
poor prognosis. • High rate of conversion to bipolar disorder: 40% by 2 years.
• Depression and conduct disorder is associated with an increased
risk of suicide, alcoholism, substance misuse, and antisocial
personality disorder.
37.19.4 Alcohol Abuse in Adolescence 37.19.8 Treatment

• Equal sex incidence. • Refer the child or adolescent to the young peo-
• 50% of adolescents taste the first alcohol at home. ple’s substance misuse service.
• 50% of 16- to 19-year-olds are regular drinkers. • The service should be user-friendly and promote
• Alcohol dependence is associated with adoles- self-referral.
cent suicide. • Strategies include harm reduction, needle
exchange, motivational enhancement, detox
37.19.5 Volatile Substances regimes, and family therapy.
• Common volatile substances include solvent and
glue. 37.19.9 Prognosis
• 21% of adolescents have tried volatile substances.
• The effects include euphoria, disinhibition, 1. Substance misuse in adolescence is associated with
impulsiveness, giddiness, nausea, vomiting, a. Accidental deaths
slurred speech, visual hallucination, and para- b. Delinquency
noid delusion. c. Suicide
• Students prefer this method because they can be
intoxicated in school. 37.19.10 Legal Aspects of the Child
• Chronic use leads to tolerance and withdrawal
and Adolescent Psychiatry
symptoms.
• Gillick competence states that a child below the
age of 16 years can give consent to treatment
37.19.6 Cannabis
without parental agreement (e.g. contraception)
• Most adolescents in the United Kingdom, provided that the child have achieved sufficient
United States, and Australia have tried cannabis maturity to understand fully the treatment pro-
in their life. posed. The child has no right to refuse treatment
• Most adolescents will stop using cannabis in that is in his or her best interests.
their 20s. • In the United Kingdom, parents have parental
• About one-tenth will use it on a daily basis. responsibility under the Children Act (2004) to
• Regular use of cannabis may precipitate acute give consent on the child’s behalf, especially
schizophrenia. when the child is refusing treatment in the best
interest of the child.
• If both child and parents refuse treatment and
37.19.7 Other Substances
the child is at high psychiatric risk, the Mental
• Amphetamine, benzodiazepine, and hallucino- Health Act can be applied.
gen are commonly used by adolescents. • If the child is in danger, the clinician can make
• The use of cocaine and opiate misuse is less the best medical decision for the child based on
common. the Common Law.
TABLE 37.12
Compare and Contrast Childhood- and Adolescence-Onset Suicide and Self-Harm
Childhood-Onset Suicide and Self-Harm Adolescent-Onset Suicide and Self-Harm
• Suicide is very rare in prepubertal • 20,000 young people in England and Wales are referred to hospital for
children. assessment of self-harm each year.
• Rate of attempted suicide: 8%–9% in western countries.
• Rate of suicidal ideation: 15%–20%.
• Suicide is common among young people at age between 14 and 16
years.
• Male to female ratio for self-harm is 1:6.
• Male to female ratio for suicide = 4:1.
• Suicide is the third commonest cause of death for young people after
accident and homicide.
• Self-harm is the most common cause of admission to a general
hospital.
Aetiology Aetiology
• It may be caused by accident Psychiatric disorders (e.g. depression, psychosis, substance abuse, conduct
(e.g. accidental hanging by playing with disorder, isolation, low self-esteem, and physical illness). For girls,
curtain string). self-harm is strongly predicted by depressive disorder. For boys, self-harm
• The child may exhibit stereotyped is strongly predicted by previous suicide attempt.
movements to an extent that either causes Family issues like loss of parent in childhood, family dysfunction, abuse,
physical injury or marked interference and neglect.
with normal activities for at least 1 month. Increase in adolescence suicide is a result of
1. Factors influencing reporting (‘copycat’ suicides resulting from media
coverage; the fostering of illusions and ideals through internet suicide
groups and pop culture).
2. Factors influencing the incidence of psychiatric problems
(e.g. problems with identify formation, depression, substance abuse,
and teenage pregnancy).
3. Social factors (e.g. bullying, the impact of unemployment for older
adolescents, poverty, loosening of family structures, living away from
home, migration, parental separation, and divorce).
Common Self-harm and suicide methods
Self-harm: Cutting and scratching are common impulsive gestures. Cutting
often has a dysphoric-reducing effect.
Suicide: Self-poisoning is a common method used by British adolescents.
The use of firearms is more common in the United States.
Management of Self-harm and suicide (NICE guidelines)
Management of Self-laceration
• Offer physical treatment with adequate anaesthesia.
• Do not delay psychosocial assessment.
• Explain the care process.
• For those who repeatedly self-poison, do not offer minimization advice
on self-poisoning because there is no safe limit.
• For those who self-injure repeatedly, teach self-management strategies
on superficial injuries, harm minimization techniques, and alternative
coping strategies.

Compare and Contrast Childhood- and Adolescence-Onset Suicide and Self-Harm
Childhood-Onset Suicide and Self-Harm Adolescent-Onset Suicide and Self-Harm
Management of suicidal adolescent

• Consider inpatient treatment after balancing the benefits against loss of
family support.
• Involve the young person in the admission process.
• ECT may be used in adolescents with very severe depression and
suicidal behaviour not responding to other treatments.
Prognosis
Self-harm
• 10% will repeat in 1 year.
• Higher risk of repetition in older male adolescents, history of suicide
attempts, persistent suicide ideation, psychotic symptoms, substance
misuse, and use of methods other than overdose or self-laceration.
Suicide
• 4% of girls and 11% of boys will kill themselves in 5 years after first
episode of suicide attempt.
TABLE 37.13
Compare and Contrast Childhood- and Adolescence-Onset Bipolar Disorder
Childhood-Onset Bipolar
Disorder Adolescent-Onset Bipolar Disorder
• Rare. • 20% of adult bipolar patients experience their first episode of
• Associated with ADHD. mania before the age of 20.
Clinical Features • The prevalence of bipolar disorder in adolescences is
• Reduction of sleep is often 0.5–1.0%.
the first indicator for Aetiology
childhood bipolar disorder. • Genetic predisposition.
Treatment • Drug induced (e.g. illicit [amphetamine] and therapeutic
• First line of treatment is [e.g. steroid] drugs).
olanzapine. Clinical Features
Prognosis • Similar to adults.
• Childhood bipolar disorder • First rank symptoms present in 20% cases.
is ranked as having the Diagnostic Interview: K-SADS-PL
second worst prognosis Treatment
among all psychiatric • First line of treatment is olanzapine although valproate and
disorders in childhood. lithium are effective.
• For ADHD children with manic symptoms, stimulants can be
prescribed.
• Adjunctive family therapy is useful in stabilizing
symptomatology.
TABLE 37.14
Compare and Contrast Childhood- and Adolescence-Onset Anxiety Disorders
Childhood-Onset Anxiety Disorders Adolescent-Onset Anxiety Disorders
• Prevalence for separation anxiety disorder is 3.6%. • Prevalence rate for generalized anxiety disorder
• At least 50% of adult cases of anxiety symptoms had their onset in childhood. in adolescents is 3.7%.
• 2% of children have phobia.
Aetiology Aetiology
• In infancy, fear and anxiety are provoked by sensory stimuli. • In adolescence, anxiety is caused by
• In early childhood, fear is evoked by stranger and separation anxiety. performance anxiety and fear of social
• In late childhood, it is caused by fear of dark, animals (more common in girls), and situations.
imaginary creatures. • 30% of patients have family history of phobia
Comparison with older patients and anxiety disorder.
• Sleeping difficulties and somatic complaints such as headache are common. Clinical features
• Panic attacks are less common. • Clinical features are similar to adult.
Separation anxiety disorders of childhood (ICD-10 F93.0) • Somatic complaints are common.
• Onset is before 6 years. Social phobia
• Unrealistic persistent worry: possible harm befalling major attachment figures or • Common in adolescents.
about loss of such figures. The child will have anticipatory anxiety of separation • This is a fear centred on scrutiny by other
(e.g. tantrums, persistent reluctance to leave home, excessive need to talk with people when in small social groups, e.g. when
parents, and desire to return home when going out). the patient is in a restaurant.
• Symptoms in the day: persistent reluctance or refusal to go to school because of • It is often associated with low self-esteem.
the fear over separation from a major attachment figure in order to stay at home. Panic disorder
Repeated occurrence of physical symptoms (e.g. nausea, stomachache, headache, • Panic attacks are associated with agoraphobia.
and vomiting). Separation anxiety
• Symptoms at night: difficulty in separating at night as manifested by persistent • Patients may present as a case of school refusal.
reluctance or refusal to go to sleep without being near to the attachment figure. PTSD
The child also has repeated nightmares on the theme of separation. • Occur in young people exposing to a traumatic
• Minimum duration is 4 weeks. event, e.g. physical or sexual abuse and fatal
Phobic anxiety disorder of childhood (ICD-10 F93.1) accident happens to friends or relatives.
• The individual manifests a persistent or recurrent fear that is developmentally • Depression is common among older children
phase—appropriate but is abnormal in degree. and adolescents.
• It is associated with significant social impairment. • New aggression may emerge.
• Minimum duration of symptoms is 4 weeks. • Other symptoms such as nightmares, social
Social anxiety disorder of childhood (ICD-10 F93.2) withdrawal, and numbing are common.
• Persistent anxiety in social situations where the child is exposed to unfamiliar Differential diagnosis
people including peers. • Hyperthyroidism.
• The child exhibits self-consciousness, embarrassment, and over-concern about the Treatment
appropriateness of his or her behaviour. • CBT should be the first-line treatment.
• The child has satisfying social relationship with familiar people but there is • If CBT fails, the child and adolescent
significant interference with peer relationships. psychiatrist can consider prescribing fluoxetine
• Onset of the disorder coincides with the developmental phase. or fluvoxamine.
• Minimum duration of symptoms is 4 weeks. • Psychoeducation.
Childhood emotional disorder • Benzodiazepine and buspirone should be
• Prevalence is 2.5%. avoided in adolescents because this will cause
• More common in girls. disinhibition syndrome.
• It presents as anxiety and somatic complaints with good prognosis.
Post-traumatic stress disorder
• Compulsive repetitive play representing part of the trauma, failing to relieve
anxiety, and loss of acquired developmental skills in language and toilet training.
• Emergence of new separation anxiety.

Compare and Contrast Childhood- and Adolescence-Onset Anxiety Disorders
Childhood-Onset Anxiety Disorders Adolescent-Onset Anxiety Disorders
Treatment Prognosis
• Behavioural therapy for the child. • Majority have good prognosis.
• Psychoeducation for the parents. • Increase in risk of anxiety disorder and
Prognosis substance misuse.
• There is a potential link between separation anxiety in childhood and panic • Phobic disorder may persist into adulthood as
disorder in adult. phobic disorder has its origin in adolescence.
• In the United Kingdom, the Mental Capacity b. Assess the impact of abuse on the physical
Act (2005) is only applicable to people above and emotional conditions.
the age of 16 and over. c. Look for further evidence to support the
• The Mental Health Act can be applied to provide claim of abuse and consistency in the child’s
involuntary psychiatric treatment for patients accounts.
(regardless of age) who are at high psychiatric d. Explore other types of abuse and family
risk and refusing treatment. members being involved.
e. Assess cognitive and language competence
of the child.
37.20 PHYSICAL AND SEXUAL ABUSE IN f. Identify emotional and behavioural distur-
CHILDREN AND ADOLESCENTS bance in the child (e.g. conduct disorder and
truancy).
37.20.1 Epidemiology g. Recognize the emotional, physical, and
therapeutic needs of the child.
• In the United Kingdom, 7% of children were
h. Seek the child’s view on staying in a safe
rated as experiencing serious physical abuse and
and protective environment (e.g. staying in a
6% had serious emotional maltreatment.
shelter administered by the social agency).
• 3/1000 children are on the official Child
i. Assess family dynamics, family members
Protection Register for the ages between 0 and
involved, and parental psychopathology.
18 years.
3. For young children, special techniques of
• 10% of children have been victims of sexual
interviewing such as drawing and using ana-
abuse if a loose definition of sexual abuse
tomically correct dolls may facilitate disclo-
including exhibitionism, lascivious talk,
sure of sensitive information from the child’s
and being sexually active at the age of 15 is
perspectives.
applied.
4. It is important of not asking leading questions
• The male to female ratio is 1: 2.5.
that may suggest certain answers.
• Each year, 3% of children up to the age of 13
5. Psychiatrist should use age-appropriate lan-
years are brought to the attention of professional
guage and ask one question at a time.
agencies because of suspected abuse.
6. After the initial assessment, further interview
may be videotaped with the parental consent
37.20.2 Assessment and permission from the child. This will avoid
the child to mention the traumatic experience
1. There are four types of abuse: physical abuse, repeatedly to different professionals.
sexual abuse, emotion abuse, and neglect. 7. Address the dilemma whether other family
2. The assessment should include the following: members shall be involved in the assessment of
a. Evaluate and validate the claim of abuse child. Psychiatrist should always seek the child’s
from the child’s perspectives. view on this issue.
TABLE 37.15
Compare and Contrast Childhood- and Adolescence-Onset Obsessive–Compulsive Disorder
Childhood-Onset Obsessive–Compulsive Disorder (OCD) Adolescent-Onset OCD
• One-third of OCD patients have their onset in childhood. • Two-thirds of OCD patients have their onset in adolescence.
• Prevalence is 0.25%. • Prevalence is 0.6%.
• Boys have earlier onset than girls. • No predomination by male adolescents.
• Boys predominate childhood OCD.
Aetiology Aetiology
• 5% of parents have OCD. • Similar aetiology as childhood OCD.
• Four times increase in risk of OCD among relatives.
• PANDAS is caused by haemolytic streptococcal infection
and associated with OCD.
• The association between OCD and tics suggests the role of
basal ganglia lesions.
• Insidious onset. • Similar to adult-onset OCD.
• Symptoms include contamination, checking rituals, and • Adolescents usually demonstrate internal resistance to
worry about harm to self. obsessions.
• Mild obsessions and rituals (e.g. magical number of
repetition to get good exam result) is part of the normal
development.
Comorbidity Comorbidity
• Tourette’s syndrome. • Tourette’s syndrome.
• ADHD. • Conduct disorder.
• Anxiety. • Trichotillomania.
• Depression. • Nail biting.
• Bedwetting. • Body dysmorphic disorder.
• Sleep disturbance. • Depression.
• Psychomotor changes. • Anxiety.
• Joint pain. • Eating disorders.
Management Management
Investigations for PANDAS • Treatment is similar to treatment in childhood OCD.
• Measure streptococcus titer. • Treatment-resistant OCD requires further assessment at
• The antistreptolysin O (ASO) titer rises 3–6 weeks after a specialist centre.
streptococcus infection. • Consider clomipramine and low-dose risperidone.
• The antistreptococcal DNAse B (anti-DNAse B) titer rises
6–8 weeks after a streptococcus infection.
Treatment
• CBT and exposure response prevention (ERP) is the
first-line treatment.
• Train parents to supervise ERP.
• Sertraline has the licence to treat OCD from the age of 6
years onwards.
• Fluvoxamine has the licence to treat OCD.
• From the age of 8 years onwards.
• Fluoxetine is indicated for OCD with significant comorbid
depression.
• Avoid TCA (except clomipramine), SNRIs, and MAOIs.
• If antipsychotic drug is required, do not prescribe
antidepressant concurrently.

Compare and Contrast Childhood- and Adolescence-Onset Obsessive–Compulsive Disorder
Childhood-Onset Obsessive–Compulsive Disorder (OCD) Adolescent-Onset OCD
• There is a delayed onset of action up to 4 weeks and full
therapeutic effect up to 8–12 weeks.
• Duration of treatment is at least for 6 months.
• In childhood body dysmorphic disorder, fluoxetine is the
drug of choice.
Prognosis Prognosis
• 50% of children with OCD continue to suffer from OCD in • Remission in one-third of patients.
adulthood. • There is a strong continuity into adulthood in two-thirds of
• Some of them develop anankastic personality disorder. patients.
• 25% of children with OCD have remission.
• Short duration is a positive prognostic sign.
TABLE 37.16
Compare and Contrast Childhood- and Adolescence-Onset Somatization Disorders
Childhood-Onset Somatization Disorders Adolescent-Onset Somatization Disorders
• Recurrent abdominal pain occurs in 10%–25% of children • About 10% of adolescents report multiple physical symptoms.
between the ages of 3–9 years. • Prevalence of somatization disorder is less than 0.1%.
• Hysteria in childhood is rare with equal gender ratio.
Aetiology Aetiology
• Stress (e.g. bullying) and anxiety can initiate and amplify • Recent-onset somatization disorder is associated with anxiety,
somatic symptoms. depression, learning difficulty, and obsessional personality trait.
• Somatic symptoms are commonly associated with school refusal. • Chronic somatization disorder is associated with early adverse
• Factors in the child include obsessional, sensitive, insecure, experience, seeking attention from parents, and failure to recognize
or anxious personality. the connection between somatic complaints and emotion.
• Factors in the family include over-involved parent, parental • Family factors include difficulty to express emotion and abnormal
disharmony and overprotection, rigid rules, and parental beliefs on somatic complaints.
communication problems.
• Recurrent localized abdominal pain lasting for few hours is • Headache.
commonly associated with emotional disorder. • Low energy.
• For hysteria, the child may present with disorders of gait or • Stomach pain.
loss of limb function. • Joint pain.
• Secondary gain is often implicated. • Some adolescents meet the ICD-10 diagnostic criteria for
somatization disorder.
Treatment Treatment
• Medical reassurance. • Work with family to facilitate expression of emotion and change
• Psychoeducation. maintaining factors.
• Behaviour therapy. • Medical reassurance.
• CBT.
Prognosis
• Most adolescents with somatization disorder have good prognosis.
• Poor prognostic factors include chronic disorders, multiple
physical complaints, neurasthenic presentations, and onset in late
adolescence.
TABLE 37.17
Compare and Contrast Childhood- and Adolescence-Onset Eating Disorders
Childhood-Onset Eating Disorders (Fox and Carol, 2001) Adolescent-Onset Eating Disorders
• One-third of British children have mild to moderate eating • Anorexia nervosa
difficulties at age 5 years • Prevalence is 0.5%
• Male adolescents account for 5% of anorexia
nervosa
• Bulimia nervosa
• Prevalence: 1%
• Peak age is around 17 years
Aetiology Aetiology
• Male gender • Heritability is high in anorexia nervosa but not in
• Low birth weight bulimia nervosa
• Developmental delay • Neurotic personality
• Early onset of the feeding problem • Family adopts critical attitude
• History of vomiting for long duration • Cultural pressure to pursue thinness
• High social class • Perfectionism
Type of childhood-onset eating disorders: Clinical features
• Childhood-onset anorexia nervosa: weight loss and The clinical features for adolescent anorexia nervosa
abnormal cognitions on weight and shape and bulimia nervosa are similar to the criteria used
• Childhood-onset bulimia nervosa: recurrent binges, lack of in adult patients
control, and abnormal cognition Anorexia nervosa:
• Food avoidance emotional disorder: weight loss, mood • Self-induced weight loss leading to low weight
disturbance, and no features of anorexia nervosa (typically below 85% expected weight)
• Selective eating: narrow range of food and unwilling to try • Body mass index (BMI) of less than 17.5
new food • Fear of fatness or weight gain
• Restrictive eating: smaller amount than expected and • Disturbed body image
normal diet in terms of nutritional content • Amenorrhoea
• Food refusal: episodic, intermittent, or situational food Bulimia nervosa:
refusal • Recurrent episodes of binge eating
• Functional dysphagia: fear of swallowing, choking, and • A preoccupation with eating including
vomiting compulsions to eat
• Pervasive refusal syndrome: refusal to eat, drink, walk, • Compensatory behaviours to reduce weight (e.g.
talk, or self-care dietary restriction between binges and
self-induced vomiting)
• Excessive exercise
• Laxative abuse
Treatment Treatment
• Behaviour therapy can enhance the child’s motivation to Anorexia nervosa:
eat and reduce maladaptive behaviour such as expelling • CBT
food • Referral to a dietician
• Social skill training • Aim at gaining 0.5–1 kg/week
• Family therapy • Some patients require hospitalization if they
have medical risk (e.g. bradycardia)
• Mortality: 2.16%
Bulimia nervosa:
• CBT
• Fluoxetine will reduce the impulse to binge

Compare and Contrast Childhood- and Adolescence-Onset Eating Disorders
Childhood-Onset Eating Disorders (Fox and Carol, 2001) Adolescent-Onset Eating Disorders
Prognosis Prognosis
For childhood-onset anorexia nervosa, two-thirds of patients Anorexia nervosa
make good recovery • Good outcome in 50% of patients
• Intermediate outcome in 30% of patients
• Poor outcome in 20% of patients
• Younger onset is associated with better outcomes
• Poor prognostic factors include achievement of
body weight < 65% of expected weight and
admission to the hospital
• Long-term suicidal rate in adolescent anorexia
nervosa is 5%
Bulimia nervosa
• Better outcome than anorexia nervosa
• Complete remission is more likely than anorexia
nervosa
• Poor prognostic signs include borderline
personality disorder and impulsivity
8. Physical examination must be carried out by • Recognize the physical and emotional conse-
an appropriately experienced paediatrician or quences of abuse (e.g. anxiety, guilt, psychiatric
gynaecologist. morbidity secondary to sexual abuse and fears
9. If abuse is confirmed, the psychiatrist needs about the consequences of disclosure, regres-
to assess the child to determine the effects of sion to an earlier developmental stage) and make
abuse, safety issues, and recommend further appropriate referrals.
treatment. • Evaluate the continuing risk to the child and
siblings.
• Evaluate the therapeutic needs of child and parents.
37.20.3 Management
• Individual psychotherapy may help the child to
• The safety of the child is the most important and overcome symptoms of post-traumatic stress
the psychiatrist needs to discuss with the paedi- disorder and poor self-esteem.
atrician and social worker to notify the authority • Family therapy may be useful to restore the
and remove the child from danger. roles and boundaries in family.
CASC STATION IN CHILD AND ADOLESCENT PSYCHIATRY

Assessment of ADHD
Name: John Smith Age: 10
You are a specialist trainee in Child and Adolescent Psychiatry. John was referred to you as he has been very active
and disruptive in school. The school is considering suspending him because of his behaviour. Developmental
milestones are known to be normal.
Task: You are asked to talk to John’s mother to take a history of his problem. Full developmental history is not required.
The NICE guidelines suggest that the diagnostic process for ADHD involves an assessment of the person’s
needs, coexisting conditions, social, familial, educational or occupational circumstances, and physical health.
For children and young people, there should also be an assessment of their parents’ or carers’ mental health.
(continued)
(A) Core Symptoms of (A3) Impulsiveness and

ADHD (A1) Hyperactivity (A2) Inattention Other Behaviour
‘In school, do the teachers ‘In school, does he often ‘Does he tend to act before
ever say he has trouble fail to follow through thinking?’ ‘Can you give
sitting still or staying in instructions or to finish me some examples?’
his seat?’ school work?’ ‘Does he seem to be
‘Compared to other kids, ‘In schoolwork, does he impatient and have
do you find John more often fail to give close difficulty waiting for his
hyperactive?’ ‘Can you attention to details? Does turn?’
give me some examples?’ he make careless ‘Does he interrupt often into
‘Does he often climb mistakes easily? Does he conversations? How about
excessively?’ dislike homework?’ blurting out answers before
‘If so, since when have ‘Does he appear to have questions have been
you noticed this?’ difficulty to sustain completed?’
attention in tasks? Is he ‘Do you find that he talks
easily distracted by excessively and you have
external stimuli?’ difficulty to stop him?’
‘Does he have difficulty in ‘Does he have twitching
listening to what is being movement on his face?’
said to him?’ (Candidates must be
‘How good is he in considered for Tourette’s
organizing tasks? Does syndrome and make
he easily misplace his stimulants contraindicated.)
belongings? Does he If the child is a girl,
often lose thing?’ candidate is advised to
‘Does he finish one focus more on mood
activity before moving to swings because girls with
the next? Does he tend to ADHD are less aggressive
start one thing and go on and impulsive.
to the next before
finishing?’
(B) Other Aspects of History (B1) Age of Onset and (B3) Impairments in Social
to Establish the Diagnosis Duration of Symptoms (B2) Pervasiveness Functioning
‘At what age did you ‘Do these problems ‘Does he have any problem
notice problems with happen at both at home in making or keeping
hyperactivity or and school?’ friends?’
inattention?’ (Age of ‘Does he have the same ‘Does he get invited over to
onset is expected to be problems at other places? see friends or to birthday
before 7 years old.) (e.g. going to a shopping parties?’
‘How long has he been mall)’ ‘Does he have friends in
hyperactive and Hyperactivity, inattention, school?’
inattentive?’ (Duration is and impulsivity are ‘What do you think stops
expected to be at least for present for more than one him from being able to
6 months.) situation. keep friends?’
‘Does his behaviour affect
his relationships with his
siblings or family
members? How does the
family cope with him?’
(C) Current Academic

Function and (C1) Behavioural (C2) Academic (C3) Developmental
Developmental History Problems in School Background History
‘Do the teachers complain ‘Is he doing well in Although the question states
about him?’ school?’ that you do not need to take
‘Does he display any ‘Has his studies been a full developmental
conduct problem?’ affected by his history, the candidate is
symptoms?’ expected to take a brief
‘Is he in a mainstream history.
school or special school? ‘Was there any delay in his
Did the teacher say he development?’
has special education ‘How old did he start
need?’ walking?’
‘How old did he start to say
simple words?’
(D) Family Background and (D1) Family History of (D2) Parental (D3) Major Changes in
Home Environment ADHD Relationship Social Circumstances
‘Is there any family ‘How are you getting Explore:
member who is also along with your husband • Financial problems
diagnosed with ADHD?’ or partner?’ • Recent birth of young
‘Do both of you have any sibling
disagreement over John’s • Recent changes in home
problems?’ environment
‘Are you in contact with the
social service?’
(E3) Past Psychiatric History
(E) Risk Assessment and (E2) Past Medical History and Family History of
Background History (E1) Risk Assessment and aetiology Psychiatric Illness
‘I am very sorry to hear ‘Did you smoke or drink ‘Was John previously seen
what has happened to when you were by a psychiatrist before?
John and your family. I pregnant?’ How about yourself or your
would like to inquire ‘Did he have low birth husband? What advice did
safety issues. Has John weight when he was the psychiatrist offer?’
ever done anything born?’ Note: autism, mental
impulsive that may harm ‘Does John have any retardation, or mood
himself or the others? If medical problems such as disorders can be causative
yes, how do you keep having a fit?’ factors for hyperactivity
him safe?’ ‘Does he have any hearing and inattention.
‘Does John think before he problems or suffer from a Explore other psychiatric
acts? Has he ever genetic disease?’ (to rule comorbidity:
involved in any road out fragile X syndrome) • ‘Does he feel sad
traffic accident?’ ‘Is John currently taking recently?’
‘Have you or your partner any other medications • ‘Is he more nervous
ever become angry with such as inhaler for lately?’
John? If so, what would asthma?’ (e.g. ventolin • ‘Does he use
you do? Did you punish may cause hyperactivity recreational drugs?’
him physically?’ in some children)
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Shaffer D and Gutstein J. 2002: Suicide and attempted suicide. Classification of Mental and Behavioural Disorders:
In Rutter M and Taylor E (eds.) Child and Adolescent Clinical Descriptions and Diagnostic Guidelines.
Psychiatry, 4th edn, pp. 529–554. Oxford, U.K.: Blackwell. Geneva, Switzerland: World Health Organization.
38 Learning Disability
38.1 CLASSIFICATION OF MENTAL • Severe limitation in ability to understand or

RETARDATION comply with requests or instructions
• Little or no self-care
ICD-10 defines mental retardation as being a condition of • Mostly severe mobility restriction
arrested or incomplete development of the mind, which • Basic or simple tasks may be acquired (e.g.
is especially characterized by impairment of skills mani- sorting and matching)
fested during the developmental period, which contribute
to the overall level of intelligence, that is, cognitive, lan- 38.1.1 DSM-5 Adopts Similar Classification
guage, motor, and social abilities.
Mild mental retardation: able to maintain age-appro-
The following is a summary of the ICD-10 classification priate personal care
of mental retardation: Moderate mental retardation: extended period of
teaching and time is needed to teach the patient
• F70 Mild mental retardation to become independent.
• Intelligence quotient (IQ) range 50–69 Severe mental retardation: require full support for
• 85% of all learning disability basic activities of daily living.
• Delayed understanding and use of language Profound mental retardation: dependent on other
• Possible difficulties in gaining independence people for daily living.
• Work possible in practical occupations The onset of age is before the age of 18.
• Any behavioural, social, and emotional dif-
ficulties are similar to the ‘normal’ 38.2 EPIDEMIOLOGY OF LEARNING
DISABILITY
• F71 Moderate mental retardation
• IQ range 35–49 The prevalence of learning disability—defined as hav-
• 10% of all learning disability ing an IQ of less than 70—is 3.7%, which is considerably
• Varying profiles of abilities higher than would be expected from the normal distri-
• Language use and development variable bution of IQ. The prevalence of self-injurious behaviour
(may be absent) among people with learning disability is 20% and 50%
• Often associated with epilepsy and neuro- for those in institutions. The peak age of self-harm is
logical and other disabilities between 15 and 20 years and associated with male gender.
• Delay in achievement of self-care The levels of coexistence of different impairments are
• Simple practical work possible shown in Table 38.1.
• Independent living rarely achieved
38.3 AETIOLOGY OF LEARNING DISABILITY
• F72 Severe mental retardation
• IQ range 20–34 The causes of learning disability are summarized in
• 3% of all learning disability Table 38.2.
• More marked motor impairment than F71
often found 38.4 DOWN SYNDROME
• Achievements at lower end of F71
38.4.1 Clinical Case
• F73 Profound mental retardation A 6-year-old boy is referred to you. On mental state
• IQ difficult to measure but <20 examination, he is pleasant and cooperative. On physical
• 2% of all learning disability examination, he has a small mouth, small teeth, and a
663
Conductive >
Small round head
TABLE 38.1 sensorineural
Back of skull flat
deafness
Levels of Coexistence of Different Impairments
Almond-shaped eyes
Severe Mental Mild Mental – Nuchal swelling slanting laterally upwards
Retardation Retardation due to excess Brushfield spots on iris
skin in the neck
Cerebral palsy Approx. 20% Approx. 8% – Altanto-axial Prominent epicanthic
Epilepsy 30%–37% 12%–18% instability folds
Hydrocephalus 5%–6% 2% Low-set simple
Severe visual impairment 6%–10% 1%–9% Oesophageal and external ears
duodenal atresia Hearing impairment
Severe hearing impairment 3%–15% 2%–7%
One or more major impairments 40%–52% 24%–30%
Congenital
Reproduced from Puri, B.K. and Treasaden, I.H., Textbook of heart disease,
Psychiatry, 3rd edn., Churchill Livingstone, Edinburgh, U.K., 2011. especially defects
Short of endocardial
With permission.
fingers cushion
with
curved
little Reduced muscle
fingers and tone in infancy
TABLE 38.2
transverse
Aetiology of Learning Disability palmar
creases Hyperextensible
Prenatal Perinatal Postnatal joints
Inborn errors Asphyxia/hypoxia Meningitis/
of metabolism at birth encephalitis
Chromosomal Mechanical birth Head injury Wide sandal gap between
abnormalities: Numerical trauma (e.g. accidental first and second toes
abnormalities (e.g. or inflicted)
Turner’s syndrome), FIGURE 38.1 Clinical features of Down syndrome.
partial chromosomal
duplications or deletions
(e.g. cri du chat high arched palate. His palpebral fissure is oblique and
syndrome), translocation he has epicanthic folds. He has short broad hands and
(e.g. Down syndrome), hyperextensible joints (Figure 38.1).
mosaicism (e.g. Down
syndrome), and
microdeletion (e.g. 38.4.2 Epidemiology
Prader–Willi syndrome)
• Down syndrome is the most common cytogenic
Congenital infections Small babies (20% Lead poisoning
cause of learning disability.
(rubella, measles, of low birth (and other
influenza [type B], weight babies heavy metals)
• It accounts for 30% of all children with mental
Japanese encephalitis, develop learning retardation.
cytomegalovirus, syphilis, disabilities) • The prevalence is 1 in 800 live births (1 in 2500
HIV, toxoplasmosis) if the mother is younger than 30 years and
Irradiation Hyperbilirubinaemia Environmental 1 in 80 if the mother is older than 40 years).
(kernicterus) chemicals Paternal age is not an important factor.
Drugs (e.g. thalidomide, Hyperoxia Malnutrition
valproate, and lithium) (iatrogenic)
Maternal alcohol, opioid Hypoglycaemia Other infections 38.4.3 Genetic Mechanism
intake, and smoking (e.g. whooping
cough) • 94% of cases are caused by meiotic nondisjunc-
Malnutrition (including Prematurity (e.g. tion or trisomy 21 (47 chromosomes).
vitamin and iodine intraventricular • 5% of cases are caused by translocation that
deficiencies) haemorrhage) refers to a fusion between chromosome 21 and 14
(46 chromosomes).
Learning Disability 665
• 1% of cases are caused by mosaicism that refers • Hypothyroidism is also common.

to nondisjunction occurring after fertilization in • 10% of people with Down syndrome suffer from
any cell division. leukaemia.
• Robertsonian translocations are caused by fusion of • Psychiatric comorbidity includes obsessive–
chromosome 14 and 21. The extra chromosome is compulsive disorder (2% of patients, especially
usually of maternal origin (90%), and most maternal presenting with a need for excessive order or
errors occur during the first meiotic division. The tidiness), depression, autism, bipolar disorder,
risk of recurrence of translocation is around 10%. psychosis, and sleep apnoea.
• Defect at 21q21.1 leads to overexpression of • The average life expectancy of people with
genes encoding amyloid precursor protein, but Down syndrome is between 58 and 66 years. The
other enzymes such as superoxide dismutase are most common cause of death is chest infection.
underactive.
• Screening for Down syndrome: Maternal serum
markers at 16 weeks of gestation show raised 38.5 LEARNING DISABILITY AND GENETIC
human chorionic gonadotropin (HCG), lowered DEFECTS IN SEX CHROMOSOMES
α-fetoprotein, and lowered unconjugated estriol.
38.6 FRAGILE X (MARTIN-BELL) SYNDROME
38.4.4 Intelligence 38.6.1 Clinical Case
• The IQ of people with Down syndrome is A 4-year-old child is referred to you for delayed speech
between 40 and 45. IQ < 50 is found in approxi- and language. He was initially suspected to suffer from
mately 85% of cases. autism. He has gaze aversion and social avoidance. His
• Verbal processing is better than auditory processing. IQ is 60. He also has attention deficit. Physical examina-
• Their social skills are more advanced than intel- tion shows enlarged testes, large ears, long face, and flat
lectual skills. feet. Mental state examination reveals limited eye con-
• Defects in the scanning environment tend to tact, preservation of words, echolalia, and stereotypical
focus on a single stimulus. behaviour such as hand flapping.
38.4.5 Growth 38.6.2 Epidemiology
• People with Down syndrome have stunted • Fragile X syndrome is the most common inher-
growth with an average adult height of 141 cm ited cause of learning disability. It accounts for
in women and 151 cm in men. 10%–12% of mental retardation in men.
• Fragile X syndrome affects 1 in 4000 men and
1 in 8000 women. 1 in 700 women is a carrier
38.4.6 Behavioural Features for fragile X syndrome.
• Passive and affable • The prevalence is less common in women because
• Obsessional and stubborn only 1 in 5 women affected by mutation at fragile
• 25% have attention deficit and hyperactivity site is phenotypically and intellectually unaffected.
38.4.7 Comorbidity 38.6.3 Mode of Inheritance

• People with Down syndrome are at higher risk to • Fragile X syndrome is an X-linked dominant
develop Alzheimer’s disease (50–59-year-olds = genetic disorder with low penetrance.
36%–40%; 60–69-year-olds = 55%). Over the age • The fragile site is located at band q27.3 on the
of 40, there is high incidence of neurofibrillary X chromosome. Examination of karyotype in
tangles and plaques with increase in P300 latency. performed in the folate-depleted and thymidine-
• Hearing loss occurs in 50% of people with depleted medium.
Down syndrome. • The trinucleotide repeats CGG (cytosine,
• Immune system is often impaired, and they are guanine, and guanine) are found on the long
at high risk to develop diabetes mellitus. arm of X chromosome. Normal number of
repeats is 30, and the repeats for carriers range • Soft velvety skin.
from 55 to 200. Full mutation with more than • Boys with fragile X syndrome are often tall in
200 repeats leads to hypermethylation at frag- childhood, but their heights become average in
ile X mental retardation (FMR)—one gene and adulthood.
underexpression of FMR protein. • Macroorchidism (70% after puberty).
• Increased incidence of connective tissue disorders.
• Hyperextensible joints.
38.6.4 Intelligence
• Flat feet.
• Women with fragile X syndrome suffer from
mild learning disability, and men with fragile X 38.6.7 Psychiatric Features
syndrome suffer from moderate to severe learn-
• Autism-like behaviour
ing disability (in 80% of male patients, IQ is less
• Speech and language delays
than 70).
• Idiosyncratic linguistic and interpersonal styles
• Verbal IQ > performance IQ.
• Attention deficit and hyperactivity
• The length of trinucleotide repeats is inversely
• Delay in language acquisition with cluttering speech
related to IQ because shorter length (<200 trip-
• Hypersensitivity to social and sensory stimuli
lets) may not cause methylation, and hence, it
• Self-injury
results in higher IQ scores.
• Social anxiety and gaze aversion
• Idiosyncratic linguistic and interpersonal styles
38.6.8 Management
In general, men with fragile X syndrome are more likely
than women (only 50%) to exhibit the typical physical • Anticonvulsant for treating seizures.
features (Figure 38.2). • Educational package designed to meet the needs
of individual, family support, and social care.
• Genetic counselling should be offered to parents
38.6.6 Other Clinical Features and other family members at risk of producing a
• Short stature. child with fragile X syndrome.
• Seizure: 20% of patients. • Self-help group (e.g. Fragile X Society).
• Strabismus.
• Mitral valve prolapse in 80% of cases. 38.7 TURNER’S (XO) SYNDROME
• Single transverse palmar crease.
38.7.1 Epidemiology
• Prevalence: 1 in 3300 live births
Macrocephaly 38.7.2 Mode of Inheritance

• Nondisjunction of paternal XY results in sex
chromosomal monosomy.
Strabismus • 50% of patients have a karyotype consisting of
and gaze
45X or 46XX mosaicism.
aversion
Large, • 50% of patients have 46 chromosomes with one
floppy ears normal X chromosome and the other X chromo-
Mid-face
hypoplasia some, which is abnormal in the form of a ring, a
long arm isochromosome, or a partially deleted
Speech High arched X chromosome.
difficulties: palate,
perseveration long, thin face and
of words and prominent jaw
38.7.3 Clinical Features (Figure 38.3)
phrases,
echolalia,
• Most fetuses with Turner’s syndrome develop
hydrops fetalis due to delayed maturation of the
FIGURE 38.2 Facial features of fragile X syndrome. lymphatic drainage system.
38.7.6 Treatment
Short stature Characteristic facial
features
• Oestrogen replacement therapy should be intro-
Fold of skin duced from the age of 12 years onwards to
Low hairline
Coarctation of aorta promote pubertal development and prevent the
Shield-shaped onset of osteoporosis.
thorax Poor breast
Widely-spaced development
nipples 38.8 KLINEFELTER’S SYNDROME (XXY)
Elbow
deformity
38.8.1 Case Example
Shortened
metacarpal IV A 25-year-old married man with history of mild learning
disability is referred to you. His history suggests possible
fertility problems. Physical examination shows gynae-
Abnormality of the Rudimentary comastia and small testes. There is no family history of
wrist, known as madelung ovaries and similar problems.
deformity, caused gonadal streak
by partial (underdeveloped
subluxation of the gonadal 38.8.2 Epidemiology
distal ends of the structures)
radius and ulna. • The incidence is between 1 in 500 and 1 in 1000
Small fingernails Amenorrhoea live male births.
Brown spots (nevi)

38.8.3 Genetic Mechanisms
FIGURE 38.3 Clinical features of Turner’s syndrome. • 50% due to maternal and 50% due to paternal
nondisjunction.
• Paternal nondisjunction is paternally derived
• At birth, the neonate always has a normal and associated with advanced paternal age.
female feature with residue of intrauterine • 80% of males with Klinefelter’s syndrome have
oedema in the form of neck webbing and puffy a 47XXY karyotype with an additional X chro-
extremities. mosome being derived equally from meiotic
• Short stature becomes apparent in early child- errors in each parent.
hood, and average adult height is 140–145 cm • Other karyotypes include 47XXY or 46XY
without hormone therapy. mosaicism and severe X chromosome aneu-
ploidy such as 48XXXY and 49XXXXY. These
38.7.4 Intelligence karyotypes usually occur as sporadic events in
a family.
• Normal IQ
• Mild learning disability
• Subtle defects in visuospatial perception and 38.8.4 Clinical Features (Figure 38.4)
fine motor skills • Newborn boys with Klinefelter’s syndrome are
clinically normal.
• Sexual orientation is usually normal and results
38.7.5 Comorbidity
in heterosexual marriage.
• Infertility is very common in women with • Passive and compliant in childhood.
full Turner’s syndrome as a result of ovarian • Aggressive and antisocial past puberty.
dysgenesis.
• Pregnancy has been achieved in a small num-
38.8.5 Intelligence
ber of female patients by embryo transplantation
following in vitro fertilization using their part- • Mild learning disability with some difficulty in
ner’s sperm and a donor egg. acquiring verbal skills.
Tall stature (4 cm progressive muscular deterioration over 20 years,

taller than average) and the patients become wheelchair bound at the
Slightly feminized
physique
end of childhood. 20% have learning disabil-
40% have ity with impairment of verbal IQ. Depression is
taurodontism Poor beard growth common.
(enlargement • Rett syndrome is an X-linked dominant disorder
of the molar
teeth by an
(refer to Chapter 37 for details).
Gynaecomastia
extension of (50%)
the pulp)
38.10 XYY SYNDROME
Osteoporosis
Tendency to
lose chest • It affects approximately 1 in 1000 male neonates.
hairs • Up to 3% of patients in maximum security hos-
Testicular atrophy
and infertility pitals have XYY karyotype.
Female-
type • Men with 47, XYY karyotype show an
pubic increased rate of petty crime (an average three
hair times more common than in the general popu-
pattern lation). This is a result of impulsiveness, and
there is no propensity towards severe aggres-
sion or violent crime.
38.10.2 Mode of Inheritance
• Primary nondisjunction of the Y chromosome.
• About 10% have mosaic, that is, 46, XY and 47,
XYY chromosome complement.
FIGURE 38.4 Clinical features of Klinefelter’s syndrome.
• Mild physical abnormalities
• Proportionate tall stature
• 48XXXY and 49XXXXY are associated • Enlarged teeth
with severe learning disability and marked • Increased susceptibility to develop acne
hypogonadism. • Muscle weakness and poor coordination
• Normal sexual development and fertility
38.8.6 Treatment
38.10.4 Intelligence
• Fertility can be achieved using haploid sper-
matocytes obtained by testicular biopsy. • Mild learning disability.
• Verbal skills are delayed.
38.9 OTHER X-LINKED SYNDROMES
• Hunter syndrome is an X-linked recessive 38.11 LEARNING DISABILITY AND
mucopolysaccharide disorder. There are two INBORN ERROR OF METABOLISM
forms. Type A presents with progressive learn-
ing disability leading to death between 10 and 38.12 LESCH–NYHAN SYNDROME
20 years, and type B affected individuals usually
38.12.1 Clinical History
present with normal intelligence and survival.
• Duchenne muscular dystrophy is an X-linked A 16-year-old boy is referred to you because of severe
recessive disorder. Abnormalities at Xp21 lead self-mutilation including biting of lips, inside of mouth,
to failure to produce dystrophin, resulting in a and fingers. There is a failure of secondary sexual
development. His maternal grandfather and maternal 38.13 HURLER’S SYNDROME

uncle also suffer from the same disorder.
38.13.1 Case History
38.12.2 Epidemiology A 3-year-old child presents with hepatosplenomegaly,
hirsutism, corneal clouding, and recurrent respiratory
• Incidence 1/10,000–1/38,000 infections.
• Exclusive to men
One in 100,000
• X-linked recessive
• CAG trinucleotide repeats
Autosomal recessive
38.12.4 Error in Metabolism
• Defect in hypoxanthine guanine phosphoribosyl- 38.13.4 Error in Metabolism
transferase resulting in accumulation of uric acid
Deficiency in L-iduronidase mucopolysaccharidosis
type I
• Microcephaly. 38.13.5 Clinical Features
• During infancy, orange uricosuric acid sand is
found in the nappy. Short stature, hepatosplenomegaly, and hirsutism
• Then patient develops hypotonia followed by spas- (Figure 38.5)
tic choreoathetosis, dysphagia, and dysarthria.
• The age of onset of self-injurious behaviours is 38.13.6 Psychiatric Features
usually before the age of 3. Lips and fingers are
Anxiety and fearful feelings
often bitten.
38.12.6 Behavioural Features
Moderate to severe learning disability
• Generalized aggression with tantrums directed
against objects and people
38.13.8 Causes of Death
38.12.7 Intelligence Recurrent respiratory infections and death before the age

of 10 years
• Mild to moderate learning disability
Depressed nasal Bulging forehead
bridge
38.12.8 Medical Comorbidity
• Gout
• Epilepsy (50%)
• Respiratory or renal failure (often the cause of
Corneal
death) clouding
Flat and
38.12.9 Treatment coarse face
• Well planned behavioural intervention may

reduce self-injurious behaviour.
• Allopurinol reduces uric acid levels but offers no
therapeutic benefits in behavioural symptoms. FIGURE 38.5 Facial features of Hurler’s syndrome.
38.13.9 Treatment 38.14.8 Treatment
Allogeneic bone marrow transplantation • The neonates are required to take a low-
phenylalanine diet before 6 months of age.
• Initiation of low-phenylalanine diet before 3
38.14 PHENYLKETONURIA months of age may preserve normal intelligence.
38.14.1 Epidemiology Other benefits include reduction of irritability
and abnormal EEG and enhanced social
• Incidence: 1 in 4,500–15,000 responsiveness and attention span.
• Frequency among institutionalized retarded • Side effects of low-phenylalanine diet include
patients: 1% anaemia, hypoglycaemia, and oedema.
• Predominantly in people of North European origin
38.14.2 Mode of Inheritance 38.15 SANFILIPPO SYNDROME
• Autosomal recessive 38.15.1 Case History

• Phenylalanine hydroxylase gene on chromo- A 6-year-old child presents with developmental delay,
some 12 (12q22–24.1) claw hand, hypertrichosis, deafness, hepatospleno-
megaly, biconvex lumbar vertebrae, and joint stiff-
38.14.3 Error in Metabolism ness. He has claw hands. His parents mention that he
is often restless with sleep problems and challenging
• Defects in phenylalanine hydroxylase or c ofactor behaviour.
(biopterin)
• Accumulation of phenylalanine
38.15.2 Metabolic Problems
38.14.4 Clinical Features Dysfunction in the breakdown of heparan sulphate
• Symptoms absent neonatally

• Blond hair 38.15.3 Intelligence
• Fair skin Severe learning disability
• Blue eyes
• Triad: eczema, epilepsy, and vomiting (30%)
38.15.4 Cause of Death
38.14.5 Behavioural Features Respiratory tract infections (between the age of 10 and
20 years)
• Autistic features
• Stereotyped behaviour destructiveness
• Self-injury 38.15.5 Galactosaemia
• Hyperactivity
• Psychotic symptoms that resemble childhood-
onset schizophrenia One in 60,000
38.14.6 Intelligence 38.15.7 Mode of Inheritance

• Mild to profound learning disability Autosomal recessive
• Language delay
38.15.8 Metabolic Problems
38.14.7 Screening Test
Absence of galactose-1-phosphate uridyl transferase
• Guthrie immunoassay detects phenylalanine in and results in intracellular accumulation of galactose-1-
the blood soon after birth. phosphate (toxic)
38.15.9 Clinical Features 38.17.3 Course of Illness

• Jaundice, vomiting, and diarrhoea after expo- Infants initially develop normally in the first few months
sure to galactose of life followed by subsequent relentless deterioration of
• Fanconi syndromes (growth failure, renal tubular physical and mental abilities.
dysfunction, acidosis, hypokalaemia, galactosaemia)
• Increased intracranial pressure
• Ovarian failure 38.18 LEARNING DISABILITY AND
• Failure to thrive NEUROCUTANEOUS SYNDROMES
38.15.10 Behavioural Features 38.19 TUBEROUS SCLEROSIS
Increased behavioural problems, anxiety, social with- 38.19.1 Case History

drawal, and shyness A 20-year-old woman presents with white skin patches
and gingival fibromata. She has history of epilepsy.
38.15.11 Intelligence A whole-body scan shows tumours in kidney, spleen, and
lungs.
Learning disability with visuospatial deficits and
language disorders
38.16 METACHROMATIC LEUKODYSTROPHY • Men and women are equally affected.
• One in 7000 population.
Autosomal recessive
38.16.2 Error of Metabolism • Autosomal dominant with 100% penetrance.
• Spontaneous mutation in 70% of cases.
Lysosomal storage disease with problems in lipid metab- • Two tumour suppressor genes are involved:
olism resulting in accumulation of galactosyl sulphatide TSC1 (on 9q34, which codes for hamartin) and
affecting myelin TSC2 (on 16p13.3, which codes for tuberin).
38.19.4 Clinical Features (Figure 38.6)
• Infantile form: before the age of 3 and pro-
• Most common feature is skin depigmentation
gresses to severe motor retardation and learning
that is especially noted under ultraviolet light.
disability
• Hypomelanotic macules.
• Juvenile form: motor retardation and learning
• Intractable epilepsy.
disability
• Classical diagnostic triad of epilepsy, learn-
• Adult form: presents with dementia or psychosis
ing disability, and characteristic facial skin
lesions seen in 30% of people with tuberous
38.17 TAY–SACHS DISEASE sclerosis.
38.19.5 Psychiatric Features
Autosomal recessive and mainly occur in people with
Jewish origin • Autism (75%)
• Hyperactivity
• Impulsivity
38.17.2 Error of Metabolism
• Aggression
Increase in lipid storage (accumulation of gangliosides in • Self-injurious behaviours
neurons). • Sleep disturbance
Hamartomas 38.20.2 Mode of Inheritance

Facial • Autosomal dominant.
angiofibromas
in butterfly
• 50% are caused by sporadic mutations.
distribution • Mutation in neurofibromatosis (NF) allele at
chromosome 17q11.2.
• Abnormal in production of neurofibromin.
Gingival
fibromata
Tumours in
lungs 38.20.3 Intelligence
Tumours in • 30% have mild learning disability.
spleen • 10% have severe to profound learning
Depigme
nted skin
Tumours in disability.
kidneys • Verbal IQ is better than performance IQ.
patches
(Ash leaf
spots)
Fibromas
of the
• Short stature.
nails • Macrocephaly (30%–45%).
• Optic nerve glioma.
• Hypertension.
• Tumours arise from the connective tissue of
nerve sheaths.
• Café au lait spots.
• Cutaneous neurofibromas.
• Freckling of groin or armpit.
• Skeletal deformities.
• Lisch nodules.
• Depression
FIGURE 38.6 Clinical features of tuberosus sclerosis.
• Anxiety
• Speech and language difficulties (50%)
38.19.6 Intelligence • Distractibility
• 30% of people with tuberous sclerosis have nor- • Impulsiveness
mal IQ. • Hyperactivity
• If learning disability is present, it is usually
profound.
38.21 LEARNING DISABILITY AND
38.19.7 Comorbidity MICRODELETION SYNDROMES
• Seizures are common (90%). See Tables 38.3 through 38.6.

• The initial presentation is usually infantile spasms.
38.22 PRADER–WILLI SYNDROME
38.20 NEUROFIBROMATOSIS TYPE 1
(VON RECKLINGHAUSEN DISEASE) 38.22.1 Case History
A 13-year-old obese boy with learning disability is
38.20.1 Epidemiology referred. He presents with irresistible hunger drive and
• Male = female incessant skin picking with compulsion and anxiety. He
• One in 1/2500–4000 live births tends to talk to himself (Figure 38.7).
TABLE 38.3
Other Microdeletion Syndromes
Syndromes Epidemiology Chromosome Abnormalities Clinical Features
Wolf–Hirschhorn Incidence: 1 in 90,000 Short arm of chromosome 4 • Severe mental retardation
syndrome 80% arise as de novo deletions. • Microcephaly
20% is a result of parentally • High incidence of congenital heart defects
transmitted unbalanced • Severe psychomotor and growth retardation
translocations. • 70% survive beyond early childhood.
Cri du chat syndrome Incidence: 1 in 50,000 Short arm of chromosome 5 • A round face with microcephaly
A de novo deletion is present in 85% • Slanting palpebral fissures
of cases. • Broad flat nose
10%–15% of cases are familial. • Low set ears
More than 90% is a result of parental • Cardiac abnormality (50%)
translocation. • Gastrointestinal abnormalities
5% is resulted from an inversion of • Severe mental retardation
chromosome 5. • Infantile cat cry
• Severe psychomotor retardation
• Hyperactivity
• Stereotypies
• Rate of survival is low
TABLE 38.4
Summary of Clinical and Psychiatric Features and Related Syndromes
Clinical and Psychiatric
Features Syndromes
Hyperactivity and aggression (1) Hurler syndrome, (2) Soto syndrome, (3) fragile X syndrome, (4) phenylketonuria (PKU), and (5) tuberous sclerosis
Autism (1) Fragile X syndrome, (2) rubella, (3) tuberous sclerosis, (4) PKU, and (5) Cornelia de Lange syndrome
Short stature (1) Prader–Willi syndrome, (2) Williams syndrome, (3) fetal alcohol syndrome, (4) Cornelia de Lange
syndrome, (5) Rubinstein syndrome, and (6) Sanfillipo syndrome
Tall stature (1) XYY syndrome, (2) Klinefelter’s syndrome, and (3) homocystinuria (mild learning disability, ectopia lentis,
fine and fair hair, and history of thromboembolic episodes)
Microcephaly (1) Wolf–Hirschhorn syndrome, (2) cri du chat syndrome, (3) DiGeorge syndrome, (4) Rubinstein syndrome,
(5) Cornelia de Lange syndrome, and (6) Angelman syndrome
Macrocephaly NF
Obesity (1) Prader–Willi syndrome and (2) Laurence–Moon–Biedl syndrome (mild–moderate LD, short stature,
polydactyly, spastic paraparesis, hypogenitalism, night blindness, diabetes, and renal failure)
In general, 30% of people with learning disability are overweight and 25% are obese
38.22.2 Epidemiology • Imprinting error (can have a recurrence rate up

to 50%).
• 1/10,000 live births. • The main gene implicated is small nuclear ribo-
• 90% of cases are sporadic. nucleoprotein polypeptide N (SNRPN).
• Autosomal dominant transmission.
• Deletion of chromosome 15q11–13 of paternal origin. • Infancy: Hypotonia leads to feeding difficul-
• Uniparental disomy (sporadic with no risk or ties and failure to thrive. Triangular mouth
recurrence): 25%. also causes feeding and swallowing problems.
TABLE 38.5
Psychiatric Comorbidity Associated with Learning Disability and the Use of Psychopharmacological Agents
Psychiatric Comorbidity Recommended Psychopharmacological Agents
Schizophrenia Antipsychotics are useful for
1. People with learning disability have higher prevalence of 1. Comorbid psychiatric disorders (e.g. schizophrenia and related psychosis).
schizophrenia (3%). 2. Behavioural disturbances.
2. The prevalence of schizophrenia is inversely related to IQ. 3. Stereotypies that may benefit from low-dose antipsychotics.
3. S chizophrenia cannot be diagnosed reliably if IQ is less than 45.
Depressive disorder Antidepressants are useful for
1. Can be easily missed. 1. Depression or anxiety disorder.
2. B iological symptoms (e.g. anhedonia, changes in activity level, 2. Self-injurious behaviour.
changes in appetite) are more useful for diagnosis. 3. Obsessions and compulsions.
3. Negative cognition and suicidal ideation are rare. SSRIs
Fluoxetine, paroxetine, and sertraline are used.
Bipolar disorder Lithium and other mood stabilizers
1. Mania should be differentiated from other causes of 1. Control of aggression or intentional self-harm.
overactivity. 2. Mania.
2. For cyclical disorders, individualized recording schedules 3. Augmentation therapy for depression.
may be useful. 4. Valproate is used for rapid cycling bipolar disorder.
Anxiety disorders SSRIs
1. The patient may present repeated somatic complaints. Facial Fluoxetine, fluvoxamine, paroxetine, and sertraline can reduce
expression and physiological signs such as tachycardia are obsessive–compulsive symptoms.
more reliable in diagnosis. Benzodiazepines
2. Phobia may manifest as avoidance of feared situation. 1. For short-term use.
3. PTSD: sudden and unexplainable changes in arousal, 2. Avoid long-term usage of benzodiazepine.
avoidance of certain activities, fear, and evidence of trauma. Psychological treatment
1. Acknowledge the patient’s fear of the trauma.
2. Drawings may facilitate expression in people with learning disability.
3. Relaxation techniques may be helpful.
Attention deficit and hyperactivity Antipsychotic
1. Risperidone can reduce attention deficit and hyperactivity.
Stimulant
1. Methylphenidate improves attention and focus on tasks.
Severely challenging behaviour Anticonvulsants/mood stabilizer
1. The intensity and frequency of certain behaviour put the 1. Carbamazepine is useful in the treatment of episodic dyscontrol.
safety of the patient or others in serious jeopardy. 2. Valproate can reduce aggression.
2. This behaviour limits or denies access to the use of ordinary 3. Lithium can reduce aggression and self-injurious behaviour.
community facilities. β-adrenergic receptor antagonists
Propranolol can reduce explosive rages.
Behaviour therapy
Shaping social behaviours and minimizing destructive behaviours.
Opiate antagonist
Naltrexone is used in the treatment of repetitive self-injury.
Antilibidinal medication
Cyproterone acetate and medroxyprogesterone reduce testosterone levels and
can be used in the treatment of sexual offending. Side effects include liver
toxicity and hyperglycaemia.
Stereotypical motor movements SSRIs
Repetitive ritualized behaviour is common among people with SSRIs such as fluoxetine or fluvoxamine can reduce repetitive behaviours.
learning disability.
TABLE 38.6
Prevention of Learning Disability
Primary prevention 1. Population screening, carrier detection, and prenatal diagnosis have been improved by the advances in molecular
genetics and used to prevent diseases like fragile X syndrome.
2. Prevention of Down syndrome by genetic counselling is limited to potential cases with translocation abnormality
inherited from the parent.
3. Prevention of exposure to ionizing radiation and teratogenic drugs.
4. Reduction of birth trauma by positive family planning, better obstetric care, hospital deliveries, and regular
maternal and fetal monitoring.
5. Vaccination to reduce infection such as measles, mumps, and rubella (MMR).
6. Prevention of neural tube defect by taking folate during pregnancy.
7. Smoking cessation and avoiding alcohol and opioid misuse during pregnancy.
8. Prevention of head injury by wearing bicycle hamlet and enforcing the use of safety car seat for children.
Secondary prevention 1. Advances in molecular genetics, amniocentesis, ultrasonic imaging, and chorionic villous sampling allow prenatal
diagnosis of fetuses affected by genetic diseases in the first trimester.
2. Maternal serum alpha-fetoprotein level is a reliable indicator of neural tube defect.
3. Triple tests: HCG, estriol, and alpha-fetoprotein as well as the nuchal translucency scan allow detection of Down
syndrome in the first trimester.
4. Metabolic diseases like PKU, galactosaemia, Lesch–Nyhan syndrome, maple syrup urine disease, Hunter’s
syndrome, Hurler’s syndrome, and Tay–Sachs disease are identified prenatally.
5. Neonatal screening may detect endocrine diseases like congenital hypothyroidism and metabolic diseases like
PKU and maple syrup urine disease in newborns.
Tertiary prevention 1. At the community level, active resettlement programmes with expansion of support networks, special educational
services, training placements, and day and residential services can prevent long-term hospital care.
2. At the individual level, the use of computer and electronic aids can promote independence and provide opportunity
for alternative methods of communication may improve the quality of life of people with learning disability.
3. Education for the child that addresses adaptive skills, social skills, and communication skills.
4. Family interventions such as family education about the condition and family therapy to enhance self-esteem and
allow expression of feelings (e.g. guilt).
Source: Day, K., Mental handicap, in Paykel, E.S. and Jenkins, R. (eds.) Prevention in Psychiatry, London, U.K., Gaskell, 1994, pp. 130–147.
• Childhood: Orthopaedic problems such as congen- 38.23 ANGELMAN SYNDROME

ital dislocation of hip and scoliosis are common.
• Adolescence: Behavioural disorders such as 38.23.1 Case History
overeating and obesity, self-injurious behaviour, A 10-year-old boy presents with severe learning d isability,
compulsive behaviour, aggression, excessive frequent hand flapping, happy disposition, paroxysmal
daytime sleepiness, skin picking, hoarding, and laughter, and microcephaly. He has history of epilepsy.
anxiety. Insatiable appetite is diagnostic.
• Prevalence is 1/20,000–1/30,000.
• Mild to moderate learning disability
• Speech abnormalities
• Autosomal dominant transmission
38.22.6 Comorbidity
• Deletion on chromosome 15q11–13 of the mater-
• Obsessive–compulsive disorder nal origin
• Frequent deletion of GABA B-3 receptor subunit
• Mutations in ubiquitin–protein ligase E3A
38.22.7 Treatment
(UBE 3A) and associated with severe psychomo-
• Dietary restriction to reduce obesity tor retardation
Fair hair and light skin Subtle facial

Low forehead features Flattened occiput
Almond
Deep set and blue and fair hair
shaped eyes
Round face eyes
Mouth shaped
like a fish, Thin upper lip Pointed chin
Increase in inverted V Wide mouth and
appetite shaped upper widely spaced
lip teeth
Hand
flapping
and
clapping
Truncal
obesity Ataxia (jerky
limb movements,
gait problems) Axial hypotonia
Small
hand and Microorchidism, and
feet cryptorchidism
(hypogonadism)
FIGURE 38.8 Clinical features of Angelman syndrome.

FIGURE 38.7 Prader–Willi syndrome.
38.23.4 Intelligence 38.24 WILLIAMS SYNDROME

• Severe or profound learning disability 38.24.1 Case Scenario
A 13-year-old girl with an ‘elfin’ facial appearance pres-
38.23.5 Clinical Features (Figure 38.8) ents with obsessions, compulsions, impulsive behaviour
including hyperphagia, aggression, and skin picking.
• Angelman syndrome is known as happy puppet
Mental state examination reveals a talkative and over-
syndrome characterized by paroxysms of laugh-
friendly child. Echocardiogram shows pulmonary ste-
ter, cheerful disposition, and ataxia.
nosis and mitral valve regurgitation. Blood tests show
• Axial hypotonia.
hypercalcaemia. She was born at full term. She has
• Jerky movements.
developmental delay and retarded growth.
• Epilepsy (90%): EEG changes develop during
the first year of life.
• Gastrointestinal problems (reflux, rumination, pica).
• 1 in 20,000 live births
• Autism
• Attention deficit syndrome • Autosomal dominant transmission
• Sleep disturbance • Small deletion of one elastin allele at chromo-
• Nightmares some 7q11.23
38.24.4 Physical Features (Figure 38.9) 38.25 DIGEORGE (VELO–CARDIO–FACIAL)

• Short stature SYNDROME
• Hypercalcaemia (50%) 38.25.1 Epidemiology
• Microcephaly (30%)
• Supravalvular aortic stenosis Incidence: one in 4000 live births
• Kidney and bladder complications
38.25.2 Genetic Defect
Microdeletion in chromosome 22q11.2
• Cocktail-party and hyperverbal speech char- 38.25.3 Intelligence
acterized by fluent and well-articulated speech More than 50% of patients have mild to moderate learn-
with overfamiliar manner ing disability.
• Anxiety
• Fears 38.25.4 Clinical Features (Figure 38.10)
• Poor peer relationships
• Hypersensitivity to sound • Cardiac abnormalities include tetralogy of Fallot,
• Outgoing, sociable, and disinhibited character ventricular septal defect, interrupted aortic arch,
• Excessive friendliness and pulmonary atresia.
• Hypocalcaemia.
• Seizures (60%).
38.24.6 Intelligence • Short stature.
• Moderate to severe learning disability 38.25.5 Psychiatric Features

• Verbal skills often better than motor and visual–
spatial skills • There is an increased incidence of schizophrenia.
38.26 RUBINSTEIN—TAYBI SYNDROME

38.24.7 Association 38.26.1 Epidemiology
• Anxiety disorder • Male = female
• Phobia • Incidence: one in 125,000
Broad forehead Medial eyebrow

flare
Stellate pattern
in the iris,
cataract,
retinal
yascular
tortuosity and
reduced
binocular
Depressed nasal vision
bridge Full prominent
cheeks
Prominent lips
Wide mouth Short turned-up nose
Widely-spaced Long philtrum
teeth
FIGURE 38.9 Facial features (elfin face) of Williams syndrome.

Microcephaly 38.26.4 Psychiatric Features

• Happy, loving, and sociable personality in
Long face
childhood
• Mood lability and temper tantrums when patient
gets older
• Poor concentration
Minor ear
• Distractibility
abnormalities
Prominent • Expressive language difficulties
tubular • Self-stimulating behaviour
nose,
bulbous • Obsessive–compulsive disorder
nasal tip
Small mouth
• Performance IQ > verbal IQ
FIGURE 38.10 Facial features of DiGeorge (velo–cardio–
facial) syndrome. 38.27 SMITH–MAGENIS SYNDROME
38.27.1 Case History
A 4-year-old boy presents with poor attention, over-
• Autosomal dominant transmission
activity, and bruxism. He has history of chronic otitis
• Microdeletions in chromosome 16p13.3
media and conductive and sensorineural deafness. He
also exhibits stereotyped self-hugging and self-injurious
38.26.3 Clinical Features (Figure 38.11) behaviour including skin picking, pulling out nails, biting,
• Feeding difficulties in infancy and slapping. During the interview, he licks his fingers
• Congenital heart disease initially. Then he finds a book in the consultation room
• EEG abnormalities and seizure and repeatedly licks and flips the pages (lick and flip). His
mother reports that he has insomnia at night and feeling
sleepy in the day time.
Ptosis
Microcephaly
Prominent nose,
broad nasal bridge,
1/25,000
hypertelorism
38.27.3 Genetic Defect
Complete or partial deletion of chromosome 17p11.2
Short stature 38.27.4 Clinical Features (Figure 38.12)

• Hearing problems
• Hoarse and deep voice
• Renal problems
• Inguinal/umbilical hernia
• Hypospadias (10% of male patients)
Broad thumb and • Short, broad hands and small toes
big toes Frequent fractures
• Hypotonia
FIGURE 38.11 Clinical features of Rubinstein–Taybi syndrome. • Hyperextensible fingers
Broad, square- Continuous

Microcephaly
shaped face eyebrows,
hypertrichosis
Small upturned (hirsuitism,
nose, anteverted long eyelashes)
nostrils Thin down-
Low set ears turning upper lip,
Deep-set
Flattened down-turned
eyes
nose mouth, prominent
bridge Short stature philtrum, high
Full arched palate
cheeks
Prominent Malformed upper

lower jaw Mouth tends to
limbs, small hands
turn downwards
and feet
with full lips
FIGURE 38.12 Facial features of Smith–Magenis syndrome. FIGURE 38.13 Facial features of Cornelia de Lange
syndrome.
• Schizophrenia like psychosis
• Inappropriate affect 38.28.5 Intelligence
• Aggression Severe to profound learning disability
• Seep disturbance (decreased REM sleep)
• Self-harm (pulling out finger and toenails)
38.28.6 Comorbidity
38.27.6 Intelligence Obsessive–compulsive disorder, gastrointestinal
Moderate to severe learning disability problems, congenital heart defects, visual and hear-
ing problems, skin problems, epilepsy, and death in
38.27.7 Treatment infancy
Naltrexone is useful in reducing self-injurious behaviour.

38.29 FETAL ALCOHOL SYNDROME
38.28 CORNELIA DE LANGE SYNDROME
• Variable incidence
One in 40,000 to 1 in 100,000; males = females • Leading cause of learning disability in Western
countries
38.28.2 Genetic Mechanism • One in 3000 live births in Western countries
Mutations in chromosome 5p; production of plasma pro-
tein A (PAPPA) and associated with infertility
38.29.2 Pathogenesis
38.28.3 Clinical Features (Figure 38.13) • It is not known whether the amount, frequency,
or timing of alcohol consumption during preg-
nancy causes a difference in the degree of
Autistic behaviour, self-injury, language delays, limited damage.
speech in severe cases, feeding difficulties, avoidance of • Mothers consuming more than 100 g/week (>10
being held, stereotypic movements, temper tantrums, and Units/week) in early pregnancy associated with
mood disorders low birth weight.
Small head BIBLIOGRAPHY

Besler RC and Sudhalter V. 2001: Conversational characteristics
Epicanthal of children with fragile X syndrome: Repetitive speech.
Short eyelid
opening folds American Journal of Mental Retardation 106:28–38.
Braddock D. 1999: Aging and developmental disabilities:
Demographic and policy issues affecting American fami-
lies. Mental Retardation 37:155–161.
Clarke AM, Clarke ADB, and Berg JB (eds.) 1985: Mental
Handicap: The Changing Outlook. London, U.K.: Methuen.
Day K. 1994: Mental handicap. In Paykel ES and Jenkins R
(eds.) Prevention in Psychiatry, pp. 130–147. London,
U.K.: Gaskell.
Low nasal
bridge
Dickinson M and Singh I. 2010: Learning disability psychia-
Flat midface try. In Puri BK and Treasaden IH (eds.) Psychiatry: An
Evidence-Based Text, pp. 1079–1099. London, U.K.:
Hodder Arnold.
Smooth Short nose
Emerson E. 1995: Challenging Behaviour: Analysis and
philtrum Intervention in People with Learning Disabilities.
Thin upper lip
Under developed Fraser W. and Kerr M. 2003: Seminars in the Psychiatry of
jaw Learning Disabilities, 2nd edn. London, U.K.: Gaskell.
Gasson EJ, Sullivan SG, Hussain R. et al. 2002: The chang-
FIGURE 38.14 Facial features of fetal alcohol syndrome. ing survival profile of people with Down’s syndrome:
Implications for genetic counselling. Clinical Genetics
38.29.3 Clinical Features (Figure 38.14) 62:390–393.
Hangerman RJ, Ono MY, and Hangerman PJ. 2005: Recent
• Prenatal and postnatal growth retardation advances in fragile X: A model for autism and neurode-
• Retrognathia in infancy generation. Current Opinion in Psychiatry 18:490–496.
• Micrognathia in adolescence Laking PJ. 2002: Psychiatry of disability. In Puri BK, Laking PJ,
and Treasaden IH (eds.) Textbook of Psychiatry, 2nd edn,
pp. 347–362. Edinburgh, Scotland: Churchill Livingstone.
38.29.4 Psychiatric Features McGuffin P, Owen MJ, O’Donovan MC, Thapar A, and
Gottesman II. 1994. Seminars in Psychiatric Genetics.
• Infants show withdrawal symptoms from birth. London, U.K.: Gaskell.
• Irritability during infancy. Roth MP, Feingold J, Baumgarten A et al. 1983: Reexamination
• Hyperactivity, hypotonia and poor coordina- of paternal age effect in Down’s syndrome. Human
tion, distractibility, and poor attention during Genetics 63:149–152.
childhood. Russell O. 1985: Mental Handicap. Edinburgh, Scotland:
• Memory impairment. Churchill Livingstone.
Sadock BJ and Sadock VA. 2007: Kaplan & Sadock’s Synopsis of
Psychiatry. Behavioural Sciences/Clinical Psychiatry, 10th
38.29.5 Intelligence edn. Philadelphia, PA: Lippincott Williams & Wilkins.
Young ID. 2005: Medical Genetics. Oxford, U.K.: Oxford
• Mild to moderate learning disability University Press.
39 Old-Age Psychiatry
39.1 EPIDEMIOLOGY Free radical theories

Free radicals commonly result from oxidative reactions in
In 2010, 17% of the population was aged 65 and over in normal cellular processes, particularly in the inner mem-
the United Kingdom, and the size of ageing population branes of mitochondria and during phagocytosis. The
has increased by 20% since 1985. The number of people resulting damage includes lipid peroxidation, which can
aged 85 and over is the fastest growing segment of popu- result in cell death. In animal experiments, antioxidants
lation, and the size has doubled in the past years. By 2035, (free radical scavengers) have been shown to increase life
the number of people aged 85 and over is projected to be expectancy but not to increase maximum life span, rais-
almost 2.5 times larger than in 2010, reaching 3.5 million ing doubt about the role of free radicals in the primary
and accounting for 5% of the total population. In 2006, ageing process.
the life expectancies of British at birth were 77.2 years The only method proven to increase the maximum life
for men and 81.6 years for women. The shorter life expec- span in experimental animals is calorie restriction. This
tancy in men is caused by male-predominant risk factors mechanism is unknown, but it may involve the delayed
such as alcohol dependence, cardiovascular diseases, maturation of the immune system or reduced free-radical
motor vehicle accidents, and suicide. Within the elderly damage secondary to reduced metabolic rate.
population, disability rises steeply with age, from 16 per
1000 who are in their 60s to 133 per 1000 who are aged
over 80 (Table 39.1) (Office for National Statistics, 2011). 39.2.4 Neurobiology of Ageing
In normal ageing, there is a slow reduction in weight and
39.2 PHYSICAL PROCESSES OF AGEING volume of the human brain (reduction by 5% by the age
of 70, 10% by the age of 80, and 20% by the age of 90),
39.2.1 Theories of Ageing with a proportionate increase in the size of the ventricles
and subarachnoid space after the age of 50 years.
There are two theories of ageing, Hayflick limit and sto-
The brain is overprovided with neurons, so a loss of
chastic damage. The mechanisms and outcomes are sum-
neurons does not necessarily result in a loss of function.
marized in Table 39.2.
Some parts of the brain show no loss in the number of
neurons with normal ageing (e.g. dentate nucleus of cer-
39.2.2 Genetic Factors ebellum). Great losses in neurons and neuron connection
are found in the frontal cortex (executive function), hip-
It is speculated that this effect is caused by the progres-
pocampus (memory), locus coeruleus (sleep), and sub-
sive loss of DNA sequences in the telomere involved
stantia nigra (gait). In normal ageing, especially after the
in the maintenance of DNA stability and replication.
age of 85, a shrinkage of nerve cells is known to occur in
Changes in ageing may involve errors in the control of
the cerebral cortex and putamen.
DNA expression, and this is known as epigenetic defects.
The rate of loss of nerve cells is around 1% per year
after the age of 60. Nerve-cell connections are reduced in
39.2.3 Nongenetic Theories some cells with compensatory increases seen in others in
normal ageing.
Age-related decline in organ function is no longer thought
Lipofuscin accumulates in the cytoplasm of nerve
tenable as a central cause of ageing; it is probably second-
cells from childhood.
ary to ageing.
Tau protein, involved in linking neurofilaments and
Mitochondrial decline microtubules, accumulates in a small proportion of
Across species, mitochondria show a reduction in num- ageing nerve cells particularly in the hippocampus and
ber, an increase in size, and structural changes in old entorhinal cortex, resulting in neurofibrillary tangles
organisms. Damage to mitochondrial membranes caused (NFTs). NFTs are composed of paired helical fila-
by free radicals is thought to contribute to these changes. ments with no amyloid. NFTs are found in Alzheimer’s
681

Summary of the Prevalence of Psychiatric Compare and Contrast the Hayflick Limit
Morbidity in Those Aged 65 and Over and Stochastic Damage
Other Psychiatric Hayflick Limit Stochastic Damage
Dementia Delirium Disorders
Concept Programmed ageing Wear and tear as a result
The prevalence of • The 3 year • Depression of ageing
dementia rises incidence is 13%. 13.5% Mechanism 1. Human diploid cells 1. There is a decline in
exponentially with • 5%–10% incidence • Phobic disorders cultured in vitro have basic metabolic rate
age, doubling every during 10% a finite life span. when a person gets
5 years hospitalization • Generalized Upon repeated older.
• 1.5% (65–69 years) • 6%–14% anxiety 4% subculture of normal 2. There is an
• 3% (70–74 years) long-term care • Personality cells, mitosis ceases accumulation of toxic
• 6% (75–79 years) home residents disorder 1% independently of substances (e.g.
• 12% (80–84 years) • 10%–15% general • Paranoid states culture conditions. lipofuscin), leading to
• 24% (85–89 years) surgical patients 0.5% 2. This finding suggests free-radical damages
• 48% (90–94 years) • 10%–20% • Panic that there is a finite in the processing of
prevalence at time disorder—rare number (the Hayflick ageing.
of admission to a limit) of 3. The macromolecules
medical unit subcultivations and distort the physical
• 30% cardiac the cells cannot divide and chemical
surgery patients further. properties of a normal
• 50% hip fracture 3. Cells derived from human body.
patients tumour tissue do not
• 70% intensive care display this limit.
unit patients Outcome • The Hayflick limit • The accumulation of
• 80% palliative causes irreversible the earlier adverse
patients with cessation of mitosis events in the process
advanced cancer and, ultimately, the of ageing ultimately
death of an leads to the end of
organism. survival.
• The Hayflick limit
disease (AD), normal ageing, progressive supranuclear supports the theories
of genetically
palsy (PSP), Pick’s disease, punch-drunk syndrome
programmed ageing.
(dementia pugilistica), Parkinson’s disease, dementia
of Lewy bodies (DLB), and Down syndrome. Senile
plaques are made up of a core of extracellular amyloid
surrounded by abnormal collections of neuritic pro- Lewy bodies are hyaline, eosinophilic concentri-
cesses. Senile plagues are formed from an aggregation cally laminated inclusions. Lewy bodies are found
of beta A4 amyloid. In the normal ageing brain, these characteristically in the substantial nigra and locus
are found in the neocortex, amygdala, hippocampus, coeruleus in patients with idiopathic parkinsonism and
and entorhinal cortex. normal old people. They comprise a spherical body in
Rod-shaped Hirano bodies are intracellular crystalline the cytoplasm of a nerve cell. They have a laminated
deposits and found near the hippocampal pyramidal cells. appearance with a dense granular core and fibrillary
These comprise the microfilament actin. Accompanying material radiating to the periphery, creating a pale
their presence is a granulovacuolar degeneration in the peripheral rim.
pyramidal nerve cells. In normal old brains, amyloid can be found deposited
Pick bodies consist of a hyaline eosinophilic mass of in the walls of blood vessels. Deposits are usually small,
neurofilaments, paired helical filaments, endoplasmic widespread, and in superficial cortical and leptomenin-
reticulum, and microtubules that distend the cytoplasm of geal vessels overlying the cerebral lobes. Amyloid and
affected neurons and displace the nucleus to the periphery. senile plagues are deposited in irregular patches in the
Pick bodies are argyrophilic. normal ageing cerebral cortex (Table 39.3).
Old-Age Psychiatry 683
rapidly than verbal IQ. Factors thought to account for this

TABLE 39.3 pattern include the following:
Summary of Histological Changes in Various Types
of Dementia • Speed of processing. This makes some contri-
Dementia AD Pick’s Disease DLB
bution to the age-related decline but is not the
whole explanation.
Neuro- Granulo- Pick bodies Lewy bodies • Familiarity/novelty. Tasks that have been learnt
pathological vacuolar Hirano bodies DLB is the
over a lifetime, relying on overlearned abilities, are
features degeneration Amyloid only dementia
most resistant to age-related changes (crystallized
(vacuoles in deposition that is
the cytoplasm NFTs characterized
intelligence). Tasks requiring the less-practised
in the Granulovacuolar by inclusion processing of new information are the most sensi-
pyramidal degeneration bodies in its tive to age-related decline (fluid intelligence).
cells in pathology
hippocampus) Although intelligence declines with age, there are consid-
Hirano bodies erable individual differences.
NFTs
Senile plaques • Problem-solving. The ability to abstract a con-
cept and apply it to a new situation declines with
age, most prominently after the age of 70.
• Creativity. Scientific creativity peaks in the
TABLE 39.4 30s, whereas artistic creativity peaks in the 50s.
Summary of Changes in Sleep Architecture in Ageing Humans seem to be most creative when they are
producing the greatest volume of work: intellec-
Sleep Parameters That Sleep Parameters That tual vigour.
Increase among Old People Decrease among Old People
↑ Sleep latency or the time to fall ↓ Duration of slow-wave sleep
asleep
39.3.2 Psychomotor Speed
↑ Frequency of awakenings ↓ Sleep efficiency Reaction time increases with age, with most slowing
at night occurring in the central processing of information. Older
↑ Episodes and fragmentation ↓ Total sleep time people are less able to maintain a state of readiness and
of REM sleep
less likely to choose flexible active information process-
ing than younger people.
39.2.5 Changes in Sleep Architecture 39.3.3 Memory

The changes in sleep architecture as a result of ageing are • Short-term memory. Short-term memory as
summarized in Table 39.4. tested by the digit span does not change with age.
• Working memory. Memory tasks requiring moni-
toring or complex decision-making are performed
39.3 PSYCHOLOGY OF AGEING more poorly in the elderly than in the young.
39.3.1 Cognition Decline is increased with the complexity of the
task or increased memory load.
39.3.1.1 Intellectual Functioning • Long-term memory. The retrieval of information
Intelligence peaks at the age of 25 years. It levels off until in the elderly is impaired; thus, uncued recall
the age of 60–70 and declines thereafter. Many studies shows an age-related decrement, but cued recall
have demonstrated an accelerated decline in cognitive reduces the extent of the decrement. Memory is
functioning in those who are closest to their death. This more durable if it is encoded at a semantic level,
has been referred to as the terminal drop, and poor health rather than at a phonological or orthographic
may be the cause. level. Older subjects are less likely to code at
Using the WAIS-R, a classic pattern of intellectual the semantic level. Memory performance in the
decline is seen, with performance IQ declining more elderly is best if the meaning is easily extracted.
from a more biological origin, whereas insecure per-

TABLE 39.5 sonalities arise more from early environmental events.
Summary of Changes in Neuropsychological Dysthymic personalities seem to persist into old age.
Functions in Elderly
Neuropsychological Functions Neuropsychological Functions 39.4 SOCIAL AND ECONOMIC
That Are Preserved in Old That Are Declined in Old FACTORS IN OLD AGE
People People
• Implicit or procedural memory • Acquisition of new 39.4.1 Attitudes
(e.g. riding a bicycle) information Western culture and young-/middle-aged adults in Western
• Registration • Problem-solving
countries devalue old age, with women perceived more
• Semantic memory (e.g. • Fluid intelligence
negatively than men. Old women are more likely to live
crystallized intelligence or • Retrieval of new information
factual knowledge)
alone and are more likely to be poor.
• Short-term recall The majority of old people cope well with ageing, report-
ing high life satisfaction, good cognitive skills, and open-
ness to new experience. These are considered to display
Memory of source is impaired in the elderly, which is an integrated personality. Those that cope less will display
thought to be related to deficits in frontal lobe functioning. either passive–dependent or disintegrated personalities.
The poorer the memory of distant events becomes, the Deviance from social norms generally decreases with age,
more remote the patient is from the event. while the prevalence of stigmatizing conditions increases.
Retention of knowledge is retained with age. Knowledge-
based skills are relatively preserved into old age (Table 39.5). 39.4.2 Status
As people age, the number of social roles they occupy
39.3.4 Importance of Loss decreases. This may reduce their social worth. Much of
the decline in the status of the elderly is associated with
After the age of 65, the ageing individual increasingly
their reduced socioeconomic circumstances.
suffers the loss of physical strength, employment, and
The status of elderly people is high in preliterate soci-
grief as a result of loss of loved ones through death.
eties and low in modern societies. The factors thought
Erikson describes the psychosocial changes that indi-
to contribute to this effect include the reduction in the
viduals negotiate as they develop. The last of these—
usefulness of the elderly as repositories of knowledge, the
integrity versus despair—is concerned with the way the
breakup of the extended family, and the reduced impor-
individual approaches death. A well-lived life is more
tance of land inheritance.
likely to result in a sense of integrity and wholeness at
this time of reflection upon life achievements. Those with
regrets and thoughts of opportunities missed are more 39.4.3 Retirement
likely to approach death with a sense of despair. Retirement in itself is not a cause of increased morbidity.
The main problem experienced in retirement is substan-
39.3.5 Personality Changes tial income reduction: the relative value of pensions today
has fallen compared with 50 years ago. In 1997, a retiree
Most studies of personality in older age support the con- who had paid £200 a month into a personal pension for
cept of the stability of personality with age. 20 years received a typical annuity of £20,500 per year. In
Adjustment to ageing can be explained by different 2007, a retiree making the same amount of contributions
models, which may apply in different individuals. The only received £4,613 per year. The pension received in
activity theory entails the successfully adjusted individual 2007 was 78% less as compared to 1997 (Barrow, 2007).
as being fully engaged with life, with interests, and with
social contact. The disengagement theory suggests that the
39.4.4 Accommodation
individual focuses increasingly on his or her inner world as
adjustment is made to diminished family and social roles. The likelihood that elderly people will live alone and
High anxiety levels in the elderly are correlated with away from their families is relatively common in Britain.
physical ill-health, but most chronic neurotic conditions The ageing population is living longer and is thus more
improve in old age. Anxiety-prone personalities arise likely to live alone at some stage in their later years.
For health reasons, large proportions of the very old • ↑ Proportion of body mass that is composed of
live in institutional care or with relatives or friends. Old adipose tissue
people living alone make more use of statutory services • ↑ First-pass availability
than those living with others. • ↑ Gastric pH
Disengagement theories hold that older people gradu- • ↓ Gastric acid secretion and intrinsic factor
ally withdraw from society in preparation for death have (associated with increased risk of vitamin B12
now lost favour. Instead, activity theories encourage the deficiency)
maintenance of social interaction and role. Elderly people • ↓ Rate of gastric emptying
do maintain a high level of social contact with others. • ↓ Blood flow in splanchnic circulation
Unhappiness is associated with a lack of friends in a • ↓ Gastrointestinal absorptive surface
social network. • Changes in plasma-protein concentration: this
may be the result of illness
• ↓ Metabolically active tissue
39.4.5 Sociocultural Differences
• ↓ Hepatic mass and blood flow
39.4.5.1 Social Class • ↓ Demethylation
Almost half of pensioners from social classes I and II • ↓ Hydroxylation
have money in addition to the state pension, from private • ↓ Renal blood flow
pension schemes and savings, compared to only 5% of • ↓ Glomerular filtration rate and rate of
those in social classes IV and V. elimination
• ↓ Tubular secretion
39.4.5.2 Ethnicity
There are competing theories about the effect of ethnicity 39.5.1.1 Absorption
and ageing: There is no evidence that the rate or extent of absorp-
tion of orally administered psychotropic medications is
• The age as leveller hypothesis argues that, changed in the elderly.
because all old people are socially disadvan-
taged, the relative disadvantage experienced by 39.5.1.2 Clearance
ethnic minorities reduces in old age. Reduction in clearance may increase the steady-state
• The double jeopardy hypothesis argues that dis- plasma drug concentration in old people. Because of low-
advantages are exacerbated with age. ered renal clearance, lithium doses in the elderly should
be approximately 50% lower than in the young. Diuretics
Language difficulties are common in ethnic minority may reduce renal clearance even further, increasing the
groups, and lack of income is most common in Asian risk of lithium toxicity.
people who have travelled from abroad to join their fami-
lies and lack pension entitlement. 39.5.1.3 Metabolism
All other psychotropic drugs are cleared by hepatic bio-
transformation, which is variably reduced with age. As
39.5 PSYCHOPHARMACOLOGY
a result, the half-life of psychotropic medications (e.g.
OF OLD AGE clonazepam) can be markedly prolonged, having residual
39.5.1 Pharmacokinetics and Pharmacodynamics effects for weeks after discontinuation.
Age-related changes in drug handling 39.5.1.4 Distribution

Changes with ageing that may affect pharmacokinetics This is determined by the drug’s relative solubility in lipid
include as opposed to water, proclivity for various body tissues,
and plasma–protein binding. Most psychotropic drugs,
• ↓ Total body mass being lipophilic, have a relatively small plasma concen-
• ↓ Proportion of body mass that is composed of tration compared to the total amount of drug in the body.
water Nevertheless, the increased fat over muscle ratio causes
• ↓ Proportion of body mass that is composed of lipophilic drugs to have increased distribution volume
muscle and risk of accumulation.
39.5.2 Drug Interactions Benzodiazepines

Accumulation in the elderly is not more likely to occur
The incidence of side effects and adverse drug reactions than in the young. The elderly are at an increased risk of
increases with age. For example, the combination of lith- delirium and falls.
ium and NSAIDS increases the lithium level in elderly
markedly. The causes that may contribute to this include
underlying physical illnesses, polypharmacy in old people, 39.6 DISTRICT SERVICE PROVISION
poor compliance, reduction of hepatic metabolism, and
renal clearance.
39.6.1 Principles of Service Provision
The planning of services for the elderly must take into
account the age distribution of the population, including
39.5.3 Side Effects
the numbers of the very elderly who are most likely to
Old people are more sensitive to side effects as a result of need the most costly institutional care.
altered receptor and neurotransmitter function. For exam- The elderly require accurate medical, psychological,
ple, tricyclic antidepressants are more likely to cause ortho- social, and functional assessment; specialist knowledge;
static hypotension as a result of blocking α2 adrenergic least disruptive solutions; and prompt interventions.
receptor in elderly. Furthermore, the presence of medical Informal carers should be considered and supported, and
comorbidity may affect their ability to metabolize or toler- liaison between all aspects of service is paramount.
ate side effects of medications. For example, an old person
with chronic obstructive lung disease is less able to tolerate 39.6.2 Needs of Carers
respiratory depression associated with benzodiazepine.
Community care of the mentally ill, especially demen-
tia sufferers, results in significant strain on an infor-
39.5.4 Practical Considerations mal carer or a very close relative, such as a spouse or a
child. Female carers outnumber males 2:1. The carers of
Antipsychotics demented elderly people have more problems than others,
The elderly are more sensitive to anticholinergic side which increase with the degree of dementia.
effects. Parkinsonian side effects are more likely in the The sources of stress include
elderly, in women, and in those with organic brain dis-
ease. The prevalence of tardive dyskinesia increases • Practical—for example, elderly person requir-
with age and is more common in women. The length of ing help with personal and household tasks and
treatment is more strongly related than the absolute dose. care
Acute dystonias, although common in the young, are rare • Behavioural—for example, nocturnal distur-
in the elderly. bance, incontinence, wandering, and aggression
An alert has been issued on the use of antipsychotics • Interpersonal
in dementia-related psychosis and dementia-related behav- • Social—for example, restrictions on the carer’s
ioural disturbance because of the increase in mortality and personal life
cerebrovascular adverse events compared to placebo.
Prescribers should consider carefully the risk of cere-
brovascular events before treating any patient with a pre- 39.7 ASSESSMENT OF A REFERRAL
vious history of stroke or TIA, hypertension, diabetes,
39.7.1 Psychiatric Assessment
current smoking, and atrial fibrillation.
The most informative setting for the initial assessment
Tricyclic antidepressants
is within the person’s home. Coordination is required
Heart disease is a relative contraindication. Again, the
to ensure that informants are available, and that is
elderly are particularly prone to postural hypotension and
essential in those with organic brain syndromes. The
anticholinergic side effects, which may result in acute
interview should be unhurried, allowing the patient to
brain syndromes, urinary retention, and glaucoma.
relate a full family and personal history. An assess-
MAOIs ment of how the patient deals with questioning is made
Extreme caution is needed if considering prescribing throughout.
these to patients with hypertension and cardiovascular The psychiatrist should be vigilant for unrecognized
disease. physical illness presenting with psychiatric symptoms and
• Basic activities of daily livings (BADLs) (mne-

TABLE 39.6 monics: DEATH): dressing, eating, ambulation,
Information to Be Assessed in a Psychiatric toileting, and hygiene (Bookman et al., 2007)
Interview for an Old Person • Instrumental activities of daily livings (IADLs)
Source and nature of referral
(mnemonics: SHAFT): shopping, housework,
Who made the referral?
accounting, food preparation, and transporta-
What the referrer wishes to know? tion (Bookman et al., 2007).
What the patient and the carers have been told to expect?
Description of presenting complaints Past psychiatric history
Onset, frequency, intensity, duration, location (home, nursing home, etc.)
Antecedents and consequences • Past psychiatric disorders (e.g. schizophrenia,
Ameliorating and exacerbating factors mood disorders, anxiety disorders)
• Current psychiatric medications
• History of heavy drinking, alcohol misuse, sub-
if this is suspected should ensure that the patient receives stance misuse, and smoking
the appropriate medical interventions. Examination at • Premorbid personality
home allows an assessment of the patient’s coping in
the immediate environment, including visuospatial ori- Past medical history
entation and the ability to manage independently. It also
allows assessment of local resources such as neighbours’ • The history of chronic medical illnesses, for
and relatives’ availability and any evidence of the unwise example, diabetes, cardiovascular diseases, and
use of alcohol. metabolic syndrome
If the first assessment occurs on a medical ward as • The history of neurological disorders, for exam-
a liaison visit, the medical notes should be read and the ple, Parkinson’s disease, multiple sclerosis, epi-
medical and nursing staff should be interviewed before lepsy, and cerebrovascular accidents (CVAs)
the patient is seen. Carers should be contacted to supple- • The history of head injury and related operations
ment the information gathered on the ward. The patient • Current medications
interview should take place in the most private conditions
available (Table 39.6). 39.7.1.1 Mental State Examination
Supporting features to suggest underlying medical
Appearance and behaviour
causes for a psychiatric or cognitive symptom
• Careful observation is important in a person
• History of trauma or exposure to toxic substance
with difficulties with verbal exchange (e.g.
• Presence of focal neurological symptoms
severe dementia, delirium, aphasia, severe hear-
• Rapid onset and progression
ing and/or visual impairments).
• Recent illness or history of chronic illnesses
• Observe for signs of psychomotor retardation or
• Younger age of onset than expected
agitation, perplexity, or behavioural disturbance.
• Poor hygiene, incontinence, or inadequate nutri-
Description of the elderly current interpersonal relation-
tion gives an indication of the patient’s ability to
ship and activities of daily living (ADL)
live independently.
• An inability to focus or sustain attention appro-
• Behaviours that can jeopardize placement in
priately may be a sign of clouded consciousness.
the community (e.g. day/night reversal, wander-
ing, aggression, sliding or throwing themselves
Speech: Cognitive impairment may result in circumlo-
to the floor, stripping off their clothes, and the
cution, paraphrasia, and polite evasions hiding a lack of
smearing of faeces)
depth and detail in speech.
• Emotions: negative and positive
Thought patterns of early dementia include a repeti-
• Peer and staff relationships for old person who
tion of themes, a lack of internal logic, and a limitation
stays in a nursing home facility
of discussion inconsistent with the level of intelligence.
• Family relationships for old person who stays
at home Mood: Depression or mania that can be easily missed.
Hallucinations and delusions

TABLE 39.7
• Auditory hallucinations are less descriptive and Information to Be Assessed during Cognitive
contain less details when compared to those Examination
reported by young schizophrenia patients.
• Orientation—to time, place, and person
• Visual hallucinations may suggest dementia
• Attention and concentration—assessed using ‘serial sevens’ or naming
with Lewy bodies (DLB).
months of the year backward if numerical abilities are not good
• Paranoid delusion is common among old people.
• Immediate memory—assessed using digit span
Physical examination • Short-term verbal memory—assessed using name and address with
six parts, repeated immediately to assess registration, then again
• Check the person’s temperature (using a low- after 5 min with intervening distraction to prevent rehearsal, also
reading thermometer). using Babcock sentence
• Short-term nonverbal memory—assessed by immediate recall
• Check the state of hydration if clouding of con-
(registration) of a geometric shape, then recall after 5 min with
sciousness is suspected.
intervening distraction to prevent rehearsal
• The presence of hemiparesis may suggest large- • Long-term memory—assessed during history taking (ask date and
vessel infarct. place of birth)
• The presence of parkinsonism may suggest DLB. • General knowledge—assessed by asking historical and recent
• Pseudobulbar palsy is found in patients with commonly known facts (e.g. the current prime minister, monarch
human immunodeficiency virus (HIV)-associated and family, the President of the United States, the colours of the
dementia, PSP, vascular dementia (VaD), and Union Jack, the names of capital cities)
Parkinson’s disease. • Verbal fluency—number of words beginning with T in 1 min or the
• Tremors and involuntary movements (e.g. be number of four-legged animals in 1 min
alert to the possibility of a cerebrovascular event, • Calculation—assessed by asking a simple calculation such as a
the onset of Huntington’s or Wilson’s disease, or, subtraction
more commonly, l-dopa for Parkinson’s disease). • Writing
• Check gait that may indicate fall risk. Gait changes • Spatial—including bodily awareness
• Recognition—of objects and faces
occur in chronic alcoholism, DLB, normal-pres-
• Appropriate use of everyday objects
sure hydrocephalus, multiple sclerosis, Parkinson’s
• Naming things—to detect nominal dysphasia
disease dementia, tertiary syphilis, and VaD.
• Receptive and expressive use of written and spoken language
• Myoclonus is found in HIV-associated dementia
• Perseveration—suggestive of frontal lobe dysfunction
and Creutzfeldt–Jakob disease (CJD).
• Tests of praxis—such as drawing a square or a clock face
• Primitive reflexes and frontal release signs (constructional apraxia) and asking the patient to make a fist, oppose
are found in patients with frontotemporal lobe thumb and little finger, fold a piece of paper, and place it in an envelope
dementia (FTD). Examples include the palmo- • Tests of gnosis—such as picture recognition, tactile recognition
mental reflex, grasp reflex, pout reflex, sucking
reflex, and glabellar tap.
• Check visual or hearing impairments. syndrome. Cambridge Cognition Examination (CAMCOG)
is a neuropsychological screening instrument used in
The NICE guidelines recommend that clinical cognitive the United Kingdom. CAMCOG is part of Cambridge
assessment should include the examination on attention, Mental Disorders of the Elderly Examination (CAMDEX).
concentration, orientation, short- and long-term memory, CAMDEX incorporates the MMSE, Blessed Dementia
praxis, language, and executive function (Table 39.7). Rating Scale and Hachinski Ischaemic Score, National
Standardized instruments for formal cognitive test- Adult Reading Test (NART), Kendrick Object Learning
ing include the mini-mental state examination (MMSE), Test for memory, and Wisconsin Card Sorting Test for exec-
Addenbrooke’s Cognitive Examination Revised (ACE-R), utive function. Detailed psychometrics may be necessary if
Montreal Cognitive Assessment (MoCA), Clinical Dementia screening tests are positive (Table 39.8).
Rating Scale (CDRS), General Practitioner Assessment of
Cognition (GPCOG), 6-Item Cognitive Impairment Test
39.7.2 Investigations
(6-CIT), and 7 Minute Screen. Patients with learning dis-
ability require different tests such as dementia questionnaire Routine investigations in the hospitalized elderly should
for mentally retarded person or dementia scale for Down include full blood count (FBC) with differential white
TABLE 39.8
Compare and Contrast MMSE, ACE-R, MoCA, and Clinical Dementia Rating Scale
Clinical Dementia
MMSE (Folstein et al., ACE-R (Mioshi et al., MoCA (Nasreddine Rating Scale (CDRS)
1975) 2006) et al., 2005) (Morris, 1993)
Person(s) assessed Patient only Patient only Patient only Patient and carer
Components and domains 1. Orientation 1. Orientation 1. Orientation 1. Memory
2. Registration and recall 2. Registration 2. Attention 2. Orientation
3. Attention and calculation 3. Attention 3. Memory 3. Judgement
4. Language 4. Recall 4. Executive function 4. Community affairs
5. Visuospatial ability 5. Anterograde and (verbal fluency, 5. Home and hobbies
6. Praxis retrograde memory abstract thinking) 6. Personal care
MMSE is lack of frontal 6. Verbal fluency 5. Visuospatial abilities
lobe assessment 7. Language (writing, 6. Attention and
comprehension, calculation
reading, naming) 7. Language
8. Visuospatial ability
9. Perceptual abilities
10. Recognition
Time required 10–15 min 10–15 min 10–15 min 30 min
Scoring Normal score >24 Two cutoffs were Normal score >26 The score is calculated
(sensitivity = 0.44–1; defined: (sensitivity = 1, based on an algorithm.
specificity = 0.46–1) 88: sensitivity = 0.94, specificity = 0.87) Normal: 0
Score is determined by specificity = 0.89 and AD: 11–21 Possible dementia: 0.5
education. For patients with 82: sensitivity = 0.84, Mild dementia: 1
only primary school specificity = 1.0 Moderate dementia: 2
education, the following Severe dementia: 3
cutoffs are used:
Ages 18–69: median MMSE
score 22–25; ages 70–79:
median MMSE score
21–22; age over 79: median
MMSE score 19–20
Mild cognitive impairment (MCI) Normal score >24 MCI patients to be Score between 21 and 26 Not applicable
impaired in areas (e.g.
attention/orientation,
verbal fluency, and
language) other than
memory
cell count (WCC), erythrocyte sedimentation rate (ESR), A CXR is required in all sick elderly people, even if
urea and electrolytes (U&E), creatinine, liver function the chest is apparently clear on physical examination.
tests (LFTs) with calcium and proteins, glucose, TSH, Pneumonia, tuberculosis, and carcinoma can all present
electrocardiogram (ECG), chest x-ray (CXR), and a mid- with acute confusional states or depression. An ECG is
stream urine examination. also required because some psychotropic medications
The prevalence of thyroid disease increases in old age. may prolong the corrected QT (QTc) interval.
Physical signs are often unreliable in the elderly, so TSH
screening should be performed in all. Hyperthyroidism
39.7.3 Structural Imageing
can be mistaken for anxiety states, hypomania, or delir-
ium. Hypothyroidism can present as depression with psy- In normal ageing, there is progressive cortical atrophy
chomotor retardation, dementia, or delirium. and increasing ventricular size. Imaging can identify
potentially treatable intracranial lesions. The indications

for imaging in a person present with cognitive impairment TABLE 39.9
are summarized as follows (Clair and Seitz, 2011): Comparison of Different Imaging Modalities
• Age of patient: younger than 60 years in Old-Age Psychiatry
• Duration of cognitive impairment: short duration Brain Volume
• Focal neurological sign: urinary incontinence Imaging and Structural Oxidative Glucose
and gait disorder Targets Changes Metabolism Metabolism
• History of anticoagulant use, bleeding disor- Clinical • Normal-pressure • Differentiating • Detecting
ders, head injury, and cancer examples hydrocephalus: AD, VaD, and changes in
• Onset of cognitive impairment: rapid decline (e.g. enlarged FTD radioligands
1–2 months) ventricles • Assessing in specific
• Specific symptoms: frontal lobe signs, progres- without cortical synaptic areas of the
atrophy strength (e.g. brain affected
sive aphasia, new onset headache, and seizure
• Huntington’s protein by AD
Conventional structural imaging is helpful in discover- disease: gross synthesis,
ing the aetiology of dementia, although it does not estab- shrinkage of the axonal
lish the diagnosis, which is determined clinically. The caudate nucleus transport, and
distribution of cerebral atrophy helps to distinguish dif- • Lacunes synaptogenesis)
• White matter
ferent types of dementia.
hyperintensities
Recently, fludeoxyglucose 18F (FDG) is one of the most
Imaging • CT and MRI • SPECT is 85% • FDG-PET
commonly used radiotracers in imaging. It is an analogue methods are useful in accurate in
of glucose and concentrated in metabolically active tissue detecting differentiating
such as the brain. After absorbed in cells, phosphorylation clinically AD, FTD, and
prevents the glucose from being released from the cell. significant VaD
Fluoro-2-deoxy-d-glucose-positron emission tomogra- structural
phy (FDG-PET) is more sensitive than SPECT in sepa- lesions
rating normal elderly individuals from dementia patients • MRI has better
when areas in the temporoparietal and posterior cingulate resolution than
are scanned. Changes on FDG-PET scans appear closely CT
related to histopathological changes (Table 39.9).
39.7.4 Electroencephalography In Pick’s disease, the EEG is more likely than in AD to be

normal and shows less slowing of the a waves.
In normal ageing (after the age of 60), the following In VaD, the tracing shows asymmetry and localized
changes occur in the Electroencephalography (EEG): slow waves, with a sparing of background activity.
• Slowing of α rhythm In CJD, a slow background rhythm with paroxysmal
• Increased θ activity particularly in the left tem- sharp waves is characteristic.
poral region In Huntington’s disease, a low-voltage pattern may
• Increased δ activity particularly in the anterior be seen.
regions
• Diminished β activity (only in those aged over 80) 39.7.4.2 Delirium
39.7.4.1 Dementias Most conditions causing delirium cause slowing of the
In Alzheimers disease (AD), the EEG may be normal EEG tracing:
(6%) or show minor nonspecific changes. The following
1. Metabolic causes
changes may occur:
a. Hepatic encephalopathy—slowing of rhythm
• Diffuse slowing in early stages with posterior preservation; triphasic waves
• Reduced α and β activity, plus increased θ and δ are highly indicative.
activity as the disease progresses b. Acute renal failure—low-voltage activity
• Paroxysmal bifrontal δ waves (more common with posterior slowing.
than in normal ageing) c. Bursts of θ activity.
d. Hypocalcaemia—slowing with bursts of • Predicting outcome: Various scales, such as the

spikes. Clifton Assessment Procedures for the Elderly
e. Hypercalcaemia—runs of 1–2 s waves. (CAPE), can predict survival, placement, and
f. Hyperthyroidism—acceleration of a rhythm. decline in elderly subjects. The Kew Cognitive
g. Hypothyroidism—low-voltage EEG. Map assesses parietal lobe function and language
2. Drugs functions in the dementing patient. This success-
a. Phenothiazines increase voltage, slow α fully predicts 6 month survival (McDonald, 1969).
activity, and reduce β activity; in overdose, • Predicting need: The CAPE assesses the level of
paroxysmal slow waves are characteristic. disability and thus allows for prediction of need
b. Antidepressants increase EEG activity but for support services. Identification of impair-
reduce a rhythm; in overdose, widespread a ments allows for interventions that may over-
activity and spikes. come the problems posed by the impairment.
c. Benzodiazepines—increase β waves, espe- Assessments can be used to provide objective
cially frontal; in overdose, prominent fast evidence for allocation of resources.
activity unresponsive to stimuli. • Monitoring change: The NART is used to deter-
d. Lithium—slow α rhythm with occasional, mine premorbid IQ, thus aiding in the initial assess-
sometimes focal, spikes; in overdose, dif- ment of apparent cognitive impairment. Premorbid
fuse slowing, triphasic waves, and paroxys- function is compared to current functioning using
mal abnormalities. the Wechsler Adult Intelligence Scale (WAIS).
Of those with delirium, 90% of patients have abnor- Repeating tests over time can give an estimate of deteriora-
mal traces. Delta activity, asymmetry in δ waves, and tion, but this can be unreliable since even the elderly with
localized spike and sharp wave complexes occur more dementia can show practise effects with repeated testing.
frequently in those with intracranial pathology. Alpha
activity correlates with cognitive functioning, and δ 39.7.5.2 Experiential Assessment and Analysis
activity correlates with the length of illness. of Function
Experimental assessment tries to clarify the nature of
impairment. By understanding the nature of the impair-
39.7.5 Psychological Assessment ment, it is possible to develop interventions that amelio-
rate the impairment.
39.7.5.1 Psychometric Testing and Measures Experiential analysis of function is used to explain
of Function dysfunction and to develop strategies for intervention.
Psychometric testing quantifies the level and range of abil-
ity. Serial measures can be used to monitor the effect of • Explaining dysfunction. A finding in a psycho-
interventions or to measure progress of the patient’s con- metric test may conclude that a patient is unable to
dition over time. It is essential, when any particular test is carry out a task but does not try to establish why.
used in the elderly, that both the test itself and its predic- The decomposition of impaired performance
tions have been validated in the local elderly population. is used to establish which ability is impaired.
Psychometric measures of function are used to clarify A hypothesis of what the disability comprises is
the diagnosis, to predict outcome, to predict need, and to tested before a conclusion is reached.
monitor change: • Developing strategies for interventions. A behav-
ioural approach may be used with an ABC (ante-
• Clarifying the diagnosis: Batteries of tests have cedents, behaviour, and consequences) analysis
been devised to distinguish between different before attempting an intervention.
diagnostic groups: the Kendrick Battery was
developed to distinguish normal, functionally 39.7.5.2.1 Social Assessment
impaired, and demented elderly groups. The Assessment is usually conducted by a social worker. This
Geriatric Depression Scale (GDS) is a 30-item involves a detailed assessment of living conditions, per-
self-administered rating scale, with cut-off sonal care, dynamics of family/carer, support network,
score determining whether depressed (exten- financial situation, family structure, level of independence,
sively validated and highly discriminant). and physical functioning in the person’s environment.
39.7.5.2.2 Occupational Therapy Assessment 39.8.3 Psychiatric Consequences of Specific

Occupational therapy assessment provides a base- Physical Disorders
line of functioning in areas of basic and instrumental
ADLs. An important part of the assessment is to iden- 39.8.3.1 Cerebrovascular Disease
tify strengths that can be built on to overcome deficits. Mood disorders may follow a stroke. These are mixed
The best place to conduct ADL assessments is within and affect different patients differently. General dys-
the person’s own home, as early in the illness as pos- phoria and worry are common. Poststroke depression
sible in order to establish baselines. ADL assessment and anxiety are recognized. Mania following stroke is
is invaluable in helping to establish the most appro- described but uncommon. Apathy and social withdrawal
priate placement on discharge and to determine those are seen in the absence of depression.
packages of care that are most likely to enable ongoing Syndromes more characteristic of stroke include
independent living. emotional lability and the denial of handicap
(anosognosia).
39.8 PSYCHOLOGICAL REACTIONS
TO PHYSICAL DISEASE 39.8.3.2 Sensory Impairment
Most commonly seen are impairments of hearing and/
Theories of ‘successful ageing’ maintain that elderly
or vision. These have a dramatic impact upon the indi-
people select a range of activities they want or need to
vidual’s ability to communicate with others, which may
do, then optimize their performance of these activities,
cause social withdrawal, reduced activity, and appar-
and compensate for losses of physical or mental abilities.
ent cognitive decline. They may increase the risks of
depression and paraphrenia in the elderly although this
39.8.1 Adjusting to Physical Illness
is not proven.
Several factors contribute to the experience of a physical
illness:
39.9 MILD COGNITIVE IMPAIRMENT (MCI)
• The meaning of the illness, both generally and
specifically to that patient 39.9.1 Epidemiology
• The response of those close to the patient
• Physical symptoms • The conversion rate from normal ageing to Mild
• Social consequences of the illness cognitive impairment (MCI) is around 15%.
• Coincidental life events and difficulties • The conversion rate from MCI to dementia is
around 5%–10% per year.
39.8.2 Responses to Physical Illness
There are three components to coping style:
39.9.2 Pathology
• Atrophy of hippocampus
• The exercise of autonomy and independence • Beta-amyloid deposition
• The sense of personal responsibility or locus of • Depression
control • Vascular atherosclerotic changes
• Activity versus passivity
Psychiatric disorder may arise as a consequence of the 39.9.3 Clinical Features

stresses imposed by the physical condition, but it may
also arise as a direct physical consequence of the patho- • MMSE: 24–30.
logical process. For example, • Subjective complaint of memory loss.
• Objective evidence of cognitive impairment.
• Hyperthyroidism may give rise to an anxiety state. • Decline from previously normal level of function.
• Hypercalcemia, infection, hypoxia, or organ • Preserve basic ADL.
failure may give rise to delirium. • No underlying medical or surgical conditions
• Steroids may give rise to depression, elation, or causing reversible dementia.
emotionalism. • Cognitive impairments are not severe to meet the
• Frontal lobe lesions are likely to result in apathy. diagnostic criteria for dementia (Table 39.10).
cerebral cortex, which plays a key role in memory and

TABLE 39.10 language. AD, frontal lobe dementia, and CJD are exam-
Classification of MCI ples of cortical dementia. Subcortical dementias result
MCI (Amnesic Type) MCI (Nonamnestic Type) from dysfunction in neuroanatomical structures that are
beneath the cortex. Memory impairments and language
This is the most common form Nonamnestic MCI may involve
difficulties are not the early signs of subcortical demen-
and manifests as preclinical multiple cognitive domains
manifestation of AD. (e.g. executive function) rather
tias. Examples of subcortical dementias include HIV-
Patients present with impaired than amnesia. related dementia, Huntington’s chorea, and Parkinson’s
performance on delayed recall. This type of MCI manifests as disease. Examples of mixed cortical and subcortical
There is objective evidence of localized impairment of other dementias include VaD, DLB, and neuropsychiatric
impairment of short-term cognitive domains rather than sequelae after carbon monoxide poisoning (Table 39.11).
memory, but general cognitive memory. The DSM-5 (APA 2013) classifies dementia into
functions are normal. Nonamnestic MCI may develop major and minor neurocognitive disorders. Major
There is no substantial into non-Alzheimer’s neurocognitive disorder involves significant decline
interference with work, usual dementias. from previous level of cognitive performance and
social activities, or other ADLs.
There is absence of the diagnosis
of dementia. TABLE 39.11
Amnestic MCI has higher Compare and Contrast Cortical and Subcortical
chance to convert to Dementia
dementia compared to
nonamnestic MCI. Cortical Dementia Subcortical Dementia
Classical • The ‘A’s’: amnesia, • The ‘D’s’:
Source: Loewenstein, D.A. et al., Dementia and Geriatric Cognitive
symptoms agnosia, acalculia, dysexecutive
Disorders, 27, 418, 2009.
apraxia, and aphasia function, dysarthria,
and depression
Memory deficits • Primarily a storage • Forgetfulness or
39.9.4 Treatment and recall deficit failure of retrieval is
initially amenable to
• Cognitive rehabilitation prompting
• Physical exercise and healthy lifestyle Executive • Late executive • Early executive
• Treat underlying vascular risk factors (e.g. dysfunction function impairment function impairment
hypertension, hyperlipidaemia) (except FTD)
• Treat underlying depression Gnostic–practic • Agnosia, acalculia, • Agnosia, acalculia,
• Yearly follow-up on instrumental ADL and abilities and apraxia are and apraxia are less
cognition common common
Language • Aphasia • Dysarthria
39.10 DEMENTIA IN OLD AGE Movement • Fine and gross • Abnormal
movements are movements are
Dementia is defined as a global deterioration in brain func- generally preserved common and
tions in clear consciousness, which is usually progressive until later in the manifest as a
and irreversible. It results in the deterioration of all higher course of dementia slowing or as chorea
brain functions including memory, thinking, orientation, or tremor early in
comprehension, calculation, the capacity to learn, lan- the course of
guage, and judgement and is accompanied by deteriora- dementia
Personality • Personality often • Personality change
tion in emotional control, behaviour, and motivation.
remains intact or is often marked
The dementias become more prevalent with increas-
displays minor
ing age. The most common dementia in the elderly is AD variations (except
(50%), followed by mixed AD and VaD (15%), VaD (5%), FTD)
frontotemporal dementia (FTD) (10%), DLB (2%), and Affective • Affective expression • Major depression or
other types of dementia (18%). expression is generally mania occurs
Dementia can be broadly classified into cortical and preserved frequently
subcortical dementia. Cortical dementias arise from the
interference with ADL. Minor neurocognitive disorder 39.10.2.1.2 Genetic Factors

is associated with mild cognitive decline and no inter- Genetic factors must account for the disease in some
ference with ADL. patients. It is familial in some families, especially those
in which the onset is early (under 65, presenile dementia).
39.10.1 Risk and Protective Factors The finding of AD in many patients with Down syndrome
for Dementia who reach middle age has focused interest on chromo-
some 21 on which is located the amyloid precursor pro-
See Table 39.12.
tein (APP) gene. The following genes are involved:
39.10.2 Alzheimer’s Disease • APP gene on chromosome 21 (accounting for
39.10.2.1 Aetiology 20% early-onset AD)
• Presenilin 1 (PS 1) gene on chromosome 14
39.10.2.1.1 Neurotransmitter Abnormalities
(presenilin is implicated in β-amyloid produc-
Of most interest is the loss of cholinergic neurons in tion and accounting for 70% early-onset AD)
basal forebrain, low cortical cholinergic activity, and • Presenilin 2 (PS2) gene on chromosome 1
reduced choline acetyltransferase especially in the
temporal cortex. This is thought to be secondary to It is also hypothesized that late-onset AD is an autoso-
the degeneration of neurons in the nucleus basalis of mal-dominant trait with age-dependent expression and
Meynert, which provides the cortex with its cholinergic low penetrance, resulting in apparent sporadic cases.
projection.
Other neurochemical changes in AD include 39.10.2.1.3 Environmental Factors
Aluminium. The brains of those with AD contain more total
• ↓ Dopamine beta-hydroxylase. aluminium than those of controls. Aluminium is found in
• ↓ Dopamine. the areas of the brain most affected in AD, particularly in
• ↓ Noradrenaline and serotonin in the cortex. the neurons containing tangles and in the core of senile
• ↓ Cortico-neuropeptides such as somatostatin. plaques. Those receiving haemodialysis accumulate alu-
• ↑ Glutamate and hyperexcitation leads to neuro- minium from the dialysate. Before this was recognized,
nal toxicity and impair learning. patients developed severe dementia. Steps are now taken
to reduce the burden of aluminium accumulation in those
receiving haemodialysis. Aluminium probably accumulates
TABLE 39.12 in the brains of those with AD secondary to the disease pro-
Classification of Risk and Protective Factors cess rather than being directly causative. It remains possible
of Dementia that aluminium is a contributory factor in some cases of AD.
Modifiable Risk Nonmodifiable Head injury. In sporadic AD, there is an increased risk in
Factors Risk Factors Protective Factors those who have experienced head injury within the pre-
Endocrine: history of Demographics: Bilingualism ceding 10 years.
diabetes advanced age and Cognitive Infection. It is hypothesized that an infectious agent
Lifestyle: exposure to female gender engagement and late
entering via the transolfactory route may be responsible
pesticides, lack of Genetics: retirement
for some cases of AD. Herpes simplex type 1 is known
physical activity, Apolipoprotein Fish intake (more
repetitive head E4 on than once a week)
to have a predilection for those brain areas particularly
injury, and smoking chromosome 19; High level of affected in AD and is suspected by some as a possible
Psychiatric: history of abnormalities in education (longer cause. However, this remains speculative.
depressive disorder chromosomes 1, than 15 years)
Vascular: 14, and 21; and High level of 39.10.2.2 Neuropathology
hypertension, family history of physical activities
hyperlipidaemia, dementia (more than three
The neuropathological findings in AD include (Graham
high homocysteine Intelligence: low times a week) et al., 2006)
levels, and stroke intelligence and Use of NSAIDs and
limited education statin • Amyloid deposition: Amyloid deposition is pre-
History of MCI disposed by apolipoprotein E e4 allele on chro-
mosome 19. Amyloid is deposited as extracellular
plaques that comprise a central core of amyloid, 39.10.2.3 Clinical Features

silica, and aluminium. These plaques are found AD is a diagnosis that can be made with accuracy only
in the neocortex (layer 3 and 4), amygdala, hip- at postmortem. However, it is possible to make a reason-
pocampus, and entorhinal cortex. The amyloid ably accurate diagnosis on the basis of clinical findings
deposition in the walls of blood vessels leads to (Table 39.13).
amyloid angiopathy. The brain of a patient with
AD has more than 10 plaques/mm2. 39.10.2.4 Diagnostic Criteria (Table 39.14)
• NFTs: Intracytoplasmic NFTs are found in the Behavioural and psychiatric symptoms (BPSDs) associ-
cortex, hippocampus, substantia nigra, and locus ated with AD (Butler and Pit, 1998):
coeruleus. The diagnostic significance of amy-
loid plaques is greater than that of the tangles. • Psychiatric symptoms: paranoid delusions
• Granulovacuolar degeneration of the neurons is (15% of AD patients), hallucinations (10%–
caused by inflammation. 15% of AD patients, with visual hallucina-
• Hirano bodies: Rod-shaped actin found in hip- tions being more common than auditory
pocampal pyramidal cells. hallucinations).
• Neuronal losses: There is significant loss of neu- • Behavioural disturbances: aggression, wander-
rons in the brains of AD patients compared to ing, explosive temper, sexual disinhibition, and
controls. Most neuronal loss is found in the supe- searching behaviour.
rior, middle, and inferior frontal gyri; superior and • Personality changes: exaggeration of premorbid
middle temporal gyri; and the cingulate gyrus. personality.
TABLE 39.13
Summary of Clinical Features of AD in Different Stage of the Illness
Early Stage—Until About
2 Years Intermediate Stage Late Stage Final Stage
• Impaired concentration • Further deterioration in the • All intellectual functions • No personality
• Memory impairment aforementioned grossly impaired • No communication
• Fatigue and anxiety • Neurological abnormalities start • Considerable neurological • Emaciated
• Fleeting depression of mood to appear disability • Incontinent
• Exaggeration of preexisting • 5%–10% develop epilepsy • Increased muscle tone • Limb contractures
personality traits • Apraxias and agnosias develop • Wide-based unsteady gait • Death often from pneumonia
• Unusual incidents cause • Disorientation in time and space • Personality changes, often and inanition
increasing concern • Get lost in familiar surroundings with fatuous gross euphoria
• Occasional difficulty with word • Speech problems with nominal • No communication
finding dysphasia, receptive dysphasia, • Failure to recognize self or
• Altered handwriting expressive dysphasia, dysarthria, family
• Perseveration of words and and reduced vocabulary • Speech replaced by jargon
phrases • Groping for words, dysphasia
mispronunciation, reiteration of
parts of words (logoclonia), and
echolalia
• Reduced ability to read and write
• Concurrent progressive memory
loss involving recent and past
events
• Misidentification (e.g. mirror sign)
• Emotional lability
• Catastrophic reaction (extreme
anxiety and tearfulness when
unable to complete a task)
• Motor restlessness or inertia
protein, ESR, vitamin B12, folate, fasting lipid and glu-

TABLE 39.14 cose, calcium, LFTs, renal function tests (RFTs), and
Compare and Contrast the ICD-10 and NINCDS– thyroid function tests (TFTs). These tests would help to
ADRDA Criteria identify reversible causes of dementia. Clinicians are
advised not to routinely order VDRL, HIV, and cerebro-
ICD-10 Criteria for Dementia NINCDS–ADRDA Criteria
in AD (F00) (WHO, 1992) for AD (Blacker et al., 1994)
spinal fluid (CSF) analysis unless there are indications.
A midstream urine test should be ordered if delirium
1. A decline in memory that is 1. Cognitive deficits are affected
is a possibility. CXR and ECG are ordered if there are
most evident of learning new in more than two areas:
indications.
information Recall of learnt amnesia plus one or more
information is affected in additional features (aphasia,
Imaging (McMahon et al., 2003; Petrella et al., 2003)
severe cases. This impairment apraxia, agnosia, executive
applies to both verbal and dysfunction).
nonverbal materials. 2. No disturbance of • CT scans of brain do not reliably differentiate
2. A decline in judgement, consciousness. normals from those with AD, with approxi-
thinking, planning, and 3. Resultant disability. mately 20% overlap between these groups.
organizing. 4. Gradual onset and progressive Generally, cortical atrophy and ventricular
3. Awareness of environment and deterioration. enlargement are greater than in controls, with
consciousness are preserved. 5. No systemic disorders or increasing cognitive dysfunction correlating
4. Decline in emotional control exclusion of other general with increasing cerebral atrophy, but more so
and motivation (emotional medical conditions. with increasing ventricular size. An increase in
lability, irritability, apathy, and 6. Dementia does not occur
ventricular size over a span of 1 year is sugges-
coarsening of social exclusively during delirium.
tive of AD.
behaviour). 7. Exclude other mental
5. Dementia is classified as mild disorders.
• The clinical usefulness of neuroimaging can be
(able to live independently), improved by using a temporal lobe orientation
The age of the patient is
moderate (dependent on others in CT scanning, which allows an accurate mea-
expected to be between 40 and
in ADL), and severe (unable to 90 years.
surement of the medial temporal lobe. In AD,
retain information and absence a dramatic thinning of the width of the medial
of intelligence). temporal lobe in the region of the brain stem
6. Exclude other causes of is seen.
dementia. • Magnetic resonance imaging (MRI) scan
7. ICD-10 classifies DAT as early may reveal atrophy of the hippocampus.
onset (<65 years old) and late
MRI is the preferred modality to assist with
onset (>65 years old).
early diagnosis or detect subcortical vascular
NINCDS–ADRDA: National Institute of Neurological and changes.
Communicative Disorders and Stroke and the Alzheimer’s Disease • PET scan may show reduced O2 and glucose
and Related Disorders Association. uptake in parietal and temporal lobes.
• SPECT scans also reveal significantly reduced
parietotemporal perfusion in these subjects.
Combining SPECT scans with temporal-lobe-
• Orientation: if disorientation occurs, it is more oriented CT scans improves the diagnostic
common for time than for place. accuracy of AD.
• Neurological features: epilepsy (75%) and extra- • The NICE guidelines recommend the use of
pyramidal symptoms (60%). perfusion hexamethylpropyleneamine oxime
• Sleep disturbance: reduction of REM sleep, fre- (HMPAO) SPECT to differentiate AD, VaD,
quent nocturnal waking periods, and shortened and FTD. If HMPAO SPECT is not available,
sleep periods. consider 2[18F] FDG-PET as an alternative.
39.10.2.5 Investigations 39.10.2.6 Management

Memory assessment service should be the single point A multidisciplinary team is essential, as are close links
of referral for all people with a possible diagnosis of AD. with physicians, general practitioners (GPs), social ser-
Routine blood tests should include FBC, C-reactive vices, and the voluntary sector. The Alzheimer’s Disease
Society can provide carers with valuable information similar in efficacy, and they are chosen based on their
about local facilities and often run local counselling and costs, side effect profiles, and patients’ preferences.
sitting services. Driving should cease as soon as there is The specialist should consider an alternative AChEI if
any evidence that it may be unsafe. The patient should adverse events or drug interaction occurs. MMSE and
be asked to inform the Driver and Vehicle Licensing global, functional, and behavioural assessment should be
Authority (DVLA), but if they fail to do so, the doctor performed every 6 months. Treatment will be continued
has a duty to inform them. if either the MMSE score remains at or above 10 points
For patients suffering from mild to moderate AD or global, functional, and behavioural conditions indicate
(MMSE > 20), the NICE guidelines recommend to offer worthwhile effects (Table 39.15).
them the chance to participate in a structured group cog- Common side effects of AChEIs include excessive cho-
nitive stimulation programme irrespective of the pre- linergic effects such as nausea, diarrhoea, dizziness, uri-
scription of drug treatment for cognitive symptoms. nary incontinence, and insomnia. Other side effects include
For patients suffering from moderate AD (MMSE headache, parasympathetic stimulation, and bradycardia.
score of 10–20 points or score >20 with significant Pretreatment ECG is required. Donepezil is contraindi-
impairment in functions or learning disability), the NICE cated in people suffering from asthma, but rivastigmine is
guidelines recommend the specialist to prescribe the ace- safe in asthma and chronic obstructive pulmonary disease.
tylcholinesterase inhibitors (AChEIs) including donepezil, For patients suffering from severe AD (MMSE
galantamine, and rivastigmine. The three major benefits score <10 points), memantine is indicated in a well-
of AChEIs include stabilization of cognitive decline, established clinical setting based on recommendations
improvement of the ADL, and reduction of behavioural from the NICE guidelines. Memantine is a NMDA
problems. Treatment should be started in the specialist receptor antagonist, and it has neuroprotective proper-
dementia clinic. The NICE guidelines recommend patient- ties (Figure 39.1). Memantine may be useful in patients
centred care, and the specialist has to consider issues relat- suffering from VaD. The usual treatment dose of
ing to informed consent to pharmacological treatment. memantine is 10 mg B.D., and its half-life is 60–100
The specialist should also seek carer’s view on the h. Memantine is available in oral tablets and droplets. It
patient’s functions at baseline. AChEIs are broadly metabolism is nonhepatic.
TABLE 39.15
Comparison of the Pharmacokinetics and Pharmacodynamics of AChEIs
Donepezil Rivastigmine Galantamine
Indications AD, VaD AD, DLB (improve hallucinations AD
and delusions), and dementia
related to Parkinson’s disease
Pharmacokinetics
Preparation Oral tablets Oral capsules, solution, and patches Oral tablets and
solution
Plasma half-life 70 h 10 h 6h
Frequency of administration Once per day Twice per day Twice per day
Daily dose 5–10 mg/day 3–6 mg/day 8–12 mg/day
Metabolism P450CYP 2D6 Not by P450 system P450CYP 2D6
P450CYP 3A4 P450CYP 3A4
Organ of elimination Liver Kidney Both liver and kidney
Pharmacodynamics
Specific for CNS Selective Selective Selective
Reversibility Reversible Pseudoirreversible Reversible
Enzymes inhibited AChE AChE and BChE AChE
Nicotine receptor modulation No No Yes
Source: Taylor, D. et al., The Maudsley Prescribing Guidelines, 10th edn., Informa Healthcare, London, U.K., 2009.
G G
G G G G
G G G G G
G G
G G G G
G G G G
G G
NMDA G G G G
GG Ca Ca Ca G G Ca
Ca Ca Ca receptor Ca Ca G
G Ca G Ca Ca G
Ca Ca G Glycine Ca G Glycine Ca Glycine
G
Ca Mg2+ Ca G Mg2+ Ca G Mg2+
M
M
Ca2+ Ca2+
Ca2+
Neuronal excitotoxicity: The release of Memantine (M) is a low-affinity voltage- Its low affinity to the NMDA receptors with
glutamate (G) from presynaptic neuron dependent uncompetitive antagonist at the rapid off-rate kinetics allows NMDA
stimulates N-Methyl-D-aspartic acid(NMDA) NMDA receptors. It may be neuroprotective receptors to be activated by the relatively
receptors which have high affinity for Mg 2+ and disease modifying. high concentrations of glutamate released
ions and leads to prolonged influx of Ca2+ ions. following depolarization of the presynatic
neurons.
FIGURE 39.1 Pharmacodynamics of memantine.
39.10.2.7 Management of Behavioural • Resolution therapy is a companion to reality orien-

and Psychological tation and looks for meaning in the ‘here and now’
Symptoms of Dementia in the behaviour and confused talk of the patient.
Small of antipsychotic medication may be needed in • Reminiscent therapy involves reliving the past
those patients who are agitated, distressed, and aggres- experiences with old TV set, radio, and home
sive or who have sleep reversal. If antipsychotic drug is environment.
ineffective, you may consider giving him or her AChEIs. • Validation therapy empathizes with the feelings
According to the NICE guidelines, intramuscular loraz- and meanings hidden behind their confused
epam can be used as a single agent (not diazepam or speech and behaviour.
chlorpromazine). Those with AD are predisposed to • Snoezelen involves the utilization of specially
developing depression, which may require treatment designed room with soothing and stimulating
with antidepressant medication, preferably using prep- environment.
arations with few antiadrenergic and anticholinergic • Art therapy (painting and drawing), aroma-
(antimuscarinic) side effects (e.g. SSRIs). therapy (lavender and Melissa balm), and music
The following nonpharmacological treatments may be therapy (singing or playing an instrument) may
useful: be useful.
• Reality orientation involves consistent use of 39.10.2.8 Prognosis

orientation devices such as signposts, notices, Disease progression varies considerably from subject to
and other memory aids to remind the patients subject. The younger the age of onset, the more rapid the
and environment. decline. In those aged under 50, the mean survival time is
about 7 years, whereas in those aged between 55 and 74, lack of hypertension or neurological signs is more sug-
the mean survival is increased to about 9 years. gestive of AD. VaD is more likely than AD to produce
Poor prognostic factors include coexistent depression, persecutory delusions, anxiety,
and emotional disturbance.
• Significant language impairment Based on clinical presentation, history and CT
• Poor cognitive functioning scan findings of VaDs have been subdivided into
• Clinical evidence of parietal lobe involvement Binswanger’s disease, leukoaraiosis, and multiple lacu-
• CT scan showing reduced density of left parietal nar states.
region
39.10.3.2.1 Binswanger’s Disease
39.10.3 Vascular Dementia This is a progressive subcortical vascular encephalopa-
thy with CT scan revealing markedly enlarged ventricles
39.10.3.1 Aetiology secondary to infarction in hemispheric white matter.
There is an excess of VaD in males, which is probably Infarcts are observed to affect periventricular and central
caused by an increased prevalence of cardiovascular dis- white matter. The age of onset is 50–65, with a gradual
ease in men. Hypertension is the most frequent risk fac- accumulation of neurological signs, dementia, and distur-
tor among those with VaD (contributing to 50% of VaD). bances in motor function including pseudobulbar palsy.
Risk factors known to increase the risk of stroke also There is often a history of severe hypertension, systemic
increase the risk of VaD, for example, cigarette smok- vascular disease, and stroke.
ing, heart disease, homocystinuria, hyperlipidaemia,
metabolic syndrome, low levels of high-density lipopro- 39.10.3.2.2 Leukoaraiosis
tein, moderate alcohol consumption, polycythaemia, and This was used by Hachinski to describe CT scan appear-
sickle cell anaemia. ances of reduced density of white matter. It differs from
Cerebral autosomal-dominant arteriopathy with sub- infarcts in that it affects only white matter, is patchy
cortical infarcts and leukoencephalopathy (CADASIL) is a and diffuse, and does not result in the enlargement of
genetic disease with Notch 3 mutations in chromosome 19 cerebral sulci or ventricles. It is found in nondemented
and results in recurrent subcortical CVAs (80%), cognitive subjects as well as those with degenerative and vascular
deterioration (50%), mood changes (30%), epilepsy (10%), dementia.
and gait abnormalities.
39.10.3.2.3 Multiple Lacunar States
39.10.3.2 Clinical Features These are CT scan appearances of small well-localized
VaD is characterized by a stepwise deteriorating course subcortical infarcts. It is associated with dementia char-
with a patchy distribution of neurological and neuropsy- acterized by dysarthria, incontinence, and explosive
chological deficits. There is evidence of vascular diseases laughing, secondary to frontal lobe disturbance.
on physical examination (hypertension, hypertensive
changes on fundoscopy, carotid bruits, enlarged heart, 39.10.3.3 Diagnostic Criteria
focal neurological signs suggestive of CVA). National Institute of Neurological and Communicative
Three presentations occur: Disorders and Stroke and the Alzheimer’s Disease and
Related Disorders Association (NINCDS–ADRDA)
• Dementia follows a stroke. (Table 39.16).
• Dementia gradually develops following multiple The ICD-10 criteria (WHO, 1992) emphasize on
asymptomatic cerebral infarcts. unevenly distributed cognitive impairment and signs of
• Neuropsychiatric symptoms gradually become focal brain damage (unilateral spastic weakness, uni-
evident. laterally increased tendon reflexes, an extended plan-
tar response, and pseudobulbar palsy). In multi-infarct
Distinguishing between VaD and AD can be difficult; dementia, the onset is gradual with minor ischaemic epi-
indeed, in a certain proportion of cases, both coexist. A sodes. In acute onset VaD, the onset of dementia is within
more insidious onset with a continuous rather than step- 1 month of CVA. In subcortical VaD, there is evidence of
wise course, less insight, fewer affective symptoms, and deep white matter lesions.
studies. Donepezil may be beneficial but not

TABLE 39.16 licenced in VaD.
Comparison of NINDS-AIREN Criteria • It is worth attempting to treat the underlying
and Hachinski Ischaemic Score cardiovascular condition in order to slow or halt
the progression of VaD. The treatment of hyper-
NINDS-AIREN Criteria Hachinski Ischaemic Score
(Roman et al., 1993) (Moroney, 1997)
tension is important.
• Depression may respond to an antidepressant.
A relationship between the Course of the illness
aforementioned dementia and 1. Abrupt onset of symptoms
CVAs manifested or inferred by (two points) 39.10.3.6 Prognosis
the presence of one or more of 2. Stepwise deterioration (one Prognosis of VaD is worse than that of AD. The mean
the following point) survival of AD is 6 years, while the mean survival of VaD
3. Fluctuating course (two points) is only 3 years.
1. Amnesia and cognitive
impairment in at least 1 Symptoms Poor prognostic factors include
domain with resultant 1. Nocturnal confusion (one
disability point) • Severity of dementia
2. Focal sign and image findings 2. Personality relatively • Being bedridden
3. Onset of dementia within 3 preserved (one point) • Urinary incontinence
months following a recognized 3. Depression (one point)
stroke 4. Somatic complaints (tingling,
4. Abrupt deterioration in clumsy) (one point) 39.10.4 Frontotemporal Lobe Dementias
cognitive functions (fluctuating 5. Emotional lability (one point)
and stepwise)
History Dementia of frontal lobe type and Pick’s disease both mainly
Clinical features consistent with 1. Presence of hypertension (one
affect the frontal and anterior temporal areas of the brain. In
the diagnosis of probable VaD point)
a large-scale neuropathological study over 20 years, 10% of
2. Stroke (two points)
1. Early presence of a gait
3. Atherosclerosis (one point)
dementia cases had dementia of the frontal lobe type, and a
disturbance further 2.5% had Pick’s disease (the Lund study, 1987).
2. History of unsteadiness and Focal neurological symptoms:
frequent unprovoked falls hemiparesis, hemianopia,
3. Early urinary symptoms not aphasia (two points) 39.10.4.2 Aetiology and Classification
explained by urologic disease Focal neurological signs: See Figure 39.2.
4. Pseudobulbar palsy unilateral weakness, sensory
5. Mood changes or abulia loss, asymmetric reflexes, 39.10.4.3 Neurochemistry
Babinski’s sign (two points)
Note that the early presence of FTD is associated with cortical and striatal serotoniner-
A total score > 7 suggests of VaD
gait disturbance and early
and score < 4 suggests DAT
gic deficits but not cholinergic deficit.
urinary symptoms are not
included in Hachinski
Ischaemic Scale 39.10.4.4 Diagnostic Criteria (Table 39.17)
The similarities and differences between AD and
Frontotemporal lobe dementias (FTD) (Orrell and Sahakian.,
39.10.3.4 Investigation 1991)
• CT and MRI may show infarcts, lacunes, and
leukoaraiosis. • Patients with FTD have younger age of onset,
• SPECT and PET scans may show patchy more severe apathy, disinhibition, reduction
hypoperfusion. in speech output, loss of insight, and coars-
ening of social behaviour but less spatial dis-
orientation as compared to patients with AD.
39.10.3.5 Management Primitive reflexes such as grasp, pour, and
• The NICE guidelines do not recommend the use palm mental reflexes often reappear in FTD.
of AChEIs or memantine for cognitive decline • Patients who suffer from AD have more
in VaD except in properly constructed clinical impairment in calculation and constructions,
FTD
Semantic dementia Progressive non-fluent aphasia Frontotemporal lobe degeneration
Semantic dementia involved Patients suffering from progressive 1. Pathology: neuronal loss and reactive
impairment in understanding nonfluent aphasia have difficulty astrocytosis.
of word meaning or object with initiation but not
2. Characterized primarily by personality
identity with lesions in the comprehension of speech due to the
change and disordered social conduct.
temporal lobe. Other clinical lesions in dorsolateral pre-frontal
features include: cortex. Other clinical features
Pick’s disease
include:
1. Age of onset: 45–65 years; F:M = 2:1
1. Anomia: loss ability to
recognize or understand 1. Hesitant, effortful speech. 2. 50% of patients are caused by autosomal-
words. dominant inheritance of tau gene on
2. Speech apraxia. chromosome 17. This results in abnormal
2. Dominant temporal lobe insoluble tau isoforms which accumulate in
lesion: fluent aphasia or 3. Stutter (including return of a
childhood stutter). neurons and glia.
semantic paraphasia. For
example, a patient names 4. Anomia. 3. Pathology: atrophy of frontotemporal lobe,
‘elephant’ as ‘cat’. swollen achromatic neurons (balloon cells),
5. Phonemic paraphasia (sound pick bodies with tau and ubiquitin positive
3. Nondominant temporal errors in speech, e.g. ‘gat’ for ‘cat’). neurons.
lobe dementia: associative
6. Agrammatism (using the wrong
agnosia and prosopagnosia. 4. ICD-10 criteria: slow onset, steady
tense or word order).
deterioration, frontal lobe symptoms
4. Memory is better for recent
7. As the disease develops, speech (emotional blunting, coarsening of social
events than remote events.
quantity decreases and many behaviour, disinhibition, apathy, aphasia),
Episodic memory is not
patients will become mute. sparing of memory and parietal lobe in the
affected.
beginning stage.
5. Onset age is 50–65 years.
5. Seizure and apraxia are uncommon.
6. Orientation is normal.
6. CT brain shows knife-blade atrophy
in frontotemporal lobe.
7. SSRIs or trazodone are beneficial for
behavioural symptoms.
FIGURE 39.2 Classification of frontotemporal lobe dementia (FTD).
lower MMSE scores, and higher prevalence 39.10.4.6 Management

of depression (20%) as compared to patients • There is no specific pharmacological interven-
with FTD. tion for cognitive impairments in FTD. SSRIs or
• Both AD and FTD have insidious onset. trazodone is indicated for noncognitive features.
• Kluver–Bucy syndrome consisting of emo- • Psychosocial interventions is often useful.
tional placidity, hyperorality (bulimia and pica),
hypersexuality, and tendency to place things 39.10.4.7 Prognosis
in the mouth may occur concurrently with AD The mean duration of dementia of frontal lobe type is
or FTD. 8 years, and of Pick’s disease 11 years.
39.10.4.8 Diogenes Syndrome

39.10.4.5 Investigations Diogenes syndrome or senile squalor is associated with
• Psychometry will show characteristic impair- frontal lobe dysfunction and compulsive collecting
ments in higher executive function, verbal flu- (syllogomania or hoarding rubbish). Thus, it is usually
ency, and agnosia. inappropriate to invoke the Mental Health Act; instead,
• Structural imaging may not show characteris- Section 47 of the Public Health Act is usually used to deal
tic lesion in early stage, and functional imaging with these situations if required. The prognosis is poor
shows anterior hypoperfusion. EEG is usually with almost inevitable relapse. Day care may help, and
normal in FTD. institutional care is often required.
ubiquitin positive. α-Synuclein is aggregated and

TABLE 39.17 insoluble protein, which is pathognomonic of LBD
Summary of the Lund–Manchester Consensus and idiopathic Parkinson’s disease.
on Diagnosis of FTD
39.11.1.3 Neurochemistry
Frontotemporal Lobe
Features Affective Features Supporting Features The cholinergic deficits are more pronounced in DLB
than DAT:
1. H
igh executive 1. Depression 1. Age of onset <65
functions: loss of 2. Anxiety years
• The dopaminergic deficits are more pronounced
interest, preservation, 3. Hypochondriasis 2. Family history of
in idiopathic Parkinson’s disease than DLB.
disinhibition 4. Emotionally FTD
(jocularity and unconcerned 3. Bulbar palsy
hypersexuality), 4. Akinesia, rigidity,
39.11.1.4 Clinical Features (McKeith’s
inflexibility and and tremor Criteria) (Barber et al., 2001)
impulsiveness, and 5. Early incontinence • Differences between DLB and Parkinson’s dis-
lack of personal and ease dementia: The cognitive and extrapyra-
social awareness midal signs develop concurrently in DLB, but
2. P
remotor cortex: cognitive symptoms occur at least 1 year after
primitive reflex and the development of extrapyramidal signs in
stereotypies
Parkinson’s disease dementia.
(compulsion without
• Cognitive symptoms: Enduring and progressive
obsessions) and
strange eating habits
cognitive impairment with impairments in con-
3. B
roca’s area: sciousness, alertness, and attention. Cognition
progressive reduction is fluctuating and short-term memory is not
in speech, poor affected in early stage. Patients suffering from
verbal fluency, and DLB have less episodic amnesia, more execu-
echolalia tive dysfunction, and more apraxagnosia as
4. Preserved compared patients suffering from AD.
visuospatial ability • Common noncognitive features: Apathy, depres-
Source: Miller, B.L. et al., British Journal of Psychiatry, 158, 76, 1991. sion, hallucinations (complex visual hallucina-
tions: 80%, auditory hallucinations: 20%), and
delusions (paranoid delusions: 65%).
39.11 DEMENTIA WITH MOVEMENT • Extrapyramidal signs and parkinsonism: Loss of
facial expression, changes in the strength and tone
DISORDERS of the voice, slowness, muscle stiffness, trembling
39.11.1 Dementia with Lewy Bodies of the limbs, a tendency to shuffle when walking
(mild parkinsonism: 70%, no parkinsonism: 25%).
39.11.1.1 Epidemiology • Serious clinical events: Neuroleptic sensitivity
• Dementia with Lewy bodies (DLB) is the third (60%), falls, syncope, and spontaneous loss of
most common cause of late-onset dementia and consciousness.
less common cause of early-onset dementia.
• DLB occurs frequently in combination with AD. 39.11.1.5 Investigations
• DLB more commonly affects men than women. • Psychometry will be useful with more impair-
ments in visuospatial tests.
39.11.1.2 Neuropathology
There are two scans that can help to establish the diag-
• There is little atrophy in the early stage of DLB. The
nosis of DLB as recommended by the NICE guidelines:
neuroanatomical areas affected in DLB include
hippocampus, temporal lobes, and neocortex. • Dopaminergic iodine-123-radiolabelled
• Lewy bodies are located in cingulated gyrus, cor- 2β-carbom ethoxy-3β-(4-iodophenyl)-N-(3-
tex, and substantia nigra. They contain eosinophilic fluoropropyl) nortropane (FP-CIT) SPECT is be
inclusion with high amyloid content but absence of used to help establish the diagnosis in those with
tau pathology. Lewy bodies are α-synuclein and suspected DLB if the diagnosis is in doubt.
• DaTSCAN is a radiopharmacological drug com- Cognitive deficits in Parkinson’s disease include

posed of ioflupane (123I) 74 MBq/mL and is used
in SPECT to detect loss of functional dopaminer- • Slowness in comprehension and response
gic neuron terminals in the striatum. DaTSCAN (bradyphrenia)
is able to differentiate probable DLB from AD. • Impaired abstract reasoning
DaTSCAN is unable to discriminate between • Memory impairment, including poor retrieval
DLB and Parkinson’s disease dementia. and poor short-term memory, especially frontal
• 90% of DLB patients have EEG abnormalities. lobe working memory
• Impaired remote memory (only in the late stages)
39.11.1.6 Management
• Antipsychotics are not indicated for mild-to-mod- Patients with typical extrapyramidal signs of Parkinson’s
erate noncognitive symptoms in DLB because of disease who later develop cognitive impairment, especially
the risk of severe adverse reactions. If it needs of a subcortical type, are given a diagnosis of dementia of
to be used, consider quetiapine and monitor for Parkinson’s disease.
extrapyramidal side effects.
• AChEIs: Consider for people with DLB who 39.11.2.3 Management
have noncognitive symptoms causing significant Exclude treatable pathology, such as depression or acute
distress or leading to behaviour that challenges. brain syndrome.
Rivastigmine has the best research evidence for Treatment with anti-parkinsonian drugs does not
improvement of cognitive functions in DLB. It improve the cognitive manifestations of the disease. Avoid
may also improve cognitive symptoms, delu- anticholinergic drugs if possible.
sions, and hallucinations. Transplants of fetal nerve cells are experimental and
• Chlormethiazole is used for night sedation. may improve the outlook for those with Parkinson’s dis-
ease. It is not known how helpful this will be in the treat-
ment of dementia of Parkinson’s disease.
39.11.2 Parkinson’s Disease Dementia
It is difficult to distinguish dementia specifically asso- 39.11.2.3.1 Corticobasal Degeneration
ciated with Parkinson’s disease from other causes of Clinical features include extrapyramidal signs such as
dementia, which are likely to occur coincidentally in poor coordination, akinesia, rigidity, disequilibrium, and
elderly people suffering from Parkinson’s disease. It is limb dystonia. Other symptoms include cognitive impair-
estimated that dementia occurs in 15%–20% of those ments, visual–spatial disturbance, apraxia, hesitant and
with Parkinson’s disease, compared to 5%–10% of the halting speech, myoclonus, and dysphagia. The patient
normal population, corrected for age. may lose their ability to walk.
The pathology involves large swollen achromatic neu-
39.11.2.1 Aetiology rons in the cortex, and tau positive glial inclusions are
This is not known. It is known that in Parkinson’s disease, found in the frontal and parietal lobes. Neuronal inclusions
there is damage to the ascending monoaminergic system are also found in the substantia nigra and basal ganglia.
affecting central dopamine, serotonin, and noradrenaline Drugs used to treat Parkinson’s disease do not produce
systems. There is also damage to substantia innominata, any significant or sustained improvement in corticobasal
causing cortical cholinergic disruption. degeneration. Clonazepam may reduce the myoclonus.
All patients with Parkinson’s disease have Lewy bod-
ies in their cerebral cortex, with a subset having more 39.11.2.3.2 Progressive Supranuclear Palsy
Lewy bodies than most. Not all of these have dementia, Patients suffering from Progressive supranuclear palsy
although it appears that all have some evidence of cogni- (PSP) present with mild cognitive deficits, apathy, slowing
tive decline. of cognitive processing, and memory deficits. It is distin-
guished from AD and DLB by prominent parkinsonism,
39.11.2.2 Clinical Features gait and poor balance, and brain stem abnormalities (oph-
Cognitive deficits seem to occur in most subjects with thalmoplegia and pseudobulbar palsy).
Parkinson’s disease; it is possible that those considered The pathology is located in neocortex and cerebral cor-
to be suffering from dementia are simply those at the tex (e.g. frontal lobe). Microscopic lesions include neuronal
extreme end of cognitive decline in this condition. loss astrocytosis, tau positive NFTs, and glial inclusions.
39.11.3 Normal-Pressure Hydrocephalus their condition. Mental and physical improvement is

likely after surgery.
39.11.3.1 Clinical Features One-third of those undergoing surgery will develop
There is insidious onset of dementia with psychomotor complications such as
retardation, unsteady gait, and urinary incontinence.
Onset is usually in the 60 or 70s. Behavioural distur- • Shunt infection and malfunction
bance, hallucinations, and paranoia are uncommon. • Epilepsy
The diagnosis is made on the basis of clinical pre- • Subdural haematoma
sentation, with a CT scan of the brain revealing dilated
ventricles (especially the third ventricle) without cortical
atrophy, with normal CSF pressures. 39.11.4 Creutzfeldt–Jakob Disease
39.11.3.2 Aetiology
• Creutzfeldt–Jakob disease (CJD) is extremely
There is obstruction to outflow of CSF from the sub- rare and affects only 1–2 per million.
arachnoid space, but the ventricular system remains in • CJD is most common in Libyan and Tunisian Jews.
communication with the subarachnoid space, thus allow-
ing CSF to flow out of the ventricular system. This sce- 39.11.4.2 Aetiology
nario is associated with • CJD is transmissible to laboratory animals by
intracerebral inoculation, with symptoms devel-
• Subarachnoid haemorrhage oping years later. The effect is similar to spon-
• Cerebrovascular disease giform encephalopathies observed in animals
• Meningoencephalitis (scrapie in sheep, bovine spongiform encepha-
• Post-intracranial surgery lopathy [BSE] in cows).
• A form of CJD known as the BSE variant has
39.11.3.3 Management been identified in humans. It has a slightly dif-
Insertion of a shunt will allow the drainage of CSF from ferent clinical presentation. There can be onset
the ventricles to the heart. in younger people. It is rapidly progressive and
is thought to be associated with eating or being
39.11.3.4 Prognosis otherwise exposed to cattle infected with BSE.
The best results are seen in those with a full clinical • The aetiology of CJD is classified into familial
syndrome, a short history, and an obvious cause for and environmental causes (Figure 39.3):
CJD
Familial causes Environmental causes
Familiar CJD: about 10% of cases appear to Sporadic CJD

be familial.
Iatrogenic CJD is related to pituitary-
Gerstmann–Straussler–Scheinker syndrome derived growth hormone, through cross
is characterized by neuronal loss, astrocytosis, contamination from instruments used in
spongiform degeneration, and extensive brain biopsy or through dural grafts with
multicentric amyloid plaques. Cerebellar ataxia 2 years of incubation period.
forming is a prominent clinical feature.
Kuru is caused by ritual cannibalism in
This syndrome is rare.
New Guinea with prion plague formation
Familial fatal insomnia is characterized by in cerebellum. Kuru is rare.
lesions in the thalamus. Patients have early New variant CJD is characterized by
onset at the age of 20–40 and the course of extensive prion plaque formation in
disease is slow progression. cerebellum.
FIGURE 39.3 Classification of the aetiologies of Creutzfeldt–Jakob disease.

39.11.4.3 Pathology Gross atrophy is seen in the frontotemporal regions

• The prion protein (PrP) is responsible for trans- (knife-blade atrophy) in Pick’s disease, but the diagnosis
mission. This is an unusual infective agent since cannot be made on this evidence alone.
it does not appear to contain nucleic acid, being
made up entirely of protein. 39.11.4.6 Management
• PrP differs from normal cell-membrane-derived There is no specific pharmacological intervention for CJD.
proteins in that it is highly resistant to degrada-
tion by cellular proteases, heat, or conventional 39.11.4.7 Prognosis
chemical disinfectants. There is terminal decline.
• The PrP gene mutations are located on chromo-
some 20, and this mutation produces protein with
conformational change into PrPCJD, which are cyto- 39.11.5 Human Immunodeficiency
toxic, insoluble, and often deposit in cerebellum. Virus Dementia
• Microscopy of brain material reveals vacuolar
changes in grey matter particularly in cerebral
and cerebellar cortex, creating characteristic • This is one of the most prominent features
spongiform appearances. of Human immunodeficiency virus (HIV)
• There is a loss of nerve cells and reactive encephalopathy.
astrocytosis. • Prevalence of dementia is 30% among HIV-
• In CJD, there is rapid brain shrinkage and reduc- infected patients.
tion in size due to diffuse and focal atrophy and
39.11.5.2 Aetiology
neuronal loss.
The encephalopathy of HIV is thought to be directly
39.11.4.4 Clinical Features caused by HIV, which is a neurotropic virus.
CJD is a very rare cause of a rapidly progressive dementia.
39.11.5.3 Pathology
There may be a brief prodromal period of anxiety,
depression, or hallucinations. Sudden onset and rapid Pathology is found in the white matter of cerebral
progression of dementia, pyramidal, and extrapyramidal and cerebellar hemispheres and in deep grey matter.
deficits present usually in the 50–60-year age group. Multinucleated giant cells deriving from macrophages
Physical features include limb spasticity, muscular are found in the affected brain tissue.
wasting and fasciculation, tremor, rigidity, choreoath-
etoid movements, myoclonus, dysarthria, and dysphagia. 39.11.5.4 Clinical Features
Convulsions may occur. • The onset of HIV dementia is usually insidious
In addition to the previously mentioned classic form, and occurs later in the course with significant
three variant forms are described: immunosuppression. There is initial lethargy,
apathy, cognitive disturbance, reduced libido,
• Heidenhain form. Prominent visual defects may and general withdrawal. As the condition pro-
result in cortical blindness. Extrapyramidal gresses, evidence of dementia becomes appar-
symptoms and myoclonus occur. ent with cognitive disturbance, incontinence,
• Ataxic form. There is rapidly progressive cer- ataxia, hyperreflexia, and increased muscle
ebellar ataxia, with involuntary movements and tone. Clinical features can be classified into cog-
myoclonic jerks. Finally, muteness and general- nitive, behavioural, and motor symptoms.
ized rigidity occur. • Cognitive symptoms include memory, concentra-
• Cortical form. This includes parietal lobe tion impairment, and mental slowing. The patient
symptoms. may need a written reminder to help them to recall.
• Behavioural symptoms include apathy, reduced
39.11.4.5 Investigations spontaneity, and social withdrawal. Depression,
The EEG is always abnormal in CJD, showing an increase irritability or emotional lability, agitation, and
in slow-wave activity and a reduction in a rhythm; as the psychotic symptoms may occur.
disease progresses, bilateral slow spike wave discharges • Motor symptoms include loss of balance and
may accompany myoclonic jerks. coordination and clumsiness and leg weakness.
• At a later stage, HIV dementia results in a global 39.11.5.7 Investigations

deterioration of cognitive functions as mani- MRI and CT scans usually show the cerebral atrophy and
fested by word finding difficulties. Patients may white matter abnormalities in HIV dementia.
exhibit psychomotor retardation and mutism.
Speech becomes slow and monotonous. 39.11.5.8 Management and Prognosis
• Neurological examination reveals that patients Therapeutic trials of antiviral treatment suggest that
become unable to walk as a result of parapare- improvement in HIV dementia may occur, but the prog-
sis. Patients usually lie in bed indifferent to their nosis is poor.
illness and to their surroundings. Bladder incon-
tinence and bowel incontinence are common 39.11.6 Huntington’s Disease (Chorea)
findings. Myoclonus and seizures may occur. 39.11.6.1 Epidemiology
39.11.5.5 Classification This is a genetic disorder resulting in a condition char-
See Table 39.18. acterized by continuous involuntary movements and
a slowly progressive dementia. There are 5 cases per
39.11.5.6 Differential Diagnosis 100,000 in the United Kingdom.
The presentation of the following differential diagnosis may
be more acute as compared to AIDS-associated dementia: 39.11.6.2 Aetiology
Transmission is mostly by a fully penetrant single auto-
• Opportunistic infections: cerebral toxoplasmo-
somal-dominant gene (located on chromosome 4), affect-
sis, Cryptococcal meningitis, CMV encephali-
ing 50% of offspring (see Chapter 19 for more details).
tis, and herpes simplex encephalitis
Occasionally sporadic cases occur.
• Neoplasms and cerebral lymphoma
Pathological appearances include a marked atrophy of
• Metabolic encephalopathies
head of caudate nucleus and putamen and severe generalized
• HIV encephalitis or leukoencephalopathy
neuronal loss resulting in cortical atrophy, which is most
marked over the frontal lobes, with ventricular dilatation.
TABLE 39.18
Comparison of Diagnostic Criteria of 39.11.6.3 Clinical Features
HIV- Associated Cognitive Motor Disorder The onset is usually between the ages of 35 and 45, but
childhood onset accounts for 10%–20% of cases. The
and AIDS Dementia Complex
onset is insidious, with fidgety movements or nonspecific
HIV-Associated Cognitive AIDS Dementia Complex psychiatric symptoms in the early stages.
Disorder (Grant et al., 2005) (Brew, 2004) Movement disorder consists of choreiform movements
Two or more of the following for Acquired abnormality in at least in the head, face, and arms; ill-sustained and jerky vol-
>1 month two of the following cognitive untary and involuntary movements affecting all muscles;
• Impaired attention or abilities for at least 1 month and a distinctive wide-based gait with sudden lurching.
concentration • Attention/concentration Psychiatric disturbance is variable but common. Initial
• Mental slowing • Speed of information processing insight may result in depression. Prodromal personality
• Impaired memory • Abstraction/reasoning changes, antisocial behaviour with substance misuse, and
• Slowed movements • Visuospatial skill affective and schizophreniform disorders are sometimes seen.
• Incoordination • Memory/learning Insight gives way to mild euphoria with explosive outbursts,
• Personality change, irritability, • Speech/language
irritability, and rage. There is a slowly progressive intellectual
and symptoms must be verified
At least one of the following impairment, with some patients profoundly demented in the
by neurological examination or
neuropsychological testing • Acquired abnormality in final stages, whereas others remain reasonably aware.
• Accompanied by mild motor function
• Decline in motivation or
39.11.6.4 Investigation
impairment of functional status
(e.g. work or ADL) emotional control or change in • In Huntington’s disease, the EEG consists of an
• Emotional lability behaviour absence of rhythmic background activity, along
with low-voltage intermittent random activities
Absence of clouding of
consciousness (delirium)
(θ and δ wave).
No evidence of other aetiology • CT scan may show a characteristic shrinkage of
caudate nuclei.
39.11.6.5 Management It is most common at the extremes of life both in

Tetrabenazine helps to reduce the movement disorder. the very young and the elderly. This may be caused by
The main side effect of tetrabenazine is depression. reduced cerebral reserve, a concurrence of multiple phys-
Antidepressants, ECT, and minor tranquillizers may be ical problems, and a higher prevalence of polypharmacy
helpful in the early stages, with phenothiazines in low dose in the elderly.
in later stages to control behavioural disturbance. It affects 10%–25% of the over-65s admitted to medi-
Genetic counselling for family members should be cal wards. Those with dementia are particularly vulner-
offered. able to developing superimposed delirium.
39.11.6.6 Prognosis
39.12.1 Aetiology
The duration to death is 12–16 years.
Although delirium presents with global disturbance of
cognitive function, certain neurological pathways seem
39.11.7 General Paralysis of the Insane
to be specifically involved. Autonomic disturbance impli-
This is a rare condition and can be missed. cates the brain stem. Cholinergic and adrenergic path-
ways are also thought to mediate delirium.
39.11.7.1 Aetiology Any physical insult can result in delirium particularly
The disease is a terminal consequence of syphilis. There in a predisposed individual. In the elderly, the following
is marked cerebral atrophy with meningeal thickening, causes are the most common:
resulting from neuronal loss and astrocyte proliferation.
The presence of iron pigment in microglia and perivas- • Hypoxia
cular spaces is specific for the disease. Spirochetes are • Infection
found in the cortex in 50% of cases. • Metabolic disturbance
• Iatrogenic
39.11.7.2 Clinical Features • CNS disease
The condition develops 5–25 years after primary infection • Epilepsy
with Treponema pallidum. The onset is usually gradual
with depression as a dominant symptom. There is then
slowly progressive memory and intellectual impairment.
Frontal lobes are particularly involved, resulting in charac- • There is rapid onset with a fluctuating course.
teristic personality change with disinhibition, uncontrolled Lucid intervals occur.
excitement, and overactivity, which may be mistaken for • The delirium tends to be more marked at night
hypomania. Grandiose delusions are present in only 10%. particularly in conditions of poor illumination.
Physically there is slurred speech, a tremor of lips and • Awareness is always impaired. Alertness tends
tongue, and Argyll Robertson pupil in 50%. As the condi- to fluctuate and can be both increased and
tion progresses, there is increasing leg weakness leading decreased.
to spastic paralysis. • Orientation is always impaired, particularly
The Wassermann reaction on CSF examination is for time.
always positive, with lymphocytosis, raised protein, and • Recent and immediate memory is impaired with
raised globulin. poor new learning and lack of recall for events
occurring during the delirious period. However,
39.11.7.3 Management and Prognosis the knowledge base remains intact.
Treatment is with high-dose penicillin under steroid • Thinking may be slowed or accelerated.
cover to prevent Herxheimer reaction. Following treat- • Misperceptions, particularly visual, are common.
ment, mental symptoms may diminish. • Hallucinations and delusions may occur.
• Heightened anxiety and fear are often prominent.
• The sleep–wake cycle is always disturbed,
39.12 DELIRIUM IN OLD AGE
with daytime drowsiness and nocturnal
This is a state of fluctuating global disturbance of the cere- insomnia.
bral function, abrupt in onset and of short duration, arising • Physical illness or drug intoxication is usually
as a consequence of physical illness or toxic effects. present (Table 39.19).
39.12.5 Management
TABLE 39.19
Comparison between Dementia and Delirium The treatment of delirium is the treatment of the underly-
ing condition.
Clinical Features Dementia Delirium
Presence of acute Usually absent Usually present (e.g.
physical illness infection, electrolyte 39.12.5.1 Nonpharmacological Treatment
disturbance) • Avoid physical restraints.
Onset Insidious Acute • Avoid sensory deprivation and overload.
Attention Normal attention Poor attention and • Adequate oxygenation.
distractible • Correct sensory deficits.
Memory Impairment in Impairment in recent and • Encourage normal sleep pattern.
immediate recall remote memory • Environmental cues such as signposting.
and recent memory • Family involvement.
Perceptual Usually no Visual hallucinations are
• Maintain hydration and electrolyte balance.
disturbances hallucination common.
• Mobilization of the patient.
Duration Long, months to Short, hours to weeks
• Pain management.
years
Course of illness Stable Fluctuation
• Presence of familiar objects.
• Psychoeducation on delirium.
• Reorientation strategies (clock, access to window).
39.12.3 Classification • Repetition of information in a slow and regular
manner.
There are three types of delirium: • Staff consistency.
• Well-illuminated environment.
• Hyperactive delirium (30%), which is character-
ized by agitation, aggression, autonomic arousal,
hyperactivity, and restlessness. 39.12.5.2 Pharmacological Treatment
• Hypoactive delirium (40%), which is character- • Vitamin supplements, particularly thia-
ized by apathy, drowsiness, confusion, and leth- mine, should be administered if there is
argy. Hypoactive delirium is often mistaken for any possibility of previous alcohol abuse or
depression. malnutrition.
• Mixed hyperactive and hypoactive delirium (30%). • Drugs known to exacerbate delirium should be
avoided if possible. Benzodiazepine should be
avoided because it can exacerbate delirium. The
39.12.4 Investigation
use of benzodiazepine is only indicated in delir-
Delirious patients should be fully investigated physically: ium tremens.
• Behaviour not amenable to other interventions,
• Laboratory investigations include FBC (raised such as gentle reassurance, may respond to
white blood cells may indicate infection), electro- treatment with an antipsychotic.
lytes (sodium, potassium, calcium, magnesium, • Haloperidol is the most frequently used in this
phosphate), RFTs, LFTs, TFTs, and arterial situation because it is generally effective and
blood gases. safe. A baseline ECG is required to check QTc
• Infection screen includes syphilis, blood cul- interval. Side effects include QTc prolongation,
ture, and urinalysis. extrapyramidal side effects, orthostatic hypo-
• ECG. tension, and sedation.
• Imaging include CXR, CT (space occupying • Second-generation antipsychotics such as
lesions, cerebral haemorrhage), or MRI scan risperidone, olanzapine, and quetiapine are
(white matter lesions). indicated for patients who are prone to extrapy-
• Electroencephalogram: diffuse slowing of brain ramidal side effects (e.g. DLB, Parkinson’s dis-
activity. ease). Side effects include sedation, orthostatic
• Lumbar puncture and CSF analysis (if signs of hypotension, and metabolic syndrome if used
meningitis or encephalitis). for a long duration.
• General principles of prescription in delirium symptoms, and a higher death rate at 2 years than elderly
include monotherapy, prescription with the low- depressives without ventricular enlargement. CT scan
est dose, and tapering off the medication when appearances in late-onset depressives are more comparable
delirium resolves. to those with AD than to those with early-onset depression
• Treatment of hypoactive delirium with psycho- or normal controls. Thus, early- and late-onset depression
tropic medications is not recommended. may be different disorders, and the late-onset type may have
a stronger association with neurological dementing disor-
ders than the early-onset type.
39.12.6 Prognosis
Depressed patients with ischaemic brain lesions have
• Delirium is associated with an increase in mor- more vascular risk factors and less family history of
tality. 1 month after delirium, the mortality rate mood disorders than those without.
is 16%. 6 months after delirium, the mortality In a proportion of elderly depressives, subtle brain dis-
rate is 26%. ease is a risk factor.
• Between 30% and 50% of delirious patients on
medical wards die of the underlying condition 39.13.2.3 Physical Illness
in 6 months. Depression can present secondary to a variety of physical
• Those who recover have a good prognosis, and conditions and may sometimes be the first indication of
only 5% go on to develop dementia. ill-health. The following are the main causes of second-
ary depression, which is more common in the elderly:
39.13 DEPRESSION IN OLD AGE • Occult carcinoma, particularly of lung and
pancreas
• Chronic obstructive airway disease (COAD)
Depressive symptoms affect 11%–16% of the over-65s. • CVA
About 3% suffer major depression. • Myocardial infarction (MI)
Female first admissions for affective illness peak at age • Hypercalcaemia
80, then fall off. Male first admissions continue to climb • Cushing’s disease
until the end of life, overtaking women at the age of 85. • Hypo- and hyperthyroidism
The prevalence of depression declines with advancing • Alcoholism
age despite the earlier findings. This may be because of • Pernicious anaemia
a survivor effect with fewer young depressed surviving • Iatrogenic—steroids, β-blockers, methyl-dopa,
to old age, or it may imply that depression in older age is reserpine, clonidine, nifedipine, digitalis, l-dopa,
more likely to require inpatient admission. and tetrabenazine
• Infections—brucellosis, neurosyphilis, and
influenza
39.13.2 Aetiology
39.13.2.1 Genetic Factors 39.13.2.4 Personality
The genetic contribution to depressive illness reduces It is suggested that personality dysfunction is associated
with age. The risk of depression in first-degree relatives with some late-life depression.
is lowered with the increasing age of onset of depression
39.13.2.5 Environmental Factors
in the proband. The risks to relatives are also lower if
there has been only a single episode, whereas they are Murphy (1982) found an association between the onset of
increased with recurrent depression in the proband. depression and severe life events occurring significantly
more commonly in the previous year compared to healthy
39.13.2.2 Neurobiological Factors controls. These included physical illness, separation, bereave-
ment, financial loss, and enforced change of residence.
Felix Post (1968) suggested that subtle cerebral changes
may make ageing persons increasingly liable to affective
disorders.
A subgroup of elderly depressives has ventricular enlarge- Elderly depressives present with much the same features
ment on a CT scan of the brain. They are characterized as of depression as younger people, but some features may
being older, with a later age of onset, more neurovegetative be more common in the elderly (Tables 39.20 and 39.21).

Summary of Similarities and Differences in Comparison between Dementia and Depression/
Depression between Young and Old People Pseudodementia in Old People
Similarities Differences Depression/
Clinical Features Dementia Pseudodementia
The following features are The following features may be
similar between young and old more common in old people: Personal or family Usually absent Usually present
people: • Behavioural disturbance history of mood
• Sleep disturbance (e.g. early (e.g. food refusal, aggressive disorder
morning awakening, frequent behaviour, shoplifting, alcohol Onset Insidious Acute
awakening, and subjective poor abuse) Response to memory Cooperative and Lack of motivation
sleep quality) • Complaints of loneliness assessment attempt to answer and does not
• Poor appetite • Complaints disproportionate to questions with attempt to answer
• Weight loss organic pathology and pain of incorrect answers the questions.
unknown origin (e.g. confabulation) Answer ‘don’t
• Depressive pseudodementia know’ for most of
(e.g. poor concentration and the questions.
memory) Memory deficits Memory deficits are
• Hypochondriacal are reported by often reported by
preoccupations relatives or patients.
• Irritability or anger caregivers.
• Loss of interest often replaces Mood Labile mood or no Low mood and
depressed mood in elderly mood changes irritability
• Minimization/denial of low Anhedonia Capacity to enjoy Cannot enjoy things
mood things in life in life and
• Neurovegetative symptoms maintained preoccupied with
• Onset of neurotic symptoms somatic complaints
(e.g. excessive worry) Aphasia May be present Absent
• Psychomotor retardation or (e.g. word finding
agitation difficulties)
• Paranoid and delusional Perceptual No hallucinations Mood congruent
ideation disturbance hallucinations
(e.g. auditory
hallucinations with
negative content)
39.13.4 Diagnosis Other Acalculia Intact arithmetic
neuropsychological Agnosia skills
Because the elderly commonly suffer from coexistent findings Impaired in Intact paired
physical disorders affecting neurovegetative function- visual–spatial associate learning
ing, the diagnosis of depression can prove more diffi- organization (e.g. shape and
cult than in the young. A careful history usually suffices name of objects)
to address this difficulty. The GDS is helpful since it Intact visual–spatial
focuses almost entirely on cognitive rather than physi- organization
cal symptoms of depressive disorder. The GDS-30 score Suicidal ideation Absent Present
Course of illness Slow progression Rapid progression
> 11 or GDS-15 score > 5 indicates depression (Sheikh
and Yesavage, 1986). The Cornell Scale for Depression
in Dementia (CSDD) was developed to assess signs
and symptoms of depression in patients with dementia 39.13.5 Management
(Alexopoulos et al., 1988). The CSDD uses an interview- The depressed elderly person should be treated in much
ing approach that derives information from the patient the same way as a depressed younger person, with anti-
and the informant. Scores below 6 as a rule are associ- depressants in an adequate dose for an adequate duration.
ated with absence of significant depressive symptoms. The choice of antidepressant will depend on concurrent
physical morbidity, and the dose is generally lower, par- relapse. Only 10%–15% are considered to suffer from
ticularly when commencing a new drug. treatment-resistant depression. The death rate is higher
Newer antidepressants such as SSRIs and SNRIs are for late-life depressives than for nondepressed patients.
better tolerated than TCAs because SSRIs have low anti- Chronicity in late-life depression is more common in
cholinergic activity. Examples of antidepressants and those with
daily starting dose for old people are listed as follows:
escitalopram (5 mg), mirtazapine (7.5–15 mg), sertraline • Male sex
(25 mg), and venlafaxine (37.5 mg). Old people are prone • Active medical illness or poor physical health
to hyponatraemia. Baseline and regular blood pressure • High severity and frequent episodes of depression
measurement, ECG, and sodium level are required for old • Atypical features of depression
people. If a TCA is required, lofepramine is the treatment • History of dysthymia
of choice. • Delusions
Deluded depressed patients require the addition of an • Cognitive impairment
antipsychotic. • Morphologic brain abnormalities
ECT remains the most effective treatment for depres-
sion and is the treatment of choice in those with life- The development of a transient dementia syndrome dur-
threatening depression. It is generally well tolerated, ing a depressive episode, the onset of the first depressive
although memory problems may follow, so unilateral episode in very old age, and abnormalities in brain mor-
electrode placement is sometimes considered preferable. phology may be predictors of dementia in an elderly per-
The seizure threshold increases with age, and older peo- son with major depression.
ple have shorter seizure duration. It is contraindicated in
those with raised intracranial pressure and is inadvisable
within 3–6 months of a CVA, pulmonary embolus, or MI. 39.14 MANIA IN OLD AGE
However, the anaesthetist’s views should be sought in any In most elderly people suffering from mania, the age
patient over whom there is particular concern. The liable of onset was usually in their young adult life. However,
consequences of inadequately treated or resistant depres- in the elderly population, the onset of the first manic
sion should be weighed against the potential adverse episode is bimodally distributed with peaks at ages 37
effects of a general anaesthetic and ECT. Monoamine and 73. Mania in the elderly is relatively uncommon,
oxidase inhibitors should be discontinued at least 10 days comprising about 5% of elderly psychiatric admissions.
prior to giving ECT.
About two-thirds of cases resistant to first-line ther-
apy show an improvement with lithium augmentation. 39.14.1 Aetiology
Generally, this is well tolerated, although the levels need
careful monitoring in those with impaired renal function 39.14.1.1 Genetic Factors
or those on diuretics. Late-onset cases appear to have less genetic loading than
Psychotherapy can be considered, although this younger-onset cases, with fewer of the former giving a
should usually be in addition to drug therapy. The focus family history of affective disorder.
of psychotherapy should support self-esteem, instil hope,
and encourage adequate nutrition and healthy lifestyle. 39.14.1.2 Organic Factors
Problem-solving may be useful and advise the elderly Secondary mania is that arising in a patient with no pre-
depressed patient to postpone major life decisions. vious history of affective disorder, soon after a physical
Socially isolated elderly depressed patients are at a illness such as cerebral tumour or infection. However,
high risk of committing suicide, so it is important that evidence suggests that this is more likely to arise in those
they be treated energetically. genetically predisposed to a bipolar affective disorder by
virtue of a family history of such.
People with late-onset mania have a greater num-
39.13.6 Prognosis ber of large subcortical hyperintensities on brain MRI
Depression in old age is a heterogeneous condition and compared to controls. It is thought that some cases of
therefore has a heterogeneous outcome. Seventy per cent late-onset mania are a subtype of secondary mania attrib-
of elderly depressives recover within a year, but 20% utable to changes in the brain’s deep white matter.
39.14.2 Clinical Features 39.15 PARAPHRENIA OR PSYCHOSIS

These are similar to the features in younger adults, but it IN OLD AGE
is thought that the following are more common in elderly 39.15.1 Explanatory Note
manic patients:
Paraphrenia is a term introduced originally by Kraepelin
• Garrulousness in 1909 to describe a psychotic condition characterized
• Slow flight of ideas by the relatively late age of first onset, chronic delusions
• Speech more circumstantial and less disorganized and hallucinations, the preservation of volition, and a lack
• More paranoid delusions of personality deterioration. The term quickly lost favour
• Less hyperactivity until Roth reintroduced it in 1955 to describe late para-
• Cognitive impairment phrenia, a condition with age of first onset after 60 years,
• Irritable surliness, anger, and less euphoria well-organized delusions with or without hallucinations,
• Mixed affective states and a well-preserved personality and affective response.
• Depression following soon after mania recovers In ICD-10 (WHO, 1992), late-onset disorders are not
• Longer duration and higher frequency of acute differentiated from early-onset disorders, so most para-
episodes phrenias are coded in ICD-10 under schizophrenia or
• Presence of neurological abnormalities espe- delusional disorders. Nevertheless, evidence suggests that
cially old male patients some late-onset delusional disorders are distinct from
schizophrenia, and the use of the term late paraphrenia
therefore persists.
39.14.3 Management
Acute manic episodes may require treatment in hospital. 39.15.2 Epidemiology
Old-age psychiatrists need to rule out underlying medi-
Good epidemiological studies in this area have not been
cal causes and order RFT, TFT, and ECG and measure
completed. It is estimated that in Camberwell (London),
baseline body weight. The old-age psychiatrist needs to
there is an annual incidence of late paraphrenia of 17–26
check potential drug interactions from existing medica-
per 100,000. There is a well-established preponderance
tions such as diuretics and NSAIDS. Treatment is with
of females over males in late paraphrenia. Late para-
antipsychotics and/or lithium. Lithium should be started
phrenics are more likely to be unmarried and have a
at 150 mg daily if the old person is frail or 300 mg/day if
lower fecundity than controls.
the old person is physically fit. The dose is increased by
150 mg on a weekly basis. The maximum total daily dose
is recommended to be less than 600 mg/day. The blood 39.15.3 Aetiology
lithium level is aimed between 0.6 and 0.9 mmol/L during
acute mania and 0.4–0.6 mmol/L during the maintenance 39.15.3.1 Genetic Factors
period. The old person requires monthly monitoring There is an increased risk of schizophrenia in the first-
of blood lithium levels in the initial period and regular degree relatives of paraphrenics, but it is less than the risk
monitoring of thyroid, renal, and cardiac status and mea- to the relatives of younger-onset schizophrenics.
surement of body weight. The response rate for lithium is Paraphrenia is partly genetically determined, but the
similar between young and old people. Addition of carba- part played by inheritance requires further study.
mazepine is recommended if the combination of lithium
and antipsychotics is not fully effective. 39.15.3.2 Personality
If the person is unresponsive or intolerant to this combi- In a subset of paraphrenic patients, there is a history of
nation, ECT can be effective for manic or mixed affective those who have long-standing paranoid personalities,
states. Lithium prophylaxis is advisable in the longer term. which are thought to predispose to the development of
paraphrenia in old age.
39.14.4 Prognosis 39.15.3.3 Sensory Impairment

The outlook is the same as in bipolar disorder. Recurrence Hearing impairment is associated with the development
is usual, and therefore mood stabilizers are advisable in of paranoid symptoms. The characteristics most strongly
the longer term. associated with late paraphrenia are the early age of onset
of hearing impairment and long-duration and profound 39.15.5 Management

hearing loss. Auditory hallucinations are most consis-
tently associated with hearing loss. It is thought that Assessment and management are usually best undertaken
deafness may exert its action through increased social in the patient’s home where the psychopathology is most
isolation, withdrawal, and suspiciousness. Late paraphre- likely to be evident. Time must be spent developing a rap-
nia has also been associated with visual impairment. port and trying to engage with the patient.
39.15.3.4 Brain Disease 39.15.5.1 Pharmacological Treatment

Compared to normal controls, late paraphrenics have sig- The treatment of metabolic disorders or other physical
nificantly larger cerebral ventricles and are more cogni- conditions may bring about an improvement in the mental
tively impaired. state. The treatment of hypertension may prevent a deteri-
Miller et al. (1991), in an MRI study of nondemented oration if this is caused by silent cerebrovascular disease.
late paraphrenics, found that organic brain pathology was Antipsychotic medication may bring about an improve-
common. In a group selected to exclude obvious organic ment. Antipsychotics with low anticholinergic, low hypo-
pathology, the following abnormalities were found: tensive potential are recommended for old people. First-line
treatment includes risperidone (1–3 mg/day). Second-line
• Forty-two per cent had structural brain abnor- treatment includes olanzapine (2.5–7.5 mg/day) and que-
malities, with white matter lesions particularly tiapine (50–300 mg/day). A substantial minority show no
evident in temporal, occipital, and frontal areas. significant response, and about one-quarter show a full
• Fifty-eight per cent had neuromedical illness, response to treatment. Treatment response is associated
such as tumours and metabolic disorders. with improved compliance, the use of depot medication,
• Twenty-five per cent had evidence of silent cere- an involvement of a CPN, and lower medication doses.
bral vascular disease, most commonly associ- 39.15.5.2 Nonpharmacological Treatment
ated with hypertension.
• Day-care centre attendance may be helpful in
• Neuropsychological testing revealed deficits in
increasing socialization.
intellectual, frontal lobe, and verbal memory
• If sensory impairment is present, there is evidence
functions.
that the condition can improve upon treatment of
the deficit (e.g. a hearing aid for the deaf person).
Osvaldo et al. (1995) studied the psychopathology of late 39.15.6 Prognosis
paraphrenics and found the following:
Some patients make little or no response to treatment,
while others make a full response. Long-term contact
• All had at least one type of delusion. These most
with psychiatric services is required.
frequently involved persecution and self-refer-
ence; delusions of thought broadcast, sin, guilt,
and grandiosity were also present.
• Forty-six per cent had at least one Schneiderian 39.16 ANXIETY IN OLD AGE
first-rank symptom. 39.16.1 Epidemiology
• Eighty-three per cent had some hallucinatory
experience, most commonly auditory, but also Anxiety disorders are often chronic, but about one-third of
visual, somatic, and olfactory. cases in the elderly have an onset after the age of 65 years.
• Thought disorder and catatonic symptoms were
almost never seen. 39.16.1.1 Phobias
• Inappropriate affect was not seen. Phobias are quite evenly distributed across the age
• Negative symptoms were seen frequently but groups, with lower rates in the over-75s compared to the
were mild. 65–75-year group. Phobias are the most common psychi-
• Other psychiatric symptoms such as worry, irri- atric disorder in elderly women in a community sample.
tability, poor concentration, self-neglect, and Specific phobias are more common than agoraphobia or
obsessive features were all seen more commonly social phobia. The 1 month prevalence for phobic disor-
in late paraphrenics than in controls. ders is approximately 10%.
39.16.1.2 Generalized Anxiety Disorder • Anxious preoccupation with physical illness,

Prevalence increases with age and is more common in finance, crime, and family.
women. The 1-month prevalence for generalized anxiety • Subjectively impaired sleep, which may be a
disorder (GAD) is approximately 4%. normal part of ageing.
• Somatic symptoms of anxiety may be misattrib-
39.16.1.3 Panic Disorder uted to physical causes.
• Abuse and overprescription of sedative drugs.
This is rarely encountered in the elderly. The 1 month
prevalence for panic disorder is <1%.
39.16.4 Management
39.16.2 Aetiology Although there is less formal evaluation of therapies for

anxiety disorders in the elderly, there is evidence that
39.16.2.1 Environmental Factors they do respond to psychological interventions includ-
Early parental loss is associated with phobic disorders in ing behavioural, cognitive, and anxiety-management
younger and older adults. training.
Benzodiazepines and other sedatives are not gen-
39.16.2.2 Physical Illness erally indicated in the treatment of persistent anxiety
Anxiety disorders and neuroses are associated with disorders, particularly not in the elderly because of
increased mortality and increased cardiovascular, respi- the problems of tolerance, dependence, confusion, and
ratory, and gastrointestinal morbidity. falls.
The onset of agoraphobia after the age of 65 is often Some anxiety disorders will respond to treatment with
associated with a physical insult such as an MI, a surgery, an antidepressant, particularly the SSRIs, which are spe-
or a fracture. cifically helpful in depression associated with anxiety
Anxiety symptoms can be caused by a number of physi- and panic disorder.
cal disorders, and a full physical examination should form Antipsychotics (e.g. quetiapine) are sometimes helpful
a part of the assessment of the elderly anxious patient. for their anxiolytic properties, but caution is required in
Causes include the elderly (e.g. orthostatic hypotension).
• Cardiovascular (e.g. MI, cardiac arrhythmia,

postural hypotension) 39.17 FURTHER CONSIDERATIONS
• Respiratory (e.g. pulmonary embolism, asthma, IN OLD-AGE PSYCHIATRY
hypoxia, COAD)
• Endocrine (e.g. hyper-/hypothyroidism, hypo- 39.17.1 Suicide and Attempted Suicide
glycaemia, phaeochromocytoma) Suicide is overrepresented in the elderly. The elderly com-
• Neurological (e.g. epilepsy, cerebral tumour, prise 15% of the U.K. population, yet they account for
vestibular disease) 25% of all completed suicides and only 5% of attempted
• Drug induced (e.g. caffeine, sympathomimetics, suicides. Ninety per cent of those completing suicide in
sedative withdrawal) old age were depressed, and two-thirds of those attempt-
ing suicide in old age had a psychiatric disorder. Suicide
39.16.2.3 Comorbidity rates increase with age until very old age, when they
There are high levels of comorbidity with other psy- seem to tail off, more so for women.
chiatric conditions, particularly depression. Late-onset The suicide rate is greater in men than in women;
cases of anxiety are almost always associated with men are more likely to use a violent method and to use
depression, which may be either a primary or second- alcohol.
ary association. The depressed elderly who complete suicide tend to
suffer from a moderate, often first-episode depression
with the clinical picture often comprising severe agita-
tion, hopelessness, guilt, insomnia, hypochondriasis, and
Features are generally similar to those seen in younger delusion of guilt. Prior to suicide attempt, the old person
adults, but the following are more common in the elderly: may have an increase in alcohol intake, giving away
possessions, reviewing will, and taking risk. The times of worth attempting to wean even elderly persons from their
highest risk include drug of addiction, since abstinence can greatly improve
the quality of life. However, there is a group, particularly
• Bereavement and their anniversaries the very elderly, who are better left on the drug if they
• The first few weeks after antidepressant treat- strongly object to withdrawal.
ment when the person develops the ability to
enact his or her thoughts prior to full recovery 39.17.3 Somatization and Somatoform Disorders
• In the first few weeks after discharge from hospital
Five per cent of old people suffer from somatoform dis-
Eighty per cent of those completing suicide had seen their orders. The most common somatic complaints in elderly
GP before their death. include pain, constipation, fatigue, headache, impaired bal-
The incidence of physical illnesses in completed ance, dry mouth, nausea, change in appetite, and difficulty
elderly suicides is higher than expected. Chronic pain is in urinating. Somatic complaints may be a presentation of
often a contributory factor, particularly postherpetic neu- underlying depressive (masked depression) and anxiety dis-
ralgia. Living alone, a widowed or separated status, and orders. Three-quarters of old people suffering from psychi-
alcohol abuse are also risk factors. atric disorders also present with somatic complaints. The
Cultural factors probably play a role since suicide presentation of somatoform disorders (e.g. somatization dis-
rates among some elderly populations, such as elderly order, pain disorder, conversion disorder, and hypochondri-
Indian people, are extremely low. asis) in old people is similar to young adults. Management
Thus, suicidal elderly patients should always be taken includes reducing unnecessary visits and assigning the care
seriously. Depression should be adequately treated, isola- to one GP. Medical reassurance is important and avoids
tion should be ameliorated if possible, and pain should be unnecessary investigations. Modified cognitive behavioural
properly managed. therapy with shorter session may be useful for old people.
39.17.4 Sexual Activity
39.17.2 Alcohol and Drug Abuse
39.17.4.1 Normal Sexual Behaviour in Old Age
39.17.2.1 Alcohol
Sixty per cent of married couples aged 60–75 and 25% of
Alcohol abuse reduces with ageing, especially in men.
those over 75 are sexually active. One-fifth of men aged
However, about 3% of the over-75s in a general practise
over 80 have sexual intercourse at least once a month. Thus,
survey drank above the safe limits.
sexual activity and sexual interest continue into old age.
The reasons for this apparent decline in alcohol abuse
The determinants of sexual activity in old age include
with age include the selective death of early-onset alcohol-
ics, reduced tolerance to the effects of alcohol secondary • Age
to reduced liver enzymes, increased sensitivity of the age- • Sex—men are more sexually active than age-
ing brain to sedatives, increased poverty in old age, and matched women
reduced opportunities to drink in elderly social circles. • Married status
New cases of alcoholism in old age tend to be more • Own physical health
neurotic with less evidence of personality disorder than in • Physical health of partner
younger-onset cases. Physical ill-health and psychiatric ill- • Enjoyment of sex
ness may be a trigger to excessive alcohol use in old age.
Loss of, or illness in, a partner is a common reason for the
39.17.2.2 Drugs cessation of sexual activity in the elderly.
Illicit drug abuse is not a great problem in the elderly,
but addiction to prescribed benzodiazepines, opiates and 39.17.4.2 Physiological Changes with Ageing
other analgesics, barbiturates, cough syrups, and laxa- The female genitalia atrophy with age particularly after
tives is problematic. In the United States where the very the menopause. Blood flow is also reduced during arousal,
elderly comprise 12% of the population, they are respon- resulting in reduced vaginal lubrication. However, regu-
sible for the consumption of 50% of prescribed hypnotics. lar sexual intercourse or masturbation protects the female
Doctors need to take care in their prescribing, to pre- genitalia from these changes. Clitoral sensitivity and
vent the initiation of prescribed drug addiction. It is often orgasm do not change with ageing.
In the male, erections are slower to develop and Sleep apnoea is associated with increased morbid-
require more tactile stimulation than in youth. The erec- ity and mortality. It is associated with daytime fatigue,
tion is less firm and persistent than in youth. The plateau memory problems, hypertension, and cardiac arrhyth-
phase can be prolonged longer, and, although ejaculation mias. It is further associated with the increased risk of a
is less forceful, orgasm remains unaltered. The refractory stroke, even after controlling for other risk factors such
period is much longer than in youth. as hypertension, cardiac arrhythmia, and obesity.
39.17.4.3 Sexual Problems in Old Age

Physical illness may impair sexual activity because of 39.17.5.1.2 Circadian Rhythms
Some sleep disturbance in old age is associated with
• Fear of the risk involved in sexual intercourse changes in the systems that regulate circadian rhythm.
(e.g. MI) In older age, the body’s circadian rhythms lose strength,
• Difficult or painful intercourse (e.g. arthritis) with a breakdown in timing and amplitude. Proposed
• Impaired responsiveness of genitalia (e.g. interventions include
neuropathy)
• Reduced feelings of sexual attractiveness (e.g. • Fitness training
after mastectomy or colostomy) • Evening bright-light exposure
• Reduced sexual desire (e.g. dementia) • Melatonin supplementation in those deficient
• Drug effects (e.g. antidepressants, antipsy-
chotics, antihypertensives, thiazide diuretics, All these methods have brought about an improve-
benzodiazepines) ment but are of only limited usefulness. Fitness train-
ing and bright-light exposure require a lot of time and
Elderly people in residential homes or hospitals should effort and are continued after trials in only a minor-
be provided with the privacy required to continue sex- ity of subjects. Melatonin is not commercially avail-
ual expression with a consenting partner or by mastur- able in reliable formulations and in some can cause
bation if they wish. The attitudes of staff and family depression.
may need to change through a process of education and
discussion.
39.17.5.2 Secondary Sleep Disorders
The significant numbers of complaints of disturbed
39.17.5 Sleep Disorders
sleep are secondary to other conditions such as medical
Forty per cent of older adults complain of chronic sleep or psychiatric illness, drug and alcohol use, and behav-
problems and use a disproportionate amount of nighttime ioural and environmental factors. It is essential that the
sedation, often on a long-term basis. primary problem be identified and treated, rather than
The cause of sleep disturbance in the elderly is multi- treating the secondary sleep disturbance. The use of
factorial. Assessment therefore requires a careful history, hypnotics should be avoided whenever possible. Sleep
with selective investigation. disturbance is typically associated with poor physical
health and depression.
39.17.5.1 Primary Sleep Disorders In some elderly people, the apparent sleep distur-
These include sleep apnoea and nocturnal myoclonus, bance is simply the unrealistic expectation that they
both of which are age related. should sleep for as long and as soundly as when they
were younger. This often responds well to reassurance.
39.17.5.1.1 Sleep Apnoea In other patients, attention to issues of sleep hygiene is
Sleep apnoea is an extremely common disorder affecting required. This involves addressing behaviour such as the
a quarter of independently living old people and higher excessive use of caffeine-containing drugs and environ-
proportions of those in institutional care. However, the mental conditions improving the conduciveness to sleep,
presence of sleep-related breathing disturbance in the such as ensuring the bedroom is peaceful and dark, with-
absence of daytime sleepiness or impaired daytime func- out stimulation, and keeping regular sleep hours without
tioning is probably not clinically significant. daytime napping.
39.17.6 Bereavement ill-health, and impending death. They also have to strug-

gle with unresolved unconscious psychological conflict
Mood disorders associated with bereavement are preva- and intergenerational difficulties.
lent in later life and are associated with morbidity and With age, the ego adapts by deploying increasingly
chronicity similar to other late-life depression. In a study mature defence mechanisms. The superego similarly
of late-life widows, 24% were depressed at 2 months after adapts. However, the unconscious id is largely unchanged
the loss, 23% at 7 months, and 16% at 13 months. Risk with time. Inner psychological conflict can persist from
factors for depression at 13 months included a past history childhood.
of mood disorder, intense grief or depression early after
the loss, and few social supports (Zisook et al., 1993).
It is important to understand the differences between 39.18.3 Transference and Countertransference
depression and bereavement. Based on clinical expe- Early in therapy with elderly patients, the transfer-
rience, the following features are more common in ence and countertransference are likely to be reversed
depression but not in bereavement: compared to therapy with younger patients. With the
younger patient, the therapist unconsciously assumes
• Active suicidal ideation the position of a powerful parent. With the elderly
• Depressive symptoms ‘out of proportion’ with patient, the transference is likely to be reversed
loss whereby the therapist experiences the unconscious
• Feelings of guilt not related to deceased transference of their own parental relationships. It is
• Marked functional impairment for long period essential that supervision be provided such that the
• Marked psychomotor changes lasting for long therapist is aware of these issues as they arise in ther-
period apy. Similarly, early in therapy, the patient is likely to
• Preoccupation with worthlessness transfer past experiences with younger people, such as
his or her own children, but as the therapy progresses,
the patient will develop the more classical transference
39.18 PSYCHOTHERAPY WITH OLDER relationships.
ADULTS
39.18.1 Individual Psychodynamic Therapy 39.18.4 Common Themes
Older adults can be treated with psychodynamic therapy. In older age, an increasing number of threatening and loss
Conditions suitable for treatment include neurotic and events occur. The therapist must work with the patient to
personality disorders rooted in unconscious, unresolved mourn the losses, thus freeing the patient to continue to
childhood conflict. take up new opportunities and relationships. Decreasing
independence and increasing dependence are often cen-
tral themes in therapy. Coming to terms with the past
39.18.2 Adaptations in Therapy
and changed relationships and power structures is also
Patients treated include those suffering from depression, relevant.
phobias, anxiety neurosis, and hysteria. Psychosomatic For the isolated elderly person, group work may be
disorders in patients over the age of 60 are not considered more appropriate than individual therapy.
treatable with psychotherapy.
It is suggested that the treatment of choice for neu-
rotic disorders in the 55–75-year age group is one to two
50 min sessions per week for between several months 39.19 MEDICOLEGAL ISSUES
to 2 years. In those with reactive crises, short-term low- IN OLD-AGE PSYCHIATRY
frequency dynamic therapy of 5–20 sessions is indicated
39.19.1 Elder Abuse
until the age of about 80.
Older adults have completed their psychosexual and The abuse of elderly people by their carers has received
psychosocial development but still have to cope with increasing attention since the 1970s. Its prevalence is
psychosocial tasks such as retirement, loss of partner, difficult to estimate and depends on the definition of
abuse—which can range from irritability and verbal 39.19.2 Management of Financial Affairs
abuse to sexual and physical abuse.
Among patients referred for respite care to geriatric Mental disorder from whatever cause can restrict a
wards in London, there was a high morbidity for demen- person’s ability to handle financial affairs and is more
tia. Almost half of the carers admitted to some form common in the elderly, particularly among those suffer-
of abuse, verbal more commonly than physical. Verbal ing from dementing conditions. Various options exist to
abuse was associated with poor premorbid relations help deal with the financial affairs of people unable to do
between patient and carer and depression and anxiety in so themselves because of mental disorder. See Chapter
the carer. Physical abuse was associated with poor com- 11 in which mental capacity, the powers of attorney, the
munication by the patient and high alcohol consump- Court of Protection, and testamentary capacity are con-
tion in the carer. Few patients admitted to any abuse by sidered. The effect of psychiatric disorders on driving
their carers. capability is also considered in that chapter.
CASC GRID: ESTABLISH THE DIAGNOSIS OF DEMENTIA

An 80-year-old man is brought by his children because they are concerned about his memory. They worry that
he suffers from dementia and seeks your assessment.
Task: Take a history from his son to establish the type of dementia.
(A) AD/cortical (A5) Acalculia and

Dementia (A1) Amnesia (A2) Alogia (A3) Apathy (A4) Apraxia Family History
‘How do you find ‘How do you find ‘How do you find ‘Does he show any ‘Does he have
his memory?’ his command of his expression of difficulty to using difficulty to perform
‘Can he recall language?’ emotion?’ a household tool simple arithmetic
recent events? ‘Does he have word ‘Does he express a (e.g. comb or (e.g. adding up the
How about remote finding difficulty?’ full range of toothbrush)?’ prices of several
events?’ emotion?’ ‘Can he wear a shirt items from the
‘Did he forget ‘How does he spend or jacket by supermarket)?’
where he put his his time in the himself?’ ‘Does the memory
items? If yes, how daytime? Does he ‘Can he follow problem run in the
did he react? Did have motivation or instructions to family? If so, at
he accuse someone initiative to do the accomplish a what age did they
stealing his item?’ things he used to simple motor task start to have memory
‘Does he make up do?’ (e.g. collecting his loss?’
story to fill the laundry)?’
memory gaps?’
(B3) Focal (B4) Focal
(B1) The History (B2) Course of the Neurological Neurological (B5) Other Clinical
(B) VaD of CVAs Illness Symptoms Signs Features
‘Did he have a ‘Did his memory ‘Does he show ‘Does he have ‘Do you find him
stroke before?’ problems come weakness on one incontinence becoming more
‘If yes, did his abruptly or side of his body?’ (e.g. passing urine emotional after the
memory gradually?’ ‘Does his face show or motion stroke?’
impairment start ‘Is his memory asymmetry?’ involuntarily?’ ‘Does he laugh or cry
within 3 months of problems ‘Can you comment excessively?’
a stroke?’ fluctuating or on his walking?
‘Did he suffer from being consistent?’ Does he walk
hypertension or steadily?’
high cholesterol?’
(C4) Assess
(C2) Progressive Dorsolateral (C5) Temporal Lobe
(C1) Personality Nonfluent (C3) Orbitofrontal Prefrontal Symptoms/
(C) FTD Change Aphasia Syndrome Syndrome Semantic Dementia
‘Do you find that ‘How do you find ‘Do you find that ‘How do you find ‘Can he name objects
there is a change the way he he is overfamiliar his planning correctly?’
in his personality speaks?’ with other people nowadays?’ ‘Does he have
or character?’ ‘Is his speech (e.g. women)? ‘How do you find difficulty to recognize
‘Can you tell me becoming more Does he display his flexibility?’ items, for example,
which component effortful and any inappropriate ‘Does he have tools or common
changes first, his halting?’ sexual difficulty in household items?’
memory or his behaviour?’ changing topics in ‘Does he have
personality?’ ‘Is he becoming his conversation?’ difficulty to recognize
more irritable?’ ‘How do you find a person (e.g. a
‘How do you find his attention and friend, a relative, or a
his judgement?’ concentration?’ family member)?’
‘Is he easily
distractible?’
(D1) Extrapyramidal
Symptoms and (D2) Diagnosis of (D5) Sensitivity to
Cognitive Parkinson’s (D3) Visual Antipsychotic
(D) DLB Impairment Disease Hallucination (D4) Delusion Medications
‘Is he slow in his ‘Was he given a ‘Does he see ‘Has he become ‘Has he ever taken any
movement?’ diagnosis? If so, things that others more suspicious?’ medication that
‘Do you find his did the doctor say cannot see?’ ‘Does he say worsens his
hands become he suffers from a Explore the someone wanted to movements? If yes,
shaky?’ condition called nature, content, harm him?’ do you know the
‘Does he fall Parkinson’s source, timing, ‘How certain is he in nature of the
easily?’ disease?’ and his sense of his belief?’ medication? What is
‘If he has movement ‘If yes, was he reality. the name of the
problems, does his given any drug? Was it called
memory problem medication to haloperidol?’
start at the same treat his motor
time or one year problems (e.g.
after the movement carbidopa or
problem?’ levodopa)?’
(E3) Poor Task
(E1) Onset and Performance
Family History (E2) Memory and Island of (E5) Treatment of
(E) Pseudodementia of Depression Problems Normality (E4) Insight Depression
‘Did he suffer ‘Did he notice that ‘Does he have the ‘Is he aware about ‘Was he treated by
from depression he has memory tendency to give his memory his GP for
before?’ problems?’ ‘don’t know’ problems?’ depression?’
‘Does he have any ‘If he suffers from answers to ‘If yes, what kind of
‘Does he seek help
family members depression, did questions?’ treatment was
on his own?’
who suffer from the memory ‘Is there a time offered?’
‘Is he very worried
depression?’ problem start when his memory ‘Did his memory
that his memory is
before or after is perfectly improve with
not well?’
depression?’ normal?’ antidepressant
treatment?’
(continued)
(F3) Risk of
(F1) Risk of Self-Harm, (F5) Risk of
(F) Risk Wandering and (F2) Safety at Suicide, and Exploitation and
Assessment Self-Neglect Home and Fall Machinery (F4) Risk to Others Abuse
‘Does he lose his ‘Has he ever left ‘Has he ever ‘Has he been ‘Has he ever been
way home? Was the cooker or fire attempted suicide aggressive to other being taken
he ever found on?’ before?’ people?’ advantages in sexual,
wandering by the ‘Has he been a ‘Does he drive? ‘How do the other financial, or
police?’ victim of Has he ever been family members emotional ways?’
‘Was he searching burglary?’ involved in road react to his ‘Was he ill-treated in
for someone, for ‘What kind of traffic accident?’ aggressive the family?’
example, his medication does behaviour?’
spouse or a he take at home
friend?’ (e.g. water
tablets or
diuretics,
sleeping pills, or
heart medication
such as digoxin
and warfarin)?’
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40 Forensic Psychiatry
40.1 EPIDEMIOLOGY OF OFFENDING 40.3 MENTALLY ABNORMAL OFFENDERS

40.1.1 Relationship with Age 40.3.1 Epidemiology
In the United Kingdom, the peak age of offending is 14 The prevalence of mental abnormality in all offenders is
years in girls and 17–18 years in boys. Half of all indict- estimated to be 1%. The prevalence of mental abnormal-
able crimes are committed by people aged under 21 ity in those in prison in the United Kingdom is estimated
years. By the age of 30 years, 30% of males in the United to be up to 33%.
Kingdom have been convicted of an indictable offence.
40.1.2 Sex Ratio 40.3.2 Mental Disorders

Mental disorders that may be associated with offending
The sex ratio of convicted males to females in the United
include (see Table 40.1).
Kingdom is approximately 5:1.
40.2 JUVENILE DELINQUENCY

40.4 PSYCHIATRIC ASPECTS OF OFFENCES
Juvenile delinquency is defined as law-breaking behaviour
by 10- to 21-year-olds. 40.4.1 Shoplifting
Most shoplifting is a conscious and goal-directed activity
40.2.1 Aetiology without the presence of a psychiatric disorder. Possible
contributing factors include personal gain, organized
The aetiology is multifactorial and is not associated with
criminal activity, poverty, low self-esteem, frustration,
an established psychiatric disorder. Factors associated with
boredom, and thrill seeking.
the development of delinquency include the following:
Sixty per cent of the total number of shoplifting is
• Unsatisfactory child rearing committed by women, but convictions are more common
• Low IQ for men. Only 2% are referred for psychiatric assess-
• Conduct disorder in childhood ment. There are two peaks in terms of age groups: ado-
• Parental criminality lescence and adults who are 50–60 years old (Chiswick
• Large family size and Cope, 1995).
Among shoplifters with associated psychiatric
40.2.2 Management and Prognosis disorders, 33% suffer from psychiatric illnesses. Acute
situational crises and adjustment disorder are the most
Factors that may improve the prognosis with respect to
common psychiatric illnesses. About 5% of shoplift-
adult criminality include the following:
ers are depressed middle-aged women. Shoplifters
Counselling
with a depressive illness make little effort to conceal
• Establishing a good relationship with a parent their actions. Absentmindedness is an acceptable defence.
or counsellor Other psychiatric disorders include personality dis-
• Improvement in the home environment order (17%), acting on delusions (15%), learning dis-
• A good experience in school ability (LD; 11%), dementia and delirium (5%), mania,
• A good peer group influence from drugs (3%), and dissociative state
• Successful employment (Sims, 2002). Organic disorder such as epilepsy is a
• A good relationship or marriage recognized cause (Chiswick and Cope, 1995).
Distressed children steal for self-comfort. Conduct dis-
Approximately 50% have stopped their delinquent order or antisocial personality traits are associated with
behaviour by the age of 19 years. criminal stealing and the peak age of onset is 15 years.
723
TABLE 40.1
The Relationship between Psychiatric Disorders and Criminal Behaviour
Psychiatric
Disorders Criminal Behaviour
Affective disorder • Shoplifting in middle-aged offenders may be associated with depression.
• Violent offending during mild or moderate depressive episode is rare. If a candidate encounters a case of severe
depression in the CASC exam, inquiry should be made about homicidal ideation. Family members are the usual
victims of altruistic homicides.
• Offending is more common in mania and hypomania than in depression.
Schizophrenia • Schizophrenic patients have similar rate of offending as compared to the general population.
• Schizophrenia is mostly associated with minor offending secondary to deterioration in personality and social
functioning.
• Schizophrenic patients are more likely to commit violent offences as compared to the general population, but most
of the violent offences are not committed by schizophrenic patients.
• Violence is a common precipitant prior to the first admission to a psychiatric ward.
Personality disorder • The term psychopathic disorder should only be used as a legal category.
• Personality disorders in forensic psychiatry are usually mixed in types.
• A wide range of personality traits such as immaturity, inadequacy, hostility, and aggression contribute to offending
behaviour.
LD • Offending is more common in people with mild to moderate LD.
• Property offences are committed with a lack of forethought.
• Offences committed by people with LD are generally similar to offenders without LD although there have been
reports for increase in rates for sex offending and fire setting in patients with LD.
Organic state • Personality change is an early feature of frontal lobe dementia and associated with impulsivity.
• In general, offending by patients with dementia is uncommon. The most common offence is theft.
• In patients with Huntington’s disease, antisocial behaviour may appear before any sign of neurological or psychiatric
disturbance.
• For patients with epilepsy, the rate and type of offending is similar to those of offenders in general. There is no excess
of violent crimes in epileptic prisoners. Offending in epileptics is rarely ictal. The increase of prevalence of epilepsy in
prisoners (about two times of the general population) is a result of common social and biological adversity leading to
both epilepsy and crime (Whitman et al., 1984).
Substance abuse • Alcohol misuse is commonly seen in the more than 50% of perpetrators and victims of violence and rape (Coid, 1986).
• Substance misuse is common in offenders with antisocial personality disorder.
• Alcohol and drugs that have been taken voluntarily do not, in general, lessen the individual’s full legal responsibility.
While amnesia is not a legal offence, its underlying cause may well be.
Morbid delusional • This is associated with repetitive and serious injury to the spouse/partner (refer to CASC grid for further details).
jealousy (Othello
syndrome)
Source: Chiswick, D. and Cope, R., Seminars in Forensic Psychiatry, Gaskell, London, U.K., 1995.
40.4.2 Kleptomania after the act. At the same time, the urge is recognized
as senseless and wrong and the act is followed by guilt.
Kleptomania (ICD-10 F63.2) is an impulse control disor- The stealing is not an expression of anger or a part of
der characterized by repeated failure to resist the impulse dissocial personality trait.
to steal in which tension is relieved by stealing (Cooper, Pure kleptomania is extremely rare (Sims, 2002).
2001). The sex ratio of F/M is 4:1. Such compulsions are associated with depression, anxi-
Classically, the compulsion is characterized by a ety, bulimia nervosa, sexual dysfunction, and fetishistic
feeling of tension associated with an urge to steal. The stealing of women’s underwear (Cooper, 2001).
person feels excited during the theft and feels relieved
Forensic Psychiatry 725
Stolen items are usually not acquired for personal use better than longer-term prediction. Dangerousness is
(e.g. same set of T-shirts) or monetary gain. The person associated with the availability of weapons, morbid jeal-
may discard the objects, give them away, or hoard the items. ousy, and the sadistic murder syndrome.
Schizophrenic patients usually assault a known per-
son, but if they assaulted a stranger, the arresting police
40.4.3 Fire Setting
officer is the most common target. The delusional ideas
There are about 30,000 episodes in England and Wales often motivate the violent behaviours and the patients
per year. The most common motives are revenge and usually admit experiencing command hallucinations
fraud insurance claims (Johnstone et al., 2004). The other after the violent offences. Schizophrenic patients with
causes include anger and the need to relieve tension by negative symptoms commit violent offences inadver-
fire setting (Chiswick and Cope, 1995). tently and neglectfully. In clinical practice, psychia-
There is a higher representation of men with LD trists should be aware that schizophrenic patients may
(IQ 70–79) because they display passive aggression and a display persistence of their normal selves especially in
sense of power or excitement during arson. Twenty to thirty patients without past history of violence (Chiswick and
per cent of arsonists have psychiatric disorders (e.g. alcohol Cope, 1995).
misuse, schizophrenia) (Gelder et al., 2001). Pyromania is a
rare condition when the arsonist derives sexual satisfaction
through fire setting. 40.5.1 Multiagency Public Protection
Most cases of arson (80%) do not lead to criminal Arrangements
conviction and only a tiny proportion lead to psychiatric
1. Multi-Agency Public Protection Arrangements
disposal (more common in women) (Chiswick and Cope,
(MAPPA) is a collaboration of different
1995). The recidivism rate for arson is 10%. If it is a gang
responsible authorities in the United Kingdom
crime, the recidivism rate is low for the gang members but
aiming at public protection, and its main focus
high for the gang leader.
is on sex offenders or violent offenders and
offenders who pose a serious risk of harm to
40.5 DANGEROUSNESS the public.
2. The role of MAPPA involves sharing informa-
Dangerous individuals are people who have caused or who tion on offenders being referred, deciding on the
might cause serious harm to others. Its features include level of risk, setting up an action plan, monitoring
of the action plan, reviewing current risk level,
• Repetition
and considering the need of disclosure to relevant
• Incorrigibility
persons.
• Unpredictability
3. MAPPA has major differences from mental health
• Untreatability
services because it deals with its targets as offend-
• Infectiousness
ers rather than patients.
The best predictor of future dangerous behaviour is the 4. Offenders are not informed about the discussion
individual’s past behaviour. Shorter-term prediction is by MAPPA and they have no right to appeal.
CASC STATION ON MORBID JEALOUSY

A GP asks you to see a 55-year-old man who has history of alcohol misuse from when he lost his job 7
years ago. He has accused his wife of infidelity. He was diagnosed with type II diabetes six years ago and
the GP reports he is depressed.
Task:
1. Take a history to establish diagnosis of morbid jealousy.

2. Perform a risk assessment.
CASC Grid
(A) Assess Morbid
Jealousy (A3) Evidence to (A4) Degree of (A5)
Symptoms (A1) Onset (A2) Precipitants Support his Beliefs Conviction Consequences
‘Hello, I am ‘Can you describe ‘How did you arrive at ‘Could there be ‘I can imagine
Dr. Wilson. I can your recent the conclusion that your other possible that you have
imagine that you relationship with wife is unfaithful? Can explanations for her gone through a
have gone through a your wife?’ you share with me your infidelity?’ tough time. What
difficult period. Can ‘Is there any event evidence?’ ‘If I give you a scale is your plan on
you share with me which triggers off ‘Do you know the identity from 1–10, 1 means your marriage?
when you started to your suspicion?’ of the third party?’ that you do not Are you going to
suspect your wife is ‘Do you follow your wife? believe and 10 divorce your
having an affair?’ If yes, how often?’ means that you wife?’
Explore the temporal ‘How often do you call firmly believe that ‘Are you going to
relationship between your wife?’ your wife is confront her?’
the morbid jealousy, ‘Do you search her unfaithful, how do ‘How do you cope
alcohol misuse, and belongings? (e.g. hand you rate your with the current
diabetes. phone, text messages, belief?’ situation?’
underwear, handbag,
credit card bill)?’
(B) Risk (B2) Partner or (B5) Access to
Assessment (B1) Self Spouse (B3) The Third Party (B4) Children Weapons
‘Have you thought of ‘What would you do ‘Are you going to take ‘Do you have any ‘Do you have
harming yourself? If to your wife if she any action against the children? How old access to weapons?
yes, how would you still denies of the third party? If yes, how are they? What is If yes, what kind of
do it?’ affair? Will you be would you do it?’ their views on the weapons do you
more aggressive?’ current situation?’ have?’
‘Have you ever ‘Do you carry the
thought of harming weapon with you?’
them?’ ‘When will you
use it?’
(C4)Assess
(C) Psychiatry (C1) Alcohol and (C2) Psychosexual Psychotic
Comorbidity Drug History History (C3) Assess Mood Experience (C5) Personality
‘Can you take me ‘Do you encounter any ‘How is your mood at ‘Do you have ‘How do other
through how much sexual problem? this moment? Do you unusual experience people describe
you drink in a day?’ (e.g. cannot maintain feel sad? Can you tell such as hearing you as a person?
‘Has there been an erection during sex?) me more about your voices when no Do they say that
increase in alcohol If yes, how long did sleep, appetite and one is around? Do you are more
intake recently?’ you have this energy?’ the voices give you suspicious? Do
‘Have you developed problem? Was it ‘How do you see your instructions?’ you have problems
further problems as a related to diabetes?’ future? Do you feel ‘Do you feel that with your friends
result of drinking? ‘Can you tell me guilty? How is your someone wants to or neighbours? Do
(e.g. liver problems, more about your confidence level?’ harm you at this you trust them?’
fits, or head injury)’ past relationship? ‘Do you experience moment? Do you
‘When people are Did you suspect anxiety? Can you tell think there is plot
stressed, they turn your partners or girl me more about your behind your wife’s
into recreational friends in the past?’ fear?’ (e.g. losing his infidelity?’
drugs, have you ‘Have you been wife)
tried those drugs?’ unfaithful to your
partners in the past?’
(D1) Forensic (D2) Medical (D4) Family

(D) Past History History History (D3) Marital History History (D5) Insight
‘Do you have any ‘Can you tell me ‘Is this your first ‘Can you tell me ‘I understand that
encounter with the more about your marriage? If not, how more about your you are very
police? If yes, for diabetes? Which did it end last time?’ family? Is there affected by what
what reason?’ kinds of medication any family history had happened.’
‘What was the do you take? Do of violence?’ (Demonstrate
consequence?’ you take them empathy.)
‘Have you ever regularly? Have you ‘I have seen
appeared in court? ever experienced patients who
If yes, were you low sugar level and presented with
sentenced to the felt very giddy? similar problems.
correctional Were you violent at You are not
service?’ that time?’ alone. They seem
‘Do you feel that to have an illness
there is a change in in their belief
your sensation?’ system. Do you
(Look for peripheral think you have a
neuropathy that may similar problem?’
be related to erectile ‘If yes, do you
dysfunction.) think you need
treatment? What
kind of treatment
would you
prefer?’
5. Psychiatrists can advise the police, probation

officers, and other social agencies in MAPPA BOX 40.1 FORENSIC PSYCHIATRIC
on the appropriateness of mental health inter- ASSESSMENT
ventions with offenders suffering from psy-
1. Full history and mental state of the patient,
chiatric illnesses who may present some level
including fantasies and impulses to offend
of risk. Confidentiality remains the important
2. Objective account of offence, e.g. from
challenge.
arresting police officer or from statements
6. Based on the good psychiatric practice guide-
(depositions) in Crown Court cases
lines (Royal College of Psychiatrists, 2006),
3. Objective accounts of past offences, if any,
a psychiatrist needs to consider the follow-
e.g. obtain list of previous convictions
ing before disclosure of any information to
4. Additional information gathering, e.g.
MAPPA:
interviews with informants (e.g. relatives),
a. The crime must be sufficiently serious for
reading a social inquiry report from a pro-
the public interest to prevail.
bation officer (if prepared)
b. Without the disclosure, the prevention of
5. Review of previous psychiatric records,
crime would be seriously prejudiced or
e.g. to ascertain relationship of mental
delayed.
disorder to previous behaviour and to psy-
c. Inform the offenders before the disclosure
chiatric treatment and need for security
and seek his or her consent unless obtaining
consent would enhance the risk of harm or Source: Puri, B.K. and Treasaden, I.H., Psychiatry:
inhibit effective investigation. AnEvidence-BasedText,HodderArnold,London,
d. Reveal only minimum information neces- U.K., 2011.
sary to achieve the objective.
BOX 40.2 CLINICAL RISK ASSESSMENT AND RISK MANAGEMENT PLANNING

The aim is to get an understanding of the risk from a detailed historical longitudinal overview, obtaining infor-
mation not only from the patient, who may minimize his or her past history, but also from informants. Ideally it
should not be a one-off single interview assessment.
Reconstruct in detail what happened at the time of the offence or behaviour causing concern.
Independent information from statements of victims or witnesses or police records should be obtained where
available. Do not rely on what the offender tells you or the legal offence category—for example, arson may be of
a wastepaper bin in a busy ward or with intent to kill. Possession of an offensive weapon may have been prelude
to homicide.
Offence = offender × victim × circumstances/environment

Risk factors associated with violence to be sought in a forensic assessment have been usefully summarized and
are detailed later in the CASC Station On the Assessment of Dangerousness.
Consider also protective factors:
Practical risk assessment (history × mental state × environment) can be supplemented by standardized instru-
ments of risk, including actuarial risk instruments based on static risk factors, such as the Violence Risk Appraisal
Guide (VRAG), and dynamic risk instruments, such as the Historical, Clinical, Risk Management-20 (HCR-20),
based on factors that can change or be managed, for example, symptoms of mental illness and noncompliance.
In conclusion:
1. Aim to answer how serious the risk is (i.e. its nature and magnitude): is it specific or general, condi-
tional or unconditional, immediate, long-term, or volatile? Have the individuals or situational risk fac-
tors changed? Who might be at risk?
2. From such a risk assessment, a risk management plan should be developed to modify the risk factors
and specify response triggers. This should ideally be agreed with the individual. Is there a need for
more frequent follow-up appointments, an urgent care programme approach meeting or admission to
hospital, detention under the Mental Health Act, physical security, observation, or medication? If the
optimum plan cannot be undertaken, then reasons for this should be documented and a backup plan
specified.
3. Risk assessments and risk management plans should be communicated to others on a ‘need to know’ basis.
On occasions, patient confidentiality will need to be breached if there is immediate grave danger to others.
The police can often do little unless there is a specific threat to an individual, whereupon they may warn
or charge the subject. Very careful consideration needs to be given before informing potential victims to
avoid their unnecessary anxiety. Their safety is often best ensured by management of those at risk.
Source: Puri, B.K. and Treasaden, I.H., Psychiatry: An Evidence-Based Text, Hodder Arnold, London, U.K., 2011.
40.6 RISK ASSESSMENT static factors such as prior convictions, age at the time of the
offence and childhood factors, as well as dynamic factors
40.6.1 Actuarial and Clinical Risk Assessment such as substance abuse, access to weapons, and insight.
In general, actuarial risk assessment requires the collec- Clinical risk assessment is based on the professional
tion of a large amount of historical data that can indicate opinions of the clinician, who take a more holistic
whether the offender is likely to reoffend. approach to predicting whether an offender will reoffend.
Risk factors measured by actuarial tools can be static Clinicians may consider personality traits, presence of
(unchangeable) or dynamic (changeable). For example, an psychiatric illness, as well as biological, social, and psy-
actuarial risk prediction tool may measure a number of chological factors that are related to offending.
CASC STATION ON ASSESSMENT OF DANGEROUSNESS

You are the psychiatric registrar on call and being asked to carry out a risk assessment for a 25-year-old man
who suffers from schizophrenia. He was remanded for an offence that he is reluctant to talk about. He has just
assaulted a nurse in the forensic ward. He is calm at this moment.
Tasks:
1. Assess the causes of his aggression and violence.
2. Perform a risk assessment and explore the index offence.
Approach to this station: The candidate should establish rapport, show concern, maintain a supportive non-
threatening stance, and avoid confrontation.
(A) Assess
Contextual
Factors in the (A1) Patient’s View on (A2) Precipitants and
Ward the Event Aftermath (A3) Staff Factors (A4) Ward Factors (A5) Visitors
‘Hello. I am Dr. ‘Was there any event ‘Can you share with ‘From your views, ‘Have your friends
Patten and I am here which upset you in the me your is the ward or relatives visited
to help you. Can you ward?’ experience with the overcrowded?’ you here? If yes,
tell me what has ‘Do you have difficulty staff on the ward?’ ‘Do you feel that can you tell me
happened tonight?’ in controlling your ‘Is there a rapid the ward is too more about
‘I can imagine that it impulses?’ turnover of staff custodial?’ them?’
may be stressful for ‘How do you feel about recently? How do ‘How do you feel ‘Did they pass you
you. Why did you the nurse who is you feel about the about the other alcohol/or
attack the nurse?’ injured? Do you feel new staff? Is the patients in the recreational
sorry for the nurse?’ nurse attacked by ward? Do you feel drugs? If yes,
‘If you are going to you is a new staff comfortable with which drugs?’
harm someone again, on the ward? Do them?’ ‘Did they pass you
are you going to inform you feel ‘Do you find the sharp objects like
us before you carry out comfortable with ward too noisy?’ razor blades?’
your attack?’ the new staff? If ‘How do you find
not, why?’ the ward
‘How do the staff programme? Is it
react to you when too boring or
you are angry? stimulating?’
How do you feel
the way they are
handling you?’
‘Is there enough
staff to respond to
you promptly?’
(B) Risk
Assessment and
Historical (B2) Past History of (B3) Access to
Factors (B1) Assess Aggression Violence Weapons (B4) Forensic History (B5) Suicide
‘May I know what ‘Did you assault other ‘Do you have ‘Did you have any ‘Do you have any
kind events make people before access to knives trouble with the current thought of
you aggressive?’ admission?’ or other weapons police or the legal harming yourself?
in the ward?’ system? If yes, how If yes, how would
did you get into the you do it?’
trouble?’
(continued)
(B) Risk
Assessment and (B2)Past History of (B3) Access to
Historical Factors (B1) Assess Aggression Violence Weapons (B4) Forensic History (B5) Suicide
‘Did you feel aroused ‘Can you tell me under ‘If yes, where are (Look for vandalism, (Look for
after assaulting the what circumstances you those weapons at sexual offences, and dangerous
victim?’ would attack the others?’ this moment?’ drug trafficking methods such as
‘Did you plan for the ‘Were you under ‘Do other patients offences.) hanging.)
assault beforehand?’ supervision in the know about it?’ ‘What happened after ‘Did you attempt
‘Is there any goal you community by the public ‘Do you own those the court hearing? suicide in the
can achieve by being protection panel?’ weapons? Do you Were you sentenced past? If yes, how
violent?’ share weapons with to the correctional many times?’
‘Are you hostile to the other patients?’ services? If yes, for ‘What made you to
victim?’ how long?’ attempt suicide in
the past? Did you
attempt suicide in
the prison?’
(C3) Motor Agitation
(C) Clinical (C2)Paranoid Accompanied
Factors Leading to (C1) Auditory Misinterpretation by Poor (C4) Depression or (C5) Substance
the Violence Hallucinations of Staff Concentration Mania Abuse
‘Do you have any ‘Do you feel that the ‘Have you been ‘How do you feel ‘Have you ever used
unusual experience staff are doing feeling restless about yourself at any drug or
such as hearing voices something behind you? lately?’ present?’ alcohol prior to
when no one is Do you feel that they ‘What has caused ‘How’s your sleep admission to the
around? If yes, what want to harm you? If that? Could it be and appetite?’ ward?
do the voices say?’ yes, what is their related to ‘Do you feel low in ‘How do you feel if
‘Do the voices give motive?’ psychiatric your mood?’ you do not have
you any instruction? ‘Do you feel that the staff medications?’ ‘How about feeling those drugs? Do
Do they ask you to or other patients are ‘How do you find high? Have you you feel shaky?’
attack the nurse?’ talking behind you?’ your attention or ever felt as if you ‘Do you want to go
‘How certain you are concentration?’ are on top of the out of the ward to
about your suspicion? world or as if you get those drugs?’
Could it be a have special
misunderstanding?’ powers?’
(D) Background (D1) Childhood (D2) Socioeconomic (D4) Past Medical
History and Family Status (D3) Personality History (D5) Insight
‘Were you bought up in ‘Can you tell me your ‘Can you tell me ‘Did you suffer from ‘In general, do
a violent employment status prior more about your any head injury?’ you feel that you
environment?’ to admission?’ (Look for character?’ ‘Did you have fit are aggressive?’
‘How do you feel about occupations that have ‘Are you concerned before?’ ‘Do you think
your parents? Is your access to firearms.) about the safety of your violent or
father an alcoholic? ‘Do you have difficulty to other people?’ aggressive
Does he have trouble stay in one job?’ ‘Are you an honest behaviour is
with the law?’ person? Do you acceptable?’
‘Were you cruel to tend to tell lies?’ ‘Could it be related
animals?’ ‘How often do you to an underlying
‘Did you set fire in the feel frustrated? psychiatric
past?’ What would you do condition? If yes,
‘Did you have difficulty if you are do you want
to follow school rules?’ frustrated?’ treatment?’
Legal systems
in the
United Kingdom
Adversarial Inquisitorial system:

system ascertain the facts
and then arrive at
eventual decision
Prosecution Defence
All criminal and (evidence is (evidence is
civil courts in heard first) heard second) Death Mental health
England follow
inquiry review
adversarial system
tribunal
Crown Court Magistrates’ Court

(Judge [My lord or My Lady] with jury (Legally qualified magistrates [Sir or Madam])
composed of 12 adults)
1. All adult defendants appear here first and
1. Deal with indicatable (serious) offence decision will be made to remand on bail or in
2. Appeals from Magistrates’ Court custody
3. For offenders with psychiatric disorder, 2. Here all summary (minor) offences and
assess treatment response some indictable (serious) offences
3. Youth Court for Juvenile Offenders: run by
Yes No specially trained Magistrates
Hospital Alternative to hospital
order order
Admision to any ward
Restriction
order
To protect
public from
serious harm
FIGURE 40.1 Legal systems in the United Kingdom.
40.7 LEGAL SYSTEMS IN THE responsible for his or her actions unless

UNITED KINGDOM caused by
a. A mistake
See Figure 40.1. b. An accident
c. Duress
40.8 CRIMINAL RESPONSIBILITY IN d. Necessity
THE UNITED KINGDOM e. Mental disorder
2. Actus reus. This is an unlawful act.
In England and Wales, criminal responsibility starts at 3. Mens rea. This is guilty intent and is required in
the age of 10 years. In Scotland it starts at the age of addition to an unlawful act for certain offences,
8 years. such as murder and rape.
40.8.1 Definitions 40.8.2 Forensic Psychiatric Assessment

and Court Reports
1. Doli incapax. Criminal responsibility is par-
tial between the ages of 10 and 14 years. After Before the assessment, the psychiatrist needs to empha-
the age of 14 years, an individual is legally size to the offender that his or her role is to write a
medical report to the court. The psychiatrist needs to d. Ability to challenge the juror: ‘Do you know
state that the assessment is similar to other clinical what it means if they say you can object to
interviews except that he or she has to share the infor- some of the members of the jury in your
mation with the court. case?’
These should include the following: e. Ability to challenge a witness: ‘If you dis-
agree with what a witness is saying in court,
1. A full history and mental state examination what could you do about it?’
2. Obtaining an account of the offence from the f. Ability to follow the course of the trial and
offender understand the evidence: ‘Will you be able
a. Assess mental state during the offence and to follow the procedures in the court?’
explore the possible influences of substances There are instruments to assess fitness to stand trial:
on mood and perception.
b. Explore details of the offence such as degree 1. Fitness Interview Test—Revised (FIT-R): a reli-
and quality of violence, use of weapons, pre- able and sensitive semistructured instrument
meditation, and planning. to screen for fitness to stand trial (McDonald
c. Aftermath of the offence: Did the offender et al., 1991).
offer any help to the victim? Explore guilt 2. The Nussbaum Fitness Questionnaire (NFQ):
and victim’s empathy. Assess defence mech- a 19-item self-report measure focusing on legal
anisms and insight. issues typically addressed during fitness inter-
d. Relationship with the victim: Was the vic- views (Nussbaum et al., 2008).
tim provocative? (e.g. the victim was drunk Mental state at the time of the offence is irrelevant to
and violent). Was the victim the intended the fitness to plead. Although the prevalence of men-
target? tal illness is high among the defendants, the number of
3. Obtaining an objective account of the offence cases found unfit to plead and given a restriction order
from police statements is less than 50 per year in the United Kingdom. Rates of
4. Obtaining an objective account of previous mental illness are higher in remanded prisoners com-
offences pared to sentenced prisoners as ill offenders are often
5. Additional information from relatives, friends, diverted. Among those on remand, female prisoners
social workers, probation officers, etc. show more behavioural disorder than male prisoners.
6. Assessing the current circumstances In criminal cases, medical report (Table 40.2)
a. Assess current impulse control. requested by the court or the Crown Prosecution
b. Assess his or her relationship with other Service will be disclosed in the court to the defendants
offenders in the custody. and prosecutors. On the other hand, the medical report
c. Assess his or her views towards custody offi- requested by the defence solicitor may be retained by
cers and other mental health professionals. the solicitor if the report does not help his or her client.
d. Explore current stressors. In civil cases, the medical report is always the property
e. Assess risk to self and others. of the person who requests it.
7. A review of previous psychiatric and other relevant
records 40.8.3 Classification of Homicide
8. Assessing fitness to plead
(Stone et al., 2000)
a. Understanding of the charge and its implica-
tion: ‘Do you understand what the police say In the United Kingdom, there are 600–700 homicides
you have done wrong?’ per year. There are around 220 manslaughter verdicts per
b. Understanding and appreciating the impor- year with a wide discretion in sentencing. Homicides are
tance of entering a plea: ‘Do you know the divided into normal and abnormal homicides based on
difference between saying guilty and not the legal outcome. Normal homicides include a convic-
guilty?’ tion for murder or manslaughter. Abnormal homicides
c. Ability to instruct counsel: ‘Can you tell include a conviction of diminished responsibility or
your solicitor your side of story?’ infanticide (Figure 40.2).
TABLE 40.2
Psychiatric Court Report Model
Para 1 Introduction: Inform the court of when and where the patient was seen; at whose request; what information was available,
e.g. statements related to the case; who were the informants; and sometimes what information was not available. State the
current offence(s) with date for which it is charged.
Para 2 Inform the court of his or her past medical history and of the result of medical examination, e.g. ‘Physical examination
revealed no abnormality’.
Para 3 Report the important, relevant points of the family history, including family psychiatric disorder and criminality.
Para 4 Personal history: Report the important points of his or her personal history, i.e. physical development, e.g. birth, milestones,
bedwetting (enuresis), schooling (e.g. bully/bullied, truancy), and occupational history (which will include difficulties
sustaining employment or with colleagues at work).
Para 5 Report his or her sexual and marital history: Be reasonably discreet as the report may be read in open court.
Para 6 Report details of his or her personality in terms of social interaction, emotions, and habits, e.g. drinking, gambling, and
drugs.
Para 7 Report past forensic history, e.g. past convictions. This is, however, inadmissible.
Para 8 Report past psychiatric history (dates, diagnoses, relevant details, and relationship of mental disorder and treatment to
offending).
Para 9 Report circumstances leading to current offence(s) and the defendant’s state of mind at the time of the offence. Restrict
discussion to the phenomena observed, e.g. ‘For the time of the offence he gives a history of tearfulness, loss of hope, poor
sleeping’ and ‘These are symptoms of the mental illness of depressive disorder’.
Para 10 Report the result of the interview: ‘He showed/did not show evidence of mental illness or mental impairment.’ Then give a brief
outline of the evidence, e.g. ‘He muttered to himself, looked around the room as though hallucinating’, or list symptoms detected
and say ‘These are symptoms of the severe mental illness of schizophrenia’.
Information in paragraphs 1–10 should be factual, verifiable, and ideally agreed by all, even if others’ opinions of these facts differ from your
own.
Para 11 The final paragraph should express your opinion. The court will be interested particularly in your opinion regarding the
following:
(a) Is the defendant fit to plead and stand his or her trial?
(b) Is he or she suffering from a mental disorder, i.e. mental illness, a form of mental impairment, or psychopathic disorder?
(c) Where appropriate, comment on issues of responsibility, e.g. not guilty by reason of insanity; diminished responsibility in
cases of homicide.
(d) If suffering from mental disorder, can arrangements be made for his or her treatment in the National Health Service?
(Arrange this if you think they can.)
Make suggestions to the court about which Mental Health Act order would be appropriate, e.g. Sections 37/41 in England and Wales, or suggest
treatment as a condition of a Probation Order, e.g. ‘In my opinion this man suffers from the severe mental illness schizophrenia, characterized by
delusions (false beliefs) and hallucinations (voices, or visions). I consider he would benefit from treatment in a psychiatric hospital. I have made
arrangements for a bed to be reserved for him at X hospital under Section 37 of the Mental Health Act 1983 if the court considers that this would be
appropriate. I additionally recommend, if the court so agrees, that he be made subject to restrictions under Section 41 of the Mental Health Act 1983
to protect the public from serious harm and to facilitate his long-term psychiatric management, including specifying the conditions of his discharge
from hospital, e.g. of residence and compliance with out-patient psychiatric treatment’. As an alternative: ‘In my opinion this man does not suffer from
mental illness, mental impairment nor psychopathic disorder and is not detainable in hospital under the Mental Health Act 1983. He has an anxious
and dependent personality disorder, requires considerable support and would benefit from group psychotherapy as an out-patient. The court may
consider that it would be an appropriate disposal to help this man if he were to attend an out-patient group under my direction at X Health Centre as a
condition of probation’.
Comment should be made on any mitigating circumstances, e.g. marital/work stress, and on the prognosis. Express any doubts you may have
as to the likelihood of benefit from treatment.
If you have no psychiatric recommendation, say so, e.g. ‘I have no psychiatric recommendation to make in this case’.
Finally, if essential information is lacking or if time is not sufficient to make the necessary arrangements for a hospital bed, then do not hesitate
to state your findings up to date, state what you would like to do, and ask for a further period of remand.
Source: Reproduced from Puri, B.K. and Treasaden, I.H., Textbook of Psychiatry, 3rd edn., Churchill Livingstone, Edinburgh, U.K., 2011. With
permission.
Homicide
Lawful Unlawful Voluntary Involuntary Gross Infanticide

homicide: homicide: manslaughter: manslaughter: negligence:
e.g. on behalf of Murder is an Murder is reduced An unlawful and The actus reus When a
the state, e.g. offence under the to manslaughter by dangerous act; the consists of a woman by
taken by people common law. It is diminished actus reus breach of a duty any wilful act
in the army or the defined as an responsibility as a (committing an act of care that the causes the
police; excusable, unlawful killing result of abnormality of which is known to accused owes to death of her
e.g. a pure accident with malice mind, provocation, be against the law) the victim, with child under
or an honest or aforethought (an killing in pursuance consists of an the result that this the age of 12
reasonable intention to inflict of a suicide pact. unlawful act that is breach leads to months. She
mistake. grievous bodily Diminished dangerous and the victim's death. has not fully
harm or to kill). responsibility can causes death. recovered
only be used in a from the
charge of murder. effect of
Offender has the
giving birth
intention to kill,
to the child
without prior
or the effect
provoc ation and
of lactation.
psychiatric illness.
–Life imprisonment
or
–Lesser prison
Life sentence or
imprisonment –Probation or
–Hospital order
under MHA or
–Restriction order.
FIGURE 40.2 Classification of homicide.
40.8.4 McNaughton Rules (Puri et al., 2012) reason, memory and understanding’ and disease refers
to ‘organic/functional, permanent/temporary, treat-
In this defence, the offender is arguing that he or she is able/not treatable’, and is ‘internal’. Criticisms of the
not guilty by reason of his or her insanity. The offender McNaughton Rules include a small number of offend-
meets the McNaughton Rules if he or she fulfils the fol- ers meeting the rigid criteria and ignoring the linkage
lowing criteria: with other higher mental functions (e.g. emotion and
1. That by reason of such defect from disease of cognition).
the mind, the person did not know the nature or
quality of his or her act. 40.8.4.1 Diminished Responsibility
2. The person did not know that what he or she was (Puri et al., 2012)
doing was wrong (forbidden by law). In the case of a charge of murder, a defence of dimin-
3. If the person was suffering from a delusion, ished responsibility (Homicide Act 1957) may be brought
then his or her actions would be judged by the in, whereupon it has to be shown that, at the time of the
relationship to the delusion, that is, if he or she offence, the offender suffered from:
believed his or her life to be immediately threat-
ened, then he or she would be justified in strik- such abnormality of mind, whether caused from a con-
ing out, but not otherwise. dition of arrested or retarded development of mind or
any inherent causes or induced by disease or injury, as
In the legal concepts, the term ‘disease of mind’ substantially impai red [the individual’s] mental respon-
is divided into two parts. Mind refers to ‘mind for sibility for [his or her] act.
Diminished responsibility is determined by the court (usu-

ally by the jury or by the judge if both prosecution and TABLE 40.3
defence agree on plea). Examples of diminished respon- Outcome of Sentencing of Mentally Abnormal
sibility include killing a spouse in a state of depression. Offenders
The abnormality of mind substantially impairs criminal (a) The law takes its course, e.g. a fine and prison
responsibility of the person’s acts. If a person is found to (b) Conditional or absolute discharge, possibly with voluntary
have diminished responsibility, it may imply that the court psychiatric treatment
will return such a person to society earlier than a ‘respon- (c) Probation order, with or without condition of psychiatric treatment
sible’ offender. In England and Wales, 7% of homicides (e.g. under Section 3 of the Powers of the Criminal Courts Act
result in diminished responsibility or infanticide and 50% 1973 in England and Wales)
of these cases result in hospital disposal. Criticisms of (d) Detention under the Mental Health Act, e.g. under Section 37 with
diminished responsibility include the problem of balanc- or without a Section 41 Restriction order under the Mental
ing the concept of responsibility with ‘determinism’. Health Act 1983 of England and Wales
Source: Reproduced from Puri, B.K. and Treasaden, I.H., Textbook of

40.8.5 Automatism (Johnstone et al., Psychiatry, 3rd edn., Churchill Livingstone, Edinburgh, U.K.,
2004; Puri et al., 2012) 2011. With permission.
Under the British law, automatism is a legal concept.

Automatism is different from automatic behaviour,
which is a clinical concept, and there is no relation- 40.9.3 Contracts
ship between these two terms. The defendant pleads A contract requires free full consent and is void if an
that his or her behaviour was automatic at the time of individual was of unsound mind at the time of making
the offence (i.e. no mens rea/guilty mind or no decision the contract.
making). Automatism refers to unconscious, involuntary,
non-purposeful acts where the mind is not conscious of
what the body is doing. There is a separation between the 40.9.4 Marriage
mind and the act. Sane automatism is a once-only event,
resulting from external causes, for example, hypoglycae- Being a contract, marriage is void if an individual had
mia caused by insulin. Insane automatism is caused by a mental disorder at the time of marriage such that the
diseases of the mind such as mental illness or brain dis- nature of the contract was not appreciated at that time.
ease (intrinsic factors), for example, epilepsy, dissociative A marriage may be annulled for any of the following
fugue states, and sleepwalking and night terrors in slow- reasons:
wave sleep. Insane automatism tends to recur. Voluntary
intoxication by itself does not constitute a defence. • The partner has a mental disorder at the time of
marriage so as not to appreciate the nature of
40.8.6 Outcome of Sentencing the contract.
The outcome of sentencing of mentally abnormal offend- • One partner did not disclose that he or she suf-
ers in England and Wales is shown in Tables 40.3 and 40.4. fered from epilepsy or a communicable venereal
disease.
• Either party was under 16 years at the time of
40.9 CIVIL ASPECTS
marriage.
40.9.1 Testamentary Capacity • Pregnancy by another male at the time of mar-
riage was not disclosed.
This is considered in Chapter 11. • There was non-consummation.
• One of the partners was forced to agree to the
40.9.2 Tort marriage by duress.
A mentally disordered person is considered incapable of
committing a tort (a civil wrong to an individual or to the Readers are advised to refer to Table 76.10 in Treasaden
reputation or estate of an individual) unless the disorder (2011a). The table provides an excellent summary on
did not preclude an understanding of the nature or prob- the civil treatment orders under the Mental Health
able consequences of the act. Act (1983).
TABLE 40.4
Forensic Treatment Orders for Mentally Abnormal Offenders
Eligibility for Appeal
Medical Maximum to Mental Health
Grounds Made by Recommendation Duration Review Tribunal
Section 35—Remand Mental disorder Magistrate’s or Any doctor 28 days; renewable
to hospital for report Crown Court at 28 day intervals;
maximum 12 weeks
Section 36—Remand Mental disorder (not Crown Court Two doctors: one 28 days; renewable
to hospital for if charged with approved under at 28 day intervals;
treatment murder) Section 12 maximum 12 weeks
Section 37—Hospital Mental disorder— Magistrate’s or Two doctors: one 6 months; During second
and guardianship accused or convicted Crown Court approved under renewable for 6 months; then every
orders (Section 37(3) of an imprisonable Section 12 further 6 months year; mandatory
without conviction) offence and then annually every 3 years
Section 41— Added to Section 37 Crown Court Oral evidence from Usually without limit As Section 37
Restriction order to protect public one doctor of time; effect—
from serious harm leave, transfer, or
discharge only with
consent from the
Justice Secretary
Section 38—Interim Mental disorder— Magistrate’s or Two doctors: one 12 weeks; renewable None
hospital order for trial of Crown Court approved under at 28 day intervals;
treatment Section 12 maximum 12
months
Section 47—Transfer Mental disorder Justice Secretary Two doctors: one Until earliest date of Once in the first
of sentenced approved under release (EDR) 6 months; then once
prisoner to hospital Section 12 from sentence in the next 6 months;
thereafter, once a year
Section 48—Urgent Mental disorder Justice Secretary Two doctors: one Until date of trial or Once in the first
transfer to hospital approved under sentence 6 months; then once
of remand prisoner Section 12 in the next 6 months;
thereafter, once a year
Section 49— Added to Section 47 Justice Secretary Until end of Section As for Sections 47
Restriction direction or Section 48 47 or 48; and 48 to which it is
effect—leave, applied
transfer, or
discharge only
with consent of
Justice Secretary
Source: Puri, B.K. and Treasaden, I.H., Psychiatry: An Evidence-Based Text, Hodder Arnold, London, U.K., 2011.
CASC STATION ON STALKING

You are the registrar in forensic psychiatric service. The police has asked you to see a 35-year-old man who was
arrested for stalking on a female nurse with threats to harm her.
Task:
1. Assess his stalking behaviour

2. Perform a risk assessment
3. Explain your management
(A1) Ask the

(A) Assess Person to
Stalking Describe Stalking (A2) Unsolicited (A5) Assess
Behaviour Behaviour Telephone Calls (A3) Electronic Mail (A4) Gifts Motive
‘Hello, I am Dr. ‘Do you know her ‘Do you know her ‘Have you sent any ‘Why do you
Trench. Can you phone number? email address? How gift to her? If yes, need to take
tell me why you are How often do you often do you send what kinds of gifts the above
under the police call her?’ her an email?’ did you send? actions? Do
custody at this ‘Do you call her ‘Did she respond to How often do you you want to
moment?’ constantly even your email? How do send her a gift?’ be close to
‘What is your though she does not you feel if she does ‘Has she rejected her?’
relationship with respond to your not respond? Do you your gift? How do ‘From your
the nurse? What call?’ continue to send you feel after that? views, how
have you done to ‘Do you usually emails if she does Were you upset? If does your
her so far?’ leave a voice mail? not respond?’ you were upset, behaviour
‘What is her name?’ Would you mind to ‘Would you mind to what would you affect her
‘Do you feel tell me the content tell me the content of do next?’ life?’
desperate for her?’ of the message?’ the message?’ ‘Do you feel
‘Did she encourage sorry for
you to follow her?’ her?’
(B) Risk (B5) Harm
Assessment (B1) Plan (B2) Threats (B3) Violence (B4) Self-Harm on Others
‘Are you planning to ‘Do you plan to harm ‘Have you ever ‘Have you ever ‘Has anyone
do something to the her? If yes, what applied force on her? thought of tried to stop
nurse? If yes, would would you do?’ What was her harming yourself? you
you mind to tell me ‘Is this part of your reaction? Did she Have you ever following
the details?’ fantasy?’ defend herself? Will thought of ending her? If yes,
you do it again in the your life?’ what did
future?’ you do? Do
you carry a
weapon?
Will you
use it to
harm those
who try to
stop you?’
(continued)
(C3) Intimacy (C5) Insight of

(C) Four Types (C1) Incompetent (C2) Rejected Seekers and (C4) Resentful Current
of Stalkers Stalker Stalker Erotomania Stalker Problem
‘Did you encounter ‘When you are ‘Are you in love with ‘Have you tried to ‘You have done
any difficulty in ignored or rejected her?’ frighten her?’ a lot in
having a by the nurse, how ‘Do you think she is ‘Are you taking following her.
relationship in the do you feel?’ love with you? How revenge on her’ Do you feel
past?’ ‘Do you feel that about the future? Do stressed?’
‘Does the nurse both of you were in you think she will ‘Do you want
remind you of the a relationship?’ love you?’ to continue
unpleasant past?’ ‘Do you hope to ‘How certain you are this
reconcile by that she is in love behaviour?
following her?’ with you? Could it Have you
be a thought of
misunderstanding?’ changing
‘Do you have sexual yourself?’
feelings towards ‘Do you think
her?’ that you need
treatment?’
(D) Background (D1) Forensic (D2) Past (D3) Substance (D5) Organic
History History Psychiatric History Misuse (D4) Personality Causes
‘Did you have ‘How is your mood ‘How often do you ‘How do your ‘Have you
trouble with the at this moment?’ drink?’ friends describe ever had a
police in the past? ‘Have you ever felt ‘What kind of alcohol you as a person?’ head injury?
If yes, what was the high in the past? If do you drink?’ ‘Are you concerned If yes,
reason? Were you yes, did have high ‘What would you do about safety of which part
charged sexual drive? Were if you are drunk?’ other people in of the brain
subsequently?’ you more ‘What would happen general?’ was
(Explore past impulsive?’ if you do not drink ‘Are you a honest affected?’
history of violent ‘Do you have any for a day?’ person?’ ‘Did you
behaviour and unusual experience ‘Do you use any ‘How do you have fits
sexual offences.) such as hearing recreational drug compare yourself before?’
‘Did you break any voices in the past? before?’ with other ‘Do you have
court order in the If yes, what did the people? Are you other
past?’ voices say to say? entitled to be medical
Do they give you treated specially? problems
instruction to follow Was it a blow to such as
her?’ your ego when diabetes?’
‘Did you receive any the nurse rejected
psychiatric you?’ (narcissistic
treatment?’ personality and
narcissistic
injury)
(E) Explain (E1) Biological (E2) Psychological (E3) Social

Management Treatment Treatment Management (E4) Legal (E5) Victim
‘Thanks for sharing ‘I can refer you to ‘I will also refer you ‘Do you have a ‘Will you look for
with me. I see a psychologist to see a social lawyer her again if you
understand that you for psychotherapy. worker who will representing you are released from
have gone through I would recommend address your social at this moment? here? She is also
a lot of stress. I cognitive and occupational The court will under tremendous
would like to share behavioural therapy needs in long run’. decide whether the stress. Would you
with you some of (CBT). It will help treatment will take mind to cancel
the treatment you to change your place in a hospital your plan to visit
which I can offer to behaviour and you or in the her? Do you have
you. Are you will be more community’. other concerns?’
interested to hear sympathetic to the
about it? There are nurse’.
medications like
antidepressants,
mood stabilizers or
antipsychotic
which could help
you’.
40.10 PRISON PSYCHIATRY Nussbaum D, Hancock M, Turner I, Arrowood J, and Melodick S.

2008: Instruments, and cross-validation of the Nussbaum
Readers are advised to refer to Treasaden (2011a). This chap- fitness questionnaire fitness/competency to stand trial: A
ter provides an excellent summary of prison psychiatry. conceptual overview, review of existing. Brief Treatment
and Crisis Intervention 8(1):43–72.
Puri BK, Brown R, McKee H, and Treasaden, IH. 2012: Mental
REFERENCES Health Law Handbook, 2nd edn. London, U.K.: Hodder
Arnold.
Chiswick D and Cope R. 1995: Seminars in Forensic Psychiatry. Puri BK and Treasaden IH. 2011: Psychiatry: An Evidence-Based
London, U.K.: Gaskell. Text. London, U.K.: Hodder Arnold.
Coid J. 1986: Alcohol, rape and sexual assault: Socioculture Royal College of Psychiatrists. 2006: Good psychiatric practice:
in alcohol related agression. In Brain PF. Alcohol and Confidentiality and information sharing. Council Report
aggression. London, U.K.: Croom Helm. CR133.
Cooper JE. 2001: ICD – 10 Classification of Mental and Sims A. 2002: Symptoms in the Mind: An Introduction to Descriptive
Behavioural Disorders with Glossary and Diagnostic Psychopathology, 3rd edn. London, U.K.: Saunders.
Criteria for Research. London, U.K.: Churchill Livingstone. Stone JH, Roberts M, O’Grady J, Taylor AV, and O’Shea K.
Faulk M. 1988: Basic Forensic Psychiatry. Oxford, U.K.: 2000: Faulk’s Black Forensic Psychiatry, 3rd edn. Oxford,
Blackwell. U.K.: Blackwell Science.
Gelder M, Mayou R, and Cowen P. 2001: Shorter Oxford Textbook Taylor PJ and Gunn J. l984: Violence and psychosis. I: Risk of
of Psychiatry. Oxford, U.K.: Oxford University Press. violence among psychotic men. British Medical Journal
Johnstone EC, Cunningham ODG, Lawrie SM, Sharpe M, and 288:1945–1949.
Freeman CPL. 2004: Companion to Psychiatric Studies, Treasaden I, 2011a: Forensic psychiatry. In Puri BK and
7th edn. London, U.K.: Churchill Livingstone. Treasaden I (eds.) Psychiatry: An Evidence-Based Text,
Kingham M and Gordon H. 2004: Aspects of morbid jealousy. pp. 1153–1213. London, U.K.: Hodder Arnold.
Advances in Psychiatric Treatment 10:207–215. Treasaden IH. 2011b: Forensic psychiatry. In Puri BK and
McDonald DA, Nussbaum DS, and Bagby RM. 1991: Treasaden IH (eds.) Textbook of Psychiatry, 3rd edn, pp.
Reliability, validity and utility of the Fitness Interview 391–426. Edinburgh, U.K.: Churchill Livingstone.
Test. Canadian Journal Psychiatry 36(7):480–484. Whitman S, Coleman TE, Patmon C et al. l984: Epilepsy in
Mullen PE, Pathé M, and Purcell R. 2001: The management of prisons: Elevated prevalence and no relationship to vio-
stalkers. Advances in Psychiatric Treatment 7:335–342. lence. Neurology 34:775–782.
41 Preparation for Psychiatric
Examinations
Preparation for the various parts of the MRCPsych • Try to keep up with a good selection of journals.
examination or similar psychiatric examinations should Try to make a habit of at least skimming the
ideally begin early during one’s psychiatric higher titles and abstracts of relevant papers published
training. This brief chapter mentions some important in journals such as
key points that should enable a candidate to perform well • American Journal of Psychiatry
in these examinations: • JAMA Psychiatry
• British Journal of Psychiatry
• Familiarize yourself with the format of the • Lancet
examinations. Always check the latest version • New England Journal of Medicine
of the examination regulations.
• Particularly early on during your training, it is If you are interested in biological psychiatry, then
invaluable to clerk as many patients as you can, Nature Neuroscience Reviews is an excellent source of
including in the psychiatric subspecialties. Try to high-quality up-to-date erudite review papers.
find suitable opportunities to present such cases, for
example, in ward rounds and at case conferences. • Make it a regular habit to attend (and present at)
• Being on call in a busy psychiatric rotation can journal clubs and relevant research meetings.
offer an excellent opportunity to see a wide vari- • There are many books and online sources of
ety of different patients and to make numerous multiple-choice questions, extended matched
clinical decisions that cause you to learn about items, etc. Obtain those of a high quality,
or revise your knowledge of different conditions preferably sources that give explanations to
and different treatments. Rather than avoiding the answers, and try to work through these
the busiest jobs on the rotation, you might wish diligently. Whenever you make a mistake, go
to consider volunteering for those placements, back and reread the corresponding textbook
seeing them as valuable learning opportunities. material until you understand the relevant
• Try to begin your study of suitable textbooks as subject matter.
early as possible during your training. • In the 6 months leading up to a clinical exam-
• There may be good courses available locally. ination, try to find the opportunity to see and
You should supplement the course material with present cases under examination conditions to
detailed textbook learning. senior colleagues.
741
Psychiatry
Revision
notes in
PsychiatRy
Third EdiTion
Revision Notes in Psychiatry, Third Edition continues to provide a clear and contemporary summary of
clinical psychiatry and the scientific fundamentals of the discipline. It is an essential study aid for all those
preparing for postgraduate examinations in psychiatry and a superb reference for practising psychiatrists.
Structured to follow the entire MRCPsych exam syllabus, the book covers the key areas in Papers 1, 2,
and 3, along with the CACS examination. Fully updated with recent references and many additional
figures, this third edition features a wealth of new material (including NICE guidelines) and updates the
DSM-IV-TR criteria to the new DSM-5.
Designed to meet the needs of today’s candidates, Revision Notes in Psychiatry, Third Edition continues
to provide a source of trusted expert information to ensure examination success for all those taking higher
examinations in psychiatry.
BasaN t K. PuRi, MA, PhD, MB, BChir, BSc (Hons)

MathSci, DipStat, PG Dip Maths, MMath, FRCPsych,
FSB, Hammersmith Hospital and Imperial College
London, UK
aNNi E Hall, BA, MB BCh, MRCPsych,

South Kensington and Chelsea Mental
Health Centre and Chelsea and Westminster Hospital,
London, UK
Ro gER Ho, MBBS, DPM, DCP, Gdip Psychotherapy,

MMed (Psych), MRCPsych, FRCPC, Department of
Psychological Medicine, National University of Singapore
K18182
ISBN-13: 978-1-4441-7013-9
90000
9 781444 170139

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Chapter 1 Descriptive Psychopathology.....................................................................................................................1

1.8.5 Disorders of Consciousness..............................................................................................10

2.5.1.11 DSM-IV-TR and DSM-5: Eating Disorders......................................................23

Chapter 3 Basic Psychology......................................................................................................................................25

3.1.6.5 Secondary Reinforcement................................................................................28

Chapter 4 Social Psychology.....................................................................................................................................57

4.2.2 Self-Perception Theory....................................................................................................58

Chapter 5 Human Growth and Development............................................................................................................63

5.3.7.2 Physical Abuse/Nonaccidental Injury..............................................................66

Chapter 6 Description and Measurement.................................................................................................................83

6.4.6.4 Wisconsin Card Sort Test.................................................................................96

Chapter 7 Cognitive Assessment and Neuropsychological Processes.................................................................... 103

7.6 Alexia and Agraphia....................................................................................................................107

Chapter 8 Social Sciences and Stigma.................................................................................................................... 115

Chapter 9 Dynamic Psychopathology and Psychoanalytic Theories......................................................................129

9.2.10 Psychosexual Development............................................................................................ 133

9.6 Psychodynamic Theory of Defence Mechanisms.......................................................................136

Chapter 10 History of Psychiatry.............................................................................................................................. 139

Chapter 11 Basic Ethics, Principles of Law, and Philosophy of Psychiatry............................................................. 145

Chapter 12 Neurology and Neurological Examination............................................................................................. 159

12.2.4 Medial Longitudinal Fasciculus..................................................................................... 161

Chapter 13 Neuroanatomy........................................................................................................................................ 175

13.2.2 Neuroglia........................................................................................................................ 176

13.9.1.2 Hippocampus.............................................................................................. 182

13.12.2.2 Lateral........................................................................................................ 188

Chapter 14 Neuropathology...................................................................................................................................... 195

14.3.1.2 Brain Length................................................................................................... 198

Chapter 15 Neuroimaging Techniques.....................................................................................................................205

15.4.2 Type of Imaging.............................................................................................................206

16.3.6 Hunger............................................................................................................................ 213

Chapter 17 Neurochemistry...................................................................................................................................... 219

Chapter 18 General Principles of Psychopharmacology..........................................................................................237

Chapter 19 Psychotropic Drugs and Adverse Drug Reactions................................................................................. 251

20.16 Linkage Analysis.......................................................................................................................266

Chapter 21 Psychiatric Epidemiology.......................................................................................................................277

21.1.3 Population at Risk..........................................................................................................277

22.2.2.2 Calculation of χ2.............................................................................................307

Chapter 23 Research Methodology and Critical Appraisal...................................................................................... 313

23.3.5.1 Definition................................................................................................... 316

Chapter 24 Physical Therapies.................................................................................................................................. 321

24.5 Complications of ECT.................................................................................................................326

Chapter 25 Advanced Psychological Process and Treatment................................................................................... 331

25.2.12 Research and Brief Psychodynamic Therapy................................................................ 335

25.8.4 Types of Family Therapy.............................................................................................343

Chapter 26 Schizophrenia and Delusional Disorders............................................................................................... 351

26.5.9.2 Cross Sectional Measures............................................................................366

26.9 Schizoaffective Disorders............................................................................................................373

Chapter 27 Mood Disorders, Suicide, and Parasuicide............................................................................................377

27.4.8.2 Bipolar Disorder.............................................................................................390

Chapter 28 Neurotic and Stress-Related Disorders..................................................................................................405

28.4.2.1 Genetic Factors...............................................................................................407

28.7.2.4 Psychological Factors.................................................................................. 417

Chapter 29 Personality Disorders............................................................................................................................. 437

29.6.5.4 Elicit Histrionic Personality Disorder in CASC............................................. 451

Chapter 30 Cross-Cultural Psychiatry...................................................................................................................... 459

Chapter 31 Liaison, Organic, and Neuropsychiatry.................................................................................................469

31.5 Hepatology and Psychiatry.......................................................................................................... 475

9.6 Psychodynamic Theory of Defence Mechanisms.......................................................................136

HMSN Hereditary motor and sensory oxime

PE Physical examination SNRI Serotonin–noradrenaline reuptake

1.5 ABNORMAL BELIEFS AND to a delusion that a person known to the patient

FIGURE 1.7 Negative autoscopy. 1.6.2.3 Pseudohallucinations (Coined

1.7 DISORDERS OF SELF-AWARENESS • Psychogenic amnesia. This is a part of the

2.1 HISTORY OF CLASSIFICATION SCHEMES • Adynamias

DSM-III was revised (and corrected) and pub- 2.4.2 Schizophrenia, Schizotypal,

2.4.6 Disorders of Adult Personality F98

2.5.1.1 DSM-IV-TR and DSM-5: Disorders Usually

sychotic disorder associated with another

• Mood disorders 2.5.1.8 DSM-IV-TR and DSM-5:

301.2 Schizoid personality disorder 2.5.4 Axis IV: Psychosocial and

3.1.6 Concepts of Extinction and Reinforcement In a fixed ratio schedule, reinforcement occurs