Strub Black Mental Status

THE MENTAL STATUS
EXAMINATION IN
NEUROLOCY
FOURTH EDITION
Richard L. Strub, MD
Chairman, Department of Neurology
Ochsner Clinic
Clinical Professor of Neurology
Tulane University
New Orleans, Louisiana
F. William Black, PhD

Professor of psychiatry and Neurology
Director, Neuropsychology Laboratory
Tulane University Medical Center
New Orleans, Louisiana
Foreword by Norman Geschwind

Illustrations by Ann Strub
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library of Congress Cataloging-in-Publication Data
Strub, Richard L., 1939The mental status examination in neurology / Richard L. Strub, F.
William Black: foreword by Norman Geschwind : illustrations by Ann
Strub. - 4th ed.
p.
cm.
Includes bibliographical references and index.
ISBN 0-8036-0427-0 (alk. paper)
1. Mental status examination. 2. Neurobehavioral disordersDiagnosis. I. Black, F. William. II. Title.
[DNLM: 1. Neurologic Examination. 2. Delirium, Dementia,
Amnestic, Cognitive Disorders-diagnosis. 3. Nervous System
Diseases-diagnosis. 4. Neuropsychological Tests. WL 141 S925m
1999)
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FOREWORD
The testing of mental status has a curious, not to say anomalous, position
in the examination of patients. Every medical student has had the experience
of being given a long and detailed outline, or an even longer booklet, containing a seemingly endless list of items. Even if he should go to the trouble
of memorizing these miniature compendia, he is likely to discover that his
teachers, both neurologic and psychiatric, are disinclined to be concerned
with the detailed examination, and often rely, at best, on fragments. The
examinations themselves seem to differ from those in other fields of medicine. The student rapidly comes to appreciate the direct relevance of rectal
tenderness to the diagnosis of appendicitis or of pulsus paradoxus to pericardial effusion. The mental examination seems to him to be much more
indirectly and diffusely related to diagnostic categories.
Equally striking, or even more so, is the usual lack of direct correlation
. between the test items and disorders of structure or physiology. Orthopnea,
swollen neck veins, rales at the lung bases, cardiac enlargement, characteristic
murmurs, and auricular fibrillation not only mean congestive failure, but all
the findings on examination come to blend almost imperceptibly and effortlessly with knowledge of normal cardiac structures and physiology and awareness of lawful derangements in disease. This easy understanding of the relationship of abnormal findings on examination to anatomy and physiology
seems to be lacking in the mental examination.
There is, however, no reason that this situation should persist. The
growth of knowledge concerning disorders of the higher functions has been
rapid over the past quarter century. Not only has our ability to specify anatomic systems involved in different behaviors increased, but even more important, we have come to a deeper understanding of the mechanisms underlying disordered function.
This book, therefore, represents a valuable synthesis. For the attentive
reader, it will yield important advantages. Not only does it shift the emphasis
V
vi
THE MENTAL STATUS EXAMINATION IN NEUROLOGY
to those methods of examination that have proven their worth in the clinic
but it provides wherever possible a link to known anatomic and physiologic
mechanisms.
Several final comments are appropriate. There is a widespread, usually
tacit but often openly expressed, view that mental examination is a long and
arduous task. Most physicians have learned that although a "complete" survey
of the heart, lungs, abdomen, and other structures can take hours, intimate
knowledge of the examination and repeated practice enable them to obtain
essential information in a very brief time. Those who have learned the mental
examination and have practiced it often can equally well obtain vital information rapidly and efficiently when necessary. There is another common view
that mental examination can be handed over to others. We should remember,
however, that the real measure of a physician's usefulness lies in his capacity
to make critical decisions when he is alone with the patient in the small
hours of the night. Furthermore, unless he can screen patients effectively, he
will fail to refer intelligently to others. Finally, if the ultimate decisions lie in
his hands, he will fail to use adequately the opinions of his consultants unless
he has a basic understanding of all aspects of his patient's problems. The
newer knowledge of mental examination set forth within this book is essential not merely to the neurologist or psychiatrist, but to all physicians.
Norman Geschwind, MD
James Jackson Putnam Professor of Neurology
Harvard Medical School
1977
PREFACE
The basic purpose and scope of this book have not changed since the first
edition was published in 1977. In the intervening years, we have gained considerable additional clinical experience with the mental status examination
and have standardized most of its sections. Some of the standardized items
have been compared with the objective data generated from formal neuropsychological tests. These comparisons have been very rewarding because the
mental status examination has been proved an accurate and valid method for
identifying and diagnosing organic brain disease as well as for describing
relative levels of functioning. Age-related norms are presented for most aspects
of the examination. These data are important because we have found that our
patients aged 70 and older do perform less adequately on some of the critical
items, especially new learning, than do the younger patients. This difference
is important to take into account when assessing the elderly for early dementia. False positive results can occur and must be minimized.
In the first edition, we assured the reader that after reading and using
the book he or she would be able to perform a brief screening examination.
It has been suggested that we provide more concrete guidelines for tailoring
the examination for brief administration. Therefore, in the summary section
of this edition, we have included some ways to use the examination as a
screening procedure, particularly in the extremely important areas of diagnosing dementia and differentiating between organic and functional disorders. A shortened form of the examination is presented, with standardization
for normals of various ages and for patients with Alzheimer's disease.
We have updated the references in all chapters; this is particularly the
case in those sections in which new studies have refined the neuroanatomic
and neuropsychological aspects of cognitive functions. The section on neuropsychological testing has been fully revised to include a survey of the most
commonly used tests, to drop some tests that have fallen from general use,
vii
viii
and to make this section more clinically relevant to both physicians and other
health-care providers and to psychologists.
In general, we feel that the earlier editions were good and have demonstrated their value in widespread clinical use. With each edition we have
tried to refine both the process of the examination and its clinical usefulness.
We hope this text will prove as useful to others who are interested in neurobehavior as it has been to our students, residents, and professional
colleagues.
RL
FW
STRUB,
MD
PhD
NEW ORLEANS, LA
BLACK,
CONTENTS
CHAPTER 1.
THE MENTAL STATUS EXAMINATION: A RATIONALE

AND OVERVIEW ..................................................................................... 1
CHAPTER 2.
HISTORY AND BEHAVIORAL OBSERVATIONS ........................................ 7
CHAPTER 3.
LEVELS OF CONSCIOUSNESS ............................................................... 29
CHAPTER 4.
AnENTION ......................................................................................... 40
CHAPTER 5.
LANCUACE ........................................................... 47
CHAPTER 6.
MEMORY ............................................................................................. 74
CHAPTER 7.
CONSTRUCTIONAL ABILITY ................................................................. 93
CHAPTER 8.
HICHER COCNITIVE FUNCTIONS ........................................................ 116
CHAPTER 9.
RELATED COCNITIVE FUNCTIONS ................................. 130
CHAPTER 10.
SUMMARY OF EXAMINATION ........................................................... 146
CHAPTER 11.
FURTHER EVALUATIONS ................................................................... 157
APPENDIX 1.
STANDARD NEUROPSYCHOLOCICAL ASSESSMENT

METHODS .......................................................................................... 166
APPENDIX 2.
MENTAL STATUS EXAMINATION RECORDINC FORM ............. 183

INDEX .................................................. 199
ix
THE MENTAL STATUS

EXAMINATION:
A RATIONALE
AND OVERVIEW
Human behavior is extremely complex and multifaceted. Because of its complexity, it is not surprising that brain disease or dysfunction can significantly
affect a patient's behavior in a variety of ways. Understanding this behavioral
disruption caused by brain disease is a substantial and often frustrating problem for the clinician faced with the tasks of diagnosis and management. Patients with organically related changes in cognitive or emotional behavior
have often fallen just outside the limits of traditional psychiatry and neurology. These borderline cognitive behavior changes have long been called organic brain syndromes, a general term that covers any possible behavior
change resulting from brain damage or dysfunction. In the American Psychiatric Association's Diagnostic and Statistical Manual of Mental Disorders, Fourth
Edition (DSM-N) , 1 such conditions are categorized as delirium, dementia, and
amnestic and other cognitive disorders. The DSM-IV classifies noncognitive
behavior changes, such as the personality disorder seen in patients with frontal lobe disease, as mental disorders due to a general medical condition. Neurologists now use the term neurobehavioral disorders to include both cognitive and noncognitive organically based behavior changes.
In the past several decades, particularly because of the focus on Alzheimer's disease, there has been a renewed interest in these organic syndromes.
It is now possible, owing to a greater understanding of these conditions, to
relate particular behavioral deficit patterns to specific diseases and to damage
in particular regions of the brain.
The magnitude and social impact of these neurobehavioral disorders are
enormous. These disorders are very common in the hospital and office practices of primary care physicians, neurologists, and psychiatrists. In clinical
1
practice, dementia, aphasia, and confusional states (delirium) are very commonly encountered. Primary organic brain disease accounted for at least 30%
of all first admissions to psychiatric hospitals in the 1950s,2 and this incidence is increasing. 3 Dementia is now the fourth leading cause of death in
the adult population in the United States, a trend that can only worsen as
the lifespan increases. Students should now be able to recognize the signs of
early dementia as readily as they do those of acquired immune deficiency
syndrome (AIDS) or congestive heart failure.
For examiners to understand organically based behavior changes adequately and to apply this understanding to individual clinical cases, they must
use a systematic behavioral examination called the mental status examination,
an orderly assessment of the important cognitive and emotional functions that are
commonly and characteristically disturbed in patients with organic brain disease.
WHEN SHOULD A MENTAL STATUS EXAMINATION

BE PERFORMED?
Because the mental status examination is not always included in a routine
neurologic evaluation, it is important that the clinician be able to determine
when inclusion of the mental status examination is appropriate. lust as the
patient with otitis extema does not routinely require an electrocardiogram,
the patient with a peripheral neuropathy does not usually need a full mental
status examination. Conversely, any patient who complains of memory or
other cognitive difficulties should receive a comprehensive mental status examination, just as the patient with a fever, headache, and stiff neck requires
an immediate computed tomography (Cf) scan and lumbar puncture.
Known Brain Lesions

Full mental status testing is definitely indicated for many patients. Patients with
known brain lesions such as tumors, trauma, or vascular accident should have
an initial screening mental status evaluation to document any cognitive or
emotional changes. Even with the current state of neurobehavioral knowledge, subtle behavioral deficits secondary to brain lesions are sometimes overlooked by the treating physician. Many patients with mild aphasias or memory deficits after craniotomy, increased irritability and decreased ability to
concentrate after head trauma, or marked emotional lability after infectious
neurologic disease are released from the hospital without adequate recognition of these cognitive and emotional deficits. Such patients frequently become emotionally frustrated, have difficulty with social readjustment, and are
unable to carry out the routine demands of home and vocation. Early recognition of the neurobehavioral sequelae of known brain lesions helps the
physician explain the totality of the patient's disability to the family and
employers. This prevents needless frustration on the patient's part, as well as
THE MENTAL STATUS EXAMINATION: A RATIONALE AND OVERVIEW
misunderstanding of the patient's behavior by family members. Such documentation helps immeasurably in planning social and vocational rehabilitation when indicated.
suspected Brain Lesions

Another large group of patients requiring mental status testing consists of
those in whom a brain lesion is suspected because of recent onset of seizures,
headaches, behavior change, or head trauma. Brain tumors, subdural hematomas, small infarcts, or cerebral atrophy may go undetected on the routine
neurologic examination, whereas the cognitive effects of these lesions are often readily apparent on a complete mental status examination. We have seen
a 46-year-old man who was admitted to the infectious disease isolation unit
because of fever, jumbled speech, and confusion. His admitting diagnosis was
"probable encephalitis." Mental status testing the morning after admission
revealed an aphasia rather than a confusional state. Because the finding of
aphasia is almost pathognomonic of significant left hemisphere disease, a left
carotid arteriogram was performed and a large subdural hematoma found.
With appropriate treatment (surgery), the patient had an uneventful and complete recovery. Because of the widespread use of noninvasive neuroimaging
techniques, particularly CT and magnetic resonance imaging (MRI), it is now
much less likely that a mass lesion would remain undetected in such a setting;
in patients in whom the diagnosis of neurologic disease is equivocat however, the mental status examination can be as specific in documenting a brain
lesion and indicating its location as the elicitation of Babinski's sign.
psychiatric patients
A full mental status examination should be performed on all psychiatric patients, particularly those whose psychiatric symptoms have appeared rather
acutely and are superimposed on a life history of normal emotional functioning. Patients with organic brain disease frequently initially present with
emotional and behavioral changes and come first to the attention of the
family physician or consulting psychiatrist. 3 This presentation is especially
characteristic of frontal and temporal tumors, hydrocephalus, or cortical
atrophy.
The most common emotional change seen in such patients is depression;
therefore, brain disease should be strongly suspected in any patient with a middleor late-life depression that is not clearly related to a recent emotional or social crisis
(i.e., adjustment disorder with depressed mood). In our clinical practice, we
have seen a number of patients being treated for an apparent depressive illness who have, in fact, demonstrated signs of primary organic disease on
mental status testing and subsequent neurodiagnostic procedures (e.g., CT,
MRI, and neuropsychologic evaluation).
Although the differentiation between psychiatric and organic disease is

critically important, unfortunately it is sometimes difficult and not always
possible. The functionally depressed patient with psychomotor retardation
may perform poorly on some aspects of the mental status examination and
in this way superficially present the picture of a true dementia rather than a
pseudodementia. Other patients have elements of both organic and functional disease; for example, patients with early Alzheimer's dementia often
present with significant associated depression or anxiety. At times, considerable effort is required to separate the respective components, even on careful
clinical examination. The mental status examination is not infallible, even in
the hands of an experienced examiner. The fact remains, however, that most
of these patients with combined problems can be correctly classified if appropriate mental testing is done.
vague Behavioral Complaints

A final group of patients in whom mental status screening is extremely important is those who initially present, or are brought in by their families, with vague
behavioral complaints that are difficult clinically to substantiate and quantify
on standard neurologic examination.
Complaints such as memory problems, difficulty in concentration, declining interest in family or work, and various physical complaints having no
obvious organic etiology should alert the clinician to the possibility of organic
brain disease. The determination of the etiology of such problems involves a
difficult but important differentiation among functional, neurologic, and
other medical causes. Again, this can often be best accomplished with the aid
of data provided by the mental status examination.
HOW SHOULD A MENTAL STATUS

EXAMINATION BE PERFORMED?
Just as with any comprehensive medical examination, mental status testing
must be arranged systematically. The mental status examination differs somewhat in that it must be performed in a hierarchic manner, beginning with the
most basic function-level of consciousness-and proceeding through the
basic cognitive functions (e.g., language, constructions) to the more complex
areas of verbal reasoning and calculating ability.
When the patient shows impaired performance on early sections of the
examination (e.g., in language), it is difficult, if not impossible, for the examiner to assess accurately verbal memory (an extremely important function)
or any other function that requires language. Similarly, the inattentive patient
will miss important details during much of the higher-level testing, especially
on memory and calculation items. If the mental status examination is per-
THE MENTAL STATUS EXAMINATION: A RATIONALE AND OVERVIEW
formed in a haphazard manner, without regard for the hierarchic nature of

cognitive performance, erroneous conclusions can be drawn.
The mental status examination as presented in this book may seem exceptionally detailed, and it may appear that the examination would take
hours to complete in its entirety. This conception is similar to the beginning
clinician's first attempts to understand the evaluation of the cranial nerves or
the brachial plexus. When first learning to administer the examination, it is
wise to evaluate several patients fully, to gain experience in performing and
interpreting all test items. With time, the examination can be completed relatively rapidly (within 15 to 30 minutes) and will yield considerable valuable
data. In Chapter 10, we have summarized the examination and indicated
ways to tailor it to meet the demands of time and of specific patients.
In many cases, a brief examination will provide sufficient definitive data
to allow the correct diagnosis and appropriate medical treatment. As an example of the ease of administering a meaningful examination in a brief period of time, a psychiatrist, called in the middle of the night to see a patient
who was "talking out of his head," started to examine the patient's language
and found that the patient was actually aphasic and not psychotic. At this
point, the psychiatrist consulted with a neurologist, who admitted the patient
to the neurology service rather than to the psychiatric unit. In this case, the
psychiatrist had properly evaluated the patient and averted an inappropriate
type of hospitalization and treatment. We were called to see a similar case,
in which a young man had been admitted to the psychiatric service because
he was answering all questions inappropriately and did not make sense in
conversation. This behavior had initially disturbed his parents, who had
brought him to the emergency room. On evaluation, the patient had little, if
any, comprehension of language and was producing fluent paraphasic speech
(aphasia). An MRl scan revealed a large hematoma in the dominant temporal
lobe. His apparent "craziness" was due to a readily diagnosed organic disorder, and his psychiatric hospitalization had resulted from the admitting physician's lack of recognition of the patient's actual condition. In this case, demonstration of a typical pattern of aphasia not only indicated the presence of
organic disease, but also strongly suggested the location of the lesion.
These examples illustrate that even a brief examination by a skilled examiner can be of critical clinical importance for some patients. Other patients,
however, may require a more comprehensive assessment. The patient who is
referred after a head injury requires a detailed elucidation of cognitive
strengths and deficits to allow for appropriate social and vocational rehabilitation. This need for a comprehensive mental status examination is amply
demonstrated in the following case. The physical medicine service requested
a consultation on a 32-year-old woman who had suffered a severe basilar
skull fracture several months previously and was not progressing satisfactorily
in the inpatient rehabilitation program. The staff also noted her "difficult"
and "uncooperative" behavior. Mental status testing revealed an apathetic patient without insight or concern, who had moderately impaired attention.
Multiple significant cognitive deficits were demonstrated, including a mild
generalized dementia, moderately impaired recent and remote memory, severely impaired new-learning ability, and a moderate to severe impairment
of all higher-level cognitive functions (abstraction, calculations, and so forth).
The documentation of an organic behavior change and significant cognitive
deficits explained both the patient's difficult ward behavior and her inability
to participate fully in a demanding rehabilitation program. Her program was
restructured and her treatment goals were altered relative to the limitations
caused by her cognitive and behavioral deficits.
In complicated situations, when extensive and quantitative data regarding cognitive and emotional functioning are required for proper patient management, consultation should be obtained from relevant ancillary professionals. These frequently include neuropsychologists and speech pathologists. The
bedside or office mental status examination as outlined in this book is very effective
for diagnosing organic disease and for evaluating major areas of deficit. By its nature, the examination is qualitative and does not offer the advantages of standardized quantitative data, which are necessary in evaluating subtle deficits,
planning for comprehensive rehabilitation efforts, and assessing improvements in levels of functioning. The neuropsychologist can provide these data
and additional valuable consultation whenever a definitive evaluation is
required. Discharge planning and vocational or educational re-entry are
also greatly aided by the findings of a comprehensive neuropsychologic
assessment.
For patients with significant communication problems, referral to a
speech pathologist is important for comprehensive evaluation of language,
possible treatment, and counseling to facilitate communication between the
patient and other family members. Chapter 11 deals in detail with the specifics of the consultation process.
REFERENCES
1. American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders, ed
4 (DSM-IV). American Psychiatric Association, Washington, DC, 1994.
2. Malzberg, B: Important statistical data about mental illness. In Arieti, S (ed): American Handbook of Psychiatry, Vol 1. Basic Books, New York, 1959, pp 161-174.
3. Strub, RL: Mental disorders in brain disease. In Vinken PI. Bruyn, GW, and Klawans, HL (eds):
Handbook of Clinical Neurology, Vol 2, Neurobehavioral Disorders. Elsevier, New York, 1985,
pp 413-441.
CHAPTER
HISTORY AND
BEHAVIORAL
OBSERVATIONS
Most sections of the mental status examination involve the evaluation of

specific cognitive functions such as memory and language. Before beginning
formal testing, however, the examiner must obtain a clinical history and make
specific observations regarding the patient's physical appearance, mood, and
behavior. These observations provide important information for the interpretation of data from subsequent parts of the examination.
HISTORY
The histol}' should be directed toward four primal}' areas of clinical concern. First,
the presence or absence of the classic behavioral changes indicative of organic dysfunction (e.g., memory impairment or language disorder) must be established.
Second, the possibility of both adjustment and functional psychiatric disorders must
be considered. Although this book is primarily concerned with the changes
in emotions and behavior that are seen as a result of organic brain disease,
the consideration of classic psychiatric syndromes is important for several
specific reasons:
1. At times, a specific lesion of the brain (e.g., a tumor of the left frontal
lobe) may produce a clinical picture that is superficially indistinguishable from that of a major functional illness. 26 ,27 Diagnoses of depression or mania, schizophrenia, and personality disorders have all been
described in patients with brain disease. These diagnoses are classified
in the DSM-Wl respectively as mood disorder, psychotic disorder, and
personality change due to a general medical condition (not substanceinduced).
7
2. Patients with primary organic disease also commonly develop associated or secondary emotional symptoms such as depression, anxiety,
or paranoia.
3. Another important area in which the symptomatology of organic disease and that of emotional disorders overlaps is pseudo dementia, a
condition in which the patient has symptoms and mental status findings that initially suggest a diagnosis of dementia but eventually prove
to be secondary to depression, anxiety, or other psychiatric disorders.
4. Some patients with a major psychiatric disease (e.g., schizophrenia)
will demonstrate cognitive deficits on the mental status examination.
This may be due to a concomitant acquired brain lesion or may, in
fact, be a part of the total clinical picture of these diseases. The incidence of cognitive dysfunction in nonfamilial schizophrenic patients
is substantially higher than expected. When significant cognitive deficits are found in psychiatric patients, a neurodiagnostic evaluation
including a mental status examination should be conducted.
The third focus of the history is to establish the patient's premorbid behavior
and level of functioning. Information such as education and vocational history
are important for establishing expected levels of functioning on the mental
status examination. For example, the patient with a third-grade education and
an inconsistent low-level work history would not be expected to perform at
a high level on arithmetic or abstract reasoning tests.
The fourth area of importance is the patient's general medical status. Many
medical conditions such as endocrine diseases, chronic renal or hepatic disorders, acquired immune deficiency syndrome (AIDS), and chronic alcohol
or drug abuse adversely affect mental functioning. In some instances, particularly in elderly individuals, the use of multiple prescription and nonprescription medications can also deleteriously affect mental status. 16 When such
conditions do affect mental functioning, they usually produce a confusional
state, but they may mimic a dementia, depression, or other mental disorder.
It is very important to diagnose these conditions early, when they are often
completely reversible.
History Outline
The following elements in the history are particularly important in evaluating
a patient with behavior change. Because such patients may not be able to
provide a complete and accurate history, it is prudent to obtain the initial
information from a family member or other individual who is very familiar
with the patient. Even if the patient is able to give a history, corroborative
information from a second source is advisable to ensure accuracy.
HISTORY AND BEHAVIORAL OBSERVATIONS
1. Description of present illness

A. Nature and date of onset
B. Duration of illness
C. Description of behavioral change associated with illness
2. Other relevant organic behavioral symptoms
A. Unusual or bizarre behavior (e.g., nocturnal wandering)
B. Evidence of poor social judgment (e.g., discarding new clothes in
the trash or being verbally abusive at social gatherings without
provocation); this information should be obtained from someone
other than the patient
C. Attention and concentration problems
D. Language problems (e.g., word-finding difficulty, comprehension
deficits, or tangential verbal responses)
E. Reading, writing, or calculation difficulty (e.g., inability to balance
checkbook)
F. Memory difficulty (recent and remote)
G. Difficulty with geographic orientation (i.e., getting lost)
H. Trouble driving or carrying out simple activities such as using the
microwave or 1V remote control.
3. Psychiatric symptoms
A. Paranoia
B. Hallucinations
C. Delusions
D. Depression
E. Anxiety, agitation, or violence
F. Other
4. Past history
A. Previous neurologic disease or psychiatric problems
B. Other medical disease
C. Drug and alcohol use and abuse
D. Use of prescription medications and over-the-counter medications
E. Head trauma (comment on severity)
F. Seizures
G. Central nervous system infections
H. Toxic exposure
5. Birth and developmental history
A. Brain damage from birth
B. Developmental delays
(1) Motor
(2) Language
(3) Intellectual
( 4) Academic
(5) Emotional or social
10
6. Educational and vocational history

A. Highest school grade attained
B. Adequacy as a student
C. Vocation
(1) Types of jobs
(2) Frequency of job changes
(3) Recent problems with job
7. Family history
A. Neurologic or psychiatric disease in other family members
B. Familial neurologic disease (e.g., Huntington's disease, Alzheimer's disease)
C. Familial predilection for a particular disease process that may involve the central nervous system (e.g., hypertension and stroke)
BEHAVIORAL OBSERVATION
The primary purpose of this section is to provide a formal framework to assist
the examiner both in systematically observing behavior and obtaining reliable
and valid reports on the patient's behavior from other observers, such as the
spouse, children, and so on. A careful observation and report of behavior is
important because:
1. Several specific neurobehavioral syndromes (e.g., acute confusional
state [delirium], frontal lobe syndrome, and the denial-neglect syndromes) are diagnosed primarily on the basis of their behavioral
manifestations.
2. Such observations provide crucial data to aid in the differential diagnosis between organic and functional disorders.
3. A significant behavioral disturbance may dramatically interfere with
subsequent formal testing (e.g., a patient in an organic confusional
state will perform poorly on memory testing because of inattention).
The discussions of behavior in this chapter are primarily concerned with
the identification and description of organic disease (physical brain disease)
and its effects. Extensive discussions of behavior from a psychiatric viewpoint
are included in all major psychiatric texts (e.g., references 2, 13, 18, and 24).
See also Trzepacz and Bake~l for a thorough presentation of a comprehensive
psychiatrically oriented mental status examination.
Physical Appearance
Many patients with either brain disease or functional disorders show characteristic patterns of physical appearance. Classic examples range from that of the
patient with unilateral neglect who exhibits a total lack of attention to dress
and care (e.g., shaving and washing) one side of the body, to that of the
11
obsessive-compulsive patient who may be scrupulously groomed and unnecessarily fastidious in matters relating to cleanliness and manner. Obvious
neurologic signs such as hemiplegia or chorea are not specifically mentioned
in this text. The following aspects of appearance should be noted:
1. General appearance
A. Descriptive data
(1) Age
(2) Height and weight
B. General impression of appearance
(1) Appearance for chronologic age
(2) Posture
(3) Facial expression
(4) Eye contact
2. Personal cleanliness
A. Skin
B. Hair
C. Nails
D. Teeth
E. Beard
F. Indications of unilateral neglect
3. Habits of dress
A. Type of clothing
B. Cleanliness of clothing
C. Sloppiness in dressing
D. Excessive fastidiousness in dressing and grooming
E. Indications of unilateral neglect
4. Motor activity
A. Level of general activity
(1) Placid versus tense
(2) Hyperkinetic versus hypokinetic
(3) Evidence of psychomotor retardation (seen in the subcortical
dementias of AIDS, progressive supranuclear palsy, and so on)
B. Abnormal posturing
(1) Tics
(2) Facial grimaces
(3) Bizarre gestures
(4) Other involuntary movements
Mood and General Emotional status

Mood is the prevailing and conscious emotional feeling expressed by the
patient. Emotional status is a general term to indicate the patient's behavior;
it may be evaluated through direct observation of the patient during the examination. Certain brain diseases (e.g., frontal lobe disease), as well as some
12
psychiatric conditions, may be distinguished by rather characteristic disturbances of mood and emotional status. Such disturbances may adversely affect
performance on subsequent portions of the mental status examination. The
following outline is intended not to be a complete and definitive psychiatric
examination but rather to provide a framework for the brief assessment of
emotional status.
1. Mood
A. Normal for the situation
B. Sadness (hopelessness, grief, or loss)
C. Elation (inappropriate optimism or boastfulness)
D. Apathy and lack of concern
E. Constancy or fluctuations in mood
F. Inappropriate mood: expressed affect inconsistent with the content
of thought
2. Emotional status
A. Degree of cooperation with examiner
B. Anxiety
C. Depression
D. Suspiciousness
E. Anger and/or hostility
F. Specific inappropriate emotional responses to particular situations
G. Reality testing
(1) Delusions (false beliefs)
(2) Illusions (misperceptions of real stimuli)
(3) Hallucinations
( 4) Paranoid thinking
H. Indications of specific nonpsychotic emotional symptoms
(1) Phobias
(2) Chronic anxiety (generalized or specific)
(3) Obsessive-compulsive thinking, behavior, or both
( 4) Depression
(5) Mania
(6) Somatic preoccupation
(7) Dissociative symptoms
I. Abnormalities in language or speech
(1) Neologisms (personal formation of a new word without real
meaning except to the patient)
(2) Flight of ideas in thinking and speaking
(3) Loose associations in thinking and speaking
Clinical Syndromes
Several distinct clinical entities are recognized primarily through behavioral
observation rather than by specific cognitive testing. These syndromes pri-
13
marily involve disturbances in mood, personality, and emotional reaction

more than alterations in cognition. The diagnosis, therefore, is made by systematic behavioral observation.
Acute Confusional state (Delirium)

The most common of the neurologically based behavioral syndromes seen in
a general hospital population is the acute confusional state (also known as
delirium or toxic-metabolic encephalopathy). The acute confusional state has
a characteristic constellation of behavioral and historical findings. The onset
of symptoms is usually fairly acute, appearing over hours or days.
Generally, the most reliable clinical feature distinguishing the acute confusional
state from other organic or functional disorders is a clouding of consciousness. Although this term may seem somewhat vague, it does accurately describe the
mental state of the confused patient. Specifically, clouding of consciousness
refers to both a dulling of cognitive processes and a general impairment of
alertness. 25 These patients are inattentive and produce incoherent conversations that drift from the central point; they are inconsistent and confabulatory
in reporting recent events (e.g., patients may tell the examiner that they have
just come back from a walk with a friend when, in fact, they have been in
their hospital bed for the entire day); and they often demonstrate fluctuations
in their level of consciousness. Hallucinations (often visual) and agitation are
often present. Patients who are grossly confusional may be severely agitated
and shout incoherently; these patients usually require restraints to prevent
them from disrupting intravenous lines, urinary catheters, and other apparatus. Patients with mild confusion may appear normal superficially, but on
systematic examination may demonstrate mild degrees of inattention and
disorientation and may have difficulty holding a coherent conversation. On
specific questioning, they may admit to nocturnal hallucinations and delusions. Confusional behavior is rarely stable, characteristically waxing and
waning throughout the day and night. At night, when environmental stimuli
are reduced, the confusion and agitation often become accentuated.
The confusional state is a very important abnormal behavioral pattern to recognize because it is usually the behavioral manifestation of an acute medical problem
rather than of a neurologic or psychiatric condition. Toxic reactions to drugs
or drug withdrawal, sepsis, metabolic imbalance, or early heart, pulmonary,
or hepatic failure are common causes. Postoperative confusional behavior is
also extremely common. In general, elderly patients, especially those with
signs of early dementia, are the most likely to develop confusional states in
the aforementioned medical situations. 11 ,15,22
We have developed a delirium scale (Table 2-1) that can be particularly
. useful to house officers when they are first exposed to confusional patients.
This scale consists of the most common clinical features of the confusional
state. The examiner must determine the presence or absence of each feature
14
History
l. Speed of onset of behavior change
2. Fluctuation over 24 hours
3. Sleep-wake disturbances
4. Hallucinations (visual or tactile)
5. Inappropriate behavior
Clinical Features
6. Level of consciousness
7. Psychomotor activity level
8. Incoherence and disorganization
9. Attention
10. Intelligibility of speech
11. Misinterpretation of surroundings
12. Orientation
a. Time:
Year
Month
Date
Day
b. Place:
State Town
County Hospital
Scale: (3) 9-10, (2) 6-8, (1) 3-5, (0) 0-2
13. Construction ability-dock drawing
Total (39 maximum)
3
3
3
3
3
0
0
0
0
0
3
3
3
3
3
3
3
2
2
2
2
2
2
2
0
0
0
0
0
0
0
Season
Floor
3 is normal; 0 is grossly abnormal.
and judge its severity based on several variables. This scale has proved clinically reliable and valid and is useful in differentiating delirium from dementia
(Fig. 2-1).
Although psychiatrists or neurologists are often asked to see these patients because of their abnormal behavior or change in mental status, most
patients require primary medical treatment in addition to medication for behavioral control. The confusional state may linger for many days, even after
initiating appropriate medical treatment; during this period tranquilizers may
be used to calm the patient's agitation.
The confusional state usually results from widespread cortical and subcortical neuronal dysfunction. Cortical dysfunction causes an alteration in the
content of consciousness, whereas involvement of the ascending activating
system leads to the disturbances of basic arousal. With focal brain disease,
confusional behavior may also be seen. This is particularly true in the first
few days after an acute cerebrovascular accident (especially where medial temporallobe or inferior parietal or prefrontal cortex is involved) or in patients
who have brain tumors with associated increased intracranial pressure.
Further mental status testing results are adversely affected in patients in
a confusional state. Owing to inattention and general cortical dysfunction,
patients cannot perform adequately on memory, abstract reasoning, calculation, drawing, or writing tasks. 5 If the full test is performed while the patient
is confused, a misdiagnosis of dementia can easily be made inadvertently.
Because the changes in the brain are physiologic rather than structural, the
patient's level of functioning should eventually return to premorbid levels.
15
FREQUBNCY COUNT
10
20
15
25
30
35
40
T01I\.L SCORES
ALZ
DELIRIUM
FIG U R E 2 - 1. Distribution of total delirium scale scores of patients with Alzheimer's disease
versus patients with delirium. In a series of patients, patients with delirium scored an average of
20 points, whereas age-matched patients with Alzheimer's disease averaged 35.
However, the confusion is often slow to clear, and definitive mental status
testing to evaluate a possible underlying dementia should be postponed
accordingly.
Although the acute onset of inattention, agitation, fluctuating levels of
alertness, incoherent speech and train of thought, and visual hallucinations
is most often due to a medical condition, the differential diagnosis must
include various functional psychiatric disorders such as acute schizophrenic
episode, severe anxiety or panic state, agitated depression, and mania. Differentiating between the acute organic confusional states and acute severe
functional disorders is difficult but is usually done accurately with data provided from the patient's medical and psychiatric history, the medical examination, and some aspects of the mental status examination. Alterations in the
level of consciousness are almost invariably associated with organic brain
disease. Visual hallucinations are more typically seen in organic brain disease,
whereas auditory hallucinations are more common in functional psychoses.
Systematized delusions and organized paranoid ideation are infrequent in
patients in an acute confusional state. Whenever the etiology is unclear, the
psychiatrist, neurologist, and primary physician should work closely together
to conduct a full evaluation.
Frontal Lobe Syndrome

Patients with bilateral frontal lobe disease typically do not show dramatic cognitive
deficits on formal mental status testing but often demonstrate specific personality
16
changes. 3, 17 The most common features of the frontal lobe personality are
(1) apathy, demonstrated both during the examination and toward work
and family; (2) euphoria, with a tendency toward jocularity; (3) short-lived
irritability; and (4) social inappropriateness. 8
Some patients with frontal lobe disease are predominantly apathetic,
showing little interest in any aspect of their environment. 29 In such patients,
the apathy is sometimes misconstrued as depression, a common error by both
family and medical personnel. Although these patients are primarily apathetic, they may briefly become very irritable and argumentative when sufficiently stressed.
Conversely, other patients are primarily loud, jocular, inappropriately
intrusive, or socially aggressive. Because of their outgoing behavior, these patients may give the initial impression of interest and productivity. However,
this emotional disinhibition and euphoria does not result in constructive
activity. In general, patients with frontal damage have lost both their interest
in their environment and their productive social drive. Such patients often
fail to maintain job performance, normal family relations, or even personal
cleanliness. Because the frontal lobes are the areas of the brain in which
reason and emotion interact,20 bilateral damage may leave the individual with
apathy, unchecked emotions, and an intellect that lacks social and emotional
guidance. Other deficits that have been described in patients with frontal lobe
damage are higher-order cognitive problems, inattention, memory disorders,
and executive motor deficits. 17
Behavioral features of the frontal lobe syndrome vary from patient to
patient, depending partly on the locus of the lesion. Basal-orbital lesions
more frequently result in dis inhibited, euphoric behavior, with a lack of concern and quick irritability. In contrast, lesions involving the dorsolateral convexities tend to produce apathy, reduced drive, depressed mentation, and impaired planning. 28 See Damasio and Anderson for an excellent comprehensive
review of this topic. 7
The following are two clinical examples of patients with frontal lobe
syndromes.
Mrs. L, a 58-year-old housewife, was brought to the hospital by her daughter, who
reported that for the past year her mother had shown a decreased interest in caring
for her house and personal needs. The patient lived alone in a rural area with few
neighbors. The daughter, during an infrequent visit, had noticed a change in her
mother's behavior; she showed a lack of interest in conversation and had an unkempt appearance, with a lack of concern about family affairs and total neglect of
personal and household cleanliness. Neighbors had noticed that the patient had
stopped attending church, did very little shopping, and no longer made social visits.
On examination at hospital admission, Mrs. L was awake but markedly apathetic. She
offered no spontaneous conversation and answered all questions with only singleword responses. She walked with a slow, shuffling gait and had several episodes of
17
incontinence. Neurodiagnostic evaluation (computed tomography [CTl scan) demonstrated a large frontal cyst. Surgical exploration with drainage produced a marked
behavior reversal. Within 2 weeks, the patient was walking well, was conversing spontaneously, and was no longer apathetic or incontinent. Mrs. L represented the primarily apathetic variation of the frontal lobe syndrome.
The next case demonstrates the disinhibition, social inappropriateness,

and jocularity that may be associated with the underlying apathy in some
patients with this syndrome.
Mr. N was 65 years old when his wife brought him to the hospital. Her chief complaint was that her husband's mind was deranged. She stated that her husband had
always been a great joker, but had used proper social restraint until about 4 or 5
years ago, when he had begun to show excessive candor in his remarks to friends
and acquaintances. His usual outgoing personality gave way to flippancy and arrogance. His prior restraint was decreased, and he approached each social situation
with an almost aggressive egotism, with much showing off and boasting. Over the
past years, he had lost regard for his personal cleanliness, bathing and shaving only
at his wife's behest. His wife also reported that his memory had started to fail and
that he confabulated on occasion. At one point, she had bought a new lawn mower
and brought it home with the handle disassembled. She had asked him to put the
handle together and to put it on the mower; he had been totally unable to do so.
Later in the course of his disease, Mr. N became quite agitated and paranoid. He
wandered around the neighborhood and often told strangers fantastic tales, the
most recent being that he "was an undercover agent for the FBI." Hisjudgment in
other matters also deteriorated. The last time he drove the car, he went through a
stop sign and joked about it with his wife. These latest events prompted his referral
to the hospital.
Examination revealed an inattentive, restless, socially inappropriate man who was
physically unkempt with uncombed hair, uncut fingernails and toenails, and messy
clothes. He exhibited some paranoia, asking if his medicine (Thorazine) was some sort
of poison. Several times during the examination he attempted to leave the room and
was obviously agitated. His thought processes were extremely concrete, and he performed poorly on virtually all aspects of the mental status examination.
During the hospital period, he became quite upset and irritable, especially at
night, and was somewhat aggressive with several nurses. The CT scan revealed frontotemporal atrophy with greatly enlarged frontal horns and widened sulci. The presumptive clinical diagnosis in this case was Pick's disease. He died several years later,
and the autopsy verified the diagnosis.
If the behavioral manifestations of the frontal lobe syndrome are present,

certain neurologic diseases should be considered in the differential diagnosis:
(1) tumors-subfrontal meningiomas, pituitary adenomas, or primary brain
18
tumors; (2) head trauma with frontal contusions; (3) Pick's disease; (4) general paresis; (5) communicating hydrocephalus; (6) Huntington's disease; and
(7) AIDS. Any patient with extensive cortical disease (e.g., late Alzheimer's
disease, multiple cortical infarcts, or traumatic or postinfectious encephalopathy) exhibits some of the behavior changes seen in patients with frontal lobe
disease. However, such patients also show evidence of severe cognitive dysfunction and other indications of pathologic involvement of other brain areas. Interestingly, after mild to moderate closed head injury with frontal lobe
contusion, the subsequent behavioral change in certain patients is seen by
family members as positive. During the past several years we have seen a
number of young adult patients (usually, but not always, male) whose parents
and spouses describe "improvements" in mood, reaction to environmental
stress, and interactional style after head injury. Unfortunately, the opposite
reaction is far more likely.
Disease of the frontal lobes may be difficult to evaluate clinically because
of the relative absence of clear-cut cognitive changes associated with lesions
in this region. 3 ,30 However, some clinical tests, primarily "go-don't go" and
alternating motor sequencing tasks, can be used to assess frontal lobe function. Luria 19 and others have shown that patients with extensive frontal lobe
disease have an impaired ability to perform these tasks.
Alternating Sequences-Visual Pattern

Completion Test
DIRECTIONS:
Present the patient with the visual patterns from Figure
2-2 on individual sheets of white paper. Tell the patient to reproduce the
stimulus figure and then to continue the alternating sequence. If necessary,

give additional elaboration of the directions to ensure that the patient understands the nature of the test. Do not correct any errors or provide additional cues after the patient begins the task.
SCORING: Patients with intact motor and sensory systems should be able
to complete these sequences without error. A loss of the sequence or perseveration in the reproduction of sequences suggests a loss of the ability to move
from one motor movement to another and an inability to shift sets efficiently.
Examples of common errors are shown in Figure 2-3.
Alternating Motor Patterns Test

DIRECTIONS: This test consists of a series of changes in hand position.
They have been adapted from Luria 19 and are described in greater detail in
that source.
1. Fist-Palm-Side Test: Tell the patient to hit the top of the desk repeatedly, first with a fist, then with an open palm, and then with the side
of the hand. Demonstrate the task once, and then tell the patient to
19
+0++0+++ 0
FIG U R E 2 - 2. Test items for the Visual Pattern Completion Test.
perform the task until told to stop. Performance for 15 to 20 seconds

should suffice to assess the adequacy of these alternating movements.
2. Fist-Ring Test: Instruct the patient to extend his or her arm several
times, first with the hand in a fist, and then with the thumb and
forefinger opposed to form a ring. Demonstrate the action, and then
tell the patient to perform the action. With successive extensions of
the arm, the patient alternates between these two positions.
3. Reciprocal Coordination Test: This alternation test uses both hands.
Initially the patient places both hands on the desk, one in a fist and
one with the fingers extended palm down. Tell the patient to alternate
the position of the two hands rapidly (simultaneously extending the
fingers of one hand while making a fist with the other). Demonstrate
the task.
SCORING: Normal individuals should have no difficulty in easily mastering these alternating sequences after one or two attempts. 19 Therefore, any
appreciable disruption of the smooth performance of these tasks indicates
dysfunction of the premotor areas of the cerebral cortex.
20
+04 b++t\CXXIbO 0
00
~o-K-DO-\ \ ~ COO ~
FIG U R E 2 - 3. Common errors in the Visual Pattern Completion Test.
21
Denial and Neglect

In some patients, a brain lesion may produce a striking degree of denial of
illness. The following case is an excellent example:
A surgeon was finishing an operation when his assistant noticed that the surgeon's
left arm had suddenly become weak and his speech slurred. The surgeon was immediately put on a stretcher and was brought to the intensive care unit, where one of
us saw him within minutes. The patient's arm and face were still weak, but, when
asked, he replied, "It is OK." When his weakness was specifically pointed out to him,
his comment was, "I really don't recognize any weakness."
This degree of denial seems to result not from a strengthening of normal

psychologic defense mechanisms but rather from a more basic and unusual
organic behavior change. Clinically the spectrum of denial and neglect syndromes ranges from explicit denial of illness (e.g., the foregoing example), as
the most severe behavioral abnormality, to a mild inability to recognize stimulation on one side of the body during bilateral simultaneous stimulation
(inattention or extinction). The patient with gross denial may deny total cortical blindness (Anton's syndrome) or a severe hemiparesis (anosognosia).
In many patients with denial, the denial is more implicit than explicit.
For example, when asked about the illness, the patient may not actively deny
that he or she is ill but may say that he or she is in the hospital for tests to
evaluate mild joint pain or some similar benign condition, when in fact they
have metastatic cancer. Some patients state that they are not really in a hospital at all, but rather in a rest facility or hotel (reduplication of place or
paramnesia). Such patients often make elaborate excuses of fatigue when
asked to perform with the paralyzed limb (confabulation) and on occasion
will even claim that the weak arm is not theirs at all (reduplication of body
parts). The surgeon mentioned earlier, for instance, claimed the next day that
he "had some arthritis" in his left arm and that was the reason for his not
moving it.
Hemiplegic patients who deny weakness are a great problem in rehabilitation because they are overtly unaware of their weakness and tend to fall
repeatedly. One of our patients tried to walk to the bathroom on the first
day after his right hemisphere stroke and fell, fracturing his left clavicle.
Some patients do not demonstrate frank denial but do have a dramatic
neglect of one side of the body. They may shave only one side of the face,
use only one sleeve of their robe, and fail to use one side of the body, even
though paralysis is not present. These patients also neglect one half of the
extrapersonal environment, even in the absence of a visual field defect. For
example, patients may fail to respond to a visitor who approaches them from
their involved side. Patients may also show neglect on drawing tasks, examples of which are shown in Figure 2-4.
The most subtle form of neglect is an inattention to one side of the body
22
FIG U R E 2 - 4. Examples of neglect on the drawing test.
23
when both sides are simultaneously stimulated. This tendency to suppress or

to extinguish the stimuli on the involved side is discussed in Chapter 4.
The type of lesion that most frequently causes the denial and neglect
syndromes is a nondominant hemisphere lesion, usually vascular in etiology. 6
A specific lesion locus within the nondominant hemisphere has not yet been
established; subcortical as well as cortical structures may be involved. Gross
explicit denial is an uncommon behavioral finding that is most often seen
during the acute stages after a vascular accident and is often associated with
a degree of confusion. Significant unilateral neglect is also rather uncommon
but may be seen as a chronic effect of parietal lesions, predominantly in the
non dominant hemisphere. (Patients with frontal lobe disease may also demonstrate denial.) The actual neuropsychologic and neurophysiologic mechanisms underlying these syndromes are not completely understood. For a review of this problem, see references 9, 10, 32, and 33.
Apathy versus Depression

or Dysthymia
Apathy, lack of interest in the environment, and psychomotor slowing (psychomotor retardation) are frequently observed in patients with psychiatric
depressive illness. However, apathy is but a single symptom and, in isolation,
never justifies the diagnosis of depression. Essentially identical symptoms are
also characteristic of various organic brain diseases, including frontal lobe
lesions, subcortical dementias (e.g., AIDS-related dementia) and other types
of dementia, and lesions in the nondominant hemisphere. Because of the
critical difference in treatment of depression and of these organic brain diseases, the importance of differentiating apathy of organic etiology from functional
depression cannot be overemphasized.
Criteria for Diagnosing Depressive Disorders

For the purposes of this book depression refers to a generic affective disorder
that consists of several relatively distinct subdisorders and many different
symptoms. Within this context, depression includes major depressive disorder
(single episode and recurrent), depressive disorder not otherwise specified, and dysthymic disorder. The diagnostic criteria listed here, adapted from DSM-IV, are
useful in establishing a diagnosis of one of these disorders of depression,
which include but are not totally restricted to the following:
1. Major Depressive Disorder, Single Episode
By definition, this disorder is time-limited and is of sufficient magnitude to be distinguished from apathy if a careful history is taken.
A. Presence of a single major depressive episode
(1) Five or more of the following symptoms are present during
the same 2-week period, representing a change from previous
functioning:
24
(a) Depressed mood most of the day, nearly every day

(b) Markedly diminished interest or pleasure in all or most
activities
(c) Significant unplanned weight gain or loss
(d) Insomnia or hypersomnia
(e) Psychomotor agitation or retardation
(f) Fatigue or loss of energy
(g) Feelings of worthlessness or excessive guilt
(h) Diminished ability to think or concentrate, or indecisiveness
(i) Recurrent thoughts of death or suicidal ideation
(2) The symptoms do not meet the criteria for any other mood
disorder.
(3) The symptoms cause significant distress or impairment of
functioning.
( 4) The symptoms are not due to the direct effect of a chemical
substance (drugs) or a general medical condition.
(5) The symptoms cannot be accounted for by a grief reaction,
persist for more than 2 months, or are characterized by
marked functional impairment, morbid preoccupation with
worthlessness, suicidal ideation, psychotic symptoms, or psychomotor retardation.
B. The major depressive disorder is not caused by, or superimposed
on, any other major psychiatric disorder.
C. The patient has never had any type of elevated mood disorder
(e.g., mania).
2. Major Depressive Disorder, Recurrent
Behavioral changes associated with this disorder are of sufficient magnitude and duration to warrant careful differentiation from organic
apathy in any patient presenting with either "depressive" or "apathetic" symptoms.
A. Two or more major depressive episodes, as defined in the previous
section, are present.
B. The episodes are not caused by, or superimposed on, any other
type of psychotic disorder (e.g., schizophrenia).
3. Depressive Disorder Not Otherwise Specified
In general, these affective disorders do reach a magnitude that would
result in a behavioral change that could be confused with organic
apathy. This category includes examples of affective disorders with
depressive features that do not meet the criteria for any other depressive disorder:
A. Premenstrual mood disorder
B. Minor depressive disorder
C. Recurrent periods of brief depression
D. Depression following a period of active psychosis
25
E. Situations in which the clinician concludes that a depressive disorder is present but cannot determine whether it is primary, due
to a general medical condition, or substance-induced
4. Dysthymic Disorder
A. Depressed mood for most of the day, more days than not, for 2
years.
B. The presence, while depressed, of two or more of the following:
(1) Poor appetite or overeating
(2) Insomnia or hypersomnia
(3) Low energy or fatigue
( 4 ) Low self-esteem
(5) Poor concentration or difficulty making decisions
(6) Feelings of hopelessness
C. During the 2-year period, the person has not been without symptoms for more than 2 months at a time.
D. No major depressive disorder has been present during the 2-year
period.
E. The patient has never had a period of abnormally elevated mood.
F. The disturbance does not occur exclusively during the course of a
chronic psychotic disorder.
G. The symptoms are not due to the direct physiologic effects of a
substance (e.g., drugs) or to a general medical condition (e.g.,
hypothyroidism) .
Differentiating between Depression

and Dementia
Before even considering a diagnosis of neurologic disease, the clinician should
carefully evaluate any patient presenting with apathy of nonacute onset as an
initial symptom for the possible presence of a primary depressive disorder.
One of the most common diagnostic dilemmas in this regard is the differentiation between depression and early dementia. Because both conditions
are relatively common in the older population and, more importantly, share
many common features, a misdiagnosis of one for the other is all too easily
made. The significance of such an error is obvious. To tell a depressed individual that he or she is demented is a devastating mistake but one that is no
less significant than overlooking a frontal meningioma while treating the patient for depression.
One can easily see why diagnoses can become confused: patients with
either condition can present with subjective or repeated complaints of apathy,
loss of interest in work and pleasurable activities, preoccupation with minor
or imagined physical complaints, difficulty concentrating, memory problems,
and a general inability to keep up with the demands of everyday life.
The problem is further compounded in the elderly. These patients, when
26
depressed, do not always manifest an obviously depressive mood as dramatically as do younger patients. The elderly depressive patient also typically
demonstrates fewer crying spells, less expressed sadness, less suicidal ideation
(although there is no less threat of actual suicide), less expressed guilt, and
less self-deprecation.24 The elderly depressive patient may also show subtle
cognitive deficits on formal mental status testing. No specific pattern of deficits is seen, and the deficits are usually mild. 4 Mild problems with concentration, memory, and arithmetic are common; drawings may contain a paucity of details. In general, performance may be impaired on any task that
requires the marshaling of significant mental energy.
Because of the similarity of clinical presentation, it is not surprising that
many elderly depressive patients are initially diagnosed as having a dementia. 21 Pseudo dementia, or dementia of depression, refers to patients giving
the initial diagnostic impression of a dementia, but whose symptoms, on
careful evaluation and follow-up, prove to be secondary to depression or
another emotional disorder and improve with appropriate treatrnent. 14 ,23
The differentiation of true early dementia from pseudo dementia is not
always easy. Wells 34 has tabulated the major features that can help make this
distinction.
Differential Features of Pseudodementia and Dementia
Clinical course and history
Pseudodementia
Dementia
Onset fairly well demarcated

History short
Onset indistinct
History quite long before
consultation
Early deficits tiIat often
go unnoticed
Uncommon occurrence of
previous psychiatric
problems or emotional
crisis
Little complaint of
cOgrIitive loss
Struggles witiI cogrIitive
tasks
Usually apatiIetic witiI
shallow emotions
Behavior compatible witiI
cogrIitive loss
Nocturnal accentuation of
dysfunction common
Usually tries items
Rapidly progressive
History of previous psychiatric
difficulty or recent life crisis
Clinical behavior
Detailed, elaborate complaints

of cogrIitive dysfunction
Little effort expended on
examination items
Affective change often present
Behavior does not reflect
cOgrIitive loss
Nocturnal exacerbation rare
Examination findings
Frequently answers "I don't

know" before even trying
Inconsistent memory loss for
botiI recent and remote
items
May have particular memory
gaps
Generally inconsistent
performance
Memory loss for recent

items worse tiIan for
remote items
No specific memory gaps
exist
RatiIer consistently
impaired performance
27
In our experience, if the examiner takes sufficient time and encourages

optimum performance from the patient, the depressed patient with complaints of memory loss will show normal or near-normal performance that
is far better than would be expected from the nature and severity of the
complaints. In some significantly depressed patients, the mental status examination seems to verify the initial impression of dementia, hence the term
"pseudodementia." Because the cognitive examination actually demonstrates
impairment that seems organic and is probably caused by chemical (neurotransmitter) abnormalities, the terms "depressive dementia" and "dementia
of depression" have been used in preference to "pseudodementia."
The syndrome of pseudodementia is most commonly seen in the elderly
depressed patient, but somatoform disorders, manic episodes, high-level anxiety, and any psychotic disorder can produce a picture of dementia on mental
status examination. In these cases, it is the inattention, racing thoughts, and
confused thinking that preclude adequate performance on the examination.
A number of patients with mild closed head injury and major emotional
adjustment disorders may also present clinically and on screening examinations with cognitive performance resembling mild dementia because of reduced cognitive efficiency. Treating a patient with pseudodementia is rewarding because, with appropriate treatment, the patient's mental status will revert
to normal, premorbid levels.
SUMMARY
Organic brain lesions may cause a multiplicity of behavioral syndromes, some
of which are characteristic of specific clinical conditions. The examiner must
be prepared to make a systematic evaluation of the patient's behavior and be
able to recognize these major neurobehavioral syndromes. The patient's history and behavior provide essential information and serve as a framework for
the interpretation of data subsequently obtained from the mental status
examination.
REFERENCES
4 (DSM-N). American Psychiatric Association, Washington, DC, 1994.
2. Anderson, NC and Black, DW: Introductory Textbook of Psychiatry. American Psychiatric
Press, Washington, DC, 1995.
3. Black, FW: Cognitive deficits in patients with unilateral war-related frontal lobe lesions. J
Clin Psychol 32:307, 1976.
4. Caine, ED: Pseudodementia: Current concepts and future directions. Arch Gen Psychiatry
38:1359, 1981.
5. Ch>dru, F and Geschwind, N: Writing disturbances in acute confusional states. Neuropsychologia 10:343, 1972.
6. Critchley, M: The Parietal Lobes. Edward Arnold & Co., London, 1953.
7. Damasio, AR and Anderson, SW: The frontal lobes: In Heilman, KM and Valenstein, E (eds):
Clinical Neuropsychology. Oxford University Press, New York, 1993, pp 409-460.
28
8. Hecaen, H and Albert, ML: Disorders of mental functioning related to frontal lobe pathology.
In Benson, OF and Blumer, 0 (eds): Psychiatric Aspects of Neurologic Disease. Grune &
Stratton, New York, 1975, pp l37-149.
9. Heilman, KM, et al: Localization of lesions in neglect. In Kertesz, A (ed): Localization in
Neuropsychology. Academic Press, New York, 1983, pp 471-492.
10. Heilman, KM, Watson, RT, and Valenstein, E: Neglect and related disorders. In Heilman, KM
and Valenstein, E (eds): Clinical Neuropsychology, ed 3. Oxford University Press, New York,
1993, pp. 279-336.
11. Inouye, SK and Charpentier, PA: Precipitating factors for delirium in hospitalized elderly
persons. JAMA 275:852-857, 1996.
12. Janowsky, OS: Pseudodementia in the elderly: Differential diagnosis and treatment. J Clin
Psychiatry 43:19, 1982.
l3. Kaplan, HI and Sadock, BJ: Modem Synopsis of Comprehensive Textbook of Psychiatry.
Williams & Wilkins, Baltimore, 1988.
14. Kiloh, LG: Pseudo-dementia. Acta Psychiatr Scand 37:336, 1961.
15. Lerner, AI, Hedera, P, Koss, E, et al: Delirium in Alzheimer disease. Alzheimer Dis Assoc
Disord 11:16-20, 1997.
16. Levenson, AJ (ed): Neuropsychiatric Side-Effects of Drugs in the Elderly. Raven Press, New
York, 1979.
17. Levin, HS, Eisenberg, HM, and Benton, AL (eds): Frontal Lobe Function and Dysfunction.
Oxford University Press, New York, 1991.
18. Lishman, WA: Organic Psychiatry: The Psychological Consequences of Cerebral Disorders.
Blackwell Science, London, 1998.
19. Luria, AR: Traumatic Aphasia. Moulton & Co, The Hague, Netherlands, 1970.
20. Nauta, WJH: The problem of the frontal lobe: A reinterpretation. J Psychiatr Res 8:167,1971.
21. Nott, PN and Fleminger, JJ: Presenile dementia: The difficulties of early diagnosis. Acta Psychiatr Scand 51:210, 1975.
22. Pompei, P, Foreman, M, Cassel, CK, et al: Detecting delirium among hospitalized older
patients. Arch Intern Med 155:301-307, 1995.
23. Post, F: Dementia, depression and pseudo-dementia. In Benson, OF and Blumer, 0 (eds):
Psychiatric Aspects of Neurologic Disease. Grune & Stratton, New York, 1975, pp 99-120.
24. Reese, WL, Lipsedge, M and Ball, C (eds): Textbook of Psychiatry. Oxford University Press,
New York, 1997.
25. Strauss, ED: The psychiatric interview, history, and mental status examination. In Kaplan, HI
and Sadock, BJ (eds): Comprehensive Textbook of Psychiatry. Williams & Wilkins, Baltimore,
1995, pp 521-531.
26. Strub, RL: Acute confusional state. In Benson, OF and Blumer, 0 (eds): Psychiatric Aspects
of Neurologic Disease, Vol II. Grune & Stratton, New York, 1982, pp 1-21.
27. Strub, RL: Mental disorders in brain disease. In Frederiks, JAM (ed): Handbook of Clinical
Neurology, Vol 2 (46), Neurobehavioral Disorders. Elsevier Science Publishers, Amsterdam,
1985, pp 4l3-441.
28. Stuss, DT and Benson, OF: Frontal lobe lesions and behavior. In Kertesz, A (ed): Localization
in Neuropsychology. Academic Press, New York, 1983, pp 429-454.
29. Stuss, DT and Benson, OF: Neuropsychological studies of the frontal lobes. Psychol Bull
95:3, 1984.
30. Teuber, HL: The riddle of frontal lobe function in man. In Warren, J and Alert, K (eds): The
Frontal Granular Cortex and Behavior. McGraw-Hill, New York, 1964, pp 410-440.
31. Trzepacz, IT and Baker, RW: The Psychiatric Mental Status Examination. Oxford University
Press, New York, 1993.
32. Weinstein, EA and Friedland, RP: Hemi-inattention and Hemispheric Specialization. Advances in Neurology, Vol 18. Raven Press, New York, 1977.
33. Weinstein, EA and Kahn, RL: Denial of illness. Charles C Thomas, Springfield, IL, 1955.
34. Wells, CE: Pseudodementia. Am J Psychiatry l36:895, 1979.
LEVELS OF
CONSCIOUSNESS
The initial step in administering a formal mental status examination is to
determine the patient's level of consciousness. This basic brain function determines the patient's ability to relate both to self and to the environment.
Any disturbance of this elementary function almost invariably affects the
higher-level mental processes that constitute the major portion of the mental
status examination. An alteration in level of consciousness is an important
indicator of brain dysfunction and is usually caused either by primary neurologic disease or systemic medical illness.
The term consciousness is multifaceted; in testing consciousness, it is
important to distinguish between the content of consciousness and basic
arousal. 10 Content refers to higher cognitive and emotional functioning,
whereas arousal refers to the activation of the cortex from the ascending
activating system (brain stem reticular formation and the diffuse thalamic
projection system). Content and arousal can vary independently, and the final
level of consciousness represents a dynamic balance between cortical and
ascending activating systems. This chapter deals with the clinical aspects of
basic arousal.
TERMINOLOCY AND EVALUATION

Many general terms are used to describe the basic levels of consciousness,
which represent points on a continuum from full alertness to deep coma.
Most clinicians distinguish five principal levels: (1) alertness, (2) lethargy or
somnolence, (3) obtundation, (4) stupor or semicoma, and (5) coma.
Alertness implies that the patient is awake and fully aware of normal
external and internal stimuli. Barring paralysis, the patient can respond appropriately to any normal stimulus. The alert patient is able to interact in a
meaningful way with the examiner. In cases of total paralysis, eye contact or
eye movement may be adequate to establish this interaction. Because there
29
30
are unusual comalike states in which alertness is simulated, we feel that an

observation of alertness should be predicated on the clinician's impression
that meaningful interpersonal interaction is taking place. Alertness per se does
not imply the inherent capacity to focus attention, a topic to be discussed in
detail in Chapter 4.
Lethargy, or somnolence, is a state in which the patient is not fully alert
and tends to drift off to sleep when not actively stimulated. In such patients,
spontaneous movements are decreased and awareness is limited. When
aroused, these patients are usually unable to pay close attention to the examiner; their eyes are open and directed toward the examiner, yet they appear
dull and without animation. In conversation, the lethargic patient often loses
the train of thought and wanders from topic to topic. It is difficult to assess
memory, calculations, and abstract thinking with validity in these patients
because of their inattention and wandering thought processes. If a lethargic
patient takes a full mental status examination, impaired performance must
be interpreted with caution.
Obtundation is a transitional state between lethargy and stupor. The
obtunded patient is difficult to arouse and, when aroused, is confusional.
Usually, constant stimulation is required to elicit even marginal cooperation
from the patient. Meaningful mental status testing is usually futile. The obtunded patient is, by our definition, in an acute confusional state or quiet
delirium.
Stupor and semicoma are used to describe patients who respond only
to persistent and vigorous stimulation. The stuporous patient does not rouse
spontaneously and, when aroused by the examiner, can only groan or mumble and move restlessly in the bed. In such a patient, there is extensive brain
dysfunction; because of the markedly reduced level of consciousness, no
meaningful assessment of the content of mental functioning is possible.
Coma is traditionally applied to those patients who are completely unarousable and remain with their eyes closed. In coma, the patient responds
neither to external stimulation nor spontaneously to internal stimulation. If
coma is thus defined as a state in which no evidence of behavioral response
to stimulation is present, the term can serve as an absolute end point on the
scale of consciousness or arousability. Some clinicians make a distinction
between light coma and deep coma. In light coma, the patient may demonstrate reflex (e.g., decorticate or decerebrate) movements but no meaningful
or purposeful movements, whereas in deep coma, no motor response is seen
at all. Stupor and coma are not discussed further here; the interested reader
is referred to Plum and Posner; 10 Young, Ropper, and Bolton; 13 and Fisher3
for extensive discussions of these states.
Each of the aforementioned terms is qualitative and encompasses a wide
range of possible points on the continuum of consciousness. Such terms lack
the objectivity and reliability that can be achieved with a less subjective assessment scheme. We suggest amending any qualitative term such as "lethargy" with a series of short statements that describe both the level of stimulus
Level of
Consciousness
Stimulus Necessary
to Rouse Patient
PM
Lethargy
Loud voice
12 AM
Lethargy
4AM
Stupor
Loud voice plus

gentle shaking
Loud voice plus
vigorous
shaking
Movement
Vocalization
Eye Opening
Moved all limbs; got

up on elbow
Moved all limbs; no
attempt to rise
Slight movement of all
extremities, but
right arm not
moving well
Mumbled something about Yes, with eye contact

being tired
Yes, but with no sustained
Incoherent mumbling
eye contact
Attempted to open eyes to
Groans
command
Comments
Odor of alcohol on
breath
Questionable
Babinski's sign
Left pupil larger than
right, not as
reactive; now
positive Babinski's
sign on right
32
necessary to arouse the patient, the actual behavioral response elicited, and
what the patient does when the stimulation ceases.
First, the intensity of stimulation needed to arouse the patient should be indicated: (1) calling the patient's name in a normal conversational tone, (2)
calling in a loud voice, (3) light touch on the arm, (4) vigorous shaking of
the patient's shoulder, or (5) painful stimulation. Second, the patient's highestlevel responses should be described: (1) degree and quality of movement, (2)
presence and coherence of speech, or (3) presence of eye opening and eye
contact with the examiner. Finally, what the patient does on cessation of stimulation should be described.
This information can be recorded in a single statement. For example:
Patient lethargic: Patient's name called in a normal tone of voice; patient opened eyes, pulled self part way up in bed, mumbled "Why ya
bothering me?" then closed eyes and went back to sleep.
Patient obtunded: Responded to loud shouting with restless movements
of all extremities and brief eye opening; speech mumbled and incoherent; when stimulation discontinued, patient returned to sleep.
Patient stuporous: Did not respond to voice but responded to vigorous
shaking of shoulder, accompanied by loud calling of patient's name,
with groan and aimless movement of left extremities; eyes remained
closed.
These types of descriptions provide much more data on the patient's arousability and capacity for interaction than the simple terms "lethargy," "obtundation," or "stupor." It is helpful to make a chart in the progress notes so
that a rapid assessment of changing levels of consciousness can be made.
Table 3-1 is an example of a patient with head trauma who had a subdural
Category of Response
Response
Eye opening
Spontaneous
To speech
To pain
Nil
Oriented
Confused conversation
Inappropriate words
Incomprehensible
Nil
Obeys
Localizes
Withdraws
Abnormal flexion (decorticate)
Extends (decerebrate)
Nil
Best verbal response
Best motor response
Adapted from Jennett and Teasdale,6 p. 78.
Points
4
3
2
1
5
4
3
2
1
6
5
4
3
2
1
Eye opening
Spontaneous
To speech
To pain
None
Best verbal response
Oriented
Confused
Inappropriate
Incomprehensible
None
Best motor response
Obeying
Localizing
Withdraws
Flexing
Extending
None
Coma Score
"'"'""
12
11
34
hematoma. As shifts of nurses and doctors change, subtle changes in the

patient's condition are easily appreciated by comparing the notes of previous
observers. This system is applicable to any patient whose illness causes a
decrease in the level of awareness.
Teasdale and Jennett6 ,12 have demonstrated the practicality of this type
of reporting system for patients with head injury. They have developed what
has become known as the Glasgow Coma, or Responsiveness, Scale. It follows
the conceptual scheme described earlier but has the advantage of providing
a numeric score to denote the actual level of consciousness. Each level of
response in the three response categories (i.e., eye opening, verbal, motor) is
given a numeric value. The response is the patient's best response; it does
not, however, take into account the level of stimulus required for its elicitation. The scale items and the quantitative ratings for specific responses are
presented in Table 3-2. Additionally, the Rancho Los Amigos Scale4 ,7 is commonly used to track the patient's level of consciousness and responsiveness
to environmental stimuli in rehabilitation settings.
The level of responsiveness can be assessed objectively at regular intervals
and plotted as a graph. The time scale can be hourly, daily, or any selected
interval. Table 3-3 is an example of such use of the scale.
ANATOMY AND CLINICAL

IMPLICATIONS
The basic brain structure responsible for arousal is the ascending activating
system. This system originates in the brain stem reticular formation and extends to the cortex via the diffuse or nonspecific thalamic projection system. 9
A group of specialized reticular neurons in the tegmental portion of the
midbrain and upper pons has the specific capacity to activate higher centers.
These cells are located in a perimedian portion in the brain stem (reticular
formation and locus ceruleus) and receive collateral input from most ascending and descending fiber systems. Stimulation applied to the skin of the hand,
for example, will send information to the activating system as well as the
sensory nuclei in the thalamus. Reticular stimulation alerts widespread areas
of the cortex and subcortex to the fact that an external stimulus is being
applied. By this mechanism, the activating system maintains a constant, albeit
fluctuating, stimulation of the higher centers. Without this steady input, the
cortex cannot function efficiently; thus, the patient cannot think clearly, learn
effectively, or relate meaningfully. Any damage or suppression of this system
renders the patient difficult to arouse and inefficient in performance. Specific
lesions such as infarcts or hemorrhages of the reticular formation lead to total
disruption of arousal and, thus, to coma. Pressure on the midbrain from
hippocampal or uncal herniation causes a change in the level of consciousness, which starts as lethargy but may progress to coma. Drug intoxication,
LEVELS OF CONSCIOUSNESS
35
disturbances in metabolic balance, and sepsis cause alterations in both reticular and cortical functioning. This leads to alterations not only in arousal,
but also in the content of consciousness.
If there is damage to the extension of the brain stem reticular system in
the thalamus or hypothalamus, the full picture of coma will not result. Such
lesions disconnect the reticulocortical and reticulolimbic pathways and cause
patients to display various interesting alterations in arousal. Because the brain
stem portion of the system is intact, reticular activity innervates the nuclei of
the extraocular nerves, and patients can open their eyes and look about. The
cortex, however, is not sufficiently stimulated to produce voluntary movement
or speech. These patients are in a comalike state.
These unusual comalike states are interesting because of the nature and
degree of disturbed awareness. Some authors categorize all such cases as akinetic mutism or persistent vegetative states, whereas others prefer to separate
them into their many subcategories. Regardless of the terminology used, however, the pathology and clinical appearance of each subcategory are relatively
distinct. The primary feature of patients with these disorders is the uncanny
appearance of awareness. Such patients lie in bed with their eyes open and
look about the room. Eye contact with others is variable. Sometimes eye
movements seem random, but on other occasions, genuine interpersonal eye
contact appears to take place. Other than this somewhat unnerving visual
scanning, the patients remain relatively immobile and mute. It is the dichotomy between this apparent visual alertness and the lack of speech and movement that differentiates this group of patients from those in stupor or coma.
The critical defining features of this vegetative state, as with coma, are no
evidence of awareness of self or the environment and no evidence that the
patient can understand or communicate with an examiner. 1
Regardless of their superficial similarity, each subgroup of the comalike
states has its own distinct features; it is often possible to differentiate among
the various states clinically and to separate them from a true vegetative state.
The term "akinetic mutism" seems best reserved for patients in whom damage
is restricted either to the midbrain or subthalamic region or to the septal
region.
A midbrain lesion causes a syndrome called apathetic akinetic mutism.
Patients with this syndrome are difficult to arouse but, once aroused, can
move all extremities, mutter a few intelligible words, and look directly at the
examiner for a few moments. They then tum away or drift back to sleep.
Subtle muscle stretch reflex changes, extensor toe signs, extraocular muscle
involvement, and pupillary abnormalities may be seen. Although this condition was originally described in a patient with a third ventricular cyst, 2 the
most common cause is occlusion of the small vessels entering the brain stem
from the tip of the basilar artery.ll This lesion interrupts the ascending activating system but not the corticospinal and corticobulbar tracts. Accordingly,
36
the patients can open their eyes and make some movement and sound but
are unable to respond fully. Because of the akinetic mute patients' capacity
to interact with the environment, they are not in a vegetative state.
Patients with lesions that involve the septal area, anterior hypothalamus,
cingulate gyri, or bilateral orbital frontal cortex are also akinetic and mute
but appear much more alert. These patients are awake most of the day and
have insomnia at night, their eyes remaining open while they are awake.
Described as being in a coma vigil, these individuals often have violent behavioral outbursts during arousal (septal rage). This syndrome is seen in those
with rupture of anterior communicating artery aneurysms, deep frontal lobe
tumors, and anterior cingulate gyrus tumors. Increased leg reflexes, with Babinski's sign from corticospinal tract involvement, difficulty with temperature
control from anterior hypothalamic damage, and primitive reflexes (snout
and grasp) from mesial frontal lobe damage may be seen. These patients do
not have pupillary or extraocular muscle paresis. These neurologic signs, plus
the more apparent alertness of these patients, frequently differentiates them
clinically from apathetic akinetic mute patients.
Patients with diffuse damage to the cortical mantle from anoxia, hypoglycemia, or circulatory or metabolic embarrassment frequently survive in a
state clinically similar to that of coma vigil. Their eyes are open and randomly
survey the room. Brain stem reflexes are intact, but bilateral decortication with
double hemiplegia and primitive reflexes is present. This condition is called
the apallic state8 because of the diffuse damage to the isocortex. Because of
the dramatic neurologic deficit, this state should be easily distinguished from
the akinetic mute states.
The term "persistent vegetative state" has been used to describe patients
surviving severe head injury whose symptoms are clinically similar to those
in the apallic state. 5 The brain lesions are widespread at both the cortical and
subcortical levels, and neurologic findings differ in each case, depending on
the specific loci of the lesions. Because the term "apallic state" has never
gained widespread acceptance, "persistent vegetative state" is often used for
any patient with widespread brain disease and no ability to interact meaningfully with the environment.
The locked-in syndromelO is another comalike state that can be differentiated from the foregoing states. In this condition, a lesion (hemorrhage or
infarct) in the upper pontine tegmentum interrupts all corticospinal and corticobulbar fibers at the level of the abducens and facial nuclei. Clinically,
patients are unable to speak, swallow, smile, or move their limbs. In some
cases, lateral gaze is also paralyzed. The entire central nervous system above
the level of the lesion is intact, and these patients are literally disconnected
from their motor system. These patients are "locked-in" and able to communicate by eye movements only.
Table 3 -4 is a composite of the clinical features of each of these comalike
Diagnosis
Akinetic mute
(apatheticmidbrain)
Akinetic mute
(coma vigilseptal)
Apallic state
( decorticate)
Persistent vegetative
state
Locked-in syndrome
.....
Level of
Consciousness
Lethargy
Voluntary Movement
Speech
Eye Responses
Limb Tone
Reflexes
Little and infrequent; With stimulation, can Open when stimulated; Usually normal; Can be normal;
but when
produce normal,
usually good eye
sometimes
occasionally
sufficiently
short phrases
contact
slight
asymmetric
stimulated, can
increase
with
move all
pathologic
extremities
reflexes
purposefully
Wakeful, with
Open during much of Often increased Frequently
Little but purposeful; Little; can
occasional
arms usually move
occasionally
the day in most
in legs
have
patients; eye contact
outbursts; some
produce normal
increased leg
much better than
patients
legs
phrases; also can
variable
reflexes;
Babinski's
somnolent
have outbursts of
unintelligible
signs, snout,
utterances
grasp often
present
Awake: no
Open, searching, but
No or little
None or occasional
Increased in all Increase in all
meaningful
purposeful
no real eye contact
extremities;
grunting
extremities
interaction with
movement; mostly
with
extremities
environment
reflex or mass
often in
pathologic
movements
flexion
reflexes
Awake; no
None
None
Open, searching, but
Variable,
Variable,
interaction with
no real eye contact
usually
usually
environment
increased;
increased
extremities
with
often in
pathologic
flexion
reflexes
None or slight,
None
Open, with normal
Awake and alert;
Increased
Increased in all
extremities
able to
except for eye
following and good
communicate
movement
eye contact; some
patients have
meaningfully
with examiners
restricted lateral gaze
by eye
movement
38
states. These features plus the clinical history should enable the examiner to
differentiate most of these complicated cases.
A final condition that deserves mention in this section is the state of
psychogenic unresponsiveness (also called hysterical comaIike state or somatoform disorder/conversion disorder). This condition constitutes 1% of all
patients presenting to a medical emergency room in an unresponsive state. 10
Careful examination reveals normal respiration, heart rate, and blood pressure. Muscle tone is usually decreased, but inconsistent limb tone frequently
exists. All bulbar reflexes (doll's eye phenomenon, caloric stimulation, gag,
corneal, and pupil) are intact. Muscle stretch reflexes are symmetric. Frequently, the patient will make inconsistent responses, such as blinking on
corneal testing before the cornea is touched. Any inconsistent response gives
the examiner additional confidence that the patient does not have a medical
or neurologically induced coma. Psychogenic unresponsiveness should not
be diagnosed too hastily; mistakenly labeling a true coma as psychogenic
unresponsiveness is far more serious than the reverse.
All of the conditions discussed earlier represent disturbances of arousal
caused by brain lesions or psychiatric illness. Not all alterations in levels of
alertness are pathologic, however. Sleep, for instance, represents a natural fluctuation in the level of consciousness. Any degree of fatigue or sleepiness can
adversely affect performance on mental status testing, even in the absence of
an organic lesion. Patients with brain disease continue to have an underlying
diurnal sleep-wake cycle that is superimposed on any organic decrease in
alertness. It may be difficult to determine the relative effects of sleep arid
pathologic alterations in the level of consciousness, but the examiner must
consider both factors in the evaluation. For example, the patient with head
trauma who is difficult to arouse on morning rounds may only be asleep and
not suffering from increasing intracranial pressure. In these critical cases, the
observed level of awareness is not the only critical factor that determines the
necessity for therapeutic intervention. The patient's neurologic status and
overall hospital course must also be considered.
SUMMARY
Because consciousness is the most rudimentary of all mental functions, consciousness level must be determined first in any mental status examination.
Any alteration in the level of consciousness decreases the efficiency of cortical
functioning, and thereby significantly decreases the validity of the subsequent
steps in the mental status examination. In the patient with diminished alertness, only the more obvious changes in higher cognitive function can be
validly documented.
The ascending activating system controls the arousal aspect of consciousness. Any damage to or dysfunction of this subcortical system alters alertness
and thus secondarily affects cortical activity.
LEVELS OF CONSCIOUSNESS
39
REFERENCES
1. American Neurological Association Committee on Ethical Affairs: Persistent vegetative state:
Report of the American Neurological Committee on Ethical Affairs. Ann Neurol 33:386390, 1993.
2. Cairns, H, et al: Akinetic mutism with an epidermoid cyst of the third ventricle. Brain 64:273,
1941.
3. Fisher, CM: The neurological examination of the comatose patient. Acta Neurol Scand
(Suppl) 36:1, 1969.
4. Hagan, C: Language disorders in head trauma. In Holland, A (ed): Language Disorders in
Adults. College-Hill Press, San Diego, CA, 1984.
5. Jennett, B and Plum, F: Persistent vegetative state after brain damage. Lancet 1:734, 1972.
6. Jennett, B and Teasdale, G: Assessment of impaired consciousness. In Jennett, B and Teasdale,
G: Management of Head Injuries. FA Davis, Philadelphia, 1981. pp 77-93.
7. Kay, T and Lezak. MD: The nature of head injury. In Corthell, D (ed): Traumatic Brain Injury
and Vocational Rehabilitation. University of Wisconsin, Menomonee, WI, 1990.
8. Kretschmer, E: Das Appalische Syndrom. Z Gesamte Neural Psychiatr 169:576, 1940.
9. Magoun, H: The Waking Brain. Charles C Thomas, Springfield, IL, 1963.
10. Plum, F and Posner, J: Diagnosis of Stupor and Coma, ed 3. FA Davis, Philadelphia, 1982.
11. Segarra, J and Angelo, J: Anatomical determinants of behavior change. In Benton, A (ed):
Behavioral Change in Cerebral Vascular Disease. Harper &. Row, New York. 1970, pp 3-14.
12. Teasdale, G and Jennett, B: Assessment of coma and impaired consciousness. Lancet 2:81,
1974.
l3. Young. GB, Ropper AH, and Bolton CF (eds): Coma and Impaired Consciousness. McGrawHill, New York. 1998.
ATTENTION
After determining the level of consciousness, assessment of attention is the
next step in the examination. The patient's ability to sustain attention over
time must be established before evaluating the more complex functions such
as memory, language, and abstract thinking. It is of no value to ask the patient
to remember the details of a story if he or she is repeatedly distracted by
internal stimuli or by the nurse passing in the hall, a noise in the next room,
or cars in the street. The inattentive and distractible patient cannot efficiently
assimilate the information being presented during testing.
Attention is the patient's ability to attend to a specific stimulus without being
distracted by extraneous internal or environmental stimuli. 19 This capacity for focusing on a single stimulus contrasts with the concept of alertness or vigilance. The term "vigilance," however, has been used interchangeably with
both "sustained attention" (focusing on one stimulus over an extended period
of time) and also with the more common concept of "watchfulness" or "alertness."24 Vigilance in the sense of alertness refers to a more basic arousal process in
which the awake patient can respond to any stimulus appearing in the environment.
The vigilant (alert) but inattentive patient will be attracted to any novel
sound, movement, or event occurring in the vicinity; the attentive patient can
screen out irrelevant stimuli. Attention presupposes alertness, but alertness
does not necessarily imply attentiveness.
Sustained attention (concentration) is the ability to maintain attention
to a specific stimulus over an extended period. This capacity to concentrate
is very important for performing intellectual endeavors and may be impaired
in both medical and emotional disorders. A wide variety of factors have been
shown to interfere with attention; the intensity and frequency of the stimulus:
environmental stressors (e.g., noise, temperature, complexity of the environment), emotional factors (e.g., anxiety or depression), and to some extent
lower IQ. 1 The concept of inattention (distractibility) is applied to two distinct clinical situations. The first is when the patient is clinically inattentive
or is unable to sustain sufficient attention to succeed in the simple tests of
attention discussed subsequently. The second situation is when the patient
40
ATIENTION
41
has specific unilateral inattention (neglect) to stimuli on the side of the body
opposite a brain lesion.
EVALUATION
Observation
One of the most valid sources of clinical information regarding the patient's general
attentiveness may be obtained by merely observing the patient's behavior and noting
any evidence of distractibility or difficulty in attending to the examiner. A
subjective rating scale of 0 (highly distractible) to 5 (fully attentive) is useful
as a means of quantifying attention over the course of the examination.
History
A patient who is having difficulty concentrating on work or other routine
tasks is usually able to tell the examiner about the problem. A simple inquiry
as to the patient's ability to concentrate or to sustain attention often provides
revealing data.
Digit Repetition
The patient's basic level of attention can be readily assessed by using the Digit
Repetition Test. Adequate performance on this task ensures that the patient
is able to attend to a verbal stimulus and to sustain attention for the period
of time required to repeat the digits. In patients with a significant language
disorder (aphasia), this task and the "A" Random Letter Test for sustained
attention, which follows, cannot be validly applied to assess attention.
DIRECTIONS: Tell the patient: "I am going to say some simple numbers.
Listen carefully and when I am finished, say the numbers after me." Present
the digits in a normal tone of voice at a rate of one digit per second. Take
care not to group digits either in pairs (e.g., 2-6, 5-9) or in sequences that
could serve as an aid to repetition (e.g., in telephone number form, 3768439). Numbers should be presented randomly without natural sequences
(e.g., not 2-4-6-8). Begin with a two-number sequence, and continue until
the patient fails to repeat all the numbers correctly.
TEST ITEMS
3-7
7-4-9
8-5-2-7
2-9-6-8-3
5-7-2-9-4-6
8-1-5-9-3-6-2
3-9-8-2-5-1-4-7
7-2-8-5-4-6-7-3-9
9-2
1-7-4
5-2-9-7
6-3-8-5-1
2-9-4-7-3-8
4-1-9-2-7-5-1
8-5-3-9-1-6-2-7
2-1-9-7-3-5-8-4-6
42
SCORING: The patient of average intelligence can accurately repeat five to

seven digits without difficulty. In a nonretarded patient without obvious
aphasia, inability to repeat more than five digits indicates defective attention.
Specific age-related norms for this task are readily available.1O,22,23
Sustained Attention
A simple test of sustained attention that can be readily administered at the
bedside is the "A" Random Letter Test. It consists of a series of random letters
among which a target letter appears with greater-than-random frequency. The
patient is required to indicate whenever the target letter is spoken by the
examiner.
DIRECTIONS: Tell the patient: "1 am going to read you a long series of
letters. Whenever you hear the letter 'A,' indicate by tapping the desk." Read
the following letter list in a normal tone at a rate of one letter per second.
TEST ITEMS
L
A
P
Z
T
N
A
Y
P
K
F
E
A
L
M
A
B
A
U
o
F
U
S
R
0
M
T
B
R
A
A
E
A
A
S
C
A
SCORING: Currently, only preliminary standardized norms exist for this

test. The average person should complete the task without error (x = 0.2); a
sample of randomly selected brain-damaged patients made an average of 10
errors. I7 Examples of common organic errors are (1) failure to indicate when
the target letter has been presented (omission error); (2) indication made
when a nontarget letter has been presented (commission error); and (3) failure to stop tapping with the presentation of subsequent nontarget letters (perseveration error).
Another attention test that has been traditionally included in mental
status examinations is the Serial Sevens Subtraction Test (e.g., counting backward from 100 by 7s: 100, 93, 86, ... ). Results of studies of performance by
normal people suggest that errors on this test may be influenced by intellectual capability, education, calculating ability, or socioeconomic status, rather
than indicating a pathologic process. I2,I8 Excellent performance indicates adequate attention or mental control, but failure may reflect any of a number
of problems, inattention being but one. In general, this test has proved of
limited validity.
Unilateral Inattention
Unilateral inattention (suppression or extinction) should be tested during the
routine sensory examination by using double (bilateral) simultaneous
stimulation.
ATIENTION
43
DIRECTIONS: Double simultaneous stimulation is tested in all major sensory modalities. In tactile testing, corresponding points on both sides of the
body are touched simultaneously with equal intensity. Visual testing is done
by having the patient face the examiner and fix his or her gaze at a point on
the examiner's face. The examiner then wiggles a finger in right and left peripheral fields. Auditory testing is carried out by having the examiner stand
behind the patient and provide a stimulus of equal intensity to each ear.
Before undertaking bilateral simultaneous stimulation, the examiner
must ensure that basic sensation for each modality is intact bilaterally. If one
side is inferior on unilateral testing, defects found during simultaneous testing
would not necessarily reflect inattention.
Extinction is present when the patient suppresses the stimuli from one
side of the body. Extinction may occur in all modalities (polymodal neglect)
or may be restricted to a single modality. When extinction is elicited, the
degree of inattention can be assessed by increasing the magnitude of the
stimulus on the inattentive side.
When the double simultaneous stimulation includes one proximal and
one distal stimulus, the distal stimulus tends to be neglected or extinguished. 4
This is particularly true when the proximal stimulus is the face and the distal
one the hand. Normal adults under 65 often extinguish the hand stimulus
on the first trial but usually begin to identify both stimuli after several trials.
Patients with organic brain syndromes rarely recognize the hand stimulus
even after as many as 10 trials. This test (Face-Hand Testf is a very useful
simple test for organic disease. Some normal elderly individuals will also
extinguish the hand stimulus; therefore, the test must be interpreted with
caution in patients over 65.
ANATOMY AND CLINICAL

IMPLICATIONS
The basic anatomic structures responsible for maintaining an alert state are the brain
stem reticular activating system and the diffuse thalamic projection system (the diencephalic extension of the reticular formation).13
The mechanism by which this ascending activation is focused and extraneous stimuli are screened out is less certain. Cortical and limbic stimulation
can definitely influence the ascending system, so it is probable that attention
results from a balance among ascending (reticulocortical) activation, ascending inhibition, and cortical (corticoreticular) modulation. 13 Selectively focusing attention requires a widespread network of cortical neurons, particularly
the prefrontal including the posterior cingulate gyrus inferior parietal cortex
and medial temporal/occipital cortices. IS The importance of cortical influence
in focusing attention is demonstrated in the experience of every student. Concentration while studying frequently requires conscious voluntary effort that
is cortical in origin. The limbic system is also an integral part of the attention
44
process; limbic input adds emotional importance to the object of attention.

A child who watches a cartoon is stimulated to pay attention by the pleasure
and excitement generated by the spectacle. The student who is studying for a
test is aided in the need to concentrate by a fear of failure or a drive to
succeed. These limbic influences are important and may be the critical factor
that facilitates the screening out of extraneous stimuli. The principal stimulus
is of greater emotional value than the incidental events in the environment,
and therefore it attracts greater attention.
Because attention represents a complex interaction oflimbic, neocortical,
and ascending activating functions, many areas of the brain exist in which damage can disrupt the ability to attend. Damage to the ascending activating system
itself usually causes alterations in the level of consciousness. In such patients,
alterations in attention are directly related to the more basic deficit in alertness. Inattention caused by lesions in the midbrain activating system is clinically rare, although a rather profound unilateral inattention has been experimentally produced in monkeys with lesions in the midbrain. 20 Inattention
has also been observed clinically in patients with lesions of the thalamus,21
the posterior internal capsule,s and other subcortical structures. 14
Some of the patients who survived the encephalitis epidemic of 1918 to
1921, which was associated with Economo's disease, were left with lesions in
the ascending inhibitory portion of the reticular substance of the pons and
medulla. These patients developed a behavior pattern characterized by hyperactivity and distractibility, which was called "organic driveness."ll This
state is clinically similar to that seen in some children with AttentionDeficit/Hyperactivity Disorder (ADHD).
Probably the most common cause of decreased attention and vigilance in a
hospital population is diffuse brain dysfunction (delirium). This dysfunction, in
which all cells in the central nervous system are affected, is usually caused by
metabolic disturbance, drug intoxication, postsurgical states, or systemic infection. Another common cause of inattention is extensive bilateral cortical
damage of any etiology (e.g., atrophy, multiple infarcts, encephalitis, or head
trauma). In patients with advanced Alzheimer's dementia, for example, new
stimuli in the vicinity may quickly draw their attention and they then become
"stimulus bound." The cortical role in focusing and maintaining attention is
very well demonstrated in these patients.
Patients with bilateral lesions of the frontal lobes or the limbic system (e.g.,
Korsakoff's syndrome) have a type of inattention that is characterized by indifference
and perseveration. Clinically, they are apathetic toward their surroundings and
are not particularly interested in test items per se. Such patients usually perform well on the digit repetition task but cannot complete the "A" Random
Letter Test accurately. These patients often fail to recognize an "A" at the end
of a long sequence (e.g., U C J TOE A) because their attention has wandered.
Patients with a frontal lobe lesion also have great difficulty shifting from one
pattern of response to another, resulting in perseveration. This perseveration
AITENTION
45
is commonly seen both behaviorally and on the "A" Random Letter Test.
For example, the series E V A A RAT may be failed by an individual with
perseveration in the following way (italic letters indicate the patient's taps):
EVAARAT.
Right hemisphere lesions have a stronger effect on attention than do left-sided
lesions. Denial, unilateral neglect, and extinction on double simultaneous
stimulation occur more frequently and are more prominent in patients with
right hemisphere lesions. 2 ,6,7,16 The reason for this peculiar quality of the right
hemisphere is not known. It is possible that reticulocortical or corticoreticular
fibers are more dense in the right hemisphere, although there is no currently
available pathologic evidence that this is true. For a thorough discussion of
the theories of the inattention syndrome, see Weinstein and Friedland,25
Contralateral inattention to double simultaneous stimulation is seen with parietal lesions of either hemisphere. The damage to parietal tissue apparently reduces reticulocortical interaction on the damaged side, thus allowing the intact hemisphere an advantage in the stimulus rivalry.5,9 Such patients will
characteristically report not feeling the stimulation on the side opposite the
lesion even though both sides were stimulated with equal intensity.
Many functional mood alterations can affect attention. Anxiety causes distractibility and difficulty concentrating; depression produces disinterest and
reduced arousal. All such mood changes hinder performance on attention
tasks and generally decrease attention.
SUMMARY
Attention results from an interplay among brain stem, limbic, and cortical
activity that allows the patient to focus on a specific task to the exclusion of
irrelevant stimuli. Both functional and organic illness can disrupt attention
and cause a failure of attention. Assessment of attention must be done early
in the mental status examination because the valid testing of many subsequent functions relies on its integrity, Inattention and distractibility can significantly impair a patient's performance on the more demanding tasks of
new learning, calculating, and verbal abstraction.
REFERENCES
1. Ballard, IC: Computerized assessment of sustained attention: A review of factors affecting
vigilance performance. I Clin Exp Neuropsychol 18:843-863, 1996.
2. Bender, MB: Perceptual interactions. In Williams, D (ed): Modern Trends in Neurology, Vol
5. Appleton-Century-Crofts, New York, 1970, pp 1-28.
3. Bisiach, E and Vallar, G: Hemineglect in humans. In Boller, F and Grafman, I (eds): Handbook of Neuropsychology, Vol 1. Elsevier Science Publishers, Amsterdam, 1988, pp 195222.
4. Critchley, M: The Parietal Lobes. Edward Arnold & Co., London, 1953.
5. Denny-Brown, D, Meyers, L and Hornstein, S: The significance of perceptual rivalry resulting

from parietal lesions. Brain 75:433, 1952.
46
6. Ferro, J and Kertesz, A: Posterior internal capsule infarction associated with neglect. Arch
Neurol 41:422, 1984.
7. Gainotti, G: Emotional behavior and hemispheric side of lesion. Cortex 8:41, 1972.
8. Heilman, KM, Valenstein, E, and Watson, RT: The neglect syndrome. In Frederiks, JAM (ed):
Handbook of Clinical Neurology, Vol 1 (45), Clinical Neuropsychology. Elsevier Science Publishers, Amsterdam, 1985, pp 153-183.
9. Heilman, KM, Watson, RT, and Valenstein, E: Neglect and related disorders. In Heilman, KM
and Valenstein, E (eds): Clinical Neuropsychology. Oxford University Press, New York, 1993,
pp 279-336.
10. Invik, R1, et al: Mayo's Older Americans Normative Studies: WAlS-R norms for ages 56-97.
The Clinical Neuropsychologist 6:1, 1992.
11. Kahn, E and Cohen, L: Organic driveness: A brainstem syndrome and an experience. N Engl
J Med 210:748, 1934.
12. Lezak, MD: Neuropsychological Assessment. Oxford University Press, New York, 1995,
p 371.
13. Magoun, H: The Waking Brain. Charles C Thomas, Springfield, IL, 1963.
14. Mesulam, M-M: A conical network for directed attention and unilateral neglect. Ann Neurol
10:309, 1981.
15. Morecraft, RJ, Gevla, C, and Mesulam, M-M: Architecture of connectivity within a cingulofronto-parietal neurocognitive network for directed attention. Arch Neurol 50:279-284,
1993.
16. Oxbury,1, Campbell, D, and Oxbury, S: Unilateral spatial neglect and impairment of spatial
analysis and perception. Brain 97:551, 1974.
17. Simpson, N, Black, FW, and Strub, RL: Memory assessment using the Strub-Black Mental
Status Examination and the Wechsler Memory Scale. J Clin Psychol 42:147, 1986.
18. Smith, A: The series sevens subtraction test. Arch Neurol 17:18, 1976.
19. Umilta, C: Orienting of attention. In Boller, F and Grafrnan, J (eds): Handbook of Neuropsychology, Vol 1. Elsevier Science Publishers, Amsterdam, 1988, pp 115-193.
20. Watson, RT, et al: Neglect after mesencephalic reticular formation lesions. Neurology 24:294,
1974.
21. Watson, RT, Valenstein, E, and Heilman, KM: Thalamic neglect. Arch Neurol 38:501, 1981.
22. Wechsler, D: Manual of the Wechsler Adult Intelligence Test, ed 3. The Psychological Corporation, New York, 1997, pp 181-194.
23. Wechsler, D: Manual for the Wechsler Memory Scale, ed 3. The Psychological Corporation,
New York, 1997, pp 135-191.
24. Weinberg, WA and Harper, CR: Vigilance and its disorders. In Brumback, RA (ed): Behavioral
Neurology. Neurol Clin 11:59-78, 1993.
25. Weinstein, EA and Friedland, RP (eds): Hemi-inattention and hemispheric specialization.
Advances in Neurology, Vol 18. Raven Press, New York, 1977.
GHAPTER
LANCUACE
Language is the basic tool of human communication and the basic building
block of most cognitive abilities. Its integrity therefore must be established
early in the course of mental status testing. If deficits are found in the language system, the assessment of cognitive factors such as verbal memory,
proverb interpretation, and oral calculations becomes difficult, if not
impossible.
Language disturbances are commonly seen in patients with focal or diffuse brain disease; in fact, demonstration of a specific language disturbance is
pathognomonic of brain dysfunction. Language disturbances have been well studied, and a number of distinct clinical neuroanatomic syndromes have been
described. These are important to the clinician because of the relationship of
specific language syndromes to neuroanatomic lesions. The ability to communicate using language is such a critical function that any disruption thereof
results in a significant functional handicap.
To assess language function the examiner must first develop a systematic
approach to the evaluation and then become acquainted with the various
classic syndromes of language impairment. Cerebrovascular accidents
(strokes), brain tumors, trauma, dementia, and other brain lesions or diseases
may all cause language disturbances. Such disturbances are not always easily
characterized by a cursory examination, and a familiarity with testing and the
patterns of language disruption will make the aphasic, alexic, and agraphic
syndromes more understandable.
TERMINOLOCY
Dysarthria is a specific disorder of articulation in which basic language
(grammar, comprehension, and word choice) is intact. Patients with dysarthria produce distorted speech sounds that have a variable degree of
intelligibility.
Dysprosody is an interruption of speech melody (e.g., tone, accent,
47
48
tempo). Speech inflection and rhythm are disturbed, resulting in speech that
is monotonaL halting, and sometimes mistaken for a foreign accent.42
Apraxia (buccofacial or oral) is the inability to perform skilled movements of the face and speech musculature in the presence of normal comprehension, muscle strength, and coordination. When asked to show how
they would blowout a match, patients with apraxia may have difficulty approximating a pucker, inhale instead of exhale, exhale vigorously without
puckering their lips, or say the word "blow." Any of these errors would be
classified as apraxic. Oral apraxia that is evident only when the patient attempts to produce speech sounds is called verbal apraxia.
Aphasia is a true language disturbance in which the patient demonstrates
an impaired production and/or comprehension of spoken language. The basic
aphasic defect is in higher integrative language processing, although articulation and praxis errors may also be present. Aphasia usually refers to a loss
of language after brain damage, but "developmental aphasia" is used when
a child has a specific delay in language acquisition disproportionate to general
cognitive development.
Alexia is the term used to describe a loss of reading ability in a previously
literate person. Alexia does not refer solely to a total loss of reading ability,
but to any level of acquired disturbance in reading. Alexia is not synonymous
with dyslexia, which is a specific developmental learning disorder of children
who have normal intelligence but who experience unusual difficulty in learning to read.
Agraphia is an acquired disturbance in writing. It refers specifically to
errors of language and not to problems with the actual formation of letters
or poor handwriting. Disorders of spelling are also included in this disorder.
EVALUATION
The language system should be evaluated in an orderly fashion. Specific attention
must be paid to spontaneous speech, comprehension, repetition, and naming.

Verbal language should be evaluated, and then reading and writing should
be assessed. A short period of systematic testing can usually identify and
roughly characterize an aphasic deficit. Because patients with aphasia are always agraphic and frequently alexic, the testing of reading and writing may
be abbreviated in these cases. In those who are not aphasic, reading and
writing should be fully evaluated because alexia or agraphia, or both, may be
seen in isolation. Language testing can be very comprehensive; for further
information, the interested examiner is referred to the test batteries listed in
Appendix 1.
Handedness
Because of the close alliance between handedness and cerebral dominance
for language, the patient's handedness should be determined before beginning for-
LANGUAGE
49
mal language testing. First, ask the patient whether he or she is right- or lefthanded. As many natural left-handers have been taught to write with their
right hand, observation of the hand used for writing may not be an accurate
reflection of natural handedness. Next, ask the patient to demonstrate which
hand is used to hold a knife, throw a ball, stir coffee, and flip a coin. Also,
ask the patient about any tendency to use the opposite hand for any skilled
movement. In addition, a family history of left-handedness or ambidexterity
is important because handedness and cerebral dominance for language are
significantly influenced by heredity. The spectrum of handedness ranges from
strong right-handedness to left-handedness. 25 Strong or exclusive unilateral
handedness is much stronger in right-handed than in non-right-handed persons. Also, patients with a strong family history of left-handedness tend to
be ambidextrous and not strongly one-handed. 31 A statement of the patient's
handedness as well as the family history of handedness should be recorded.
Spontaneous speech
Eliciting Speech Production
The first step in language testing is to listen carefully to the patient's spontaneous
speech. If the patient offers none, open-ended questions should be asked in
order to elicit speech production. Listening to the patient's spontaneous
speech even briefly may provide invaluable information that cannot be obtained during more formal aspects of the language examination. It is wise to
ask the patient to discuss relatively uncomplicated issues, such as "Tell me
why you are in the hospital" or "Tell me about your work." This type of
general conversational question affords the patient a familiar topic and usually elicits his or her best efforts. In contrast, questions that require a mere
"yes" or "no" answer will not provide sufficient speech output for meaningful
evaluation. Pictures may be used to stimulate speech, but these can restrict
the range of language output because of the limitations of the specific
stimulus.
Observing Spontaneous Speech

Several clinical observations must be made and noted while listening to the
patient's spontaneous speech:
Is speech output present?
Is the speech dysarthric or dysprosodic?
Is there evidence of specific aphasic errors (e.g., errors of syntax, wordfinding pauses, abnormal words, or paraphasias)?
The most obviously abnormal output is the total lack of any speech, in which
patients may make some vocalizations but no meaningful linguistic utterances. This reduced output may be due to severe dysarthria, apraxia (buccofacial), or true aphasia. Of slightly less severity is a specific aphasic disorder
50
that is characterized by stereotyped output in which the patient repeats the

same utterance in response to each question. The utterance is usually a nonsense word like "bica, bica" or "a dis, a dis, a dis." Patients with very restricted
output can, however, often surprise the naive examiner by producing wellarticulated curse words or short phrases when under emotional stress.
Types of Aphasic speech

Aphasic language production is characterized by errors of grammatic structure, difficulty in word finding, and the presence of word substitutions (paraphasias). One common type of aphasic speech pattern has been classified as
nonfluent. 8 ,24 Nonfluent output is sparse and effortful, contains primarily
nouns (substantive words), is agrammatic, and contains frequent word-finding pauses. For instance, the nonfluent patient describing winter weather
might say "ah, ah, chold ... snow ... freezing ... ah, ah ... cold.
At the other end of the spectrum of fluency is a group of patients with
aphasia who produce an easily flowing speech that is remarkably empty of
content and contains many abnormal words (e.g., paraphasias). Paraphasias
are words that are either substitutions for the correct word (e.g., "I drove
home in my pen") or contain substituted syllables (e.g., "I drove home in
my lar"). The complete word substitution ("pen" for "car") is a verbal or
semantic paraphasia. The syllable substitution ("lar" for " car"') is a phonemic
or literal paraphasia. The substitution of a non-English or nonsense word is
the neologistic (new word) paraphasia ("I drove home in my strub").
Fluent aphasic speech is an easily recognizable speech pattern. The output is fluent and is characterized by normal or excessive rate of word production, often with a distinct press of speech. Content words (nouns and
verbs) are lacking, and, in contradistinction to nonfluent output, small grammatic words such as articles, conjunctions, and interjections prevail. The
nouns and verbs are often paraphasic. Because of the difficulty in producing
nouns, word-finding pauses may interrupt the easy flow of speech. A patient
with fluent aphasia who was describing a picture of a man after a shipwreck
said the following: lilt is a ... I can see it ... it is near a cold and he has a
... actually what has happened is part of a ... the rest of it there is a man
right here and he is cold being out there." Occasionally, the language of the
patient with aphasia contains so many paraphasic errors that the discourse is
virtually unintelligible and impossible to follow. The term "jargonaphasia" is
used for this heavily paraphasic but fluent speech.
The expressive language of many patients with aphasia cannot be classified strictly according to fluency. The primary goal in the evaluation of a braindamaged patient is to recognize that the language production is in fact aphasic. With
experience, the examiner can accurately recognize aphasic language and can
classify the patient's language output, which often provides important information about the locus of the brain lesion. Patients with nonfluent aphasia
are likely to have an anterior left hemisphere lesion, whereas those with fluent
II
LANGUAGE
51
aphasia usually have posterior lesions. 8 This anterior-nonfluent, posteriorfluent dichotomy holds true in about 85% of cases, but sometimes the reverse
is true (i.e., posterior lesion occurring with nonfluent aphasia, or an anterior
lesion with fluent aphasia).? The classification of an aphasia does not depend on
the output characteristics alone; a complete evaluation of all language functions is
always indicated.
Verbal Fluency
Verbal fluency refers to the ability to produce spontaneous speech fluently
without undue word-finding pauses or failures in word searching. Normal
speech requires verbal fluency in the production of responses and the formulation of spontaneous conversational speech. This ability is often impaired
after brain injury, especially that associated with anterior left hemisphere lesions. On formal testing, patients with aphasia almost invariably demonstrate
some impairment in fluency. Additionally, individuals with early dementia
or clinically silent left hemisphere lesions who exhibit relatively normal expressive speech and no other signs of word-finding difficulty may show subtle
deficits on fluency tests. Verbal fluency is a reflection of word-finding efficiency, and fluency testing evaluates the patient's ability to scan memory
traces rapidly in a specific semantic or phonemic category and to produce a
series of responses in a given time frame.
An overall impression of fluency is gained by listening to the patient's
spontaneous speech, but subtle defects in fluency can be elidted only through
specific fluency tests. Verbal fluency is typically evaluated by tabulating the
number of words the patient produces within a restricted category (e.g., animal types or words beginning with a specific letter) and within a specified
time limit. Two easily administered evaluations are the Animal-Naming
Teseo and the FAS Test (a controlled oral word association test). 14 Tests using
semantic categories such as animal names or grocery items are more sensitive
indicators of early dementia than those using words beginning with a specific
letter, such as the FAS Test. 6 We therefore usually use animal naming in clinical testing, especially when a deterioration in general cognitive functioning
is suspected.
DIRECTIONS: For animal naming, instruct the patient to recall and name
as many animals as possible. Any animal from the zoo, farm, jungle, water,
or house is acceptable, but the examiner should not suggest these various
locations, as subcategory shifting is one of the main cognitive challenges of
this test. Time the patient's performance for 60 seconds, encouraging him or
her to continue whenever necessary. The score is the number of correctly
produced animal names during the 60 seconds. Record the correct responses
as well as any paraphasic productions.
SCORING: The normal individual should produce from 18 to 22 animal
names during a 60-second period, with the expected variation being 5 to
52
7. 30,51 Age is a statistically significant factor in the expected performance on

this task. Normal individuals age 69 and under will produce approximately
20 animal names, with a standard deviation of 4.5. This level of performance
drops to 17 (::t:2.8) in the 70s and to 15.5 (::t:4.8) in the 80s. Scores of less
than 13 in otherwise normal patients under age 70 should raise the question
of impaired verbal fluency; scores less than 10 in patients under age 80 are
suggestive of a word-finding problem; in an 85-year-old, however, a score of
10 may be the lower limit of normal.
DIRECTIONS: The FAS Test consists of three separate, timed word-naming
trials, using the letters "F," "A," and "S," respectively. The patient is instructed
to name as many words as possible (not including proper names) that begin
with the stipulated letter during each 60-second trial. The patient's responses
are recorded, including any paraphasias and repeated words that were produced in the three trials. Different forms of the same word (e.g., short,
shorter) count as separate responses.
SCORING: Normal people name from 36 to 60 words, with performance
depending in part on age, intelligence, and educational level. 14 An inability
to name 12 or more words per letter is indicative of reduced verbal fluency.
Performance on this test should be cautiously interpreted in patients with
under 10 years of formal education or intelligence quotients (IQs) of less
than 85.
Comprehension
Assessing the comprehension of spoken language is the next step in the language evaluation. Comprehension must be tested in a structured fashion, without
reliance on the patient's ability to answer verbally. The most common error in
assessing comprehension is to ask the patient to answer general or openended questions. Such questions require the patient to construct complex
verbal answers that test the integrity of the entire language system and not
verbal comprehension in isolation. Comprehension testing should require the
minimum verbal response necessary for the patient to demonstrate that he
or she has understood the examiner. For example, a question such as ''What
was the weather like in January?" does not assess language comprehension
in isolation, whereas one such as "Is it snowing out today?" does.
We use two methods ottesting comprehension: pointing commands and questions that can be answered with a "yes" or "no" response. Testing the patient's
ability to point to single objects in the room, body parts, or articles collected
from the examiner's pockets (e.g., coins, comb, pencil, keys) is an excellent
way to quantify single-word comprehension. This task may be increased in
complexity by requiring that the patient point to an increasing number of
objects in sequence (e.g., "Point to the wall, the window, and your nose").
Increase the number of objects until the patient consistently fails. The patient
LANGUAGE
53
of average intelligence without aphasia should succeed in pointing to four

objects or more. Because the patient with aphasia who has comprehension
difficulty may still be able to point to one or two items accurately, it is important to continue testing until consistent failure occurs. This test provides
an evaluation of single-word comprehension, auditory retention, and sequence memory. For clarity, the level of performance should be described
accurately on the test form.
Next, a series of simple and complex questions that require only "yes"
or "no" answers should be asked. For example, "Is this a hotel?" "Is it raining
today?" "Do you eat breakfast before dinner?" Question content may be simple or complex, as necessary. Before testing, be sure that the patient can reliably indicate "yes" and "no." Many patients confuse these two responses
and cannot answer accurately or nod or shake the head appropriately. Also,
it is important to ask at least seven questions because correct responses can
occur by chance alone 50% of the time with "yes" and "no" questions. Correct
answers should alternate between "yes" to "no" randomly because of the
tendency for brain-damaged patients to perseverate. It is not uncommon for
such patients to answer "yes" to 10 consecutive questions without knowing
the correct answer to any of them.
Many clinicians test language comprehension by asking patients to carry
out motor commands such as "Show me how to light a cigarette" or "Stick out
your tongue." If the patient correctly carries out such commands, he or she
has certainly understood them; however, many patients with aphasia have
significant apraxia and fail to follow the command correctly because of a
problem in high-level motor integration and not because of poor verbal
comprehension.
Repetition
Repetition of spoken language is linguistically and, to some extent, anatomically a
distinct function. In certain types of aphasia, repetition may be either spared
or involved in relative isolation. Therefore, it is clinically relevant to test this
function specifically. Repetition is a complex process that can be affected by
impaired auditory processing, disturbed speech production, or disconnection
between receptive and expressive language functions.
DIRECTIONS: Testing should present material in ascending order of difficulty, beginning with single monosyllabic words and proceeding to complex
sentences. The following list of items provides a suitable range of difficulty.
The patient should be asked to repeat the word or sentence verbatim after
the examiner.
TEST ITEMS
1. Ball.
2. Help.
54
3.
4.
5.
6.
7.
8.
9.
10.
Airplane.
Hospital.
Mississippi River.
The little boy went home.
We all went over there together.
The old car wouldn't start on Tuesday morning.
The fat short boy dropped the china vase.
Each fight readied the boxer for the championship bout.
SCORING: The examiner must listen for paraphasias, grammatic errors,
omissions, and additions. Normal people and brain-damaged patients without aphasia can accurately repeat sentences of 19 syllables. 46 Performance is
related to intelligence and educational level, but errorless performance is expected on these specific items.
Naming and Word Finding

The ability to name objects is one of the earliest acquired and most basic
language functions. Naming ability stays remarkably stable over the decades,
with 80-year-olds performing at the same level as 25-year-olds. 45 Very old
persons (over 80) and relatively uneducated persons over 70, however, tend
to demonstrate mild naming problems. 49 Naming ability is almost invariably
disturbed in all types of aphasia. 30 Impaired naming ability is called anomia.
Word-finding difficulty, which is closely related to anomia, is a reduced
ability to retrieve the nouns and verbs used in spontaneous speech. Specific
word-finding problems can be detected by listening to the spontaneous
speech of the patient with aphasia. Asking the patient to describe a picture
that contains objects and actions usually brings out any word-finding defect.
Anomia may also be objectively tested with a confrontation naming test.
In this task, the examiner points to a variety of objects or pictures of objects
and asks the patient to name them. The examiner should select from 10 to
20 items. Several categories of objects should be used (colors, body parts,
room objects, articles of clothing, and parts of objects). Various categories are
chosen because some patients with aphasia have a curious inability to name
objects in a specific category while maintaining adequate ability to name
objects in other categories. Because the disruption of naming has varying
degrees of severity, it is important to use uncommon (low frequency of usage)
items as well as common (high frequency of usage) items. For example,
"nose," "arm," and "floor" are common, high-frequency words, whereas
"watch stem and crystal," "shin," and "coat lapel" are uncommon, lowfrequency words. Many patients with aphasia will be able to name common
objects quickly and accurately, only to show great hesitancy, paraphasia, and
circumlocutio'n with uncommon objects. Some patients obviously recognize
LANGUAGE
Colors
Red
Blue
Yellow
Pink
Purple
Clothing and Room Objects
Door
Watch
Shoe
Shirt
Ceiling
55
Body Parts
Eye
Leg
Teeth
Thumb
Knuckles
Parts of Objects
Watch stem (winder)
Coat lapel
Watch crystal (lens)
Sole of shoe
Buckle of belt
the object and are able to demonstrate and describe its use but cannot name
it. For example, a patient shown a door key responded with "Oh, you know
... the thing used to get in the ... you tum it to get in."
The 20 items in Table 5-1, listed in ascending order of difficulty, are
suggested for evaluating naming ability. Normal individuals will know all
items except the parts of objects; on this set of five words the average score
is 4.5 (O.B). The examiner should note that the names for parts of objects
are low-frequency words and will be frequently misnamed or not named by
most patients with aphasia and those with early dementia. With experience,
each examiner will develop a personal repertoire of items tailored to his or
her own office and patient population.
Reading
Reading ability is one of the few aspects of mental status testing that is directly
related to educational experience. It is important, therefore, to determine the
patient's educational background before testing reading. Demonstrating an

alexia (reading deficit) in a patient, only to discover that he or she has had
just 3 years of formal education, is merely documenting the patient's illiteracy.
Both reading comprehension and reading aloud ability should be tested. Both
are usually defective in the same patient, but either can be disturbed in isolation. If the patient is not aphasic, screen for alexia by having the patient
read a paragraph from a newspaper or magazine. To test reading in patients
with aphasia, begin with having them read aloud first short single words,
then phrases, sentences, and finally paragraphs. If they succeed at the lower
levels, then have the patients read the names of objects in the room or on
display and point to them. Finally, have patients read questions that can be
56
answered "yes" or "no" or ask them questions about what was written. For
example, if the patient read the sentence "The boy and girl walked in the
snow," the examiner could ask, "Did the boy go alone?" or "Was it raining
when the boy and girl went for a walk?"
The examiner should note any syllable or word substitutions (paralexic
errors), omitted words, and defects in comprehension. Occasionally, patients
have visual field defects or problems in ocular motility. In such cases, the
examiner must help the patient stay on the written line and ensure that the
patient completes one line before starting another. Using careful observation
and examination, the examiner can readily separate the patients with true
alexia from those having problems with the mechanics of reading.
writing
Writing must be tested in the same way as that used to test reading. If the
patient shows evidence of aphasia, he or she undoubtedly also has an agraphia.
Agraphia is diagnosed when a patient demonstrates basic language errors,

gross spelling errors, or use of paragraphias (word or syllable substitutions).
To test writing, first have the patient write letters and numbers to dictation.
Second, ask the patient to write the names of common objects or body parts.
Third, if patients can successfully write single words, ask them to write a short
sentence describing the weather, their job, or a picture from a magazine.
Asking patients to write their name is not always particularly meaningful
because name writing may be preserved even in the presence of gross
agraphia. In the literate patient without aphasia, the examination can begin
with this sentence-writing task. Patients with aphasia who cannot write spontaneously may show residual writing ability when asked to write to dictation.
Writing often shows a misalignment, in which the written line slants
upward or downward. This misalignment is an error in the mechanics of
writing but is not an agraphia per se.
Spelling
Spelling is a complex, little-studied, higher-language function that is strongly
associated with educational experience. For practical purposes, spelling can
be evaluated by asking the patient to spell dictated words. Gross errors in
spelling can be detected in bedside testing; if it is important to establish an
actual level of competence, standardized achievement tests should be used
(Appendix 1).
CLINICAL IMPLICATIONS
Cerebral Dominance
Approximately 90% of the population is considered definitely right-handed.
Of this 90%, more than 99% are strongly left hemisphere-dominant for language. 10
LANGUAGE
57
Because of this strong language dominance in right-handed individuals, left

hemisphere lesions frequently cause aphasia, whereas right hemisphere lesions
rarely result in such deficits (i.e., a crossed aphasia).52
Left-handed individuals (non-right-handers) have a far different pattern of
cerebral dominance for language. Approximately 70% are left hemisphere-
dominant, 13% are right hemisphere-dominant, and the remainder are

mixed. 28 In individuals with a strong family history of left-handedness (nonright-handedness, or sinistrality), this mixed dominance tends to be more
prominent. Strongly left-handed individuals with no history of familial sinistrality tend to have the strongest left hemisphere dominance for language
of all left-handed individuals. Accordingly, damage to either hemisphere in
a left-handed patient usually results in aphasia. Aphasia in a left-handed patient with a lesion in either hemisphere is less severe than that resulting from
a similar lesion in the left hemisphere of a right-handed patient. Knowing the
patient's cerebral dominance for language is important for localizing lesions and for
deciding the risk that neurosurgical procedures pose to language. In cases in which
documentation of hemispheric dominance for language is critical (e.g., a lefthanded patient with a right middle cerebral artery aneurysm), an intracarotid
Amytal injection (Wada test) at the time of angiography can often establish
dominance. 48
Aphasia Syndromes
The impairment of language secondary to brain damage is not a unitary process; all
components of language can show variable disruption. The extensive study of right-
handed patients with aphasia has resulted in a generally accepted schema of

cortical regionalization of language. Because some features overlap among
patients who demonstrate mixed aphasia, some aphasiologists do not believe
that this traditional neurologic classification system is suitable for neurolinguistic research. 16,50 However, this classification system follows the classic anatomic pattern, is easy for the student to understand, and is useful to the
clinician for localizing lesions.
The clinical features of a patient's aphasia change dramatically over time. The
acute destructive lesion causes maximal language disruption and is often associated with considerable disorientation and confusion, In the first several
weeks, recovery is rapid and the aphasic picture constantly changes. After
approximately 3 to 4 weeks, the aphasic pattern is more stable and may be
fully assessed, The final prognosis of language recovery, however, cannot be
given at that time bf'cause the reorganization and recovery process can continue for months or even years.
The posterior language area (area 1, Fig. 5 -1) is the cortical area primarily
concerned with the comprehension of spoken language, This area has traditionally
been referred to as Wernicke's area, although the exact boundaries of the
region have not been established. 12 The anterior language area (area 2, see Fig,
5-1) subsumes the functions of language production. Brodmann's area 44 within
58
FIG U R E 5 - 1. Anterior and posterior language areas.
the anterior language area is the classic Broca's area. Recent positron emission
tomography (PET) studies of glucose metabolism have supported this regional specialization in patients with aphasia but have demonstrated that
almost all such patients, irrespective of clinical characteristics, have evidence
of hypometabolism in the temporal region on the left.35 Such studies demonstrate that the language system is quite complex physioanatomically and is not
simply a collection of cortical centers that act independently.
Traditionally, patients with damage in the posterior speech area are said
to have "receptive aphasia" because of their primary difficulty in understanding spoken language. Patients with lesions in the anterior area are said to
have "expressive aphasia" because of their primary difficulty in producing
language. The problem with using "expressive aphasia" in this context however, is that all patients with aphasia have some type of abnormal language
expression. For this reason, we prefer to use the classification system described
hereafter rather than the expressive-receptive dichotomy.
Global Aphasia
Global aphasia, the most common and severe form of aphasia, is characterized by spontaneous speech that is either absent or reduced to a few stereotyped words or sounds (e.g., "ba, ba, ba" or "dis, a dis, a dis"). Comprehen-
LANGUAGE
59
sion is absent or reduced to only recognition of the patient's name or a few

selected words. Performance on repetition is at the same level as spontaneous
speech. Reading and writing are likewise severely impaired. Global aphasia is
caused by a large lesion that damages most or all of the combined language areas 1
and 2 (anterior and posterior shaded areas). The most common lesion causing
global aphasia is an occlusion of the internal carotid artery or the middle

cerebral artery at its origin, caused by an embolus from the heart or carotid
artery. Unfortunately, the prognosis for language recovery in these patients is
poor. Global aphasia is almost always associated with hemiplegia. Because of
these combined deficits, such patients have a severe chronic disability\
Broca's Aphasia
Patients with Broca's aphasia have nonfluent, dysarthric, dysprosodic, effortful
speech. They utter mostly nouns and verbs (high-content words), with a pau-
city of grammatic fillers. The characteristic speech has been called agrammatic
or telegraphic. For example, one patient with Broca's aphasia described a
picture of a boy on a stool stealing cookies while his mother is washing dishes
and letting the sink run over 30 in the following manner: "Boy ... ah girl
cookie ... stool falling ... water spilling ... dishes." Repetition and reading
aloud are as severely impaired in these patients as is their spontaneous
speech. Auditory and reading comprehension are surprisingly intact, although
the comprehension of complex grammatic phrases (e.g., "Do you eat lunch
before breakfast?") is often impaired. Naming may show paraphasic
responses.
This characteristic nonfluent aphasic syndrome results from a lesion in the anterior speech area (area 2, see Fig. 5 -1 ). The lesion causing Broca's aphasia
includes more than Brodmann's area 44 alone. Lesions restricted exclusively

to area 44 result in only transient dysarthria or dysprosody.3,36 Auditory and
visual (reading) comprehension are intact because parietal and temporal
lobes are not damaged. Patients with Broca's aphasia usually have right
hemiplegia.
These patients often undergo an interesting and significant emotional
change, characterized by frustration, agitation, and depression. 9 Whether this
emotional change is a psychologic reaction to the loss of speech or a specific
organic change associated with left frontal lobe damage is not yet known. 44
The prognosis for language recovery in patients with Broca's aphasia is
generally more favorable than in those with global aphasia. Because of relatively intact comprehension, these patients adjust better to life situations.
Wernicke's Aphasia
Wernicke's aphasia can be considered the linguistic opposite of Broca's aphasia. The patient with Wernicke's aphasia has fluent, effortless, well-articulated
60
speech. The output, however, contains many paraphasias and is often devoid of substantive words. Patients often feel very pressed to speak. The following is an
example of speech in Wernicke's aphasia. The patient was a ferry boat captain
with a left temporal lobe brain tumor. In describing his previous work, the
patient said, 'Yea, I walked on the ... always over ... then pull it in ... tie
the ... ah, ah over and back over wellendy catch it... ." The spontaneous
speech can range from comprehensive sentences with occasional paraphasic
errors to totally incomprehensible jargon in which most words are paraphasic
and the output is devoid of content (jargonaphasia).
The essential feature of Wernicke's aphasia is a severe disturbance of
auditory comprehension. Because the comprehension defect is so marked, the
patient answers questions inappropriately and is completely unaware that the
answers are often total nonsense. Repetition is severely impaired because of
a severe auditory processing defect. Naming is grossly paraphasic. Reading
and writing are also markedly impaired.
The lesion that causes Wernicke's aphasia is in the posterior language area (area
1, see Fig. 5-1). The more severe the defect in auditory comprehension, the
more likely it is that the lesion involves the posterior portion of the superior
temporal gyrus. If single-word comprehension is good but comprehension of
complex material and written language is impaired, the lesion is more likely
to involve the parietal lobe rather than the superior temporal lobe. 30 If the
lesion also involves the middle and inferior temporal gyri, anomia is likely
to be significant and persistent. 3 Because the damage is restricted to parietal
and temporal lobes in most patients, the person with classic Wernicke's aphasia does not have hemiplegia.
Patients with Wernicke's aphasia are sometimes initially considered to
be psychotic rather than aphasic. This confusion arises because the patient
usually does not have a hemiplegia or other neurologic signs and produces
inappropriate, but often reasonably well-formed, sentences. The gross comprehension deficit may not be appreciated, and the inappropriate answers to
the examiner's questions are judged to be due to a basic thought disorder
rather than a language disorder.
These patients often develop unusual patterns of behavior. They are frequently totally unaware of their problem and may talk endlessly without the
slightest appreciation of their language deficit. This indifference may approach
the point of euphoria. Other patients, however, develop a pronounced paranoid attitude accompanied by combative behavior. 9 This behavioral change
may become chronic and require use of major psychotropic medication or
treatment in a long-term psychiatric facility.
Patients with severe comprehension deficits do not have a good prognosis for language recovery, even with intensive language therapy. Milder
Wernicke's aphasia may evolve into conduction or anomic aphasia, in both
of which auditory comprehension is adequate but output contains paraphasias and word-finding pauses.
LANGUAGE
61
Conduction Aphasia
The hallmark of conduction aphasia is a disproportionate deficit in repetition. This
syndrome is characterized by fluent, yet halting, speech with word-finding
pauses and literal paraphasias. Comprehension is good, naming is mildly
disturbed, and repetition is severely defective. This syndrome demonstrates
that repetition and propositional speech (everyday language used to describe
events or thoughts) are distinct psycholinguistic processes that can be selectively impaired by focal brain lesions. In conduction aphasia, reading is quite
good, but writing shows errors in spelling, word choice, and syntax.
Two lesions are known to cause conduction aphasia. The first is usually
reported to involve the supramarginal gyrus and arcuate fasciculus, a long
fiber tract petween the anterior and posterior areas (Fig. 5-2). The second
22
FIG U R E 5 - 2. Arcuate fasciculus (AF) and anterior and posterior language areas.
62
lesion damages the insula, contiguous auditory cortex, and underlying white
matter. This lesion spares the arcuate fasciculus, which arches higher into the
parietal operculum. 21 This entity represents one of the clinical disconnection
syndromes 23 because it literally disconnects the auditory sensory cortex from
the motor speech cortex.
Transcortical Aphasias
The linguistic opposite of conduction aphasia is transcortical aphasia. The
transcortical aphasias are characterized by intact repetition of spoken language but
disruption of other language functions. Some patients have difficulty producing
speech while having adequate language comprehension; others produce fluent speech but have poor comprehension.
The patient with transcortical motor aphasia can repeat, comprehend,
and read well but has the same kind of restricted spontaneous speech exhibited by patients with Broca's aphasia. In contrast, the patient with transcortical
sensory aphasia repeats well but does not comprehend what he or she hears
or repeats. Spontaneous speech and naming are fluent but paraphasic, as in
Wernicke's aphasia. Occasionally, a patient may have a combination of transcortical motor and sensory aphasias. These individuals can repeat long sentences, even in a foreign language, with remarkable accuracy. Repetition is
very easy to initiate in these patients, even inadvertently, because some patients have a tendency to be echolalic (to repeat everything said within the
range of their hearing).
The lesions that cause transcortical aphasia are either extensive, crescentshaped infarcts within the border zones between major cerebral vessels (e.g.,
within the frontal lobe between the territories of the anterior and middle
cerebral arteries and posteriorly between middle and posterior cerebral arteries [Fig. 5-3]) or subcortical lesions of the white matter underlying these
areas of cortex. Transcortical motor aphasia is seen with an anterior border
zone lesion, whereas transcortical sensory aphasia indicates a lesion that resembles a reversed C (see Fig. 5-3). These lesions spare the superior temporal
and inferior frontal cortex (areas 22 and 44 and their immediate environs)
and the parietal perisylvian cortex. This spared perisylvian cortex is all that is
required for complete and accurate language repetition. When this region is
the only language area spared by combined border zone infarcts, the resulting
language deficit (echolalia) has been called the "isolation of speech syndrome."26 The most common causes of the transcortical aphasias are (1) anoxia secondary to decreased cerebral circulation, as seen in cardiac arrest;
(2) occlusion or significant stenosis of the carotid artery; (3) anoxia due to
carbon monoxide poisoning; and (4) dementia. 13A3
Recovery from transcortical sensory aphasia is relatively good, but few
data are available regarding the prognosis in the motor or mixed transcortical
aphasias.
LANGUAGE
63
FIG U RES - 3. Border zone infarct that produces transcortical aphasia.
Anomie Aphasia
In some patients with aphasia, the only language defects are word-finding difficulty
and an inability to name objects on confrontation. This condition has been labeled
anomic, nominat or amnestic aphasia. Spontaneous speech is usually fluent
and grammatically rich but contains many word-finding pauses and paraphasias of specific object names. Auditory comprehension is very good, except
when the patient is asked to point to a series of specific objects. This comprehension defect is a result of two-way dissociation of naming: the patient
cannot name objects and frequently has difficulty recognizing object names
when offered in examination. Repetition is good, with the exception of sentences that contain many nouns. Reading and writing may be impaired in
specific patients; the degree of alexia and agraphia depends entirely on the
location of the lesion that is responsible for the aphasia.
Lesions in many parts of the dominant hemisphere can cause anomic
aphasia; thus, the localizing significance of this type of aphasia is limited.
Neurosurgical mapping studies of naming have demonstrated multiple sites
where naming can be interrupted with a low-level electric current. 40 The sites
differed widely among patients, and the only area that produced naming
problems in more than 50% of the patients was the posteroinferior frontal
cortex. The most severe anomic aphasia, however, is noted in patients with
temporal lobe lesions involving the second and third temporal gyri. This area
64
cannot be considered an actual "word dictionary" but includes important

pathways from the occipital lobe to the limbic system that are critical for
object naming. 23 Lesions in the parietotemporal area also result in rather
severe anomia. Patients with these lesions also have significant alexia with
agraphia. Accordingly, the combined syndrome of alexia and agraphia with
anomic aphasia localizes a lesion to the left parietotemporal area.
Anomias may be so mild that they are scarcely detectable in normal
conversation or so severe that spontaneous output is nonfluent and devoid
of meaningful content. The prognosis for language recovery depends on the
severity of the initial defect. Because language output is relatively spared and
comprehension reasonably intact, such patients make better life adjustments
than other, more severely affected, patients with aphasia.
subcortical Aphasia
Some patients with vascular lesions (either hemorrhage or infarct) of the
thalamus, putamen caudate, or internal capsule will demonstrate aphasic
symptoms. These individuals are dysarthric and often run words together in
their speech. They have mild anomia and comprehension deficits but excellent repetition.20,37 Anterior lesions tend to produce speech-production problems, whereas posterior lesions result in comprehension difficulty.38
The mechanisms by which these subcortical lesions produce aphasia are
not clear. I7 In some cases, the disorder seems more a motor-speech problem;
in others, a true aphasia or language disturbance is present. 32 Because the
cortex is thought to be the repository of language engrams, it is most likely
that the subcortical damage alters the input to and function of the overlying
cortex, In one study of glucose uptake in patients with aphasia caused by
subcortical lesions, Metter and associates 34 demonstrated a definite decrease
in cortical metabolism in addition to the expected decreased metabolism of
the subcortical structures.
Aphasia in Left-Handed Individuals

(NOn-Right-Handers)
Owing to their mixed cerebral dominance, left-handed individuals may become
aphasic secondary to a lesion in either hemisphere. The resultant aphasia is usually
milder and is associated with greater recovery than an aphasia caused by a
similar lesion in a right-handed patient. In 35% to 40% of these cases, the
aphasia cannot be classified within the traditional scheme. Wernicke's aphasia
or the agrammatism of Broca's aphasia is rarely seen. Decreased verbal fluency
and dysarthria are common, but comprehension and repetition are usually
relatively intact. Naming and reading are defective when the lesion is in the
left hemisphere. I5,27
LANGUAGE
65
Crossed Aphasia
Crossed aphasia refers to the rare cases in which a right-handed individual
develops an aphasia from a right hemispheric lesion. In 70% of such cases,
the patients demonstrate a language syndrome similar to that of left hemisphere-dominant right-handers;5 in the other 30% of cases, however, syndromes and signs vary widely.4
Language in Alzheimer's Disease

A progressive deterioration in language facility is observed in atrophic (cortical) dementia. In the earliest stage, the patient's conversation wanders in a circumlocutory fashion and can be difficult to follow. The content of conversational
speech is simplified and reflects the general decrease in intellectual ability.
Word-finding pauses may be present and verbal fluency is reduced. As the
disease progresses, word-finding difficulty becomes prominent and paraphasic
substitutions are seen. Spontaneous speech lacks relevance and may be tangential. Intrusions of words or phrases from earlier parts of a conversation
may appear at inappropriate times. Comprehension is also decreased. Naming is reduced and may be paraphasic. Repetition, however, is preserved quite
late in the course of the dementia.
In the late stages of the disease, there is little spontaneous speech or
comprehension. Echolalia is often seen. In the final decorticate state, the patients become mute.I,IS
Progressive Aphasia
An interesting progressive language disorder called progressive aphasia is
caused by relatively restricted left frontotemporal degeneration. Such patients

usually show a slowly progressing nonfluent aphasia and apraxia, with good
preservation of comprehension and other cognitive functions for many years.
Many of them eventually become demented in the late stages of their illness.
Pathologically, these cases are mixed: some show findings of Alzheimer's disease; some, Pick's disease; and some, Creutzfeldt-Jakob spongiform encephalopathy or other degenerative disorders.ll,33
Pure Word Deafness

Pure word deafness is a rare syndrome in which patients do not have aphasic
speech, agraphia, or alexia, yet are lacking in verbal language comprehension.
In these patients, hearing is intact and nonlanguage sounds (auditory gnosis)
are recognized.
The lesion that produces this condition is located in the posterior lan-
66
guage area and is often bilateral. The lesion is deep in the temporal lobe and
effectively disconnects auditory input from the auditory cortex. 2
Articulation Disturbances
Dysarthria
Pure dysarthrias are caused by a disruption in any of the inputs to the muscles of
articulation: the cortex, as in Broca's aphasia; the basal ganglia, as in parkin-
sonism or cerebral palsy; bilateral striatal or pontine lesions, as in pseudobulbar palsy; or the bulbar neurons, as in amyotrophic lateral sclerosis. The
patient with pure dysarthria can communicate normally using reading and
writing.
Buccofacial Apraxia
Buccofacial apraxia may be caused by various lesions between the supramarginal gyrus and the frontal lobe in the dominant hemisphere. Lesions in these
areas appear to interrupt the motor planning necessary for the complex movements of normal speech. Many patients with aphasia, particularly Broca's or
conduction aphasia, have considerable apraxia of facial movement. Some patients with language output resembling Broca's aphasia may, in fact, have
pure buccofacial apraxia. The difficulty in separating the aphasic and apraxic
components of speech in some patients has lead some speech pathologists
to consider Broca's aphasia as merely a motor-speech disorder and not a true
aphasia. Broca's aphasia can be seen, however, in the absence of any buccofacial apraxia. Therefore, careful examination of each patient is important to separate the apraxic and aphasic components.
Dysfluency
Dysfluency (stuttering or stammering) is another speech-production problem.
Not an aphasia, apraxia, or dysarthria, it is a common speech disorder whose
exact etiology is not known, although mixed dominance is seen in many
cases. Both organic and functional explanations have been advanced. Dysfluency is usually a developmental speech disorder, but it can be acquired secondary
to a brain lesion.
Alexia
Several distinct syndromes exist in which reading ability is impaired secondary to acquired brain lesions. The classic syndrome of pure alexia without
agraphia22 23 is caused by a left posterior cerebral artery occlusion in a right-handed
individual. The resulting cerebral infarct damages the posterior portion of the
LANGUAGE
67
corpus callosum as well as the left occipital lobe. Because the left visual cortex
is damaged, all visual information enters only the right hemisphere. The right
visual cortex perceives the written material but cannot transmit it to the left
hemisphere because of the callosal lesion (Fig. 5-4). The inferior parietal
lobule in the dominant hemisphere (primarily area 39, the angular gyrus) is
the association cortex that combines the visual and auditory information necessary for reading and writing. In alexia without agraphia, the inferior parietal
lobule is disconnected from all visual input. Because the lobule and its connections within the language area are intact, the patient can write normally.
One of the dramatic aspects of this syndrome is the patients' ability to write
lengthy, meaningful messages, only to be unable to read his or her own
writing. These patients are able, however, to understand words spelled aloud.
Interestingly, most patients with this syndrome can name objects and discuss
FIG U R E 5 - 4. The cross-hatched area represents infarction of the left visual cortex and the
posterior portion of the corpus callosum. The visual information from the right visual cortex
(arrow) is unable to reach the left inferior parietal lobule (39 and 40) because of the callosal
lesion.
68
visual events that are occurring in their environment. This type of visual information must cross to the left hemisphere by some pathway other than .the
damaged posterior corpus callosum.
A second distinct type of alexia, classically called alexia with agraphia, results
from damage to the inferior parietal lobule itself (angular gyrus and environs). This
lesion renders the patient unable to read or write. These patients are not appre-
ciably aphasic but may have a certain degree of anomia. Recognition of this
syndrome is clinically important for localization; in the right-handed patient
with this syndrome, the lesion is invariably in the left inferior parietal area.
The most common acquired alexia is neither of the pure syndromes but rather
the alexia associated with aphasia.
Agraphia
Writing is a complex motor task that involves the translation of a language item
into written symbols. 29 The linguistic message to be written originates in the

posterior language area, is then translated into visual symbols in the inferior
parietal area, and is finally transferred to the frontal language area for motor
processing. Lesions within any of these language areas will cause an agraphia.
With the exception of patients with pure word deafness, all patients with aphasia show some degree of agraphia. Although the most common agraphia is the
form that is accompanied by aphasia, under certain circumstances agraphia
may be seen in the absence of aphasia.
Two syndromes are seen in patients with damage to the dominant parietal lobe: (1) agraphia with alexia, described in the previous section; and
(2) a syndrome of agraphia in association with other parietal lobe signs (dyscalculia, right-left disorientation, and finger agnosia), called Gerstmann's syndrome (discussed in detail in Chapter 9).
One rare pure agraphia occurs only in the left hand. This syndrome is
seen in patients with lesions of the anterior corpus callosum. These patients
are agraphic with the left hand only, because the right motor cortex is disconnected from the language areas of the left hemisphere. Writing with the
right hand is normal because of the intact connections of the left motor cortex
and the language areas. Figure 5-5 demonstrates the normal pathways required for writing. The callosal lesion (Fd appears to interrupt the language
message going to the right hemisphere.
Single case reports describe isolated pure agraphia resulting from superior
parietallesions. 47
psychotic Language (Bizarre

Language Output)
Rambling, disjointed, neologistic language can be seen in patients with severe psychosis (especially schizophrenia), advanced organic dementia, delirium, and fluent
LANGUAGE
69
FIG U R E 5 - 5. The written message originates in the posterior language area of the dominant
hemisphere (B,). The message is transferred via the arcuate fasciculus (e,) to the premotor area
in the same hemisphere (D,). Motor patterns are transferred to the motor strip (E,) for innervation of the right hand. The message must cross via the anterior corpus callosum (F,) to the
right motor system (D2' E2) for innervation of the left hand. F2 is not a significant pathway for
transferring the written message to the right motor area.
jargonaphasia. Differentiation among these conditions on the basis of spon-
taneous speech alone may be difficult. Historical data are invaluable: in elderly persons an acute onset of gross language disturbance with aphasia or
delirium favors the diagnosis of a stroke; a prolonged history of language
deterioration in the young patient indicates schizophrenia or an unusual organic lesion such as a left hemisphere glioma; a gradual deterioration of language in the older patient suggests dementia or a focal brain lesion such as
a left hemisphere tumor or subdural hematoma. Unfortunately, detailed historical information is often unavailable, and a tentative diagnosis must at
such times be based on mental status findings alone.
Each of the aforementioned conditions has certain features that help to distinguish it from the others. Systematized paranoid delusions may be seen in both
70
aphasia and dementia, but are much more common in schizophrenia. Neologisms are used infrequently by patients with schizophrenia, but their use
is usually consistent and symbolic (e.g., one patient with paranoid schizophrenia repeatedly referred to the "frinky-franks" that were placed in the walls
to watch him). Neologisms produced by patients with aphasia tend to be
random, very frequent, and nonsymbolic (e.g., "The walret is the you know,
wimbit, lep, olla other one"). Those with dementia often have word-finding
difficulty and produce circumlocutory speech with some paraphasias. Until
the late stage of the dementia, their speech is generally more comprehensible
and less paraphasic than that of the patient with aphasia. The patient with
advanced dementia produces little speech, and what is produced may be
largely neologistic isolated words or short neologistic word strings.
Because it is difficult to differentiate among these conditions by listening
to spontaneous speech alone, complete language testing is essential. Careful
comprehension testing reveals that patients with jargonaphasia are unable to
understand even very simple commands. Delirious, moderately demented, or
schizophrenic patients have adequate comprehension but may be difficult to
evaluate because of a lack of cooperation. Patients with aphasia usually demonstrate inferior performance in repetition testing. Naming tasks clearly reveal
language problems in patients with aphasia by their production of paraphasic
errors. A patient with aphasia who is shown a key may say, "Pel, klo, klep,
kleep ... key," whereas one with schizophrenia may call it a "key sort of
watching tower thing." In this instance, the patient with schizophrenia correctly identified the object but incorporated it into his or her disordered
thought process. Patients with delirium or dementia usually have some naming trouble but not as severe as that seen in patients with aphasia nor as
bizarre as that seen in those with schizophrenia. When asked to name a key,
the patient with dementia might well answer, "Lock, no ... the lock keyer
... key!"
The differential diagnosis of these conditions is important because a misdiagnosis
may lead to gross mismanagement. For example, we saw a very robust 80-yearold retired grocer who began answering questions inappropriately at dinner
one evening. Becoming concerned, his wife continued to ask questions, which
the husband was unable to answer. He became frustrated, angry, and agitated.
The wife became frightened and called the police. Because of this aggressive
behavior, the man was jailed for 3 days. He was then transferred to a psychiatric hospital, where he remained for an additional 3 days before a neurologist diagnosed a Wernicke's aphasia secondary to a middle cerebral artery
thrombosis. Mistakes such as this can be made unless a careful mental status
examination is performed.
Differentiating patients with dementia from those with schizophrenia is
usually not difficult because of the age at onset, differences in behavior, and
distinct differences in verbal output. On complete examination, additional
data may corroborate the initial opinion. The patient with dementia may
LANGUAGE
71
show problems with praxis and drawing. The patient with schizophrenia often distorts drawings but usually can make recognizable copies of designs
and figures. Ideational apraxia (Chapter 9), which can be demonstrated by
asking the patient to fold a letter and place it in an envelope, is often present
in patients with dementia but not in those with schizophrenia.
Nonorganic Speech and Language

Disorders
Several types of functional speech disorders can be mistaken for organic language
patterns. Some neurotic patients convert anxiety into a halting, effortful, telegraphic speech pattern (e.g., "Me want go home see wife"). These patients
have normal comprehension, repetition, and naming but reduced verbal fluency. Reading and writing are also intact but are carried out in the same slow,
effortful fashion. Mild dysarthria may also be present. These patients may
require the help of psychiatrists and speech pathologists to alter their speech
patterns.
Other functional patients develop an acute aphonia (total inability to
adduct the vocal cords and make audible sounds). Aphonia may arise as a
pure conversion symptom or, more commonly, secondary to an insult to the
speech apparatus. One middle-aged patient remained aphonic for 2 months
after awakening from surgery with an endotracheal tube in place. Aphonic
patients breathe normally and show no evidence of stridor (a sign of vocal
cord paralysis). They communicate well by gesture, mouthing words, and
writing. This type of functional overlay is well known to speech pathologists
and responds well to therapy.
Elective mutism is another functional speech disorder that may be seen
in both children and emotionally disturbed adults. It is characterized by a
willful reluctance or an outright refusal to speak. The disorder may be complete (i.e., an absolute lack of speech in all situations) or relative (i.e., selective
communication with a small circle of intimates). The speech, when present,
may be limited to a mouthing of words; whispering; or a slow, labored,
halting production. The adult who elects to remain mute typically has no
language deficit and is physiologically capable of producing speech sounds.
Some patients, especially children, do have a basic organic language disorder
with considerable emotional overlay. The mutism is often resistant to the
usual forms of speech therapy and psychotherapy41 but can respond to behavior modification. 39
SUMMARY
Language is a very complex and interesting higher-cognitive function. Because
of the unique relationship of language and cerebral dominance, most acquired language disorders are pathognomonic of left hemisphere damage.
72
Careful evaluation of language functions can localize the lesion within the
dominant hemisphere. Language is critically important for many other cognitive functions; thus, the subsequent parts of the mental status examination
must be administered and interpreted with some caution in patients with
aphasia.
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1. Albert, ML: Language in normal and dementing elderly. In Obler, LV and Albert, ML (eds):
Language and Communication in the Elderly. Lexington Books, Lexington, MA, 1980,
pp 145-150.
2. Albert, ML, et al: Clinical Aspects of Dysphasia. Springer-Verlag, Vienna, 1981, pp 88-91.
3. Alexander, M: Aphasia: Clinical and anatomic aspects. In Feinberg, TE and Forah, MI (eds):
Behavioral Neurology and Neuropsychology. McGraw-Hill, New York, 1997, pp 133-149.
4. Alexander, MP and Annett, M: Crossed aphasia and related anomalies of cerebral organization: Case reports and a genetic hypothesis. Brain Lang 55:213-239,1996.
5. Alexander, MP, Fischett, MR, and Fischer, RS: Crossed aphasia can be mirror image or anomalous. Brain 112:953-973, 1989.
6. Barr, A and Brandt, I: Word-list generation deficits in dementia. I Clin Exp Neuropsychol
18:810-822, 1996.
7. Basso, A, et al: Anatomoclinical correlations of the aphasias as defined through computerized
tomography: Exceptions. Brain Lang 26:201, 1985.
8. Benson, OF: Fluency in aphasia: Correlation with radioactive scan localization. Cortex 3:373,
1967.
9. Benson, OF: Psychiatric aspects of aphasia. Br I Psychiatry 123:555, 1973.
10. Benson, OF and Geschwind, N: Cerebral dominance and its disturbances. Pediatr Clin North
Am 15:759, 1968.
11. Benson, OF and Zaias, BW: Progressive aphasia: A case with postmortem correlation. Neuropsychol Behav Neurol 4:215, 1991.
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Paper presented at the 13th Annual Meeting of the Academy of Aphasia. Victoria, BC, October 5, 1975.
13. Bogousslavsky, J, Regli, F, and AssaI, G: Acute transcortical mixed aphasia: A carotid occlusion
syndrome with pial and watershed infarcts. Brain III :631, 1988.
14. Borkowski, IG, Benton, AL, and Spreen, 0: Word fluency and brain damage. Neuropsychologia 5:135, 1967.
15. Brown, JW and Hecaen, H: Lateralization and language representation. Neurology 26:183,
1976.
16. Caramazza, A: The logic of neuropsychological research and the problem of patient classification in aphasia. Brain Lang 21:9, 1984.
17. Crosson, B: Subcortical Functions in Language and Memory. The Guilford Press, New York,
1992.
18. Cummings, IL and Benson, OF: Dementia: A Clinical Approach. Butterworth & Co, Boston,
1983.
19. Damasio, AR: Aphasia. N Engl I Med 326:531, 1992.
20. Damasio, AR, et al: Aphasia with nonhemorrhagic lesions in the basal ganglia and internal
capsule. Arch Neurol 39:15, 1982.
21. Damasio, Hand Damasio, AR: The anatomical basis of conduction aphasia. Brain 103:337,
1980.
22. Dejerine, I: Des differentes varietes de cecite verbale. Memoires de la Societe de Biologie
1892, pp 1-30.
23. Geschwind, N: Disconnection syndromes in animals and man. II. Brain 88:585, 1965.
24. Geschwind, N: Current concepts in aphasia. N Engl I Med 284:654, 1971.
25. Geschwind, Nand Galaburda, AM: Cerebral Dominance: The Biological Foundations. Harvard University Press, Cambridge, MA, 1984.
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26. Geschwind, N, Quadfasel, F, and Segarra, J: Isolation of the speech area. Neuropsychologia
6:327, 1968.
27. Gloning, K: Handedness and aphasia. Neuropsychologia 15:355, 1977.
28. Goodglass, H: Understanding Aphasia. Academic Press, San Diego, 1993.
29. Goodglass, H: Disorders of writing. In Goodglass, H: Understanding Aphasia. Academic
Press, San Diego, 1993, pp 172-192.
30. Goodglass, H and Kaplan, E: The Assessment of Aphasia and Related Disorders, ed 2. Lea &
Febiger, Philadelphia, 1983.
3l. Hecaen, H and de Ajuriaguerra, J: Left Handedness: Manual Superiority and Cerebral Dominance. Grune & Stratton, New York, 1964.
32. Luria, AR: On quasi-aphasia speech disturbances in lesions of the deep structures of the
brain. Brain Lang 4:432, 1977.
33. Mendez, MF and Zander, BA: Dementia presenting with aphasia: Clinical characteristics. J
Neurol Neurosurg Psychiatry 54:542, 1991.
34. Metter, EJ, et al: Comparison of metabolic rates, language and memory in subcortical aphasias. Brain Lang 19:33, 1983.
35. Metter, EJ, et al: Cerebral glucose metabolism in Wernicke's, Broca's and conduction aphasia.
Arch Neurol 46:27, 1989.
36. Mohr, JP: Broca's area and Broca's aphasia. In Whitaker, H and Whitaker, H (eds): Studies
in Neurolinguistics, Vol 1, Perspectives in Neurolinguistics and Psycholinguistics. Academic
Press, New York, 1976, pp 201-235.
37. Mohr, JP, Watters, WC, and Duncan, AW: Thalamic hemorrhage and aphasia. Brain Lang
2:3, 1975.
38. Naeser, MA, et al: Aphasia with predominantly subcortical lesion sites: Description of three
capsular/putaminal aphasia syndromes. Arch Neurol 39:2, 1982.
39. Norman, A and Broman, H: Volume feedback and generalization techniques in shaping
speech of an electively mute boy: A case study. Percept Mot Skills 31:463, 1970.
40. Ojemann, G, et al: Cortical language localization in left dominant hemisphere: An electrical
stimulation mapping investigation in 117 patients. J Neurosurg 71:316,1989.
41. Reed, G: Elective mutism in children: Are-appraisal. J Child Psychol Psychiatry 4:99, 1963.
42. Ross, ED: Nonverbal aspects of language. In Brumback, CA (ed): Behavioral Neurology.
Neurol Clin 11:9-23, 1993.
43. Rubens, AB and Kertesz, A: The localization of lesions in transcortical aphasias. In Kertesz,
A (ed): Localization in Neuropsychology. Academic Press, New York, 1983, pp 245-268.
44. Strub, RL: Mental disorders in brain disease. In Frederiks, JAM (ed): Handbook of Clinical
Neurology, Vol 2(46), Neurobehavioral Disorders. Elsevier, Amsterdam, 1985, pp 413-441.
45. Tombaugh, TN and Hubley, AM: The 60-item Boston Naming Test: Norms for cognitively
intact adults aged 25 to 80 years. J Clin Exp Neuropsychol 19:922-932, 1997.
46. Vargo, ME and Black, FW: Normative data for the Spreen-Benton Sentence Repetition Test.
Cortex 20:585, 1984.
47. Vignolo, LA: Modality specific disorders of written language. In Kertesz, A (ed): Localization
in Neuropsychology. Academic Press, New York, 1983, pp 357-369.
48. Wada, J: A new method for the determination of the side of cerebral speech dominance: A
preliminary report on the intracarotid injection of sodium amytal in man. Med Bioi 14:221,
1949.
49. Welch, LW, et al: Educational and gender normative data for the Boston Naming Test in a
group of older adults. Brain Lang 53:260-266, 1996.
50. Willmes, K and Poeck, K: To what extent can aphasic syndromes be localized? Brain
116:1527-1540,1993.
5l. Wilson, RS, Kaszniak, AW, and Fox, JH: Remote memory in senile dementia. Cortex 17:41,
1981.
52. Zangwill, OL: Two cases of crossed aphasia in dextrals. Neuropsychologia 17:167, 1979.
MEMORY
A disturbance in memory is the most common cognitive complaint of patients with organically based behavioral syndromes. Almost all patients with
dementia show memory problems early in the course of their disease. In dementia
the problem is insidious and can make it difficult or impossible for patients
to function effectively. They may lose track of the date, forget work details,
or fail to remember commitments extending beyond their daily routines. This
can have devastating effects on patients' social and vocational life, especially
before the nature of the problem is fully appreciated. Recognition of this
memory difficulty allows the clinician and the family to help these patients
to avoid potential personal catastrophe. Careful attention to memory testing often
reveals the presence of an organic disorder before abnormal findings are noted on
standard neurologic examination.
Various neurologic diseases result in different types of memory disturbance (e.g.,
severe memory deficit in relative isolation in Korsakoff's syndrome, memory

difficulty compounded by inattention and agitation in the confusional states,
impaired recent memory associated with general cognitive dysfunction in dementia). In each of these diseases, memory is disturbed by different pathophysiologic mechanisms.
Not all memory difficulties have neurologic origins. Depressed and anxious
patients, as well as other patients with significant psychiatric disorders, often
have difficulty with memory. Because performance on memory testing requires maximum patient cooperation and effort, the emotionally disturbed
patient often performs poorly. The misdiagnosis of depression as dementia
or the reverse is a serious diagnostic error that can lead to months or even
years of inappropriate treatment. Untangling the memory problems in patients with a psychiatric disorder is difficult; however, full neurologic, psychiatric, and psychologic evaluation can almost always lead to the correct
diagnosis. The diagnostic challenge is even greater when a problem such as
early Alzheimer's disease is compounded by a superimposed depression or
anxiety.
74
MEMORY
75
TERMINOLOGY
Merrwry is a general term for a mental process that allows the individual to store
information for later recall. 33 The time span for recall can be as short as a few
seconds, as in a digit repetition task, or as long as many years, as in the recall
of one's childhood experiences.
The memory process consists of three stages. In the first stage, the information
is received and registered by a particular sensory modality (e.g., touch, auditory,
or visual). Once the sensory input has been received and registered, that information is held temporarily in short-term memory (working memory). The
second stage consists of storing or retaining the information in a more permanent form (long-term memory). This storage process is enhanced by repetition or by association with other information that is already in storage. 25
Storage is usually an active process requiring effort through practice and rehearsal. 23 Some information, however, is stored passively throughout our
lives; this process is called incidental memory because it is acquired effortlessly. The final stage in the memory process is the recall, or retrieval, of the
stored information. This retrieval is an active process of mobilizing stored
information on request or as needed (so-called declarative memory).
Each stage in the total memory process relies on the integrity of the
previous stages. Any interruption in the hierarchy may prevent the storage or
retrieval of a memory. Formal studies of memory have demonstrated that
each aspect of memory involves separate yet interlocking neurobiologic substrates or systems. The effects on these systems differ according to the patient's
particular disease, and each produces a different clinical picture.
Clinically, memory is subdivided into three types, based on the time span between stimulus presentation and memory retrieval. "Immediate," "recent," and
"remote" are commonly used to denote these basic memory types. Unfortunately, these terms are nonspecific, and the time span each implies is not well
defined in clinical use. Immediate memory, or immediate recall, is used to
recall a memory trace after an interval of a few seconds, as in the repetition
of a series of digits. Sometimes short-term memory is also used to describe
this memory type, when the recall interval is filled with a distractor such as
having the patient count backward.
Recent memory is the patient's capacity to remember current, day-to-day
events (e.g., the current date, the doctor's name, what was eaten for breakfast,
or recent news events). More strictly defined, recent memory is the ability to
learn new material and to retrieve that material after an interval of minutes,
hours, or days.
Remote memory traditionally refers to the recall of facts or events that
occurred years previously, such as the names of teachers and old school
friends, birth dates, and historic facts. In patients with a specific defect in new
learning (recent memory), remote memory refers to the recall of events that
occurred before the onset of the recent memory defect.
76
Amnesia is a general term for a defect in memory function. Although

applied to a broad spectrum of memory defects, amnesia is used most commonly to label patients with severe and relatively isolated memory deficits
(e.g., Korsakoff's syndrome or posttraumatic amnesia). The inability to learn
new material after a brain insult is called anterograde amnesia. The inability
to remember events that occurred before the brain insult is called retrograde
amnesia. The period of amnesia in either case may be as short as a few
seconds or as long as several years. It is most commonly seen with head
trauma but may also follow any major brain insult (e.g., stroke). Amnesia
may also refer to psychogenic amnesia, in which the patient blocks a period
of time from memory. These patients do not demonstrate a recent memory
deficit, can learn items during the amnestic period, and, after the amnestic
period is over, do not have a defect in recent memory when tested. Psychologically based memory loss leaves patients with gaps, or relative gaps, in
their memory for the events that occurred during the amnestic period. Sometimes patients recall parts of the amnestic period that were not emotionally
traumatic while blocking recall of the traumatic events themselves.
EVALUATION
In the mental status examination, each aspect of memory should be assessed in some
detail. This allows the examiner to distinguish the type of memory deficit (if
any), the degree of memory loss, and the impact of the memory deficit on
the patient's ability to function.
Patients commonly perform at different levels on various memory tests,
depending on the nature of the disorder (e.g., patients with Korsakoff's syndrome can respond very adequately to questions regarding remote events but
cannot learn new material). The use of several different memory tests is also
of clinical importance. Brain-damaged patients demonstrate differences in the
incidence, nature, and degree of memory deficits based on the type of test
used and the nature and location of their lesions. 2 ,3,9,17
The accurate assessment of memory requires that any question asked by the
examiner be verifiable from a source other than the patient. For example, it is
useless to ask patients when they graduated from high school or what they
ate for lunch if the examiner cannot ascertain the accuracy of the patients'
responses. Many patients with readily demonstrable memory deficits deny
their problem and may confabulate answers. Such responses may appear perfectly appropriate to the naive examiner who is unable to verify their accuracy.
Personal information concerning the patient's social history, lifestyle, vocation, and so forth should be verified by the patient's family or friends.
Historic facts (e.g., "When was World War IE" or "Who was the President
before Mr. Clinton?") are commonly used by examiners to screen both remote
and recent memory. Because the knowledge of such information is closely
related to the patient's basic premorbid intellectual level, education, and gen-
MEMORY
77
eral social exposure, the examiner must be mindful of these factors when
considering the use of historic facts to test memory. If used at all, questions
related to historic material must be tailored to the patient's background.
The most sensitive and valid tests of recent memory are those that require the
patient to learn new material and recall it over time. The use of this technique
eliminates some of the dangers of encountering unverifiable material and
unknown social background. New learning is an active memory process that
requires more expenditure of effort by the patient than does the mere recall
of personal or historic facts.
When evaluating memory, the examiner must be aware of various factors
that can impair performance even in individuals who do not have an organic
memory deficit. Because memory test performance requires the patient's sustained attention, inattentive, distractible patients cannot perform optimally
on such tests, regardless of the etiology of their memory problem. Patients
in an acute confusional state or who have a severe psychogenic disorder usually have impaired attention, which hinders memory test performance. Disturbances of basic sensory, motor, or language functions that interfere with
comprehension or expression also cause impaired memory test performance.
Poor memory performance by patients who are deaf, aphasic, acutely confused, psychotic, anxious, depressed, or grossly inattentive may reflect defects
caused by these processes alone and should not be interpreted as evidence of
an underlying memory deficit. Valid memory testing presumes that the patient is
reasonably attentive, can relate to and cooperate with the examiner, and has no
defect that impairs language comprehension or expression. Any evidence of aphasia, whether a subtle residual effect of a more significant aphasia (e.g., after
a stroke) or a mild defect noted on examination, impairs both short-term
and long-term verbal memory.38 Extreme caution must be exercised when
interpreting a verbal memory impairment in such patients.
Because of the clinical and social importance of memory, we have selected a number of memory tests that enable the examiner to assess a variety
of memory processes. Many patients become apprehensive when having their
memory tested, so it is important to present the material slowly and in as
calm and nonthreatening a fashion as possible.
Immediate Recall (Short-Term

Memory)
Immediate recall is usually tested by digit repetition, which was covered in
detail in Chapter 4 and will not be repeated here. Although backward digit
repetition has been used by some examiners to assess verbal memory, this is
a highly complex task that requires several neuropsychologic processes in
addition to memory.4 It is useful as a general screening test for brain dysfunction but should not be considered a test of short-term memory in
isolation.
78
Orientation (Recent Memory)

The patient's orientation with respect to person (who he or she is), time (the
date), and place (where he or she is) is important preliminary information
and should be evaluated early in the examination of memory functioning.
Orientation to place and time are actually measures of recent memory, as they
test the patient's ability to learn these continually changing facts. If a patient is not
fully oriented, this alone suggests a significant recent memory deficit.

DIRECTIONS: The patient should be asked the following questions in sequence. Questions may be paraphrased when necessary to ensure clarity. If
the patient fails these items, tell the patient the correct answers and have him
or her repeat them; several minutes later, have the patient recall the answers.
Failure at this level verifies poor new learning ability and predicts deficient
performance on any subsequent memory tasks.
TEST ITEMS
1. Person
a. Name
b. Age
c. Birth date
2. Place
a. Location
b. City location
c. Address
3. Time
a. Date
b. Day of the week
c. Time of day
d. Season of the year
What is your name?

How old are you?
When is your birthday? (day, month, year)
Where are we right now?
What is the name of this place?
What kind of place are we in now?
What floor did you come to today?
What city are we in now?
State? County?
What is your home address?
What
What
What
What
is to day's date? (year, month, date)

day of the week is it?
time is it right now?
season is it now?
SCORING: Normal people usually perform perfectly on this test, with some
individuals receiving somewhat less adequate scores on time orientation. 29
The only items sometimes failed by normal individuals are the exact date of
the month and, less commonly, the day of the week. Performance correlates
with education level; normal college graduates, if they do not know the exact
date or day, usually miss by only 1 day, whereas normal people without a
high school education may miss by 2 or even 3 days.22 A small number
(7.7%) of normal uneducated individuals may incorrectly identify the month.
Remote Memory
Remote memory tests such as those included here evaluate the patient's ability
to recall personal and historic events. As previously emphasized, personal
events must be verifiable by a reliable source other than the patient, and
MEMORY
79
performance on the recall of historic information must be interpreted in light

of the patient's premorbid intelligence, education, and social experience.
TEST ITEMS
1. Personal information
a. Where were you born?

b. School information
c.
Vocation history
d. Family information
Where did you go to school?

When did you attend school?
Where is your school located?
What do you do for work?
Where have you worked?
When did you work at those places?
What is your wife's (children's) name?
Howald is your wife (children)?
What was your mother's maiden name?
SCORING: Personal information items are completed with approximately

equal accuracy by both normal patients and patients with mild, nonspecific
brain damage. Although impaired performance is pathologic, this test does
not efficiently differentiate among groupS?9
TEST ITEMS AND SCORING
Historic facts:
Ask the patient to name four people who have been president during the
patient's lifetime. The normal patient should be able to accomplish
this task without difficulty. A slightly more difficult task, and one that
is very frequently failed by patients with early Alzheimer's disease, is
asking the patient to name the last four or five presidents in proper
reverse sequence, starting with the current president.
Ask the patient to name the last war in which the United States was
directly involved. At the time of this writing, the correct response
would be the war in Iraq (Desert Storm). An older patient may name
the Vietnam War, Korean War, or World War II. If the patient gives
one of these responses, ask him or her about any recollection of the
Iraq war. If the patient has no memory for these major events, this
implies deficient memory.
New-Learning Ability
This section assesses the patient's ability to actively learn new material (to acquire
new memories). Adequate performance requires the integrity of the total memory
system: recognition and registration of the initial sensory input, retention and
storage of the information, and recall or retrieval of the stored information.
An interruption in any of these stages impairs clinically relevant new-learning
ability. A careful clinical examination of how a patient fails a particular task
may often provide valuable information as to the nature of the impaired
process. Patients with impaired memory, particularly those with Alzheimer's
80
disease, can become rather overwhelmed during extensive memory testing.

Items previously presented inhibit and confuse learning on subsequent items
(proactive interference). In such situations, the patients may provide answers
from earlier test items in later testing. These intrusion errors are characteristic
of many organic syndromes, especially dementia.
Four Unrelated Words

DIRECTIONS: Tell the patient, "1 am going to tell you four words that I
would like you to remember. In a few minutes, I will ask you to recall these
words." To ensure that the patient has heard, understood, and initially retained the four words, have him or her repeat the words after their presentation. Correct any errors made on immediate repetition. Older patients (over
age 75) may require several trials to learn the words, but when a patient must
be given four or five trials to repeat the words accurately, this usually forecasts
a significant memory problem. To eliminate possible mental rehearsal, interference should be used between presentation and recall of the words. Accordingly, the examiner may wish to present the four words before the remote
memory or orientation examination. After 5 minutes, ask the patient to recall
the four words. Information concerning the duration of memory can be obtained by asking for another recall of the words after 10 and 30 minutes. The
following sets of words have been selected because of their semantic and
phonemic diversity. Only one set of words should be used with a given patient, because of possible contamination and resultant confusion.
TEST ITEMS
l. Brown
2. Honesty
l. Fun
2. Carrot
l. Grape
2. Stocking
3. Tulip
4. Eyedropper
3. Ankle
4. Loyalty
3. Happiness
4. Toothbrush
When a patient cannot recall a given word, it is often possible to obtain an

indication of memory storage by the use of verbal cues. These include semantic cues relating to the category of the named object (e.g., "One word
was a color"), phonemic cues using syllabic components of the word (e.g.,
"Hon ... [honesty]"), and contextual cues (e.g., "A flower"). If a patient cannot recall the words either spontaneously or with cues, the examiner may
resort to asking the patient if he or she recognizes the appropriate word from
a series of words (e.g., "Was the color red, green, brown, or yellow?"). When
this yields significantly better results than spontaneous recall, the memory
problem may be due to a retrieval defect rather than to an acquisition or
storage deficit. This demonstration of good memory on recognition testing
but poor memory on free recall is called implicit memory.
SCORING: The normal patient under age 60 should accurately recall three
or four of the words after a 10-minute delay.29 Normal results for this test
MEMORY
Alzheimer's Disease
Patients (Stage)
Normal Individuals
(Age in Years)
40-49
81
50-59
60-69
70-79
80-89
II
III
IV
2.9
2.0
(1.0)
3.0
(1.0)
3.5
(0.7)
9.7
(2.6)
4.2
(0.8)
1.8
(0.8)
2.6
(0.9)
3.1
2.1
(1.4)
2.7
( 1.4)
2.9
(Ll)
7.6
(2.8)
3.8
(1.6)
0.4
(0.7)
0.7
( 1.0)
0.6
(1.0)
2.8
(2.0)
(1.3)
0
(0.1)
0.1
(0.4)
0.1
(0.3)
0.6
(1.0)
0.2
(0.5)
(1.2)
1.6
(1.2)
1.9
(1.4)
1.8
(1.4 )
5.5
(2.3)
2.3
(1.7)
3.6
(0.7)
2.3
(1.0)
3.2
(0.7)
1.7
(0.9)
2.4
(0.9)
0.9
(1.0)
0.8
(Ll)
0.1
(0.4)
4 Words
5 min
10 min
30 min
Story
5 Objects
3.1
(0.9)
3.7
(0.7)
3.7
(0.7)
10.1
(2.8)
4.6
(0.6)
(1.3)
3.5
(0.8)
4.0
(0.0)
ILl
(1.9)
4.7
(0.6)
8.2
(3.3)
3.9
(1.0)
Ll
0
0
0
0
Paired Associate Learning (Both Trials)

Easy
Difficult
3.8
(0.4)
3.3
(1.0)
3.8
(0.6)
3.2
(0.7)
3.6
(0.7)
2.6
(1.3)
3.1
(1.2)
2.1
(1.0)
0
0
'Mean and standard deviation, n = 100.
vary significantly (standard deviation 0.8 words), however, so the clinical

implication of a low score (e.g., 2 of 4) must be interpreted in light of the
patient's history and the performance on the entire examination. As shown
in Table 6-1, an age-related decline in performance on this test is seen in
normal individuals over age 60. Normal persons over age 80 retain an average
of only two of four words over 5 minutes, with a substantial variance. After
being reminded of the correct words, these individuals will improve their
performance after 10 and 30 minutes. Patients with dementia, on the other
hand, tend not to improve on subsequent trials.
Verbal Story for Immediate Recall

DIRECTIONS: Tell the patient, "I am going to read you a short paragraph.
Listen carefully, because when I finish reading, I want you to tell me everything that I told you." For older patients, read the story more slowly to give
them adequate time to process the information. After reading the story, say
"Now tell me everything that you can remember of the story. Start at the
beginning of the story and tell me all that happened." The separate items in
the story are indicated by slash (f) marks. As the patient retells the story,
indicate the number of items recalled. In patients with good immediate recall,
it may be useful to ask for another recall after 30 minutes. This is a sensitive
method of assessing short-term verbal recall.
82
TEST ITEM
It was July! and the Rogers / had packed up / their four children / in
the station wagon / and were off / on vacation.

They were taking / their yearly trip / to the beach / at Gulf Shores. / This
year / they were making / a special/one-day stop / at the Aquarium /
in New Orleans.
After a long day's drive / they arrived / at the motel / only to discover /
that in their excitement / they had left / the twins / and their suitcases /
in the front yard.
SCORING: The story contains 26 relatively separate ideas or information
bits. In our experience, the normal individual under age 70 should be expected to produce at least 10 of these items on immediate recall. For patients
in their 70s, the average score drops to 8.2, and in their 80s, to 7.6. Elderly
individuals are slower in their auditory processing and less able to store as
much information on a single presentation as are younger people. Less adequate performance than that shown by age-specific values (see Table 6 -1) by
the nonretarded patient indicates defective verbal recall ability. Story recall
significantly discriminates between normal individuals and Alzheimer
patients and also between brain-damaged and low-IQ normal groups
(Tables 6-1 and 6-2, respectively).
Variable
Total score
Digit repetition
Vigilance errors
Orientation
Person
Place
Time
Remote memory
Personal information
Historic facts
Four words-l 0 min
Four words-3D min
Visual memory
Hidden objects found (4)
Hidden objects named
Paired associate learning
Easy
Difficult
Total
*P <.05.
tP <.01.
:j:p <.001.
Brain Damaged
Mean
Low-IQ
Normal Mean
33.4
4.2
10.2
8.7
2.6
2.7
3.4
50.0
4.8
0.2
10.6
3.0
3.0
4.6
28.0:j:
1.9
s.st
l3.3:j:
7.s:j:
3.4*
8.4:j:
3.4
1.3
1.9
1.8
3.9
1.5
3.6
3.9
3.1
3.2
15.l:j:
20.4:j:
1.3
1.0
3.7
0.2
1O.8:j:
3.1
2.1
1.4
3.5
3.0
3.0
6.0
12.6:j:
9.7:j:
15.6:j:
.F
MEMORY
83
Visual Memory (Hidden Objects)

Visual memory should be tested in all patients, but it is especially useful in
evaluating the memory of patients with aphasia. It is also a good nonthreatening test to use for patients whose history has already indicated considerable
memory problems or for those with reduced verbal abilities or lack of
education.
DIRECTIONS: The examiner may use any five small, easily recognizable
objects that may be readily hidden in the patient's vicinity. We commonly
use items such as a pen, comb, keys, coin, and fork. The use of five items
provides a reasonable span for most patients. The objects are hidden while
the patient is watching. Name each item as it is hidden to ensure that the
patient is aware of which object was hidden in what place. After hiding the
objects, the examiner should provide interfering stimuli for 5 minutes by
administering another mental status task, asking the patient routine questions, or engaging the patient in general conversation. After this period, ask
the patient to name and indicate the location of each of the hidden objects.
If the patient cannot recall the location of any object, ask him or her to name
the hidden object.
SCORING: The average patient under age 60 should find four or five (4.6
: :': : 0.6) of the hidden objects after a 5-minute delay without difficulty. Older
patients (age 70 to 90) will not do quite as well (3.8 : :': : 1.3). Less adequate
performance (fewer than three objects) indicates impaired visual memory. A
patient with aphasia should be able to find and demonstrate the use of the
objects but may not be able to name them.
Paired Associate Learning

Paired associate learning (PAL) is commonly used in standard memory batteries and is another highly sensitive measure of new-learning ability.
DIRECTIONS: Tell the patient, "I am going to read you a list of words, two
at a time. Listen carefully because I will expect you to remember the words
that go together. For example, if the words were 'big' and 'little,' I would
expect you to say the word 'little' after I said the word 'big.' " When the patient
understands the directions, continue as follows: "Now listen carefully to the
words as I read them." Read the first presentation at the rate of one pair every
2 seconds. After reading the first presentation, test for recall by presenting the
first recall list. Give the first word of a pair and allow 5 seconds for a response.
If the patient gives a correct response, say "That's right" and proceed with the
next pair. If the patient gives an incorrect response, say "No," provide the
correct word, and proceed to the next pair.
After the first recall has been completed, allow a la-second interval and
give the second presentation list, proceeding as before.
84

TEST ITEMS
PRESENTATION LISTS
First Presentation
Second Presentation
Weather-Box
High-Low
House-Income
Book-Page
House-Income
Weather-Box
Book-Page
High-Low
RECALL LISTS
First Recall
Second Recall
HouseHighWeatherBook-
BookHouseHighWeather-
SCORING: The normal patient under age 70 is expected to recall the two
"easy" paired associates (high-low, book-page) and at least one of the
"hard" associates of the first recall trial, and to recall all paired associates on
the second trial. In patients over age 70, performance is slightly less adequate. 26 Some patients can learn the paired words with strong natural associations but cannot learn the pairs without such associations. This discrepancy
demonstrates a reliance on semantic cues and an inability to learn new material that cannot be associated with memories already in storage. The total
PAL score is the best measure of verbal learning.
The results of a statistical comparison of these memory tests between 25
patients with mixed brain damage and 25 normal patients with IQs less than
80 appear in Table 6-2. Differences in age and education were controlled. 29
Some aspects of the memory process are associated with certain neuroanatomic structures or neuronal systems. Pathologic studies have amply documented that limbic structures are involved in the long-term storage and retrieval of recent information. 7 ,21,26,36 However, the structures required for
immediate recall and remote memory are not as well established. Although
all memory traces-visual, verbal, tactile, and polymodal-are most likely
stored in the neocortex, many subcortical structures are necessary for the total
memory process (registration, storage, and retrieval), Damage or disruption of
different cortical or subcortical systems result in varied patterns of dysfunction,
Immediate Recall
The immediate recall of digits is a process that does not require any long-term storage
of information but does require initial registration, short-term holding, and verbal
repetition. This entire process can be performed by the language cortex surrounding
MEMORY
85
the sylvian fissure, as demonstrated in patients with transcortical aphasia. 13 The

exact mechanism by which these short-term memories are maintained within
the language system is not known. Reverberating circuits may be established,
or patterns of cortical after-image may be present. Whatever change does occur, however, is not long-lasting.
Efficient short-term memory is not a passive process, and several factors
favor good performance. A digit-sequence task is performed much better if
active mental rehearsal can take place. Also, if the patient actively groups
digits into two- or three-digit sets, performance will be improved. A third and
always very important element in all memory processing is the association of
the new material with previously stored information; for example, a digit
sequence that is similar to an old phone number or address will be much
more easily recalled than a completely unique random sequence. Short-term
memory (immediate recall) is a distinct property of the cortical sensory, motor, and integrative areas necessary to register, recall, and produce the original
stimulus. It does not require the limbic system, as do long-term storage and permanent memory formation.
If these basic sensory or motor areas are damaged or disrupted, then

short-term memory will be faulty. In digit repetition, the language system is
essential, so any degree of aphasia (excluding the transcortical aphasias) can
disrupt immediate memory functioning. This repetition failure is particularly
pronounced in conduction aphasia,35 the primary deficit of which is an inability to repeat. Whether this repetition failure is a defect of language or
short-term memory is an open question that may, in fact, reflect an argument
of semantics.
The most common cause of failure on short-term memory tasks is probably inattention. 30 If a patient's attention strays from the stimulus during presentation, the information may be imperfectly registered. Similarly, if the patient
is inattentive during the repetition phase and pauses occur, the memory trace
will fade. Inattention can be organic, as in confusional states and dementia,
or functional, as in anxiety and depression.
Patients with dementia have difficulty with immediate memory for several reasons: such patients are often inattentive; they have cortical atrophy,
which affects their basic language and other sensory-motor integration systems; and they have general intellectual deterioration. 39
Recent Memory
In general, the ability to store and then retrieve new material (recent memory,
new learning, or memorizing) presumes intact registration, retention, and

short-term storage. If the material is familiar and can be associated with information already in long-term storage, the process is easier and relies less
on short-term storage. 25
Certain limbic structures are required to ensure storage and retrieval. The medial temporal lobe, the mamillary bodies, and the dorsal medial nuclei of the thalami
86
are essential subcortical links in the storage and retrieval of both verbal and nonverbal
memories.7.26.36 The degree of memory loss is related to the extent of damage
within this system. When there is bilateral temporal lobe damage, injury to
the hippocampus is sufficient to produce memory problems; if there is also
damage to the subiculum and the perihippocampal and entorhinal cortices,
the memory loss becomes profound. 40 Actual memories are probably not
stored in these structures, but the limbic system seems to act as the mechanism to store and retrieve memories from the cortex. Frontal lobe damage
(primarily affecting the orbital cortex) also can impair recent memory; this
situation is most commonly seen after rupture of an anterior communicating
artery aneurysm.
Whenever these subcortical structures are destroyed or severely damaged,
the patient is rendered unable to learn new material (anterograde amnesia)
or to retrieve memories from the recent past (retrograde amnesia). These patients literally become fixed in time and are unable to record the passing of
events from that time onward. If these limbic structures are damaged in isolation
(i.e., with no additional damage outside the limbic system), patients develop a profound organic amnesic state. This condition is characterized clinically by
(1) severe anterograde amnesia; (2) moderate to severe retrograde amnesia,
which can extend back for several years; and, usually, (3) confabulation during the acute stage. In the face of this devastating memory impairment, such
patients have remarkably intact immediate memory, as assessed by digit repetition and similar tests. These patients also demonstrate no change in premorbid levels of intelligence. They carry on coherent, intelligent conversations
that appear abnormal only when recent events are discussed. Because these
patients do not remember the date, place, and recent events, they may appear
confused.
This dramatic amnesic state has been seen secondary to bilateral temporal lobectomy, herpes simplex encephalitis, and bilateral hippocampal infarction in which the hippocampi have been completely destroyed. A similar
memory deficit is seen clinically in Korsakoff's syndrome (a syndrome of
thiamine depletion seen in chronic alcoholism and severe malnutrition), in
which there is bilateral destruction of the mamillary bodies and the dorsal
medial nuclei of the thalami. The patient with Korsakoff's syndrome frequently, but not invariably, goes through an acute encephalopathy (Wernicke's encephalopathy) at the onset of the memory difficulty. Vascular or
traumatic lesions of the dorsal medial thalamus also cause severe organic
amnesia. 16.31.34 The patient with Korsakoff's syndrome shows good implicit
memory; that is, the patient can recognize if he or she has seen a previously
presented item, rather than recalling or retrieving it from memory. This implicit memory is strictly a cortical process, in which the memory trace has
been stored without the patient's awareness. lO 27
In Alzheimer's dementia, patients also have defects in new learning, which are
due in part to a gradual degeneration of the cells in the hippocampus and in
MEMORY
87
the basal nucleus of Meynert. The memory loss in the atrophic dementias is
more complex than that seen in the organic amnesias, and it is discussed
more fully in the section on remote memory.
The amnesia most familiar to the lay person is the memory loss that
occurs after head injury. Patients with moderate to severe closed head injury almost
always have some degree of retrograde amnesia for the time immediately preceding
the injury, and they usually have transient difficulty learning new material after the
trauma (anterograde amnesia). In head trauma, the temporal lobes are commonly concussed against the bony confines of the middle fossa. This trauma
causes a physiologic disruption of hippocampal function, which in tum disturbs memory storage and retrieval. Posttraumatic amnesia is usually reversible, but in cases of significant temporal lobe damage, the memory loss can
be permanent. Repeated concussion, such as that seen in boxers, may result
in gradual but permanent memory disturbance. An interesting feature of the
amnesia seen with acute head injury is that the retrograde amnestic period
will shorten in the days following recovery of consciousness. Initially the
patient may not recall events that occurred years preceding the accident.
Within several days, the patient may remember all but the few minutes that
immediately preceded the accident. This shrinking retrograde amnesia verifies
that the injury did not eliminate the memories from storage but merely rendered them temporarily irretrievable. us In some interesting trauma cases retrograde amnesia is profound and persistent even after the anterograde amnesia clears.19 Such cases indicate that neuroanatomic subsystems exist for the
various aspects of recent memory.
Clinically, the memory disturbance in the various types of organic amnesias is similar (i.e., the patients cannot recall recent information). On experimental tasks, however, it has been shown that patients with Korsakoff's
syndrome, whose damage is in the thalamus and mamillary body, have actually retained a considerable amount of the material presented to them, but
are unaware of this (the memory is implicit but not explicit). The deficit is
with retrieving the information and realizing that it has been presented, rather
than with the storage process. Patients with hippocampal and temporal lobe
damage have both a storage and a retrieval defect. As mentioned earlier, the
fact that the cortex of the patient with Korsakoffs syndrome has stored the
engrams for the memory does not help the patient clinically because he or
she does not realize that they are stored and thus cannot retrieve and use the
information. 37
Transient global amnesia is another type of organic memory problem. 15 This
syndrome probably involves transient ischemia of both medial temporal lobes secondary to decreased perfusion in the territory of the posterior cerebral arteries. 14,20 Single
photon emission computerized tomography (SPECT) perfusion scans usually
demonstrate this bilateral or unilateral left temporal lobe hypoperfusion. This
syndrome is characterized by an acute but temporary confusional state with
amnesia. The patients are disoriented to time and place and have a significant
88
defect in new-learning ability. Fortunately, recovery generally occurs within

hours or days, and the patient is left with a permanent amnesia only for the
duration of the episode itself. Some patients, however, may experience permanent memory loss and demonstrate bilateral hippocampal infarction. 8 The
following case illustrates some of the essential features of this syndrome:
Dr. JL was a robust 68-year-old educator who was addressing a teacher's convention.
In the middle of his speech, he stopped suddenly, became dazed, and began to ask
where he was. He repeatedly asked, "What am I dOing?" and "Where am I?" On initial
neurologic examination, he was distraught and very confused. He was unable to attend well, and he could not learn new material. He did not remember arriving in New
Orleans, but he did know that he was scheduled to attend the convention. One day
later, his mental function was essentially normal, except that he was amnesic for the
day prior to and the day of his amnesic episode.
All of the conditions discussed thus far have resulted from bilateral lesions localized in limbic structures. Although it is true that a bilateral lesion is
necessary to produce a profound memory loss, there is some loss of specific memory
functions after a unilateral lesion. Patients who have had a unilateral dominant
temporal lobectomy show a relative decrease in verbal learning, whereas those
with unilateral nondominant temporal lobectomies show a decrease in visual
memory.21 This pattern of differential deficits is also seen with unilateral subcortical lesions. 32
Various factors other than specific limbic damage can interfere with the
storage and retrieval of new material; some of these have been discussed in
the previous section, but they merit additional mention here. Inattention will
prevent any patient from accurately storing new material. Because efficient
memory storage requires close attention to the information for short-term
registration and storage, the results of memory testing in inattentive patients
must be interpreted with caution. Patients with aphasia are also at a tremendous disadvantage in any verbal learning task; if they cannot accurately comprehend or repeat verbal material, it is not valid to judge their memory capacity using that material. Nonverbal memory tasks are necessary for valid
assessment of memory in patients with aphasia. Memory-test performance
and intelligence are directly related; accordingly, patients' premorbid intellectuallevels must be considered when interpreting the results of memory testing. Deficits in basic sensory capacity (i.e., hearing and vision) are sometimes
overlooked in testing, but obviously sensory systems must be adequate for
memory testing in each specific modality.
Certain medications are also well known to produce genuine memory
deficits. Psychotropic drugs, beta blockers (e.g., propranolol), anticonvulsants,
prednisone, and any number of other medications and toxins (e.g., alcohol
and street drugs) have been implicated.
MEMORY
89
The patient's emotional state can also significantly affect new-learning

ability. Very anxious patients often make errors owing to inattention and
distractibility. Depressed patients perform poorly on memory testing because
of their inability to put forth the required effort to memorize the presented
material.
Depressed patients also tend to remember negative or sad events or ideas
more effectively than they do positive or happy ones. 5 In significant depression, the decrease in motivation and learning probably involves more than
purely psychologic mechanisms. The underlying chemical disorder postulated
in major depressive disorders undoubtedly adversely affects neuronal TImctioning at various levels. l1
Poor performance on memory tests is probably the single most important factor
that may result in the misdiagnosis of depression as dementia. 24 Accordingly, in
the patient with psychomotor retardation and memory problems, the diagnosis of depression must be considered and carefully pursued during the
evaluation process.
Remote Memory
When a memory has remained in a person's repertoire for a number of years,
it can be considered a remote, or old, memory. Old memories are stored in the
appropriate association cortex (e.g., language cortex for verbal material). In contrast
to recent memory, remote memory does not require the limbic system for retrieval
from storage. Patients with Korsakoffs syndrome or bilateral temporallobectomy can accurately discuss personal and historic events that occurred years
previously (remote memory), yet they are unable to remember what they had
for breakfast that morning (recent memory).28 There is apparently a mechanism, thus far unexplained, by which memories finally become sufficiently
well established that they can be recalled without the aid of subcortical limbic
structures. These remote memories can be lost only by damage to the cortical
storage areas themselves. This loss of remote, or old, memories is seen in patients
with the atrophic dementias (Alzheimer's and Pick's) or any disease that damages
extensive areas of the cortex. The memory disturbance in the patient with dementia is complex: such patients have difficulty with short-term memory because of atrophy in the basic sensory association cortex (e.g., language cortex
for verbal memory); they are hampered in recent memory acquisition because
of degeneration of cells in the basilar nucleus of Meynert and hippocampal
system; and they have defects in remote memory because of widespread cortical atrophy.
Functional Memory Disturbances

Not all memory disorders are of organic origin, and knowledge of the functional disturbances of memory is important. The interference with memory
90
performance that can occur secondary to anxiety and depression has been
discussed previously. In addition, studies of Vietnam War veterans have demonstrated stable memory deficits in servicemen suffering from posttraumatic
stress disorder. 5 There are, however, several psychiatric conditions in which memory
disturbances are central features. The first and most common is the dissociative state,
now called psychogenic amnesia. This is the classic amnesia that has been popularized in the press and in movies. Such patients either lose their identity
completely and travel to a new location (fugue, psychogenic fugue state, or
dissociative amnesia) or have periods of minutes, hours, or days when they
carry out their normal life routine and later become aware that they remember nothing of what transpired during this period (dissociative state or localized amnesia). During a dissociative or fugue state, the patients do not
usually act confused, as do persons with transient global amnesia, and they
are able to learn new materiat unlike patients with organic amnesia. There
should be no difficulty in differentiating patients with organic amnesia, who cannot
learn new material when tested, from those with psychogenic amnesia, who have
experienced a "memory lapse. Brief testing using the Four Unrelated Words
task or the PAL task should suffice.
One other curious pseudomemory disturbance is Ganser's syndrome, or
the syndrome of approximate answers. These patients routinely give approximate answers to all questions: for example, saying that today is Tuesday
(actually it is Wednesday), the month is March (actually it is April), or 2 and
2 are 5. Because their answers are so consistently close to the correct answer,
it is obvious that they have more knowledge of the subject in question than
they are indicating. Although giving the approximate answer is the most characteristic symptom, Ganser's original patients all had clouded consciousness,
hallucinations, and somatic conversion symptoms. 12 This uncommon syndrome was originally described in prisoners but is not restricted to this population. It is not typically seen in children. Its etiology is unclear, but some
patients have a schizophrenic disorder or an underlying brain disease. The
nature and inconsistency of their mental status findings strongly suggest a
significant component of either hysteria or malingering. Most patients have
some motivating reason to appear legally insane, incompetent or cognitively
impaired.
On occasion, professed memory loss is a conscious and motivated symptom of
malingering. It may be associated with other feigned neurologic or psychiatric
symptoms but can also be seen alone. The patients whom we have seen
usually have a very specific, well-recognized reason for their malingering (in
our experience, either avoiding prosecution by virtue of incompetence or
gaining compensation for a minor head injury). On examination, these patients may give approximate answers or very bizarre answers. Their memory
loss is usually inconsistent, in that they may fail all memory testing but remember a football score from the previous weekend. They also claim patches
of remote memory loss and at times claim not to remember their own name.
II
MEMORY
91
SUMMARY
In general, memory is a hierarchic process in which information must first
be registered in a basic sensory cortical area and then processed through the
limbic system for new learning to occur. Finally, the material is permanently
established in the appropriate association cortex. At this point, limbic retrieval
is no longer required in the recall process. The immediate recall system is
disturbed by damage to the primary sensory or motor cortex or by inattention.
Learning is prevented by damage to the hippocampi or the dorsal medial
thalamic nuclei. Old remote memories are resistant to limbic damage but will
be lost when widespread cortical damage occurs. Careful testing of the various
aspects of memory can frequently lead to both a clinical and an anatomic
diagnosis.
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CONSTRUCTIONAL
ABILITY
Constructional ability (constructional praxis or visuoconstructive ability) is

the ability to draw or construct two- or three-dimensional figures or shapes.
Copying line drawings using pencil on paper, reproducing matchstick patterns, and reconstructing block designs are all examples of routinely used tests
of constructional ability. Such constructional tasks are extremely useful for detecting organic brain disease and should be included in every mental status examination.
A high-level, nonverbal cognitive function, constructional ability is a very complex
perceptual motor ability involving the integration of occipital, parietal, and frontal
lobe functions. Because of the extensive cortical area necessary to perform con-
structional tasks, early or subtle brain damage frequently disrupts performance. In some patients, the unsuccessful attempt to copy a simple line drawing can be the only objective evidence suggesting organic brain disease.
Despite their importance and proven clinical use, constructional tasks
are not always included in bedside or office mental status testing, partly because very few patients actually complain of constructional impairment. Architects or engineers, whose professions require such abilities, might notice
difficulty when drawing plans, reading blueprints, or translating plans into
actual construction, but most patients are quite surprised to find that they
are unable to draw a clock or copy a block design when asked to do so.
Because constructional tests take only a few minutes to perform and can yield
very valuable data, we encourage every clinician to use them.
We use the term "constructional ability," rather than the more classic
term "constructional praxis," to discuss this general area of cognitive function.
"Praxis," in the strict sense, refers to the motor integration used to execute
complex learned movements. The reproduction of line drawings or block designs involves more than the organization of skilled hand movements. Such
reproduction requires accurate visual perception, integration of perception
into kinesthetic images, and translation of kinesthetic images into the final
93
94
motor patterns that are necessary to produce the construction. Patients do

not have to recognize or name the figure; they only have to develop an accurate concept or gestalt. The relations of angles and sides, the integration of
parts into a whole, orientation on the page, and three-dimensionality must
all be appreciated for accurate motor integration to occur. The final step, of
course, requires adequate limb strength and coordination.
We use "constructional impairment," rather than "constructional
apraxia," to describe the failure to perform adequately on any of these tasks.
As implied in the preceding paragraph, a disturbance in praxis (apraxia) refers
only to a breakdown in the execution of the learned movements that are
involved in the constructional task. 10 The term "apraxia" excludes the component of visual perception and organization and thus does not accurately
describe the neuropsychologic complexity of the entire process.
EVALUATION
As with any skilled motor activity, both initial exposure and repeated practice
affect the ability to reproduce paper-and-pencil designs or to complete block
constructions. Social deprivation and a lack of academic experience, therefore,
have a detrimental effect on constructional performance. The clinician who
uses constructional tests as a part of the mental status examination must be
cautious in interpreting the results of performance of patients with a history
of retardation, a poor academic background, or both. Placed in the proper
interpretive context, however, use of drawings and other constructional tests
may be productive in such patients.
selecting Tests of Constructional

Ability
Constructional ability may be tested in a variety of ways, and different levels
of performance may be found in the same patient when different tests are employed.
To show the range of test materials that may be used, Warrington 25 has listed
six basic types of tests for eliciting evidence of constructional impairment:
Two-dimensional block designs

Paper-and-pencil reproduction of geometric shapes
Spontaneous drawings
Stick-pattern reproduction
Three-dimensional block constructions
Spatial analysis tasks that require the patient to shade in the portion
of a design that is common to two or more overlapping figures
Patients with brain lesions show differences in the incidence, severity,

and quality of constructional impairment, depending on the type of test used
CONSTRUCTIONAL ABILITY
95
and the nature, size, and location of their lesions. 1 ,3,22 The clinical examination of constructional impairment in each patient ideally should include several tests to tap somewhat different aspects of constructional ability; however,
reproduction drawings and drawings to command are the easiest tests to administer and interpret.
The use of the tests outlined in this book presumes that the patient has
adequate visual acuity (at least 20/100, as objectively tested) and sufficient
motor ability to use paper, pencil, and blocks effectively. Deficits in either
motor or sensory channels can hinder performance, but such impairment
does not reflect the disruption in the integrative higher cortical function that
these tests are designed to assess.
Several constructional tests that include a memory component are available. 4 ,1l,21 Although the inclusion of the memory component does increase
the sensitivity of constructional tests, it also raises serious problems in the
interpretation of the test results. Deficits in drawings from memory may be
due to memory problems, constructional problems, or a combination of the
two. We believe that memory is an important enough variable to warrant
testing it specifically in isolation. As we have emphasized throughout this
book, a primary goal of each aspect of mental status testing is to assess each cognitive
function as discretely as possible. The reader is referred to Appendix 1 for further
information regarding the availability and description of visual memory tests.
The following brief tests of constructional ability are included for bedside
and office testing. These tests were chosen because of their ease of administration
and interpretation, their limited need for apparatus and specialized equipment, and
their proven efficacy in the detection of diffuse and focal brain lesions in patients
with a wide range of intelligence. 24
Reproduction Drawings
We suggest that reproduction drawings be administered first when assessing
constructional ability because of their apparent simplicity and familiarity.
DIRECTIONS: The drawings presented in Figure 7 -1 can be reproduced
adequately by normal individuals and are very sensitive to the effects of brain
disease. They are organized in order of increasing difficulty and should be so
administered. Both two- and three-dimensional drawings are used because of
frequent quantitative and qualitative performance differences noted on these
two somewhat different tasks. The examiner either may use a standard predrawn set of designs (probably best because the stimuli are identical for each
administration and are generally of better quality than quickly drawn bedside
examples) or may draw the stimulus figures on the left side of a piece of
blank white paper. It is helpful to use two colors of pencil or felt-tip pen, to
reduce the possibility of confusion between the drawings of the patient and
those drawn by a hurried examiner. Separate sheets of paper for each design
96
Vertical Diamond
Two-Dimensional Cross
I
Three-Dimensional Block
~
__v
Three-Dimensional Pipe
Triangle within a Triangle
FIG U R E 7 - 1. Test items for Reproduction Drawings Test.
may be needed for patients who are highly distractible or perseverative. Lined
progress-note forms, consult sheets, and other handy paper that is perceptually confusing should not be used. Patients who become frustrated with their
efforts on one grawing should be encouraged by the examiner either to start
over or to go on to the next drawing.
97
Introduce each item by saying, "Please draw this design exactly as it looks
to you" (see Fig. 7-1).
SCORING: To help the examiner quantify the adequacy of patients' performance on this test, an objective scoring system 18 is provided for rating the
relative quality of each drawing.
O-Poor
I-Fair
2-Good
3-Excellent
Given for nonrecognizable reproductions or a gross distortion of the basic

design gestalt
Given for moderately distorted or rotated two-dimensional drawings or a loss
of all three-dimensionality with moderate distortions or rotations on threedimensional designs
Given for minimal distortions or rotations with adequate integration on twodimensional designs and some evidence of three-dimensionality but lessthan-perfect reproduction on three-dimensional designs
Given for perfect (or nearly perfect) reproductions of two- and threedimensional drawings
As illustrated in Figure 7-2, drawings that show evidence of rotations of

more than 90 degrees, perseveration, or "closing in" are given ratings of o.
Standardization of these designs comparing their use with nonselected
brain-damaged individuals and with low-IQ (less than 80) normal people
has indicated highly significant (P < .0001) differences in performance by
the two groups on each design. A rating of a on any design resulted in a
100% probability of the patient being correctly classified as brain-damaged,
with a 0% probability of misclassification (false-positive). A rating of 1 resulted in an 80% probability of brain damage. 24
Although the clinician soon gains familiarity with this test and develops
his or her own scoring criteria based on experience, examples from our clinical population representing poor, fair, good, and excellent drawing reproductions are shown in Figures 7 - 3 through 7 - 7 to help the examiner rate
each design.
Drawings to Command
DIRECTIONS: The patient is required to draw three pictures, according to
verbal commands. Introduce the test by saying, "1 would now like you to
draw some simple pictures on this paper. Draw each picture as well as you
are able. Please draw a picture of a clock with the numbers and hands on it;
a daisy in a flowerpot; and a house in perspective, so that you can see two
sides and the roof."
SCORING: A simple scoring system similar to that used with reproduction
drawings may be used to aid the examiner in quantifying performance on
this test.
98
Example 1 ROTATION
Example 2 PERSEVERATION
Example 3 "Closing In"
FIG U R E 7 - 2. Examples of patient drawings with specific types of errors.
99
3
FIG U R E 7 - 3. Renderings of Vertical Diamond Test, with scores of 0 (poor) through 3
(excellent).
100
FIG U RE 7 - 4. Renderings of Two-Dimensional Cross Test, with scores of 0 (poor) through

3 (excellent).
101
FIG U R E 7 _ 5. Renderings of Three-Dimensional Cube Test, with scores of 0 (poor) through

3 (excellent).
102
3
FIG U R E 7 - 6. Renderings of Three-Dimensional Pipe Test, with scores of 0 (poor) through
3 (excellent).
103
FI G U R E 7 - 7. Renderings of Triangle Within a Triangle Test, with scores of 0 (poor) through

3 (excellent).
104
O-Poor
I-Fair
2-Good
3-Excellent
Given for nonrecognizable drawings or a gross distortion of the basic gestalt

Given for moderate distortion or rotation of any of the drawings or a loss of
three-dimensionality on the house drawing (the clock should contain an
approximately circular face or the numbers 1 through 12; the daisy should
be recognizable as a flower in a pot; and the house should be recognizable
as a house)
Given for only mild distortions with adequate integration on all pictures (the
house should contain some evidence of three-dimensionality and contain
the basic elements of a house; the clock should contain two of the
following: circular face, numbers 1 through 12, and symmetric number
placement; the daisy should be in the generally appropriate shape-a
circular center with petals around it)
Given for perfect (or near perfect) representations of the items with all
appropriate components, placement, and perspective (the house and
flowerpot should be clearly three-dimensional)
Representative clinical examples of poor, fair, good, and excellent drawings

are shown in Figures 7-8 through 7-10, to help the examiner rate each
picture.
The clock setting task can often bring out interesting errors, not only in
pure constructional ability but also in the conceptualization of time and its
abstract relation to the placement of the hands. Many patients with early
dementia can draw the clock and put in the numbers correctly, but when
asked to set the hands at 2:30, they will ponder, then put one hand on 2 and
the other on 3 and add a 0, or put in three hands (one on the 12, one on
the 3, and one on the 6), or draw a straight line from the 2 to the 6 (Fig.
7 -11 ). Freedman and Kaplan 8,14 have studied clock drawings extensively and
suggest asking patients to set a time in which one hand is on the left side of
the clock face and one on the right (e.g., 11:10 or 10:20) in order to identify
errors that might arise if a patient has unilateral neglect. In their studies,
patients over age 70 made increasingly frequent errors in clock setting.
Block Designs
The following test, although important and often a source of excellent clinical
data, does require equipment other than paper and pencil and is therefore
considered ancillary,
DIRECTIONS: The use of this test requires four multicolored cubes (obtained from the suppliers of the Wechsler's Adult Intelligence Scale [WAIS-R
or WAIS-IIIj or from many toy stores as Kohs blocks) and four stimulus
designs, which may be drawn with colored pens or pencils on pieces of heavy
white paper. The stimulus designs should be accurately drawn in the approximate size of the design completed with blocks, The designs in Figure 7 -12
are arranged in ascending order of difficulty. Take four blocks and say, "These
blocks are all alike. On some sides they are all red; on some, all white; and
on some half red and half white. I would like you to take these blocks and
3
FIG U R E 7 - 8. Renderings of Drawings to
Command Test (clock), with scores of 0
(poor) through 3 (excellent).
105
106
3
FIG U R E 7 - 9. Renderings of Drawings to Command Test
(flowerpot), with scores of a (poor) through 3 (excellent).
FIG U R E 7 - 1 o. Renderings of Drawings to

Command Test (house in perspective), with
scores of 0 (poor) through 3 (excellent).
107
108
DRAW A CLOCK FACE

WITH ALL NUMBERS.
SET CLOCK FOR
2:30.
II IZ
ID
Cr
27
.(,
FIG U R E 7 - 1 1. Common errors seen on clock-setting

task.
make a design (or picture) that looks like this picture." If the patient fails to
reproduce design 1 accurately, score the response as a failure and demonstrate
the correct reproduction. Continue with each design in turn, being sure to
mix up the blocks after each effort.
SCORING: Only perfect reproductions of the designs are considered correct. Rotations (either right-left or near-far) are scored as incorrect, as are
figure-ground (color) reversals. A score of 1 is given for each correctly reproduced design. Normal individuals are expected to reproduce each design
perfectly.
Examples of commonly seen rotation, reversal, and "stringing out" errors
are shown in Figure 7 -13.
Interpreting Test Performance

Normal individuals obtain almost-perfect scores on simple reproduction and
command drawings, but a modest yet significant dropoff in performance oc-
109
~.
4
FI G U RE 7 - 12. Test items for Block Designs Test.
curs with increasing age (Table 7-1). The three-dimensional cube and the
house are the most difficult. Close inspection of the data in Table 7 -1 shows
how much overlap exists among normal individuals (particularly the elderly),
as well as the considerable overlap between normal elderly and patients with
early dementia. Subtle evidence of constructional impairment, therefore, must be
cautiously interpreted.
Several specific types of errors on constructional tests are usually accepted as
almost pathognomonic of brain damage when made by a nonretarded patient
over age 10. Most of these errors can be seen on both paper-and-pencil and
110
~.
FIG U RE 7 - 13. Common errors seen on Block Designs Test. (1) Right-left rotation. (2) Nearfar rotation. (3) Figure-ground reversal. (4) "Stringing out."
Age
Diamond
Cross
Cube
Pipe
Triangles
Clock
Flower
House
2.9
3.0
2.5
2.3
2.1
2.6
2.7
2.5
2.2
1.9
(0.6)
(0.6)
(0.7)
(0.7)
(0.9)
2.2 (0.7)
1.9 (0.9)
1.5 (0.8)
0.5 (0.6)
1.8 (0.9)
1.4 (0.9)
0.5 (0.8)
Normal Individuals (by age group)

40-49
50-59
2.8 (0.4)
2.9 (0.3)
2.8 (0.4)
2.8 (0.4)
60-69
70-79
80-89
2.7 (0.5)
2.6 (0.5)
2.8 (0.4)
2.6 (0.5)
2.2 (0.5)
2.2 (0.6)
2.3 (0.7)
2.4 (0.5)
2.1 (1.0)
1.6 (0.7)
1.9 (1.0)
2.6 (0.5)
2.6 (0.5)
2.5 (0.7)
2.9 (0.4)
2.9 (0.4)
2.1 (0.7)
2.0 (0.8)
2.5 (0.8)
2.7 (0.5)
2.5 (0.5)
(0.3)
(0.2)
(0.7)
(0.7)
(0.9)
2.5 (0.5)
2.2 (0.7)
2.1 (0.7)
1.9 (0.8)
Patients with Alzheimer's Disease (by stage and age)

I (age 71.3 ::': 7.8)
II (age 71.6 ::': 7.1)
III (age 71.5 ::': 8.9)
2.5 (0.5)
2.4 (0.7)
1.5 (1.1)
'Mean (SD), on a scale of 0 to 3.
2.2 (0.9)
1.9 (0.8)
1.2 (1.0)
2.0 (0.7)
1.6 (0.9)
0.9 (0.9)
2.2 (0.5)
1.8 (0.7)
0.9 (0.8)
2.4 (0.6)
2.0 (0.9)
1.1 (1.0)
2.7 (0.5)
1.8 (1.0)
0.6 (0.9)
112
block-design tests. The most important of these pathognomonic signs are the
following:
1. Rotation by more than 45 degrees or the disorientation of the whole
figure or a component of it on the background
2. Perseveration or the repetition of the entire figure or part of it
3. Fragmentation of the design or the omission of parts of the figure
4. Significant difficulty in either integration or the placement of individual parts at the correct angles or location
5. Substitution or addition of "dog-ears" for angles on the drawn figure.
Any of these errors should raise a strong question of brain dysfunction requiring more detailed evaluation.
ANATOMY
The parietal lobes are the principal cortical areas involved in visual-motor integration.
The visual receptive areas of the occipital lobes and the motor areas of the
frontal lobes are necessary for the completion of all of the tests, but it is
the association cortex of the parietal lobes that is responsible for most of the
complex integration. The actual localization of the various aspects of construction within the parietal lobes is not established, but visual stimuli are
thought to spread from primary sensory area 17 to contiguous secondary
association areas of the inferior parietal lobule (areas 39 and 40), where
associations are made among visual, auditory, and kinesthetic images. 19 Kinesthetic analysis of the visual pattern is the initial task of the association area.
The kinesthetic images are then translated into motor patterns by involving
the perirolandic premotor area. Drawings to command also require input
from the auditory system. The premotor frontal association cortex would theoretically seem to be very important in these highly skilled, fine motor tasks,
but, in fact, only a small percentage of patients with lesions restricted to the
frontal lobes have constructional impairment. 7 The parietal lobes seem to be
the major areas involved in learning and programming skilled movements;
the frontal motor areas appear to be more involved in the pure executive
nature of the task. (A more extensive discussion of deficits in learned skilled
movements is in the section on apraxia in Chapter 9.)
Locating Lesions
If a nonretarded adult demonstrates constructional impairment on the tests outlined
in this chapter, parietal lobe dysfunction should be strongly suspected. Although
lesions in any quadrant of the brain can disrupt constructional performance,
the incidence and severity of the deficits in patients with lesions restricted to
113
the frontal lobes are small. Most constructional impairment is seen in patients
with cortical damage posterior to the rolandic fissure. 7 ,ls
It was once believed that the right (nondominant) parietal lobe was actually dominant for constructional ability. Many studies have been performed
comparing the relative incidence and severity of constructional impairment
in patients with lesions of the right and left hemispheres. These studies clearly
demonstrate that performance can be defective with lesions in either parietal
lobe. 20 In general, right hemisphere lesions produce a higher incidence and greater
severity of defect than do left hemisphere lesions,3 What is certain is that constructional ability is not a function exclusive to the right parietal lobe. 12
Some subtle differences in qualitative performance that are both interesting and possibly useful in clinical testing have been noted in patients with
right and left parietal lobe lesions. On the block designs test, patients with
right hemisphere lesions frequently lose the basic outline of the design and
"string out" the blocks 13 (example 4, see Fig. 7-13), These patients tend to
make scattered and fragmented drawings that show loss of spatial relations
and orientation on the page. Patients with left hemisphere lesions show more
coherent block designs, with maintenance of external configuration but loss
of accurate internal detail (example 3, see Fig. 7-13). Their drawings tend to
be simplifications of the model, lacking detail but having preserved general
spatial relationships, Obvious differences in the performance of the two
groups are not always seen, and elaborate scoring schemes have been designed to bring out the subtle differences. s Such systems are interesting but
are probably not of practical significance to the bedside clinician. The quality
of constructional impairment with right hemisphere lesions is uniform and
will not differ according to the locus of the lesion within the hemisphere. 16
Without very careful assessment of qualitative performance and using constructional tests alone, it is not always possible to determine the side of the
lesion in the individual patient unless unilateral neglect is present. When a
patient with normal language shows grossly impaired constructional ability,
right hemisphere dysfunction is strongly suggested.
Patients with lesions confined to the parietal lobes often show evidence
of significant constructional impairment on mental status testing but fail to
demonstrate abnormalities on the standard neurologic examination. Therefore, the presence of errors on constructional ability testing should lead to a more
complete neurodiagnostic workup.
Identifying Cortical Disease

The most dramatic examples of constructional impairment occur in patients with
bilateral cortical disease, particularly cerebral atrophy. Patients with Alzheimer's
disease (by far the most common dementia) may show constructional difficulty in the early stages of their disease (see Table 7 _1)?3 Patients with multiple infarct dementia, seen in cerebral vascular disease, may also demonstrate
constructional impairment, but they usually have other abnormal neurologic
114
signs as well. Patients in confusional states from toxic or metabolic factors

frequently demonstrate constructional impairment during the acute stage.
This is secondary to reversible physiologic disturbance of the cortex rather
than to structural damage.
Because of the fairly high incidence of constructional impairment in dementia, such tasks are very good screening tests in patients of advancing age
who present with vague psychiatric or neurologic complaints.
Evaluating Maturation
Standard drawing and other constructional ability tests are used not only to
detect brain disease, but also by psychologists to evaluate both the maturational stage of perceptual motor development (constructional ability) and the
presence of specific constructional problems in children. The ability to integrate visual stimuli and to construct or draw a reproduction is closely related
to both chronologic and intellectual maturation in young children,z,9,18 Errors
in construction, including poor integration of the parts, distortions or simplification, perseveration, and rotations, are common early in development
(age 5 to 7) and tend to decrease with age. 6 Relatively errorless performance
on simple drawing tests is expected by age 10 to 12.18 Measured intelligence
tends to be relatively highly correlated with constructional performance in
children; for adults of normal intelligence (i.e., IQ above 85) IQ appears to
have a limited effect on constructional ability.21 Both children and adults with
a significant mental deficiency tend to show inferior performance on most
constructional tests. 4 Formal studies have indicated that it is difficult but not
impossible to use drawing tests to differentiate intellectually impaired (e.g.,
IQ below 70) but socially and vocationally independent adults from similar
individuals with demonstrable brain damage,z4
SUMMARY
Constructional ability is a highly developed cortical integrative function that
is primarily carried out in the parietal lobes, Drawings and block constructions are easily administered tests to evaluate this function. Constructional
impairment usually suggests disease of the posterior portions of the cerebral
hemispheres, although other areas of the cortex may be involved. Because
constructional ability is so frequently disturbed in patients with brain disease,
testing this function is a very important and highly useful component of the
mental status examination.
REFERENCES
1. Arrigoni, G and DeRenzi, E: Constructional apraxia and hemispheric locus of lesions. Cortex
1:170,1964.
2. Bender, L: A Visual Motor Gestalt Test and its Clinical use. American Orthopsychiatric
Association, New York, 1983.
115
3. Benson, DF and Barton, M: Disturbances in constructional ability. Cortex 6:19, 1970.

4. Benton, A: Revised Visual Retention Test. The Psychological Corporation, New York, 1974.
5. Benton, AL: Visuoperceptive, visuospatial and visuoconstructive disorders. In Heilman, KM
and Valenstein, E (eds): Clinical Neuropsychology, ed 3. Oxford University Press, New York,
1993, pp 165-213.
6. Black, FW: Reversal and rotation errors by normal and retarded readers. Percept Mot Skills
36:895, 1973.
7. Black, FW and Strub, RL: Constructional apraxia in patients with discrete missile wounds of
the brain. Cortex 12:212, 1976.
8. Freedman, M, et al: Clock Drawing: A Neuropsychological Analysis. New York, Oxford University Press, 1994.
9. Frostig, M, Lefever, D, and Whittlesey, J: A developmental test of visual perception for evaluating normal and neurologically handicapped children. Percept Mot Skills 12:383, 1961.
10. Geschwind, N: The apraxias: Neural mechanisms of disorders oflearned movement. Am Sci
63:188, 1975.
11. Graham, F and Kendall, B: Memory for Designs Test. Psychology Test Specialists, Missoula,
MT, 1960.
12. Hecaen, H: Apraxias. In Filskov, SB and Boll, TJ (eds): Handbook of Clinical Neuropsychology. John Wiley & Sons, New York, 1981, pp 267-286.
13. Kaplan, E: Personal communication, 1973.
14. Kaplan, E: A process approach to neuropsychological assessment. In Bull, T and Bryant, BK
(eds): Clinical Neuropsychology and Brain Function: Research Measurement and Practice.
American Psychological Association, Washington, DC, 1988, pp 129-167.
15. Kertesz, A: Right hemisphere lesions in constructional apraxia and visuospatial deficit. In
Kertesz, A (ed): Localization in Neuropsychology. Academic Press, New York, 1983, pp 455570.
16. Kertesz, A and Dobrowski, S: Right hemisphere deficits, lesion size and location. J Clin
Neuropsychol 3:283, 1981.
17. Kirk, A and Kertesz, A: Subcortical contributions to drawing. Brain Cognition 21 :57 -70,
1993.
18. Koppitz, E: The Bender Gestalt Test for Young Children. Grune & Stratton, New York, 1964.
19. Luria, A: The Working Brain. Basic Books, New York, 1973.
20. Mack, JL and Levine, RN: The basis of visual constructional disability in patients with unilateral cerebral lesions. Cortex 17:515, 1981.
21. Pascal, G and Suttell, B: The Bender Gestalt Test. Grune & Stratton, New York, 1951.
22. Piercy, M, Hecaen, H, and DeAjuriaguerra, J: Constructional apraxia associated with unilaterallesions: Left and right cases compared. Brain 83:232, 1960.
23. Sjorgen, T, Sjorgen, T, and Lindgren, AGH: Morbus Alzheimer and Morbus Pick: A genetic,
clinical, and pathoanatomical study. Acta Psychiatr Scand (Suppl)82:1, 1952.
24. Strub, RL, Black, FW, and Leventhal, B: The clinical utility of reproduction drawings with
low IQ patients. J Clin Psychiatry 40:386, 1979.
25. Warrington, E: Constructional apraxia. In Vinken, P and Bruyn, G (eds): Handbook of Clinical Neurology, Vol 4, Disorders of Speech, Perception and Symbolic Behavior. American
Elsevier, Amsterdam, 1969, pp 67-83.
HICHER COCNITIVE
FUNCTIONS
Attention, language, and memory are the basic processes that serve as building blocks for the development of higher intellectual abilities. These basic
functions are necessary, but not sufficient in and of themselves, to execute
more complex cognitive functions. The higher cognitive functions, including the
manipulation of well-learned material, abstract thinking, problem-solving, judgment,
arithmetic computations, and so forth, represent the highest level of human intellectual functioning readily assessable by formal testing methods. These complex neuropsychologic functions are predicated on the integrity and interaction of
more basic processes.
Because they represent the most advanced stages of intellectual development, the higher cognitive functions are often highly susceptible to the
effects of neurologic disease. The evaluation of these functions in the mental
status examination may often demonstrate the early effects of cortical damage
before the more basic processes of attention, language, and memory are impaired. The ability to perform effectively within the environment is determined in
large part by an individual's adequacy in performing such higher-order functions.
An assessment of the patient's performance in these areas provides useful
diagnostic information, as well as information concerning social and vocational prognosis. The higher cognitive functions are evaluated initially during
the history taking, when the patient and others are asked about the patient's
adequacy in job performance, management of personal finances, ability to
solve problems, and overall judgment.
116
HIGHER COGNITIVE FUNCTIONS
117
EVALUATION
The higher cognitive functions may be formally evaluated in many different
ways. Most tests of intelligence and higher-order reasoning are based largely
on assessments of these functions. In general, the higher cognitive functions may
be categorized in the following hierarchic groupings:
1. The fund of acquired information or the store of knowledge

2. The manipulation of old knowledge (e.g., calculations or problem
solving)
3. Social awareness and judgment
4. Abstract thinking (e.g., interpretation of proverbs or the completion of
a conceptual series)
The store of basic acquired information is most efficiently assessed by
simple verbal tests of vocabulary, general information, and comprehension.
Specific examples of these kinds of tests may be seen on any basic intelligence
test (e.g., Wechsler's Adult Intelligence Scale-Third Edition [WAIS-III] Vocabulary, Information, Picture Completion). General intelligence, education,
and social exposure are closely related to performance on these tasks, and the
results of any evaluation must be interpreted in light of this background
information.
The manipulation of old knowledge is a more active process, which
requires both an intact fund of general information and the ability to
apply this information to new or unfamiliar situations. Questions concerning
social comprehension and calculation ability may be used to assess this
function.
Abstract thinking, which is perhaps the highest level of cognition, may
be readily assessed by the use of proverbs, conceptual series, or analogy
interpretation.
The following tests are recommended to evaluate a spectrum of relevant
higher cognitive functions.
Fund of Information
DIRECTIONS: The questions asked in this test provide a reasonable estimate of the patient's store of knowledge or fund of general information. They
are presented in order of increasing difficulty and should be so administered.
Continue to ask questions until the test is completed or until the patient has
failed three successive questions. If the patient's response is unclear, ask him
or her to explain more fully. The examiner may repeat the question if necessary but should not paraphrase the question or spell or explain words that
are unfamiliar to the patient.
118
TEST ITEMS
Questions
Acceptable Responses
1. How many weeks are in a year?

2. Why do people have lungs?
3. Name four people who have been president
of the United States since 1940.
4. Where is Denmark?
5. How far is it from New York to Los
Angeles?
6. Why are light-colored clothes cooler in
summer than dark-colored clothes?
7. What is the capital of Spain?

8. What causes rust?
9. Who wrote the Odyssey?
10. What is the Acropolis?
52
To transfer oxygen from air to blood; to
breathe
Any appropriate presidents
Scandinavia, Northern Europe

Any answer between 2300 and 3000
miles
Light-colored clothes reflect heat from the
sun whereas dark-colored clothes
absorb heat
Madrid
Oxidation: a chemical reaction of metal,
oxygen, and moisture
Homer
Site of the Parthenon in Athens, Greece;
ancient city on a hill in Athens
SCORING: The patient's answer must either be exact or very closely approximate the acceptable response. In our experience, the average patient with
an adequate educational background should answer a minimum of six questions appropriately (Table 8-1). Less adequate performance indicates an impaired fund of general information and suggests reduced intelligence, limited
social and educational exposure, or significant dementia. Conversely, more
Normal Individuals
Age Group
Mean Score (standard deviation)
40-49
50-59
60-69
6.7 (2.5)
6.8 (1.9)
6.5 (2.0)
6.3 (2.0)
5.2 (1.5)
70-79
80-89
Patients with Alzheimer's Disease

Stage
I
II
III
2.0 (2.9)
'Mean number correct (::':SD)
3.5 (3.9)
0.6 (1.1)
o (0)
119
adequate performance suggests above-average intelligence and education. The

fund of information is quite stable over a wide age range; only in the 80s
does one find a small yet statistically significant dropoff in this function. By
contrast, patients with Alzheimer's disease, even those with mild disease,
score only an average of 3.5 of a possible 10 on this task.
Calculations
DIRECTIONS: Calculations are complex neuropsychologic functions that
involve the somewhat distinct components of number sense and manipulation. Components of calculations include the following:
Rote tables (e.g., addition, subtraction, and multiplication)

The basic arithmetic concept of carrying and borrowing
Recognition of the signs (+, -, x, -7-)
Correct spatial alignment for written calculations 12
Because these components of calculations may be disturbed in isolation, they
are assessed separately. There are many ways of testing the basic concept of
numbers (written and verbal) as well as the actual manipulation of the numbers. We have chosen the following items for their overall ease of administration and clinical validity. When evaluating calculations, it is important to
require the patient to actually calculate and not merely to recite rote tables
(e.g., 4 + 4 = 8 or 3 X 5 = 15). This allows the observation of many different
types of errors and provides additional clinical data that are important for
describing the nature of the deficit and providing neuroanatomic implications. Performance on calculation is, of course, closely related to educational
experience. Tell the patient, 'We are now going to do some arithmetic examples. Some will be familiar to you and some will not. Try your best on
each one."
Verbal Rote Examples

Read each example in a clear voice in the following form: 'What is 4 plus
6?" Record the patient's response.
1. Addition
4
7
+ 6 = (10)
+ 9 = (16)
2. Subtraction
8 - 5 = (3)
17-9=(8)
3. Multiplication
2 X 8 = (16)
9 X 7 = (63)
120
4. Division
9 -:- 3 = (3)
56 -:- 8 = (7)
Verbal Complex Examples

Read each example in the following form only once: "What is 8 plus 13?"
Allow only 20 seconds for a response; a failure to respond within that time,
even if a correct response is ultimately given, is scored as a failure. Record
the patient's response.
1. Addition
14 + 17 = (31)
2. Subtraction
43 - 38 = (5)
3. Multiplication
21 X 5 = (105)
4. Division
128 -:- 8
(16)
Written Complex Examples

Provide the patient with the following written examples. If the patient is
inattentive and distractible, it is useful to provide each example on individual
cards or to write each new example after the patient completes the previous
example. Examples written on a single sheet of paper should be widely separated. Allow a reasonable amount of time for completion of each example.
Failure to complete the example within 30 seconds should be noted. Record
the patient's response, including errors in alignment.
1. Addition
108
+ 79
2. Subtraction
605
- 86
3. Multiplication
108
X 36
4. Division
43)559
SCORING: Each response should be scored as correct or incorrect. By comparing performance on each computation subtest, the patient's overall level
121
FIG U R E 8 - 1. Examples of calculation errors. (1) Patient

with a large right hemisphere lesion and left neglect. (2) Patient with head trauma and a right parietal hematoma. Note
poor alignment, as well as other calculation errors. (3) Patient
with 2 years of college education, now showing signs of early
dementia. (4) Patient with Alzheimer's disease. Note that rate
multiplication is good, but basic arithmetic processes have
gross problems.
63
x27
122
Age Group
Verbal Rote
Verbal Complex
Written

40-49
50-59
60-69
70-79
80-89
3.7
3.7
3.7
3.4
3.7
(0.7)
(0.6)
(0.7)
(1.0)
(0.5)
2.9
3.1
3.2
2.4
2.9
(1.3)
(0.9)
(0.8)
(1.3)
(1.4)
3.4
3.2
3.4
2.8
3.2
(1.3)
(1.1)
(0.6)
(1.3)
(0.8)
Patients with Alzheimer's Disease (by stage)

I
II
III
IV
3.6 (0.6)
3.1 (1.0)
1.6 (1.6)
o (0)
2.9 (1.3)
1.2 (1.3)
0.3 (0.8)
o (0)
2.7 (1.0)
1.9 (1.2)
0.4 (0.8)
0(0)
of calculation ability and area of adequacy and deficit can be determined

(e.g., intact rote tables, with inability to complete complex, verbally presented
examples). Errors specific to a particular aspect of computation (e.g., division)
or to a modality of presentation (e.g., intact performance on verbally presented items and impaired performance on written examples) should be
noted. Errors involving borrowing and alignment on written examples should
be recorded (Fig. 8-1). If an objective measure of arithmetic is needed, the
examiner should refer to a standard achievement test such as the Wide Range
Achievement Test, Third Edition. 11 Calculation ability is stable across all age
groups, although variable performance is seen within each group (Table 8-2).
Performance in early dementia is not significantly impaired, particularly in
older patients. Performance deteriorates dramatically in the second and third
stages of the disease.
proverb Interpretation
Interpreting proverbs accurately requires an intact fund of general information, the
ability to apply this knowledge to unfamiliar situations, and the ability to think in
the abstract.
DIRECTIONS: The following proverbs are presented in ascending order of
difficulty. Tell the patient, "I am going to read you a saying that you mayor
may not have heard before. Explain in your own words what the saying
means." Read each proverb exactly as it is written; do not paraphrase or otherwise explain the proverb. Continue only until the patient fails on two successive proverbs. If the patient's response to the first proverb is concrete (non-
123
abstract), or if he or she is unable to interpret it, the examiner should supply

the correct answer and explain that this is the expected type of response.
TEST ITEMS
1. Don't cry over spilled milk.

2. Rome wasn't built in a day.
3. A drowning man will clutch at a straw.
4. A golden hammer can break down an iron door.
5. The hot coal bums; the cold one blackens.
SCORING: The primary scoring criterion for proverb interpretation is the
degree of abstraction demonstrated by the patient in explaining the proverb.
It is helpful to rate the quality of the patient's response to each proverb.
Because the grading of "abstractness" is somewhat subjective, some investigators have questioned the reliability and therefore the validity of this test. 1
If the examiner properly adjusts his or her expectations based on the level of
education or intelligence of the patient, proverb interpretation appears quite
reliable and valid. 14 To aid in scoring, examples of abstract (2 points); semiabstract (1 point); and concrete (0 points) responses to each proverb follow.
The possible total for this section is 10 points.
a-Concrete
'The milk's all over the floor."

'When the milk is on the floor, you can't use it."
l-Semiabstract
"It's gone; don't worry ab9ut it."
"Don't cry when something goes wrong."
2-Abstract
"Once something is over, don't worry about it."
"Don't be concerned about events that are beyond control."
a-Concrete
"It took a long time to build Rome."
"You can't build cities overnight."
l-Semiabstract
"Don't do things too fast."
"You have to be patient and careful."
2-Abstract
"If something is worth doing, it is worth doing it carefully."
"It takes time to do things well."
3. A drowning man will clutch at a straw.
a-Concrete
"Don't let go when you're in the water."
"He's trying to save himself."
l-Semiabstract
"Self-preservation is important."
"It's a last resort."
2-Abstract
"A person in trouble will try anything to get out of it."
"If sufficiently desperate, a person will try anything."
4. A golden hammer can break down an iron door.
a-Concrete
"Gold can't break iron!"
"Gold is too soft to break a door."
l-Semiabstract
"Gold's worth more than iron."
'The harder something is, the more you have to work to get it."
2-Abstract
"Money can get whatever you want."
"Virtue conquers all."
"If you have sufficient knowledge, you can accomplish even the most
difficult task."
124
5. The hot coal burns; the cold one blackens.

O-Concrete
"Hot coals will burn you and leave it black."
"Hot coals get black when they're cold."
l-Semiabstract
"Coal can have many uses."
"Getting burned and dirty are both bad."
2-Abstract
"Extremes of anything can be detrimental."
"There may be bad aspects to things that appear good."
Concrete responses are pathologic in all but the retarded or illiterate

patient. The average patient should provide abstract interpretations to at least
the first three proverbs and minimally semiabstract responses to the remaining proverbs. Often, uneducated patients will initially give a concrete response
but can give abstract interpretations when specifically asked if there is another
way of explaining the proverb. Such cued responses should be scored as semiabstract responses. A total score of less than 5 on proverb interpretation is
suspicious. A concrete response or an absence of any abstract responses
should suggest an impairment of abstract ability.
Performance on proverb interpretation is stable across all ages (Table
8-3). The high standard deviation within the normal population, however,
shows how cautious the examiner must be in interpreting a low score on this
task. Familiarity with the proverb is an additional factor in judging the abstracting ability of the patient. 5 A very familiar saying that the patient has
heard all his or her life may not need much verbal reasoning to interpret
because it is merely a piece of advice that has been repeatedly applied to
a standard situation. The average score of patients with early Alzheimer's
disease is only slightly lower than the average for normal individuals.
As dementia progresses, performance drops rapidly. In general, a score of
Age Group
Proverbs
Similarities

40-49
50-59
60-69
70-79
80-89
5.1
5.1
4.4
4.3
5.6
(1.5)
(l.5)
(2.2)
(l.6)
(l.3)
6.0
5.9
5.0
4.5
5.1
(2.5)
(1.9)
(2.3)
(2.0)
(2.6)
Patients with Alzheimer's Disease (by stage)

I
II
III
4.0 (2.3)
l.8 (l.5)
0.5 (0.9)
o (0)
4.9 (2.1)
2.8 (2.1)
0.9 (1.4)
o (0)
125
2 or 3 on proverb interpretation in educated individuals indicates organic

impairment.
Similarities
In the Verbal Similarities Test, the patient must explain the basic similarity
between two overtly different objects or situations. This test of verbal abstract
ability requires analysis of relationships, formation of verbal concepts, and logical
thinking.
DIRECTIONS: Tell the patient, "1 am going to tell you some pairs of objects.
Each pair is alike in some way. Please tell me how they are similar, or alike."
If the patient mentions a difference between the items, fails to respond, or
states that they are different, score the item 0, provide the appropriate response, and continue with the next item. Give no help on succeeding items.
The following test items are presented in ascending order of difficulty.
TEST ITEMS
1. Turnip-Cauliflower
2.
3.
4.
5.
Car-Airplane
Desk-Bookcase
Poem-Novel
Horse-Apple
SCORING: The response for each item pair is scored for adequacy. Two
points should be given for any abstract similarity or general classification that
is highly pertinent for both items in the pair. One point should be given for
responses that indicate specific properties of both items in the pair and that
constitute a relevant similarity. A score of 0 is given when the response reflects
properties of only one member of the pair, differences or generalizations that
are not pertinent to the item pair, and failures to respond. Following are
examples of responses receiving 2 points, 1 point, and 0 points. Total for this
section is 10 points.
1. Turnip-Cauliflower
2 points: Vegetables
1 point: Food; grow in the ground; edible
o points: Buy in the store; one is a root, the other grows above ground
2. Car-Airplane
2 points: Modes of transportation
1 point: Drive them both; both have motors
o points: One's in the air and one's on the road
3. Desk-Bookcase
2 points: Articles of furniture; office furniture
1 point: Household objects; put books on them; made of the same
material
o points: Sit at a desk and put books in the bookcase; for studying
126
4. Poem-Novel
2 points: Literary works or types of literature; artistic works; modes of
creative expression
1 point: Write them both; tell stories; express feelings
a points: Famous things; study them in school; people like them
5. Horse-Apple
2 points: Living things; God's living objects, organic things
1 point: Both grow; both have skins; both need food
a points: Horses eat apples; one is big and one is small; we use them
The nonretarded patient with a normal educational background should
obtain a score of 5 or 6 on this test (see Table 8-3). Two concrete (a-point)
responses or a total score of less than 4 suggests reduced general intelligence
or impaired abstract thinking ability. In general, performance on this test
should be compatible with performance on the fund of information and
proverb interpretation tests. Equal impairment on this and the fund of information
test suggests retardation or educational deprivation rather than a specific deficit in
abstract thinking.
Insight and Judgment

Insight and judgment are other high-level behavioral functions that can be
affected by brain disease. These behaviors are different, yet interrelated. Insight is one's ability to understand either oneself or an external situation. Judgment
is a complex mental process whereby a person forms an opinion, makes a decision,
or plans an action or response after first analyzing the issue and comparing choices
with acceptable social behavior.
Insight can be assessed by asking patients whether they are aware of their problem, such as memory loss. A high percentage of demented patients do not appreciate the fact that they have a problem, a situation that is protective for
the patient yet often frustrating to others. Lack of insight, or denial, is also
seen in patients with large right hemisphere lesions.
Assessing judgment is more difficult, as the quality of judgment varies
widely in the normal population; what the examiner is attempting to evaluate, therefore, is a change in the patient's judgment. Basic social awareness
and problem-solving may be evaluated by questions about environmental
situations and how to deal with them effectively (e.g., What should a person
do if he or she sees smoke or fire in a grocery store?). Social judgment is a
more complex function that includes the basic knowledge of social situations,
knowledge of the socially appropriate responses in such situations, and the
ability to apply the correct responses personally when faced with an actual
social situation. Because of the reality-based nature of social judgment, it is
difficult to assess validly in an abstract test situation. The patient who, when
asked the question in the confines of an office or hospital bed, matter-of-
127
factly answers that he or she would calmly inform the store manager of the
presence of smoke or fire may act very differently in the actual situation.
Therefore, collaborative data concerning the patient's social judgment are best obtained by history from family members or other informants who have witnessed the
patient's actual performance in dealing with day-to-day events. An alternative possibility, though somewhat cumbersome and inefficient, is to place the patient
in actual, but experimental, situations that require an immediate, appropriate
social response.
ANATOMY
The higher cognitive functions rely primarily on an intact cerebral cortex, although
subcortical lesions can also affect performance. Except for calculating ability, however,
these functions have not been well localized in the way that language or constructional ability has. Abstract thinking, the ability to manipulate old knowledge,
and similar functions are probably widely represented in the cortex, and subcortical structures are also important in carrying out these highly abstract
functions. Because of this diffuse representation, lesions located in various
parts of the brain can impair these functions. Impairment is particularly
prominent in widespread bilateral disease (e.g., dementia).
Many of these higher cognitive functions are probably localized in the posterior
rather than in the frontal areas of the brain. Social judgment is the major exception.
Patients who have frontal lesions often show very poor social judgment despite normal cognitive functioning. Although a loss of abstraction has been
described in patients following frontal lobectomies 14 and has been traditionally considered a sign of extensive frontal lobe dysfunction, patients with
frontal lobe damage also have defects of attention, memory, and perseveration that may well account for the observed deficits in higher cognition. ID ,lS
In a comprehensive review of the literature concerned with the interaction of
frontal lesions and cognitive functioning, Teuber 16 concluded that such lesions generally affect intelligence less than do lesions located in the more
posterior areas of the brain. Black2 also documented the differential effects
of frontal and nonfrontal unilateral lesions on cognitive functions, verifying
again that these higher cognitive functions are more commonly impaired with
posterior lesions.
Verbal reasoning and abstraction are primarily dominant-hemisphere functions
having very close relationships with language. Thus, dominant-hemisphere lesions
frequently interfere with these high-level verbal manipulations.

Impaired performance on calculations may be seen with brain lesions that are
bilateral or unilateral on either side. 7 Lesions in somewhat different areas of the
brain may cause different types of impaired calculation ability (dyscalculia). 6 Left
hemisphere lesions in the right-handed patient typically result in more severe

impairment of calculations than do corresponding lesions of the nondominant hemisphere. 3 Because numbers are similar to words, in that they are
128
symbols representing a concept, it is not surprising that there is a strong

association between acalculia and language problems. Alexia and agraphia for
numbers, so-called aphasic acalculia, is a common finding in mild aphasia. 12
Some patients, however, are alexic for numbers and signs (i.e., +, -, x, -;-)
but not for words. This type of dyscalculia is a significant component of
Gerstmann's syndrome (described in Chapter 9), which is secondary to a
dominant parietal lobe lesion. Anarithmetria (inability to understand and
carry out the complex manipulations of numbers) is usually seen in left hemisphere lesions or in bilateral disease (e.g., dementia). Specific calculation defects have been ascribed to focal frontal, temporal, parietal, and occipital
lesions. 9 Impaired calculating ability is most commonly caused by focal lesions in the parietal lobes. Parietal lobe acalculia is characterized by a loss of
the ability to understand the meaning of numbers and numeric concepts (e.g.,
larger or smaller) and by the inability to align numbers correctly on the page,
owing to visual-spatial deficits. The malalignment in complex computations
can often be the most striking feature in the dyscalculia seen in patients with
right parietal lobe lesions. In addition to the cases with cortical involvement,
some patients with purely subcortical lesions (e.g., involving the left caudate
nucleus) have shown dyscalculia. 4
Deficits in higher cognitive functions are most frequently seen in patients with widespread brain disease of any etiology. These deficits may often be the first sign of
deterioration in progressive brain diseases such as Alzheimer's disease. Focal dominant parietal lobe lesions may produce defects in verbally mediated functions
and must be considered in the differential diagnosis in any patient presenting
with a loss of abstract ability or impaired calculations. As discussed previously, lesions of the frontal lobe typically do not interfere with the fund of
knowledge, abstract thinking, and problem solving unless other, more basic
deficits are also present (e.g., perseveration or aphasia). Conversely, social
awareness and judgment in social situations are often impaired in patients
with large frontal lesions.
Significant functional disease, particularly schizophrenia, may also cause impaired abstracting ability. Although the concreteness of the schizophrenic patient is frequently different from that of the patient with organic brain disease,
at times the deficits may be indistinguishable.
Because of the close relationship between higher cognitive function and
general intelligence, mental retardation from whatever cause will result in
impaired performance on these tests. Educational deprivation will similarly
result in substandard performance that is not of diagnostic significance. The
test of fund of information provides a reasonable estimate of current intellectual functioning, which may be combined with data from the history to
furnish this background information.
129
SUMMARY
Higher cognitive functions are measures of the patient's reasoning and problem-solving abilities. These functions are often impaired early in brain disease
and thereby offer an effective measure for detecting brain disease in patients
with relatively intact performance in other areas (e.g., language or constructional ability). Any deficits will be reflected in the patient's inability to function effectively within the environment. Thus, an evaluation of these functions will aid in making a valid social and vocational prognosis.
REFERENCES
1. Anderson, NC: Reliability and validity of proverb interpretation to assess mental status.
Comp Psychiatry 18:465-472, 1977.
2. Black, W: Cognitive deficits in patients with unilateral war-related frontal lobe lesions. J Clin
Psychol 32:366, 1976.
3. Boller, F and Grafman, J: Acalculia: Historical development and current significance. Brain
Cognition 2:205, 1983.
4. Corbett, A), McCusker, EA, and Davidson, OR: Acalculia following a dominant hemisphere
subcortical infarct. Arch Neurol 43:964-966, 1986.
5. Cunningham, DM, Ridley, SE, and Campbell, A: Relationship between proverb familiarity
and proverb interpretation: Implications for clinical practice. Psychol Rep 60:895-898, 1987.
6. Ferro, JM and Botello, MAS: Alexia for arithmetical signs. A cause of disturbed calculations.
Cortex 16:175,1980.
7. Critchley, M: The Parietal Lobes. Edward Arnold, London, 1953.
8. Grafman, J and Rickard, T: Acalculia. In Feinberg, TE and Farah, MJ (eds): Behavioral Neurology and Neuropsychology. McGraw-Hill, New York, 1997, pp 219-226.
9. Grewe!, F: Acalculias. In Vinken, P and Bruyn, G (eds): Handbook of Clinical Neurology,
Vol 4, Disorders of Speech, Perception, and Symbolic Behavior. American Elsevier, New York,
1969, pp 181-194.
10. Hecaen, H and Albert, M: Disorders of mental functioning related to frontal lobe pathology.
In Benson, DF and Blumer, D (eds): Psychiatric Aspects of Neurologic Disease. Grune &.
Stratton, New York, 1975, pp 137-149.
.
11. Kahn, HJ (ed): Cognitive and Neuropsychological Aspects of Calculation Disorders. Brain
Cognition 17:97, 1991 (special issue).
12. Levin, HS, Goldstein, FC, and Spiers, PA: Acalculia. In Heilman, KM and Valenstein, E (eds):
Clinical Neuropsychology, ed 3. Oxford University Press, New York, 1993, pp 91-120.
13. Reich, IN: Proverbs and the modem mental status exam. Comp Psychiatry 22:528-531,
1981.
14. Rylander, G: Mental Changes After Excision of Cerebral Tissue. Ejnar Munksgaards Forlag,
Copenhagen, 1943.
15. Stuss, DT and Benson, DF: Neuropsychological studies of the frontal lobes. Psychol Monogr
95:1, 1984.
16. Teuber, HL: The riddle offrontallobe function in man. In Warren, J and Akert, K (eds): The
Frontal Granular Cortex and Behavior. McGraw-Hill, New York, 1964, pp 410-444.
17. Wilkinson, GS: Wide Range Achievement Test - 3 Administration Manual. Wide Range, Inc.,
Wilmington, DE, 1993.
CHAPTER
RELATED COONITIVE
FUNCTIONS
Several specific disorders of cognitive function have been of great interest
to neurologists and neuropsychologists. Most are related to high-level motor
and sensory processing. For instance, apraxia is a high-level motor disturbance, and visual agnosia is a high-level perceptual disturbance. For years
these functions were classified, along with aphasia, as higher cortical functions, but with the advent of more sophisticated imaging techniques (i.e.,
computed tomography [eT] and magnetic resonance imaging [MRI]), it has
been shown that subcortical lesions can also affect them. Understanding these
disorders can help clinicians in cerebral localization. In addition, neurobehaviorists have considerable research interest in understanding these disorders. Because each disorder is relatively discrete, a complete discussion of
each disorder is presented, including terminology, evaluation, and clinical
implications.
APRAXIA
Apraxia is an acquired disorder of learned, skilled, sequential motor movements that
cannot be accounted for by elementary disturbances of strength, coordination, sensation, or lack of comprehension or attention. 28 It is an impairment in selecting and
organizing the motor innervations needed to execute an action. 3 Apraxia is not a
low-level motor disturbance but rather a defect in motor planning, which

involves the integrative steps that precede skilled or learned movements. Although this discussion concentrates on acquired apraxia, a developmental
form of apraxia has also been described. 22 Different types of apraxia may be
present, based on the complexity and nature of the task performed.
A motor disturbance characterized by clumsiness or involuntary grasp
reflexes in the limb contralateral to a corticallesion15 is called a limb-kinetic
apraxia. Because patients with this disturbance have difficulty with basic mo130
RELATED COGNITIVE FUNCTIONS
131
tor control and display abnormal reflexes, their movements do not meet the
classic requirements of a true apraxia.
Ideomotor Apraxia
Ideomotor apraxia is the most common type of apraxia. Patients having this form of
apraxia fail to perform previously learned motor acts accurately. Impairment can
be seen in buccofacial, upper or lower limb, or truncal musculature. The
inability to carry out such commands as "Show me how you blowout a
match" or "-drink through a straw" is called buccofacial apraxia. Difficulty
making certain arm or leg movements such as those involved in flipping a
coin, saluting, or kicking a ball is called limb apraxia. Difficulty with truncal
commands such as "Curtsy," "Swing a baseball bat," or "Stand like a boxer"
is called an apraxia of whole body movements. This disorder is not related
to a disturbance in comprehension of the verbal command.
Evaluation
There is a hierarchy of difficulty in performing these ideomotor tasks. The
most difficult level requires the patient to perform the action to verbal command (e.g., "Show me how to flip a coin"). This movement must be mimed
without the actual coin and in the absence of nonverbal cues from the examiner. If the patient fails at this level, the examiner performs the action and
asks the patient to imitate it. Most patients with apraxia find imitation easier
than miming the movements on command. If the patient again fails, provide
the actual object and again ask the patient to follow the command. Use of
the actual object is usually the easiest task for the apraxic patient, and many
who fail on verbal command and imitation will succeed with the concrete
task using the real object. The presence of the object gives the patient additional visual and proprioceptive cues that facilitate performance. Innumerable
possible commands can be used to evaluate praxis. The following tests frequently elicit apraxic movements.
Buccofacial Commands
Commands
"Show me how to_":

1. "Blowout a match."
2. "Protrude your tongue."
3. "Drink through a straw."
Errors
Difficulty giving short, controlled exhalation; saying "blow";
inhaling; difficulty maintaining appropriate mouth
posture
Inability to stick out tongue; tongue moving in mouth but
tending to push against front teeth and not protruding
Inability to sustain a pucker; blowing instead of drawing
through the straw; random mouthing movements
132
When tested for buccofacial praxis, patients may try to cue themselves by
pretending to have the object (match or straw) in their hands. This self-cuing
facilitates performance and should be discouraged by gently restraining the
patients' hands.
Limb Commands
Commands
"Show me how to-":
l. "Salute."
2. "Use a toothbrush."
3. "Flip a coin."
4. "Hammer a nail."
5. "Comb your haiL"
6. "Snap your fingers."
7. "Kick a ball."
8. "Crush out a cigarette."
Errors
Hand over head; hand waving; improper position of hand
Failure to show any proper grip; failure to open mouth; grossly
missing the mouth; using finger to pick teeth; not allowing
adequate distance for shaft of toothbrush; using the finger as
a toothbrush
Movements miming tossing the coin into the air with an open
hand; supinating or pronating the hand as though turning a
doorknob; flexing the arm without flipping thumb against
finger
Moving hand back and forth horizontally; pounding with fist
Using fingers as teeth of comb; smoothing the hair; making
inexact hand movements
Extension of fingers with patting movements; tapping of finger
on thumb; sliding finger off thumb with insufficient force
Stamping foot; pushing foot along floor; moving foot laterally
Stamping foot; kicking foot on floor
Although ideomotor apraxia is usually a bilateral phenomenon (i.e., seen in

both right and left limbs), occasionally ideomotor apraxia is unilateral. Accordingly' commands should be alternated between left and right limbs. Do
not have the patient do the same command sequentially with both hands,
because visual self-cuing will improve performance on the second trial.
Whole-Body Commands
Commands
"Show me how to-":
1. "Stand like a boxeL"
2. "Swing a baseball bat."
3. "Bow" (for a man) or "Curtsy" (for a woman)
Errors
Awkward arm position; hands at side
Difficulty in placing both hands together;
chopping movements
Any inappropriate truncal movement
Clinical Implications
The ability to perform skilled movements on verbal command is closely associated
with the language functions of the dominant hemisphere. Because adequate verbal
comprehension is a prerequisite to valid praxis testing, brain area A (Fig.
133
FIG U R E 9 - 1. The pathways for praxis in the right hand (controlled by the left motor area).
9-1) must be intact. Once the command is understood, the information

spreads to the contiguous supramarginal gyrus (area B, see Fig. 9 -1), where
the words (e.g., "flip a coin") are associated with the kinesthetic memories
present in the postrolandic parietal cortex. According to the classic model,
these sensory memories of the movement are then transferred along pathway
C to the premotor area (D), where memory for motor patterns is evoked. The
premotor area then directs the pyramidal neurons in the motor strip (E) actually to perform the action. Recent studies have shown that this classic model
should be modified, however. 36.53 Information from the parietal area is transferred to the supplementary motor area on the medial frontal lobe (not
shown) before going to the motor cortex on the lateral cortex (D&E). A lesion
along any of these pathways can cause an ideomotor apraxia. Subcortical
structures also have a role in guiding skilled movement, and cases have been
described where thalamic lesions, for example, have resulted in severe
apraxia. 41 Many patients with lesions in the dominant hemisphere are also
aphasic. Accordingly, praxis testing must be very carefully done to ensure that
a comprehension deficit is not responsible for the impaired motor performance. Lesions in the areas of the left hemisphere described above can produce a bilateral limb (not buccofacial) apraxia. 53
The previous paragraph outlined the pathways for praxis in the right
hand (controlled by the left motor area). The apraxic patient also has an
apraxia with the left hand. Figure 9-2 illustrates that a command to the right
134
motor cortex for innervation of the left hand is transferred from the left premotor area (D1) to the right premotor area (D2) via the anterior callosal fibers
(Fd. Any interruption of this pathway will render the left hand apraxic. 27,28,54
This is often called a "sympathetic dyspraxia"26 and can be readily demonstrated in the intact left hand of patients with Broca's aphasia with right
hemiplegia. Lesions of the anterior corpus callosum (F1) will cause an isolated
apraxia of the left hand; motor and praxis functions of the right hand are
intact. 3D The posterior callosal pathway (F2 to C2 ), which could theoretically
transmit the praxis information to the right premotor area (D 2), obviously
does not.
Lesions of the right hemisphere rarely result in a significant apraxia of either
hand when the patient must carry out the action to command. 14,19 Some patients
with right hemisphere lesions do, however, have difficulty carrying out actions when asked to imitate the examiner. 3 In such cases the right hemisphere's stronger visual system impairs the patient's perception of the action.
This anatomic model has been verified clinically and pathologically, and
A.
FIG U R E 9 - 2. The pathways for praxis with anterior corpus callosum lesion.
135
firmly establishes that the hemisphere dominant for language is also dominant for learning skilled movements. 28 This dominance is obvious because
most individuals have a strong hand preference for such activities as writing,
throwing, and using tools. Because a lesion of the dominant hemisphere causes
an apraxia in both hands, it is apparent that the dominant hemisphere exerts a
continual guiding role on movements that originate from the nondominant hemisphere. Because of the close relationship between language and praxis, many
aphasics have an apraxia of the buccofacial musculature. In some patients the
apraxia is confined to speech movements, a condition called verbal apraxia.
Not all patients with apraxia demonstrate a similar degree and type of
impaired performance. Some patients fail completely on command (even
when comprehension of the command is adequate), but perform perfectly
on imitation. Such patients have a type of disconnection syndrome in which
verbal input is literally disconnected from motor areas. Visual input, however,
is relayed quickly to the motor areas, and the patient can imitate without
difficulty. Most apraxic patients who fail on command, however, also have
difficulty with imitation. Some patients have such severe ideomotor apraxia
that they fail on verbal command, on imitation, and in the use of actual
objects. Some patients with lesions in the left temporoparietal area seem to
have considerable difficulty demonstrating the use of simple objects, yet may
imitate the action quite well. It has been proposed that this difficulty with
real objects is an ideational apraxia rather than a severe ideomotor apraxia
and is caused by a memory disorder (of object use) rather than true apraxia. 18
Patients with extensive dominant-hemisphere lesions who cannot carry out
movements to command or imitation often show fairly good use of objects
such as eating utensils. The performance has some problems in efficiency and
organization of movements but is adequate,23,46 implying that the right hemisphere has sufficient motor engrams for basic tool use.
Whole-body commands can sometimes be performed correctly even in
the presence of obvious limb apraxia. They can often be accurately carried
out by patients with severe auditory comprehension deficits as well. The reason for the relative sparing of performance involving whole-body commands
in some patients is unclear, but it may be due to the fact that these axial
movements are under the control of the more widespread extrapyramidal
system. 28 As a rule, however, patients with ideomotor limb apraxia also demonstrate apraxic axial movements. 44
Ideational Apraxia
Classic ideational apraxia is a disturbance of complex motor planning of a higher
order than is seen in ideomotor apraxia. It refers to a breakdown in performance of
a task that involves a series of related, but separate steps, such as folding a letter,
placing it in an envelope, sealing it, and then putting a stamp on it. The
patients can often perform each individual step of the task in isolation (e.g.
136
folding the paper) but cannot integrate the parts accurately to complete the
sequence. The patients seem to have lost the overall concept of how to go
about completing the task. Some investigators define an ideational apraxia as
any difficulty in manipulating real objects. 17,20 We feel that difficulty with
object use in simple limb commands (e.g., inability to flip an actual coin)
represents a severe ideomotor limb apraxia and not an ideational apraxia.
Some patients, however, have for various reasons lost both the concept of the
object and its proper use. These individuals are said to exhibit "conceptual
apraxia."43
Evaluation
Several simple tasks are used to demonstrate an ideational apraxia.
Tasks
Errors
1. Folding a letter, placing it in
Turning paper around without being able to fold it;

folding improperly; licking the wrong side of
stamp or envelope; inability to place paper in
envelope
Placing candle in holder wick-down; inability to
place candle in holder; inability to open or close
matchbox; striking match on candle; striking
wrong end of match; striking candle on
matchbox; blowing out candle and not match
Removing cap from toothpaste and placing cap on
toothbrush; putting toothpaste in a tootbrush
holder; placing toothbrush back in holder with
tootpaste on it
an envelope, sealing it,

addressing it, and placing a
stamp on the envelope
2. Placing candle in holder, taking
match out of box, lighting
candle, and blowing out match
3. Opening toothpaste, taking
toothbrush from holder, and
placing toothpaste on
toothbrush.
In each of these tasks, the patient can usually perform each part of the series
adequately (e.g., striking the match or brushing the teeth) but cannot coordinate the individual movements that are necessary to complete the sequence.
Ideational apraxia is a complex disability that is usually seen in patients with bilateral
brain disease. Any diffuse cortical disease, especially those diseases that affect
the parietal lobes, may result in an ideational apraxia. Although the patient
fails on a specific task (e.g., lighting a candle), it is obvious from watching
the patient's performance that his or her failure is the result of a number of
cognitive deficits. Many patients have elements of ideomotor apraxia, and
almost all have some degree of constructional impairment and spatial disorientation. Memory and auditory comprehension may also be diminished.
One interesting element in the performance of patients with ideational
apraxia is their apparent inability to recognize the use of objects. This failure
137
to recognize objects and their use has been called an object agnosia or a form
of conceptual apraxia and may be illustrated by the patient who attempts to
light a candle by striking it on the matchbox. The ability to do serial ordering
is also impaired, and the complex multistep task becomes a confusing group
of discrete parts with no logical, sequential relationship. The ambiguity and
incongruity of the formal test situation also are confusing. The patient does
not quite understand exactly what he or she is supposed to do when the
doctor brings out a toothbrush and toothpaste and pushes it benignly toward
the patient.
Neuropsychologically, ideational apraxia is the culmination of many significant cognitive deficits. Clinically, it results in the patient's inability to manipulate the environment effectively. The patient cannot cook a meal, make
a bed, light a cigarette, use the channel changer on the 1V, or do any of the
dozens of everyday activities that we all take for granted. Ideational apraxia is
not usually seen in isolation but is generally associated with the widespread intellectual deterioration seen in patients with dementia, especially Alzheimer's disease.
SUBCORTICAL COGNITIVE CHANGE

Considerable attention has been paid recently to the mental status changes
occurring with disease that primarily affects the subcortical structures of the
cerebral hemispheres (e.g., thalamus, putamen, globus pallidus, septal nucleus). Diseases that primarily affect the subcortical structures include focal infarcts
and trauma, Huntington's disease, progressive supranuclear palsy, and, more recently, acquired immunodeficiency syndrome (AIDS). Mental status changes may
be the defining illness in patients with AIDS; therefore, a specific battery of

tests has been developed to diagnose this subcortical dementia. 45 The main
feature of subcortical dementia that differs from other dementias is psychomotor
slowness. Various tests of psychomotor speed can be used, but a quick and
reliable test is to ask the patient to write the alphabet in uppercase letters.
Normal individuals should be able to perform this test in under 21 seconds. 45
RIGHT-LEFT DISORIENTATION
Right-left orientation is traditionally defined as the ability to distinguish right from
left on oneself and in the environment (e.g., on the examiner's body). This ability
is basically a capacity for spatial orientation. 9 The application of the verbal

labels "right" and "left" to the respective sides of the body is frequently used
to test right-left orientation,32 but this is a linguistic task that does not necessarily test spatial sense. Right-left disorientation may be developmental in
nature or may result from either focal or diffuse brain lesions. Although this
disorder is interesting and may be combined with other deficits to produce
Gerstmann's syndrome (discussed later in this chapter), it is oflimited clinical
utility when seen in isolation.
138
Evaluation
The following outline, which is in ascending order of difficulty, may be used
to test for right-left disorientation.
TEST ITEMS
1. Identification on self
A. Show me your right foot.
B. Show me your left hand.
2. Crossed commands on self
A. With your right hand touch your left shoulder.
B. With your left hand touch your right ear.
3. Identification on examiner (with examiner facing patient)
A. Point to my left knee.
B. Point to my right elbow.
4. Crossed commands on examiner (with examiner facing patient)
A. With your right hand point to my left eye.
B. With your left hand point to my left foot.
Most normal persons will successfully accomplish all items without difficulty,
although a significant percentage of the normal population (9% of males and
over 17% of females) has demonstrable difficulty on right-left testing. 4 ,6
If right-left disorientation is present, it is important to determine if the patient was
ever capable of adequately performing such tasks. As previously mentioned, right-left
disorientation may be developmental in nature and may also be associated with
reduced general intellectual ability.
Aphasic patients may fail on right-left commands because of their primary language disorder. Anomia can cause confusion in the use of the labels
"right" and "left." Deficits in auditory retention interfere with performance
on complex commands.
Thus far, clinical and neuropathologic case studies have failed to demonstrate
an association between right-left disorientation and any circumscribed brain lesion. 24
If an acquired disorder of right-left orientation is present, the lesion is usually located
in the parietotemporal-occipital region of the dominant hemisphere. 34 In our clinical
experience, right-left disorientation is infrequent in patients with lesions that
are restricted to the nondominant hemisphere. This is also substantiated by
Critchley's review. 9
FINGER AGNOSIA
Finger agnosia is the inability to recognize, name, and point to individual fingers on
oneself and on others. 25 This disorder may be most readily demonstrated in
139
reference to the index, middle, and ring fingers. 8 Finger agnosia is similar to
right-left orientation in that it may be developmental in nature or may result
from either diffuse or focal brain disease. Its clinical utility for localization
of cerebral lesions is relatively limited.
Evaluation
Evaluation of this function can be very extensive, but for practical purposes
a brief screening should suffice. Patients must have adequate auditory comprehension and must know or be capable of learning the names of the fingers
(thumb, index or pointing finger, middle finger, ring finger, and little finger).
TEST ITEMS
1. Nonverbal finger recognition

Directions:
With the patient's eyes closed, touch one finger. Have the patient open
his or her eyes and then point to the same finger on the examiner's
hand.
2. Identification of named fingers on examiner's hand
Directions:
The examiner's hand should be placed in various positions (e.g., palm
down on the table facing the patient; hand held vertically in the
air with the palm facing the patient; and hand held horizontally in
the air with the palm facing the examiner). The examiner should
say "Point to my middle finger," and so forth.
3. Verbal identification (naming) of fingers on self and examiner
Directions:
The patient's and examiner's hands should be placed in the various
positions as described earlier. The examiner points to the patient's
index finger and says, ''What is the name of this finger?" and so
forth.
Patients with finger agnosia usually have lesions of the dominant hemisphere. 37 Lefthanded patients or those with strong family histories of left-handedness may exhibit
finger agnosia with lesions of either hemisphere. Parietal-occipital lesions are the
most likely to cause finger agnosia. 42 As with right-left testing, aphasia will ad-
versely affect verbally mediated performance. For a more comprehensive review of this topic, see references 9 and 37.
140
GERSTMANN'S SYNDROME
Gerstmann's syndrome is a classic, albeit controversial, neurologic syndrome.
It consists of four major components: finger agnosia, right-left disorientation,
dysgraphia, and dyscalculia. Most patients with this disorder, however, demonstrate additional neuropsychologic deficits, principally constructional impairment or mild aphasia. The syndrome has localizing value; the demonstration of all four elements indicates damage to the dominant parietal lobe
or to bilateral parietal lobes. 47,5o,51 For further information about this syndrome, see references 6, 12, and 51.
VISUAL AGNOSIA
Visual agnosia is a rare, acquired neurologic syndrome in which the patient is unable
to recognize objects or pictures of objects presented visually. Visual acuity is adequate,
mentation clear, and aphasia absent. 52
Two major categories of visual agnosia have been described in the literature. In the first type, actual visual perception of the object is distorted to
the point that recognition is impossible. Such patients cannot name or tell
the use of an object when it is shown to them but can readily name and
demonstrate the use of the object when it is placed in their hands. Kinesthetic
cues provide sufficient information for recognition. To evaluate for the presence of visual agnosia, ask the patient to identify verbally common objects
presented visually. If the patient fails to recognize the object, allow manipulation of the object. If the patient then readily identifies the object, the defect
is in the visual system. It has been postulated that such patients have damage
to the visual association cortex bilaterally (areas 18 and 19). Recent studies
using positron emission tomography (PET) scanning have verified the damage
to the temp oro-occipital cortex bilaterally.31 This type of visual agnosia (apperceptive visual agnosia) has been reported in a patient with anoxic encephalopathy secondary to carbon dioxide poisonint and in patients with
Alzheimer's disease.
The second variety of visual agnosia is called associative visual agnosia.
Patients with this type of agnosia have adequate visual perception but their
visual cortex is disconnected from the language area or visual memory stores.
Accordingly, they can recognize the object and demonstrate its use, but they
cannot name it. When unable to name an object, such patients are also unable to describe its use. 49 The precise neuropsychologic defect for this disorder
is still not clear. Whether it is a disconnection syndrome or a syndrome of
subtle perceptual problems plus specific visual memory deficits remains to be
elucidated. The evaluation for this disorder is similar to that for the first type
of visual agnosia, except that adequate visual perception must be demonstrated. This can be done with a simple visual matching task. Lesions that
141
cause an associative visual agnosia may be bilateral, involving the inferior

temporal occipital junction and subjacent white matter,2 or may be an infarct
that destroys the left occipital lobe and the posterior corpus callosum. 38 This
is the same lesion that causes alexia without agraphia, and, in fact, most
patients with associative visual agnosia are also alexic. For further reading,
see references 1, 2, 4, 10, and 38.
Two additional types of visual agnosia deserve mention but will not be
fully discussed. Prosopagnosia is an unusual agnosia in which patients are
unable to recognize familiar faces. In such cases, the agnosia is so profound
that even members of the patient's immediate family are not recognized. The
patient will recognize the person, however, on hearing his or her voice. The
mechanism that results in prosopagnosia is probably a combination of a
disturbance of fine visual discrimination and a failure of memory for the
discrete category of human faces. The lesions that are responsible for this
disorder are usually in the occipitotemporal areas bilaterally. One of the lesions is usually in the right inferior temporo-occipital region. 39 For further
discussion, see references 7, 13, 16,21, and 39.
Color agnosia is an inability to recognize colors secondary to an acquired cortical lesion. Two types of color agnosia have been described. A
specific color-naming disturbance results from a disconnection of visual input
from the language area. This anomia is associated with the syndrome of alexia
with agraphia. 29 In this form, there is no damage to the primary language
area and no other evidence of aphasia.
The second and more common disturbance of color recognition is actually a defect in color perception caused by bilateral inferior temporo-occipital lesions. These are the same lesions that cause prosopagnosia, and most
patients with this type of color agnosia have concomitant prosopagnosia. 40
For further reading on this topic, refer to references 11 and 17.
ASTEREOGNOSIS
Stereognosis is the ability to discriminate the size and shape of objects and to identify
them by touch alone. This is usually tested during the routine neurologic examination by asking the patient to identify several common objects placed
in his or her hand (e.g., coin, key, paper clip, and so forth). The patient is
tested with the eyes closed and is given one object at a time. The patient is
allowed to manipulate the object freely. Each hand is tested individually.9,33
The task demands that the patient be able to integrate spatial features,
weight, and texture in order to identify the object. If a patient has a defect in
primary sensation in the hand, failure to identify the object cannot be attributed to astereognosis.
Classic astereognosis, or a failure of tactile recognition (tactile agnosia),
usually indicates a lesion in the anterior portion of the parietal lobe opposite
142
the astereognostic hand. 48 Cases have been reported in which a unilateral

lesion, either right or left, produced a bilateral defect. 9 A rare form of lefthand unilateral astereognosis has been reported in patients with a lesion in
the anterior corpus callosum. 30
CEOCRAPHIC DISORIENTATION
Geographic orientation is a complex ability that includes the patient's capacity
to find his or her way in familiar environments, to localize places on maps
or floor plans, and to find his or her way in new environments. A significant
geographic disorientation will interfere with the patient's ability to live a normal life. Such patients are unable to travel alone outside of their home and
may even become disoriented within their own houses.
Evaluation
History Obtained from Family
In evaluating geographic orientation, it is important to obtain historical information regarding the patient's ability to operate in familiar and unfamiliar
environments outside of the formal testing situation. Such information is best
obtained from family members rather than from the patient.
1. Does the patient become lost at work, in the neighborhood, or at
home?
2. Has the patient become lost traveling to a less-frequented location
(e.g., the inability to locate a restaurant not visited in a year)?
3. Does the patient have great difficulty orienting to new environments?
Localizing Places on a Map

Map localization is an abstract task that can quickly detect disturbances in
geographic orientation. It is also useful when adequate historical information
is unobtainable, and it is particularly useful in bringing out subtle defects in
unilateral attention. 8
DIRECTIONS: Have the patient draw a map of the United States. If he or
she is unable to produce a recognizable representation, the doctor should
draw one or provide a suitable outline. Ask the patient to locate the following
cities on the map outline:
Denver
New York
San Francisco
New Orleans
Chicago
143
SCORING: In reviewing the patient's performance, the following factors

should be considered: (1) Are coastal cities located on the coast? (2) Are the
cities in the appropriate states? (3) Are all cities in one half of the map (either
east or west)? (4) Are attempts made to locate all cities?
Ability to Orient Self in Hospital

Environment
Information concerning patients' ability to orient themselves in the hospital
may be obtained from nurses' reports and by observing the patients' capacity
to find their bed, ward, and bathroom. For example, we saw a patient with
communicating hydrocephalus and mild dementia who, on concluding a fifth
office revisit, walked confidently into the closet.
Geographic disorientation has been clinically associated with parietal lobe disease, 9
although good clinicoanatomic studies are few. Of the studies available, there
is some suggestion that right hemisphere lesions most frequently cause geographic difficulty.35 Other studies, however, have failed to support this finding
of lateralization and report an approximately equal incidence of geographic
disorientation in patients with right and left hemisphere lesions. 8
A consistent finding of clinical usefulness is that patients with unilateral
lesions tend to localize cities on the map toward the side of their lesion (e.g., patients
with left parietal lesions tend to place cities toward the west coast on the
map outline). This appears to be a result of neglect of the contralateral visual
field. 8 A more generalized geographic disorientation is a frequent finding in patients
with diffuse cortical disease and may be an early sign of dementing illness.
Geographic orientation is probably not a unitary cortical function but a
combination of more basic cognitive processes including visual memory,
right-left orientation, visual perception, and spatial neglect. Performance on
formal tests of geographic orientation, such as locating cities on a map outline, is closely associated with both general intelligence and social exposure
(education). General lack of geographic knowledge is the most common cause of
failure on the map test and we were surprised to find that our normal subjects
(on an average) correctly located only half of the five cities. Obviously, the
effects of educational level (and quality), as well as social experience and
exposure, are highly significant factors that must be considered when assessing geographic orientation.
One must not minimize the devastating effects that clinically significant
geographic disorientation has on the patient's ability to function effectively.
Such patients are typically unable to work, easily become lost in unfamiliar
places, and eventually have difficulty with orientation in even familiar settings
such as the neighborhood and home.
144
SUMMARY
The cortical functions of apraxia, right-left disorientation, visual and finger
agnosia, astereognosis, and geographic disorientation are interesting and may
be clinically relevant in localizing brain lesions.
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45. Power, C, Selnes, OA, Grim, JA. HN dementia scale: A rapid screening test. J AlDS Hum
Retrovirus 8:273-278, 1995.
46. Rapcsak, SZ, Ochipa, C, Beeson, PM, et al: Praxis and the right hemisphere. Brain Cogn
23:181-202, 1993.
47. Roeitgen, DP, Sevush, S, and Heilman, KM: Pure Gerstmann's syndrome from a focal lesion.
Arch Neurol 40:46, 1983.
48. Roland, PE: Focal increase of cerebral blood flow during stereognostic testing in man. Arch
Neurol 33:543, 1976.
49. Rubens, A and Benson, OF: Associative visual agnosia. Arch Neurol 24:305, 1971.
50. Strub, RL and Geschwind, N: Gerstmann syndrome without aphasia. Cortex 10:378, 1974.
5l. Strub, RL and Geschwind, N: Localization in Gerstmann syndrome. In Kertesz, A (ed): Localization in Neuropsychology. Academic Press, New York, 1983, pp 295-32l.
52. Warrington, EK: Agnosia: The impairment of object recognition. In Frederiks, JAM (ed):
Handbook of Clinical Neurology, Vol 1(45), Clinical Neuropsychology. Elsevier Science,
Amsterdam, 1985, pp 333-349.
53. Watson, RT, et al: Apraxia and the supplementary area. Arch Neurol 43:787, 1986.
54. Watson, RT and Heilman, KM: Callosal apraxia. Brain 106:391, 1983.
55. Wolf, SM: Difficulties in right-left discrimination in a normal population. Arch Neurol
29:128, 1973.
SUMMARY OF
EXAMINATION
Throughout this book, we have emphasized the importance of performing

a systematic and complete mental status examination. Although it is not always necessary to evaluate exhaustively every aspect of mental functioning,
certain critical functions should be assessed in every patient. These include:
Level of consciousness
Physical appearance and emotional status
Attention
Expressive and receptive language
Memory
Constructional ability
Abstract reasoning
Items that are adequate for evaluating these areas are shown with an asterisk
in the composite mental status examination shown in Appendix 2.
The experienced clinician can tailor the mental status examination to the
individual patient's clinical problem and, with practice, can complete an adequate screening examination in 15 to 30 minutes. In patients with a vague
history of behavioral complaints, or when emotional features predominate,
a more extensive examination may be required.
The systematic mental status examination usually allows the clinician to differentiate patients with organic brain disease from both normal persons and those with
functional disorders. In many cases, it is also possible to specify the type, locus,
and degree of disease. For example, knowledge of specific patterns of aphasia
often permits the examiner to localize a lesion within the dominant hemisphere. In other cases, the pattern of performance is suggestive of a specific
disease entity (e.g., Alzheimer's disease).
In the Clinical Implications sections of each chapter in this book, we
146
SUMMARY OF EXAMINATION
147
have attempted to describe many neurobehavioral syndromes as they relate

to specific areas of cognitive deficit. Examples of these are the acute confusional states (Chapter 2), aphasias and related language disorders (Chapter
5), amnesias (Chapter 6), and the frontal lobe syndrome (Chapter 2) These
sections of the text are not intended to be a comprehensive review of neurobehavior or an extensive discussion of anyone syndrome, but should illustrate the bridge between the data and the diagnosis. See references 1, 3,
and 8 for complete discussions of these topics.
In general, the more clinical data the examiner obtains regarding the patient's
level of functioning in a variety of areas, the more accurate the final diagnosis will
be. An examination that includes all of the items discussed in this book (out-
lined in Appendix 2) can usually be completed in an hour or less. Although

all of the data are valuable, the busy clinician may not be able to spend this
much time on all routine consultations. In most clinical settings, the initial
goal is to make a tentative diagnosis and plan an appropriate diagnostic evaluation, so the examination will be tailored to fit the clinical situation. Following are discussions of several specific clinical neurobehavioral syndromes.
Because of the magnitude of the problem of dementia, a disproportionate
amount of space is devoted to the use of the mental status examination in
diagnosing that condition.
ALZHEIMER'S DISEASE
One of the most common organic brain disorders is dementia,4 and Alzheimer's disease (senile dementia Alzheimer type [SDAT]) is the most prevalent
and well-known cause. 4,S,9 Although a cure is not yet available, it is important
to recognize the early features of this syndrome because early diagnosis can
prevent serious social and vocational embarrassment to both patient and family. The early features of this disease are apathy, vague subjective complaints, decreased verbal fluency, memory difficulties, constructional impairment, dyscalculia
(calculation problems), and problems with abstract reasoning. As the disease pro-
gresses, anomia, apraxia, agnosia, geographic disorientation, and significant

deficits in judgment typically appear, while the defects seen in the early stages
worsen. In the deteriorated stage, all deficits are accentuated; behavior is regressed; language, memory, and thought processes are severely disturbed; and
the patient requires total care. The diagnosis of Alzheimer's disease in the
advanced stages is usually made without difficulty, but mild significant dementia can go unrecognized or misinterpreted by family members and health
professionals alike.
The mental status examination for a patient with suspected dementia can
be shortened but should include the following essential components:
1. Level of consciousness: Patients with simple atrophic dementia
(Alzheimer's and senile Alzheimer's disease) are fully alert unless they
148
have a secondary decrease in the level of consciousness from medication, medical illness, or a focal brain lesion with increased intracranial pressure.
2. Behavior observations: These are important, but as they are made
throughout the history and examination, they rarely prolong examination time.
3. Language: Spontaneous speech and comprehension can be roughly
assessed during history taking, but verbal fluency, repetition, and
naming should be specifically tested. Although naming and wordfinding errors are often present in patients with dementia, repetition
is usually intact unless the disease is advanced or there is an associated
left hemisphere lesion with aphasia.
4. Memory: This is a critical term. Orientation should be tested first. If
the patient fails, particularly if the failure is significant, this strongly
suggests a new-learning or recent-memory deficit. Next, tell the patient
the correct date and location and ask him or her to remember it. Then
ask about recent news items for a few minutes, and then ask the
orientation questions again. If there is a second failure, in our experience the patient has a significant memory problem, and additional
testing will only support this initial impression and will not provide
additional substantive data. If the patient is oriented or quickly learns
his or her orientation, carry out the full memory section of the
examination.
5. Drawings: These take only a few minutes to perform and are an
invaluable aid in diagnosing brain disease, especially dementia.
6. Abstract functions
1. Calculations: These are very useful when evaluating patients with
dementia; several examples should be included.

2. Proverbs and similarities: These are also useful, and several of
each should be asked. The patient with dementia tends to provide
very concrete answers.
After many years of use and the statistical analysis of hundreds of cases
of Alzheimer's disease, the shortened form of the mental status examination
shown in Table 10-1 was developed. The items were selected on the basis of
sensitivity in diagnosing dementia. These items, although not specific to Alzheimer's disease, are highly likely to be abnormal in that population (i.e.,
highly sensitive). The total score for this test is 100 points (Table 10-2).
Because of the potential for false-positive results in elderly persons (i.e., diagnosing dementia in nondemented individuals), a total score in the 50 to
60 range in an 85-year-old must be interpreted cautiously (Table 10-3).
PATIENT INFORMATION
NAME:
DATE:
HOSPITAL OR FILE NUMBER:

AGE:
SEX:
DIAGNOSIS:
1. VERBAL FLUENCY
Animals per 60 seconds
Total animals:
2. COMPREHENSION
Check if correct:
a. Point to the ceiling.

b. Point to your nose and window.
c.
Point to your foot, door, and ceiling.
d. Point to window, leg, door, and thumb.

3. NAMING AND WORD FINDING
Parts of objects:
Watch stem (winder)

Coat lapel
Watch crystal
Sole of shoe
Buckle of belt
4. ORIENTATION
a. Date
b. Month
c.
Year
d. Day of week
5. NEW LEARNING ABILITY
Four unrelated words:
5 min
10 min
a. Brown (Fun) (Grape)

b. Honesty (Loyalty) (Happiness)
c.
Tulip (Carrot) (Stocking)
d. Eyedropper (Ankle) (Toothbrush)

6. VERBAL STORY FOR IMMEDIATE RECALL
It was July / and the Rogers / had packed up / their four children / in the station wagon /
and were off / on vacation.

They were taking / their yearly trip /
to
the beach / at Gulf Shores.
This year / they were making / a special/one-day stop / at The Aquarium / in New
Orleans.
After a long day's drive / they arrived / at the motel/only to discover / that in their
excitement / they had left / the twins / and their suitcases / in the front yard.
Number of correct memories: _ _ _ _ __
149
150
7. VISUAL MEMORY (HIDDEN OB}ECfS)

Found
Object
a. Coin
b. Pen
c. Comb
d. Key
e. Fork
8. PAIRED ASSOCIATE LEARNING
2
a. Weather-Box
b. High-Low
c. House-Income
d. Book-Page
a. House-Income
b. Weather-Box
c. Book-Page
d. High-Low
a. House _ _ _ _ _ _ _ _ _ __
b. High _ _ _ _ _ _ _ _ _ __
c. Weather _ _ _ _ _ _ _ _ _ __
d. Book _________________
a. High _ _ _ _ _ _ _ _ _ _ _ __
a. House _ _ _ _ _ _ _ _ _ _ _ __
c. Book _ _ _ _ _ _ _ _ _ _ _ __
d. Weather _ _ _ _ _ _ _ _ _ _ ___
9. CONSTRUCfIONAL ABILITY
Score ______
Daisy in flower pot
Score ______
House in perspective
Score _ __
151
10. WRITTEN COMPLEX

CALCULATIONS
a. Addition
108
79
605
86
b. Subtraction
c. Multiplication
108
x 36
d. Division
43)559
Number correct _ _ _ _ __
11. PROVERB INTERPRETATION
a. Don't cry over spilled milk.
b. Rome wasn't built in a day.
c. A drowning man will dutch at a straw.
d. A golden hammer can break down an iron door.
e. The hot coal bums, the cold one blackens.
12. SIMILARITIES
a. Turnip ............................................................................. Cauliflower

b. Car ....................................................................................... Airplane
c. Desk .................................................................................... Bookcase

d. Poem ....................................................................................... Novel
e. Horse ....................................................................................... Apple
Score
152
PATIENT:
Score
Verbal fluency-animal names

(1 point/2 animals)
Maximum: 10 points
Verbal comprehension (pointing)
4 points
Naming-parts of objects
5 points
Memory
Orientation:
2 points
2 points
1 point
1 point
Date
Day
Month
Year
6 points
Unrelated words
(2 points each) 5 min _ __
10 min _ __
16 points
Story (1 point = 1 remembered

item [l3 maximum])
l3 points
Hidden objects (1 point each)
5 points
Paired associate learning
8 points
Drawings
Pipe, daisy, house
9 points
Calculations (written)
4 points
Proverbs
10 points
Similarities
10 points
Maximum: 100 points
Normal Individuals
Age Group
40-49
50-59
60-69
70-79
80-89

80.9
82.3
75.5
66.9
67.9
(9.7)
(8.6)
(10.5)
(9.1)
(11.0)
Patients with Alzheimer's Disease
Stage
II
III
57.2 (9.1)
37.0 (7.8)
13.4 (8.1)
153
ACUTE CONFUSIONAL STATE

A history of a rapid decrease in mental status (hours to a few days) does not
usually suggest a primary dementia but more likely a delirium (acute confusional state). As discussed in Chapter 2, this condition is usually easily
recognized by its typical behavioral features and represents a specific diagnostic entity. Extensive mental status testing usually yields abnormal results
but rarely adds additional useful diagnostic information.
LESIONS OF THE DOMINANT

HEMISPHERE
Patients with lesions of the dominant hemisphere frequently show abnormalities of
language functions. In the right-handed patient, evidence of aphasia, alexia, or
agraphia almost always indicates left hemisphere disease. Gerstmann's syndrome, constructional impairment, verbal memory difficulties, ideomotor
apraxia, dyscalculia, and impairment of verbal reasoning are all findings that
can be seen with left hemisphere lesions. Denial and neglect are not commonly seen in these patients. Even left-handed patients frequently show the
aforementioned findings with left hemisphere disease, although there is a
higher frequency of bilateral representation of these functions in these
patients.
LESIONS OF THE NONDOMINANT

HEMISPHERE
Although most patients with lesions of the nondominant hemisphere do not show
evidence of language disorders, they do have a more dramatic constructional impairment than do patients with dominant-hemisphere lesions. In such patients,
denial and neglect are more common and severe in degree, malalignment is
seen in writing and calculations, and deficits are present in nonverbal
memory.
AIDS DEMENTIA
In AIDS dementia, the cognitive areas most commonly impaired are attention, psychomotor speed, and recent memory, but it is always prudent to
assess constructional facility, proverb interpretation, and reading ability.
RECORDINC, SUMMARIZINC,
AND INTERPRETINC DATA
As with any medical examination, it is very important to record both what was
specifically tested and the patient's responses to each item. A form similar to the
composite in Appendix 2 should be used as an aid in recording these data.
At the completion of the examination, the clinician should synthesize the
154
data and then summarize and emphasize the key areas of impairment. This
summary allows an identification of deficit patterns and the efficient communication of essential findings.
The clinician must summarize and organize the data in such a way that
he or she can arrive at the following four clinical implications:
1. Describe the major areas of impairment: Indicate those areas of
mental status functioning that are deficient compared with the level
expected in the patient, based on his or her education and premorbid
function (e.g., verbal memory, abstraction, or construction ability).
This is the initial step in organizing the data so that they can be
interpreted neurobehaviorally.
2. Make a tentative neurobehavioral diagnosis: Having indicated the
major areas of impairment, the clinician can now analyze the pattern
of deficits and make a specific neurobehavioral diagnosis: delirium,
dementia, organic amnesic state, aphasia, nondominant-hemisphere
syndrome, and so forth. The interpretation of the mental status findings is difficult and, as in all fields of medicine, requires clinical experience with patients who have organic brain syndromes (neurobehavioral disorders), as well as additional reading in this area.
3. Arrive at a tentative localization of the lesion: This step is of both
practical and academic importance. In a practical sense, findings that
suggest a single focal lesion (e.g., fluent aphasia without other deficits,
suggesting a left temporal or temporoparietal lesion) require a far
different neurodiagnostic evaluation than does the identification of a
global cognitive disorder such as an acute confusional state or dementia. Academically it is of great interest to attempt to correlate
clinical findings with what is known about brain function.
4. Make a tentative clinical diagnosis: This is the final step in the
diagnostic process. It requires the clinician to correlate historical and
examination data with medical knowledge to make a specific medical
diagnosis. For example, a patient with a slowly developing cognitive
deterioration, whose mental status examination shows multiple areas
of impairment suggesting bilateral brain disease (dementia), yet who
has normal results on a standard neurologic examination, most likely
has Alzheimer's disease. Similarly, an elderly patient with the acute
onset of aphasia with fluent paraphasic speech with impaired comprehension (Wernicke's aphasia) probably has had an occlusion of a
posterior branch of the left middle cerebral artery.
This entire summary process requires careful thought and considerable
clinical knowledge. When the examiner becomes proficient with the examination and familiar with the organic syndromes, this complex process of data
analysis and diagnosis becomes easier.
155
The final steps in any patient evaluation include communicating test

findings to the patient, the patient's family, and the referring physician; referring the patient for further evaluation when necessary; arranging for appropriate neurodiagnostic evaluation; and planning subsequent patient
management.
SUMMARY
As stated in our introduction, we have intended to help the clinician to un-
derstand many of the cognitive functions that can be easily tested at the
bedside. We have tried to give enough information concerning these functions and their disturbance in brain disease to allow the examiner to test the
patient and to delineate the deficits. Understanding these deficits and how to
test for them, and recognizing the common pattern in disease, often permits
the examiner to make a specific diagnosis.
After reading this book, the neurologist, psychiatrist, psychologist, or
other health care provider should be able to conduct a comprehensive examination of the patient with brain disease and use the data for diagnosis.
Although this mental status examination is qualitative, it can be quantitative
if the examiner so desires. Some screening tests (the Mini-Mental State Examination l being the most widely used) give the examiner a single score,
which is used to identify the presence and degree of organic disease. This
quantitative method, in contrast to the comprehensive qualitative examination, can provide only a gross estimate of the patient's global cognitive functioning and is restricted in its contents, scope, and sensitivity. A plethora of
screening tests to identify dementia exists, from the 7 Minute Screen? to the
test in which the patient must rearrange alphabetically the letters in the word
"world."6 All such tests assess cognitive level and can be useful for screening.
This book is designed as an educational tool to help the examiner to understand the richness of cognitive functioning and its assessment. Selection of
any number of individual items to test such as orientation, verbal fluency,
and recall of five hidden objects can serve as an excellent screening test, but
the information gained from these short tests is limited and should not be
relied on in isolation.
REFERENCES
1. Feinberg, TE and Farah, MJ: Behavioral Neurology and Neuropsychology. McGraw-Hill, New
York, 1997.
2. Folstein, MF, Folstein, SE, and MCHugh, PR: "Mini-Mental State": A practical method for
grading the cognitive state of patients for the clinician. J Psychiatr Res 12:189, 1975.
3. Heilman, KM and Valenstein, E: Clinical Neuropsychology, ed 3. Oxford University Press,
New York, 1993.
4. Katzman, R: The prevalence and malignancy of Alzheimer's disease. Arch Neurol 33:217,
1976.
156
5. Katzman, Rand Karasu, T: Differential diagnosis of dementia. In Fields, W (ed): Neurological

and Sensory Disorders in the Elderly. Stratton Intercontinental Medical Books, New York,
1975, pp 103-134.
6. Leopold, NA and Borson, AJ: An alphabetical 'WORLD': A new version of an old test. Neurology 49:1521-1524, 1997.
7. Solomon, PR, et al: A 7 minute neurocognitive screening battery highly sensitive to Alzheimer's disease. Arch Neurol 55:349-355, 1998.
8. Strub, RL and Black, FW: Neurobehavioral Disorders: A Clinical Approach. FA Davis, Philadelphia, 1988.
9. Whitehouse, PJ (ed): Dementia. FA Davis, Philadelphia, 1992.
FURTHER
EVALUATIONS
In a number of patients, completion of the mental status examination
prompts the need for one or more additional specialized evaluations or consultations. This section briefly discusses the contributions of the neuropsychologist, speech pathologist, psychiatrist, and social worker to the evaluation
and management of the patient with organic brain damage or disease. It is
beyond the scope of this book to offer more than a basic introduction to
each specialty, with suggested readings for each area.
NEUROPSYCHOLOGY
Clinical neuropsychologists are trained at the doctoral level, with a I-year
clinical internship, a postdoctoral fellowship, or both, during which formal
training is obtained in the evaluation and behavioral treatment of patients
with organic brain disease. Reference I gives more detailed information regarding recommended training for neuropsychologists. Clinical neuropsychologists are primarily concerned with the identification, description, and
quantification of changes in behavior (cognitive, motor, and emotional) that
are associated with brain dysfunction. Their primary area of expertise is the
investigation of the relationships between human behavior (whether a specific response on a formal test or in day-to-day functioning) and brain function and dysfunction. Accordingly, the neuropsychologist can aid in a variety
of important clinical problems, including differential diagnosis, lateralization
and localization of lesions, establishment of baselines of behavior and cognitive performance from which improvement or deterioration can be gauged,
determination of competence in the aged or demented, and development
of remedial methods for the rehabilitation of the individual brain-damaged
patient. 7 -9,17
The neuropsychological evaluation is a comprehensive, objective assessment of a wide range of cognitive, adaptive, and emotional behaviors that
157
158
reflect the adequacy (or inadequacy) of higher brain functions. In essence,

the neuropsychological evaluation is a greatly expanded and objectified mental status examination. The mental status examination is designed to screen
a variety of critical areas briefly, whereas the neuropsychological evaluation
assesses a wider range of performance in considerably more depth. It differs
from the mental status examination in that it generally uses tests and evaluation procedures that have been standardized with samples of either normal
people or brain-damaged patients. Because of the use of standardized tests,
the individual patient's performance can be compared to that of normative
groups, and the adequacy of a patient's performance can be compared across
a variety of neurobehavioral areas. The objective and highly quantified nature
of most neuropsychological tests aids in the detection of subtle changes in
performance over time (e.g., a slowly deteriorating dementia or the improvement in specific cognitive functions after epilepsy neurosurgery). Because of
the wide range of behaviors assessed and the depth of the evaluation, the
neuropsychological evaluation frequently can detect subtle deficits not apparent on the mental status examination.
Referral
Appropriate referrals for neuropsychological evaluation include patients in whom
brain damage is suspected but not unequivocally verified, as well as those for whom
the physician requires further information regarding diagnosis, description of the
effects of a well-verified lesion on behavior, or prognosis and rehabilitation. As with
any consultation, the questions that should be answered (e.g., "Is this patient
demented or depressed?" or "Will the effects of this head injury interfere with
the patient's ability to do his or her job?") should be stated as clearly as
possible.
Cognitive and behavioral disturbances may occur in the absence of any
clear-cut physical signs of cerebral disease on a standard clinical neurologic
examination; this is particularly true in cases of early-stage progressive neurologic disease or mild closed-head injury. In cases of early dementia, the
neuropsychological evaluation can often contribute to an appropriate diagnosis, in combination with other neurodiagnostic procedures. The dilemma
of differentiating between dementia and depression is usually readily resolved
by the data obtained from the neuropsychological assessment. In other cases,
the neuropsychological evaluation can provide data suggestive of brain dysfunction, which then serve as a basis for completing a more extensive and
specific neurodiagnostic workup.
The neuropsychological evaluation can also determine the relative impact
of the organic and functional components in patients with mixed neurologic
and psychiatric complaints, which occurs frequently in geriatric medicine.
Any patient with a documented brain lesion in whom rehabilitation is planned
should receive a complete neuropsychological assessment as part of the initial comprehensive evaluation. This assessment provides valuable information regarding
FURTHER EVALUATIONS
159
the effect of the lesion on cognitive functioning, emotional status, behavior,

and social adjustment. Objective data document both specific areas of impairment and residual abilities. This outline of strengths and weaknesses is
essential in providing information for planning cognitive, vocational, and
social rehabilitation.
Periodic reevaluations over time provide reliable, objective information regarding
the speed and degree of recovery after brain injury or the effectiveness of specific drug
treatment regimens. Similarly, repeat evaluations can assess deterioration in
patients with progressive disease or rule out such progression in equivocal
cases. Testing before and after neurosurgery helps to quantify the effects of
surgery on the patient's neurobehavioral functioning.
In any case of trauma or suspected brain damage involving litigation or compensation, the objective data obtained from a neuropsychological evaluation are of
great value in documenting and describing the presence, absence, and degree of
disability. There is considerable legal precedent for the admission of testimony
of psychologists as expert witnesses in such cases. Forensic neuropsychology
is a rapidly emerging subspecialty, requiring additional training and experience, which has proven very helpful to clinicians and attorneys alike dealing
with cases of traumatically acquired brain damage. 6 ,8,24
Contributions of the
Neuropsychological Evaluation
The following summarize the major clinical contributions of the neuropsychological evaluation.
Categorization
Categorization provides information regarding the presence or absence of
brain dysfunction, significant emotional disturbance, or both. The differential
diagnosis among a primary organic, primary functional, or mixed disorder is
made. If significant components of both organic and functional features are
present, the relative impact of each will be discussed.
Localization
Performance on the neuropsychological test battery can be analyzed to provide data to determine if the brain dysfunction is diffuse or focal. Further
analysis provides data regarding the lateralization of the lesion to the right
or left hemisphere and localization of the lesion within the anterior or posterior region of the hemisphere. With the advent of new neurodiagnostic
procedures (magnetic resonance imaging, positron emission tomography,
etc.) this traditional focus of the neuropsychological evaluation has become
less important clinically, although it continues to be of theoretical and research interest.
160
Description
The neuropsychological evaluation can provide a comprehensive description
of the patient's current level of functioning in a wide range of cognitive,
adaptive, emotional, and behavioral areas. This is perhaps the best use of
neuropsychological consultation in many cases. A comprehensive overview
of the patient's deficits and residual abilities describes current functioning,
explains present behavior, determines the relative effects of organic and functional factors, and provides a baseline of data from which to judge future
change. Answers to the question of mental competence and social independence can also be provided.
prognosis and Recommendations

Based on the nature of the neurologic disease and the pattern and degree of
deficits seen during the neuropsychological evaluation, a determination of
the probability and degree of expected recovery or deterioration can be made
for many patients. Reevaluation is very helpful in making valid prognostic
statements in case of either progression or recovery. Further evaluations, including psychiatry, speech pathology, occupational therapy, and social service, may be recommended, as may specific remedial methods or programs.
components
A meaningful review of the components of the neuropsychological evaluation
is beyond the scope of this book; see references 2, 4, 17, and 25 for additional
information regarding the specific tests used in the neuropsychological evaluation and further details about the field of clinical neuropsychology.
The amount of literature pertaining to clinical neuropsychology has increased almost exponentially during the past 20 years. The amount of available material forces the interested reader to be highly selective in choosing
books that are both current and clinically pertinent. A representative selection
might include references 2, 4, 8, 9, 11, 14, and 17.
SPEECH PATHOLOCY
Patients with significant diffiCUlty in communicating, as a result of neurologic disease
or injury (e.g., patients with aphasia, apraxia of speech, or dysarthria), should be
evaluated by a speech pathologist. Not all such patients are treatment candidates,
but, through thorough language evaluation, the speech pathologist can determine appropriate candidates for speech and language therapy and provide
other services to patients who are not selected for treatment. The speech pathologist is an important member of any comprehensive rehabilitation team,
particularly when a facility sees a large number of stroke and trauma patients.
FURTHER EVALUATIONS
161
Evaluation by the speech pathologist provides a description of the patient's communicative abilities and deficits, the possible benefits of therapeutic intervention, and a plan for family counseling to facilitate the development of alternative methods of communicating with the patient.
Referral
The major reasons for referring patients to a speech pathologist include:
The mental status examination indicates a probable organic communication disorder that requires a more thorough evaluation.
An obvious communication disorder exists that requires a screening
evaluation to determine the appropriateness of speech therapy.
A significant communication disorder is present that requires family
counseling to inform the family members about the patient's problem
and to assist in maximizing effective communication in the home.
For additional information regarding the important role of the speech pathologist in the evaluation and treatment of neurologic patients, see references 5, 10, 16, 20, and 23.
PSYCHIATRY
Many patients with organic brain disease have an associated emotional disorder that
deserves psychiatric consultation. Patients appropriately referred for evaluation
include those with the following:
Psychiatric disorders that preceded their neurologic problem
Neurologically based emotional problems (e.g., organic mood
disorder)
Emotional reactions to brain disease or trauma (e.g., adjustment
disorder)
Emotional factors complicating dementia
Functional disorders that present as neurologic conditions (e.g., conversion disorder paralysis)3
Emotional factors are frequently significant in the rehabilitation and social
reintegration of the patient with organic disease. A psychiatrist or psychologist
should be consulted to aid in the management of any patient with an emotional problem severe enough to interfere with rehabilitative efforts or home
adjustment.
Referral
Because of the relatively high incidence of both mental illness and brain disease,
many patients have coexisting psychiatric and neurologic conditions (e.g., a brain
tumor in a schizophrenic patient, a seizure patient with a manic-depressive
162
disorder). For instance, we saw a 37-year-old woman with a long premorbid

psychiatric history. The patient also suffered from alcoholism and over the
years had sustained several significant traumatic head injuries. After alcohol
withdrawaL she had several grand mal seizures and was admitted to the neurology ward. As her postictal confusion cleared, she demonstrated gross delusional and aggressive behavior. A complete history and medical evaluation
indicated that the patient had an acute neurologic condition superimposed
on a preexisting schizophrenia. Because of the underlying psychosis, a psychiatrist was consulted for treatment and long-term management.
It is not uncommon for previously emotionally stable individuals to develop a significant emotional reaction to an acute-onset neurobehavioral disorder such as aphasia. Depressive reactions, anxiety, paranoia, and aggressiveness may develop in response to brain damage. Such emotional responses
often significantly interfere with rehabilitation efforts and require appropriate
evaluation and treatment.
Patients with dementia present a particular challenge because of their
combined intellectual and emotional changes. These changes produce a variety of difficult management problems that are often best handled with the
aid of a geriatric psychiatrist or neuropsychiatrist. In the early stage of dementia, patients may retain considerable insight; this capacity to realize the
seriousness of their condition often results in profound depression. Other
patients with dementia are unaware of their deteriorating intellectual ability;
such patients often push themselves beyond their capability and thus develop
reactive frustration and severe anxiety. Anxiety or depression can greatly exacerbate the mental and social disability experienced by the patient with dementia. The psychiatrist can provide great assistance through the use of psychotropic drugs, family counseling, and general patient management.
Patients with chronic organic mental syndromes such as significant dementia, severe traumatic encephalopathy, or Korsakoffs disease may become
management problems and eventually require long-term placement in
chronic-care facilities. Early referral to the psychiatrist or medical social
worker can help the family and the primary care clinician with the administrative and legal details involved in such placement.
A final group of patients who may initially be seen by the neurologist,
but who require referral to a mental health professional for treatment, are
those with somatoform disorders (e.g., conversion disorders or pseudo dementia). Such patients will present with symptoms that mimic neurologic
disease (e.g., limb paralysis, loss of speech, or sensory loss) but demonstrate
no organic etiology after thorough evaluation. The treatment for such functional disorders is most often psychotherapy in association with psychotropic
medication.
Information regarding specific psychiatric interview, evaluation, and
treatment techniques is readily available in all major textS.13,28
FURTHER EVALUATIONS
163
SOCIAL WORK
In dealing with neurologic patients and their families in either postacute hospital settings or long-term follow-up and rehabilitation, social workers are
important resources for better patient management. The primary areas of social work input in such settings include:
Gathering and evaluating premorbid, psychosocial, and family information, crucial to understanding the patient and the effect of the neurologic illness or trauma on the patient's ability to function
Participating in patient management and family education and support processes during the early recovery stage
Serving as the primary data collator, resource investigator, and coordinator of the referral and placement process when considering a rehabilitation or long-term care facility
Although not all patients and families need all aspects of the social worker's
total role, virtually all can benefit from some degree of involvement. See
Johnson and McCown 12 for an overview of the role of family therapy in
dealing with neurologic patients and their families, and Thyer and Wodarskf 6
for a more comprehensive introduction to the various roles of the social
worker in managing patients with neurobehavioral disorders.
COGNITIVE REHABILITATION
In recent decades, the fields of cognitive retraining and neurorehabilitation
have become prominent, albeit somewhat controversial, forces in the treatment of brain-injured patients. Providing specific therapies (e.g., physical,
speech-language, psychologic) to promote maximal recovery of particular
neurobehavioral deficits after traumatic brain injury or an acute neurologic
event (e.g., stroke) is not new, but only in the last 20 years or so have comprehensive rehabilitation programs become readily available to such patients.
Discussion of the theoretical framework underlying specific cognitive retraining orientations and the nature of comprehensive programs, as well as the
practical logistics, advantages, and problems of cognitive rehabilitation programs, is beyond the scope of this book. However, the clinician dealing with
patients suffering from static neurologic disorders and traumatically induced
neurobehavioral deficits should become acquainted with this rapidly evolving
area as a potential patient-treatment resource. Decisions regarding whom to
refer, when to refer, and particularly where to refer are difficult and should
be approached with considerable understanding of the developments in this
field and an awareness of the positive and negative aspects of particular programs. We suggest references 15, 19, 21, 22, and 27 for good introductions
to and critical reviews of this important field.
164
SUMMARY
The management of patients with organic brain disease is a multidisciplinary
effort. Physicians and other health professionals are strongly encouraged to
acquaint themselves with the expertise and clinical services offered by their
colleagues in related specialized fields, who can help in understanding patients better and providing them with more comprehensive and effective evaluation and treatment.
REFERENCES
1. Adams, KM and Rourke, BP (eds): The TCN Guide to Professional Practice in Clinical Neuropsychology. Swets and Zeitlinger, Berwyn, PA, 1992.
2. Adams, RL, et al (eds): Neuropsychology for Clinical Practice. American Psychology Association, Washington, DC, 1997.
4 (DSM-IV). American Psychiatric Press, Washington, DC, 1994.
4. Anderson, RM: Practitioner's Guide to Clinical Neuropsychology. Plenum Press, New York,
1994.
5. Benson, DF and Ardila, A: Aphasia: A Clinical Perspective. Oxford University Press, New
York, 1996.
6. Doerr, HO and Carlin, AS: Forensic Neuropsychology. Guilford Press, New York, 1991.
7. Feinberg, TE and Farah, MJ (eds): Behavioral Neurology and Neuropsychology. McGrawHill, New York, 1996.
8. Filskov, SB and Boll, TJ (eds): Handbook of Clinical Neuropsychology. Wiley-Interscience,
New York, 1981.
9. Filskov, SB and Boll, TJ (eds): Handbook of Clinical Neuropsychology, Vol II. WileyInterscience, New York, 1986.
11. Heilman, KM and Valenstein, E (eds): Clinical Neuropsychology, ed 3. Oxford University
Press, New York, 1993.
12. Johnson, J and McCown, W: Family Therapy of Neurobehavioral Disorders: Integrating
Neuropsychology and Family Therapy. Haworth Press, Binghamton, NY, 1997.
13. Kaplan, HI and Sadock, BJ: Comprehensive Textbook of Psychiatry, ed 6. Williams & Wilkins,
Baltimore, 1995.
14. Kolb, Band Whishaw, IQ: Fundamentals of Human Neuropsychology, ed 4. WH Freeman,
New York, 1995.
15. Kreutzer, JS and Wehman, P (eds): Cognitive Rehabilitation for Persons with Traumatic Brain
Injury. Imaginart, Bisbee, AZ, 1996.
16. Lapoint, LL (ed): Aphasia and Related Neurogenic Language Disorders. Thieme Medical Publishers, New York, 1996.
17. Lezak, MD: Neuropsychologic Assessment, ed 3. Oxford University Press, New York, 1995.
18. McCaffrey, RJ, et al (eds): The Practice of Forensic Neuropsychology. Plenum Press, New
York, 1997.
19. Meier, M, Benton, A, and Diller, L: Neuropsychologic Rehabilitation. Guilford Press, New
York, 1987.
20. Plum, F (ed): Language, Communication, and the Brain. Raven Press, New York, 1988.
21. Prignatano, GP: Learning from our successes and failures: Reflections and comment on
"Cognitive Rehabilitation: How it is and how it might be." Journal of the International
Neuropsychologic Society 3:497, 1997.
22. Rosenthal, M, et al (eds): Rehabilitation of the Adult and Child with Traumatic Brain Injury,
ed 2. FA Davis, Philadelphia, 1990.
23. Sarno, MT (ed): Acquired Aphasia, ed 2. Academic Press, New York, 1991.
FURTHER EVALUATIONS
165
24. Spordone, RJ: Neuropsychology for the Attorney. Paul Deutch Press, Orlando, 1991.
25. Spreen, 0 and Strauss, E: A Compendium of Neuropsychologist Tests, ed 2. Oxford University Press, New York, 1997.
26. Thyer, BA and Wodarski, JS (eds): Handbook of Empirical Social Work Practice. John Wiley
and Sons, New York, 1998.
27. Wilson, BA: Cognitive rehabilitation: How it is and how it might be. Journal of the International Neuropsychologic Society 3:487, 1997.
28. Yudofsky, SC and Hales, RE (eds): Textbook of Neuropsychiatry. American Psychiatric Press,
Washington, DC, 1997.
STANDARD
NEUROPSYCHOLOCICAL
ASSESSMENT
METHODS
The primary purpose of this appendix is to introduce the physician and
other specialists to psychological tests that are commonly encountered in
neuropsychological reports and that have proved to be clinically useful in the
assessment of patients with neurologic dysfunction. It is not intended as a
comprehensive overview of neuropsychological evaluation procedures or as
an in-depth evaluation of any individual test or technique. See references 11,
28, 39, or 44 for such detailed information.
FIXED BATTERY VERSUS FLEXIBLE

ASSESSMENT APPROACHES
The two primary underlying philosophic approaches to neuropsychological
assessment at this time are the fixed battery and flexible assessment methods.
The fixed battery typically consists of a standard series of neuropsychological
tests, each of which is administered to every patient regardless of the presenting complaint or specific findings obtained during the course of the assessment. This approach grew out of the American psychometric approach to
psychological and neuropsychological evaluation. Most neuropsychologists
augment the fixed battery with additional tests to more carefully evaluate
a particular problem if it becomes apparent during the evaluation. The
Halstead-Reitan Neuropsychologic Battery is the most representative of the
fixed batteries, although few psychologists currently use this approach without the addition of various other measures.
The flexible approach most commonly uses a small core battery of tests
to provide an overview of the patient's functioning and to suggest particular
166
STANDARD NEUROPSYCHOLOGICAL ASSESSMENT METHODS
167
areas of neurobehavioral function that may require more definitive evaluation. Accordingly, it is a much more individualized approach, with the actual
battery of tests to be administered varying from patient to patient, depending
on the particular set of clinical questions raised. This "process" assessment
approach is more akin to the single-sample method of Luria and to behavioral
neurology than to the more traditional standard methods of clinical neuropsychology. The Wechsler Adult Intelligence Scale-Revised as a Neuropsychological Instrument (WAIS-RNIf2 and Christensen's adaptation of Luria's
techniques 6 are representative of this philosophic approach. In reality, the
well-trained neuropsychologist typically uses elements of both underlying
philosophies in the selection of particular tests for an individual battery, in
the general approach to patient evaluation, and in the analysis of test results.
COMPREHENSIVE FIXED BATTERIES
Halstead-Reitan Battery
This battery, comprising a well-standardized series of tests of cognitive and
adaptive ability, was originally introduced by Halstead,15 revised and standardized by Reitan and associates, and statistically refined by Reitan and
Wolfson,35 Russell and colleagues,37 and others.18 The core tests included
in this battery include: (1) the Category Test, (2) Tactual Performance Test,
(3) Seashore Rhythm Test, (4) Speech-Sounds Perception Test, and (5) FingerOscillation (Finger-Tapping) Test. Age-graded norms for the basic HalsteadReitan Battery and for many additional tests frequently used in conjunction
with this battery are now available. 18 The primary limitations of the HalsteadReitan Battery include its length, its limited emphasis on important neurobehavioral areas such as memory and language, and a lack of test results that
can be readily translated to functionally relevant descriptive information useful to the patient, physician, and others involved in patient care. Its primary
intent, which is to diagnose brain dysfunction and not to delineate and describe functional disabilities, appears somewhat dated in an era of magnetic
resonance imaging (MRI) for anatomic visualization and positron emission
tomography (PET) to assess physiologic functioning of the brain. However,
as typically augmented by the addition of tests of general cognitive ability,
language, and memory, this battery remains one of the best and most popular
standardized methods of identifying patients with neurologic dysfunction.
See references 21 and 35 for more detailed information on this assessment
technique.
Luria-Nebraska Neuropsychological
Battery
This battery,ll which was an attempt to standardize and provide normative
data on selected items adapted from the Christensen-Luria materials, has been
168
the source of both considerable clinical popularity and major criticism in the
neuropsychological literature since its inception. It represents a standardized
fixed battery application of a basically flexible approach, and accordingly incorporates some of the best and most of the worst features of both methods.
Although the battery is still available and is used by some clinicians, it is no
longer well accepted nor in frequent clinical or forensic use. 27
TESTS COMMONLY USED IN FIXED

AND FLEXIBLE BATTERIES
Luria's Neuropsychological
Investigation
Christensen6 organized some of Luria's materials and techniques into a written format, with a manual of administration instructions, within a framework
that corresponded to his conceptualization of brain function-behavior relationships. This has allowed the well-trained clinician to use and adapt Luria's experimental procedures for clinical patient examination. It is perhaps
the foremost example of the flexible assessment approach. The battery includes techniques that assess auditory-motor organization, kinesthetic functions, higher visual functions, receptive and expressive language, reading and
writing, arithmetic skill, memory, and intellectual processes. However, it is
limited in the areas of attention and vigilance, visual memory, and nonverbal
abstract reasoning. Its primary advantage is its ready adaptability to meet the
needs of each individual case, but its lack of normative data restricts the valid
interpretation of test results to very well-trained and highly experienced examiners. The use of Christensen's materials and especially Luria's approach
and techniques cannot be considered a ready-to-use test battery in the sense
of the usual psychometrically based approaches to assessment. Although very
interesting and often useful in providing detailed information about an individual patient, any clinician interested in this approach must be thoroughly
versed in Luria's philosophy, theories, and techniques, and must be prepared
to design detailed single-subject experimental investigations for each patient.
Tests of Ceneral Cognitive

Functioning
Wechsler Adult Intelligence ScaleThird Edition
The Wechsler Adult Intelligence Scale-Third Edition (WAIS-III)47 is the current revision and restandardization of the familiar adult Wechsler intelligence
scales. The test, which remains the standard for the clinical assessment of
intelligence in patients between age 16 and age 89, provides data that quan-
169
tify general intellectual functioning (Full-Scale IQ), verbal and nonverbal performance (Verbal and Performance Scale IQs), and specific performance in
the areas of verbal-comprehension, perceptual-organization, working memory
(attention), and processing speed. The Verbal Scale includes seven distinct
subtests of verbally mediated cognitive functioning; the Performance Scale
includes seven other subtests requiring visual-perceptual analysis, visual organization, comprehension, and psychomotor coordination. The summary IQ
scores derived from the WAIS-III (and most other commonly used intelligence
tests) have a normative mean of 100, with a standard deviation of 15.
Edith Kaplan introduced the WAIS-R as a Neuropsychological instrument,22 which represents a synthesis of the process-oriented flexible assessment approach and a standard psychometric test of general cognitive functioning. After administration ofthe standard WAIS-R, this technique provides
additional subtests, an alternate multiple-choice format for further assessment
of the pattern and style of patients' functioning on a number of the subtests,
a more comprehensive method of assessing specific deficits in arithmetic, and
a new symbol copy task to better delineate the visuospatial processes involved
in the standard Digit Symbol subtest. This allows a more comprehensive analysis of the nature of more specific cognitive processes underlying basic intelligence. The WAIS-RNI provides the means for a qualitative assessment of
cognitive functioning in addition to the quantitative measure provided by the
standard intelligence test.
Measures of Premorbid Intellectual

Functioning
Interpretation of the clinical significance of neuropsychological findings for
the individual patient depends in part on changes in functioning from premorbid levels. School records frequently contain the results of group tests of
general ability (e.g., Otis-Lenon Test, Scholastic Aptitude Test, American College Test [ACT], and the like), which are useful for comparison purposes.
Reports of school grades may also be used, although they tend to be less
reliable. A number of techniques for estimating premorbid intellectual functioning from demographic information and test data gathered during the neuropsychological evaluation have been devised; including use of the Wechsler
sub tests of Vocabulary and Information, performance on tests ofreading recognition (especially the National Adult Reading Test),38 reliance on the patient's highest level of functioning on any test or set of tests, and the development of statistic regression equations based on demographic information.
The use of demographic or psychometric variables to predict premorbid intelligence statistically has the advantages of using data readily generated during the neuropsychological evaluation, applying equally to virtually all patients, and not changing because of any clinical condition. Barona, Reynolds,
170
and Chastain,2 Krull et al.,26 and others have developed and refined regression
equations for predicting premorbid WAlS IQs at reasonably valid and reliable
levels.
Tests of Attention and vigilance

Digit Repetition
The number of digits repeated forward on the WAlS-III (or any other string
of single-digit numbers) provides an easily administered objective measure
of the patient's ability to maintain auditory attention for a brief period (approximately 10 to 15 seconds). The patient is verbally presented an increasing
series of random digits at a rate of one digit per second (beginning with two
digits and increasing until failure on two successive trials), and is requested
to repeat the digit string exactly as heard.
Digits repeated backward requires very different mental processes, cognitively differing appreciably from digits repeated forward. Although attention
is certainly one of the requirements of this task, it is far from the primary
component of such performance; this task should therefore not be used to
measure attention.
"Jl:' Random Letter Test for Vigilance

This easily administered test of auditory attention is well described in Chapter 4.
Letter and symbol Cancellation Tasks

Various visually presented letter, number, and symbol cancellation tasks can
evaluate the patient's ability to maintain attention to visually presented stimuli for differing periods of time. These tasks typically include an array of
randomly presented visual stimuli, with a given target item that must be
noted and crossed out (e.g., letter, number, and symbol). The arrays presented
by Mesulam 30 are particularly useful, as their format allows the examiner also
to detect unilateral visual neglect and inattention.
Paced Auditory Serial Addition Test

The Paced Auditory Serial Addition Test (PASAT)31 is a highly demanding
and sensitive test of active sustained verbal attention, information processing,
and basic ability to calculate. It consists of a taped series of randomized digit
pairs that are presented at four different rates of speed, ranging from one digit
every 1.2 seconds to one every 2.4 seconds. The patient is instructed to add
each digit pair (e.g., "2-9 (11); 5-3 (8); 4-6 (10); 7-8 (15) ... "). Derived
171
scores include the percentage of correct responses at each rate, the total correct, and sometimes the mean time per correct response for each trial. New
age-graded norms have been published recently, expanding the clinical usefulness of this test. 36
Tests of Language Functioning

peabody Picture vocabulary TestThird Edition
The Peabody Picture Vocabulary Test-Third Edition 9 is an easily administered test of single-word vocabulary comprehension. Norms are provided for
age groups between 2~ and 90 years. The test is composed of two equivalent
204-item word lists presented verbally in ascending order of difficulty. The
patient responds by indicating which of four pictures best represents the word
spoken by the examiner (e.g., "Where is 'incandescent'?"). The primary use
of the Peabody test is as an objective test of spoken language at the singleword level, with an important secondary role of providing an early estimation
of the patient's probable ability (or inability) to perform validly on both the
language-mediated components of the neuropsychological evaluation and
any other measure requiring language comprehension.
Token Test
The short version of the Token Test (see reference 44) is a well-structured,
simply administered test of language comprehension that assesses the patient's ability to respond to various sentence types, semantic relations, and
linguistic elements. The Token Test uses colored plastic tokens that are manipulated by the patient in response to a series of hierarchically ordered verbal
commands (e.g., ranging from "Show me a circle" to "After touching the
yellow square, pick up the blue triangle"). It is useful in the assessment of
aphasic patients, as well as those with language comprehension deficits secondary to dementia, other neurologic conditions, or low levels of general
intelligence.
Boston Naming Test

The Boston Naming Test (BNTf3 is an objective measure of visual confrontation naming. It requires the patient to name a difficulty-graded series of
pictured objects, ordered in increasing difficulty from "bed" to "abacus".
When the patient is unable to spontaneously name an item, the examiner
first provides a categorical cue (e.g., "It is something to eat" and then a phonemic cue (e.g., the beginning sound of the target word). Provisional norms
are provided in the manual for children, normal adults, and aphasic adults;
172
additional norms derived from both normal and clinical samples are readily
available. 43 Because of the frequent incidence of naming problems in various
neurologic conditions, the BNT has deservedly become a very popular tool.
verbal Fluency Tests

Several standardized tests of verbal fluency are currently available. The two
that have proved most effective in our setting are the Controlled Oral
Word-Association Test (FAS or CFL), adopted from the Multilingual Aphasia
Examination-Third Edition (MAE-3V and the Animal-Naming Test,
adopted from the Boston Diagnostic Aphasia Examination (BDAE).12 Both
objectively measure the patient's ability spontaneously to produce single
words under the restrictions of a limited category (e.g., "F") and time (60
seconds) (e.g., 'Tell me all the words you can think of that begin with 'F' ").
These tests are further discussed in Chapter 5. Updated norms for these procedures are available for a variety of age groupS.43
Comprehensive Aphasia Batteries

When evaluating a patient with known aphasia or with a clinically apparent
language obstacle to valid neuropsychological evaluation, a complete aphasia
battery should be conducted. In some settings, this is the responsibility of the
speech pathologist; in other instances, such batteries are administered by the
neuropsychologist or behavioral neurologist. In either case, the clinician who
deals with brain-damaged patients should be familiar with the contents, as
well as the advantages and disadvantages, of the commonly used measures.
The following is an alphabetic listing of the more popular batteries. Our
preference is for the BDAE or the similar Western Aphasia Battery, although
each of the listed tests has enjoyed considerable popularity.
BDAE12
Communication Abilities in Daily Living 19
MAE-3
Neurosensory Center Comprehensive Examination for Aphasia 43 ,44

Western Aphasia Batterf4
See references 28 and 44 for reviews of the assessment process in aphasic
patients and detailed descriptions of specific instruments.
Tests of Memory
Wechsler Memory Scale-Third Edition
(WMS-IID
The publication of the Wechsler Memory Scale-Revised (WMS-Rt S in 1987
and a subsequent reformulation and restandardization (WMS-III) in 1997 46
173
have provided neuropsychologists with a significant new omnibus measure

of memory functioning. The WMS-R and -III are currently the most frequently
used comprehensive measures of memory functioning in neuropsychological
practice, although they have been criticized regarding their psychometric
properties. The WMS-III includes a measure of general memory (actually composed of auditory and visual delayed recall), as well as indices of immediate
memory (auditory and visual), working memory (auditory and visual), and
auditory recognition (delayed). The WMS-R and -III are rather well standardized, with ample normative data provided in the test manuals and also available from numerous research studies for a wide range of age groups.
Memory Assessment Scales

The Memory Assessment Scales (MAS)4B are a comprehensive battery for assessing memory functioning in adults. The MAS includes 12 subtests, based
on seven learning and recall tasks, and provides summary scores for shortterm memory (verbal span and visual span), verbal memory (word list recall
and immediate recall of a logical paragraph), visual reproduction (IS-second
recall of visual designs and immediate visual recognition of visual designs),
and global memory. The battery also includes methods to obtain verbal processing scores, measures of intrusion errors, and recognition memory. Although the MAS is psychometrically well designed and both clinically and
theoretically interesting, clinical research data pertaining to this test are considerably more limited than for the more widely distributed WMS-R and -III.
Rey Auditory Verbal Learning Test;

California Auditory Verbal
Learning Test
The Rey Auditory Verbal Learning Test (RAVLT)40 and the California Auditory
Verbal Learning Test (CAVLT)9 are easily administered tests of immediate
verbal memory span, verbal learning, and immediate and delayed recall. In
both tests word lists are verbally presented for five acquisition trials, requiring
the patient to recall as many as possible of the verbally presented words after
each trial. The tests provide a learning curve (presuming an increasing number
of words recalled over successive trials) and document learning strategies (primacy or recency effects), retroactive and proactive interference, and intrusion
errors, confusion, or confabulation tendencies. An interference trial followed
by an immediate recall of the acquisition list and a short-term delayed recall
provide retention scores. Recognition memory is assessed after the delayed
recall trial. With additional delay trials (60 minutes, 24 hours, and so forth),
the test can also measure verbal retention over more extended periods of time.
The CAVLT offers the advantage of using a word list that can be encoded
by several different methods, allowing the examiner to further analyze learn-
174
ing and memory by measuring coding strategies, learning rates, other process
data, and short- and long-term delay. Published norms and methods to statistically analyze the learning and recall processes are more sophisticated for
the CAVLT than for the RAVLT. Neither test alone should be considered a
sufficient test of all aspects of memory functioning, but both tests together
are extremely useful for augmenting a more comprehensive memory assessment or for screening purposes.
Benton Visual Retention Test;

Memory for Designs Test
The Benton Visual Retention Test (BVRT)S.41 and the Memory for Designs
(MFD) test 13 are measures designed to assess visual perception and analysis,
short-term visual memory, and paper-and-pencil constructional ability. Each
includes a series of graduated simple-to-complex line drawings that the patient must visually analyze and then copy. Both incorporate a memory component. The BVRT includes trials with variable periods of exposure of the
stimuli as well as increasing periods of delay between exposure and reproduction, making it a more sensitive measure, albeit cognitively more complex.
Both tests include explicit scoring instructions and adequate normative data.
Because of its psychometric properties and its long history of research findings, most clinicians prefer the BVRT.
Tests of Abstraction and Higher

Cognitive Function
Category Test
Among the tests of the Halstead-Reitan battery, many consider the Category
Tese s to be the most sensitive to the effects of brain dysfunction. The test
consists of seven subtests of varying complexity, each with a different underlying principle (e.g., size, shape, color, and position). The patient is required
to learn sorting behavior based on auditory or verbal reinforcement, and must
also make conceptual shifts between categories upon reaching criteria for a
given sorting strategy. Statistical studies suggest that the Category Test measures abstract reasoning and problem solving, conceptual set shifting, and the
ability to learn from verbal reinforcement on tasks of moderate-level complexity. Category Test performance is related to age, education, and intelligence, at times resulting in interpretation problems when such variables are
not taken into consideration. We have also noted problems caused by the
effects of varying levels of attention and effort, as well as frustration and other
emotional and behavioral factors. Newer, age-based norms 18 have proved
helpful and should be used when this test is given. Short-form and paperand-pencil versions of the test have been developed; we have found the Booklet Category Test,7 which is more easily transported and administered in a
175
hospital setting, to be a useful, valid, and reliable measure of higher-order

conceptual functioning.
Wisconsin Card-Sorting Test

The Wisconsin Card-Sorting Test (WCST), 14 designed to assess abstract ability,
conceptual set shifting, and "learning to learn," using tasks of medium-level
complexity, was recently revised in terms of administration and scoring and
has been subjected to a more refined standardization study. IS The WCST requires the patient to sort a series of stimulus cards that vary in color, form,
and number by matching to a sample array containing a red triangle, two
green stars, three yellow crosses, and four blue circles. The examiner tells the
patient whether his match is correct or incorrect after each trial. The designated "correct" matches are, in sequence: color-form-number-colorform-number. This test has received renewed clinical and research attention
because (1) it provides an objective measure of abstraction and problem solving; (2) it is purported to be differentially sensitive to the effects of frontal
lobe lesions (although this has certainly not been consistently found); and
(3) it gives information on the particular reasons for difficulty on the test
(e.g., impaired conceptualization, failure to sustain the correct set, perseveration, or deficits in learning across several trials). As with the Category Test,
WCST results may be affected by the patient's general intelligence and academic background, as well as by emotional or behavioral factors; careful interpretation of results of each individual patient is therefore very important.
Raven's Progressive Matrices

Raven's Progressive Matrices 32 - 34 are a series of tests of visuospatial analysis,
spatial conceptualization, and numeric reasoning. The test is available in three
difficulty levels, ranging from the Coloured Matrices for children and impaired adults to the Advanced Matrices for well-functioning adults. Each of
the test forms requires the patient to select, from a series of alternative possibilities, the pictured pattern or segment of a pattern that best matches or
completes the stimulus figure. The matrices are useful for assessing visual
pattern analysis, matching, nonverbal reasoning, unilateral neglect, and cognitive style. Additionally, the matrices can be used to differentiate between
the visual analytic and the motor integration components in a patient who
has documented "visual-perceptual deficits."
Tests of Sensory-perceptual
Functioning
Seashore Rhythm Test
This test of auditory perception and integration, an integral component of
the Halstead-Reitan Battery and many of its derivatives, requires the patient
176
to discriminate between pairs of recorded musical tones that are either identical ("same") or different. The Seashore Rhythm Test is primarily used within
the Halstead-Reitan Battery to assess right temporal lobe functioning, although impaired performance may result also from more disparate or diffuse
lesions. Varying attention levels, as well as basic difficulty in following directions, may adversely affect test performance, sometimes to the point of invalidating the results. Many neuropsychologists now consider the Seashore
Rhythm Test to be a good test of auditory attention, notwithstanding its utility (or lack thereof) in localizing cerebral lesions.
Speech Sounds Perception Test

This subtest of the Halstead-Reitan Battery requires the patient to indicate on
an answer sheet which one of four possible nonsense speech -like syllables
he or she has heard via headphones (e.g., "heep . .. heet . . . wheep ...
wheet"). The test includes 60 sets of syllables based on the vowel sound "ee,"
but beginning and ending with different consonants. Although it has been
reported to be sensitive to the effects of brain damage, particularly left temporal lesions, considerable research suggests that it is primarily a measure of
sustained attention. The examiner who wishes to use the test for its original
purpose must ensure that sufficient basic attention was maintained over the
course of the administration to allow valid interpretation of the higher-level
component of the test. Once again, behavioral and emotional problems can
have an adverse effect on test performance, causing invalid results.
Tests of Tactile Perception

A variety of objective tests of tactile suppression, tactile recognition (stereognosis), and graphesthesia (e.g., fingertip writing recognition, palm writing)
have been developed to assess unilateral parietal lobe functioning. With the
exception of normative data for objective comparison, the measures are very
similar to clinical tests conducted during the standard neurologic and extended mental status examination.
Tests of Visual Perception

It is crucial to establish the adequacy of the patient's visual acuity and visual
perception and to rule out the possibility of unilateral neglect or inattention.

Much of this is accomplished using clinical methods identical to those used
in the standard neurologic examination. Tests of neglect, color vision, visual
recognition, facial recognition, fragmented visual stimuli,2 and figure-ground
discrimination are merely examples of the many standardized tests and procedures that can be used to assess these functions. See references 28 and 44
for reviews of available measures.
177
Tests of Constructional Ability
Bender Gestalt Test

The Bender Gestalt Test (originally the Bender Visual Motor Gestalt3 ) is a
venerable, rapidly administered screening test of paper-and-pencil constructional ability. The patient is presented with a series of simple and more difficult geometric line drawings, which are copied. The patient's design reproductions can be objectively scored for the errors of integration, distortion,
perseveration, and rotation. 2s Unfortunately, this test is still used fairly commonly as a screening measure for "organicity." This use is unwarranted given
the current state of knowledge regarding brain-behavior relationships. It is
quite appropriate to include it as a test of one type of constructional ability
within the context of a more comprehensive battery, however.
Raven's progressive Matrices

These tests are useful in assessing the visuospatial analytic component of the
constructional process.
Benton Visual Retention Test

This well-standardized test can also be used to evaluate both reproduction
constructional ability (design copying) and short-term recall reproduction
(constructions from memory). The major advantages of this test are standard
administration and scoring criteria, good normative and research data, and
the availability of alternate, equivalent test forms.
Hooper Visual organization Test

The Hooper Visual Organization Test (HVOTfO has recently gained renewed
favor in neuropsychology as a measure of visual analysis and organization
and of the ability to synthesize disparate arts into a meaningful gestalt without a motor component. The test includes a series of line drawings of increasing complexity that have been cut into a variety of separate parts. The
patient must identify the pictured object by mentally organizing the various
parts. The HVOT is essentially a "constructional" test without a motor-output
component. In addition to the patient's absolute level of performance, the
HVOT is useful in demonstrating the more specific underlying nature of a
patient's perceptual motor dysfunction.
Tests of Visual Motor Sequencing
Trail-Making Test
This test, which is included in the Halstead-Reitan Battery, is a popular measure of visual searching, visual sequencing, perceptuomotor speed, the ability
178
to make alternating conceptual shifts efficiently, and attention. Part A of the

test merely requires the patient to draw a line sequencing the numbers 1
through 25. Part B includes an element of conceptual shifting, requiring the
sequencing of numbers and letters in alternating fashion (e.g., l-A-2-B3-C-4 ... ). Both speed and accuracy are considered in the interpretation of
this test. Currently available research shows that this test (particularly Part B)
is sensitive to the effects of brain dysfunction of any type and also provides
some equivocal indication that patients with frontal lobe lesions perform
relatively more poorly than those with lesions in other loci.
Digit symbol Modalities

The Digit Symbol Modalities (DSM) test,42 essentially a symbol coding task
under timed conditions, assesses visual scanning, visual tracking (attention),
and psychomotor speed. The patient is presented with a printed key associating the numbers 1 through 9 with a different symbol, and a test form
containing an array of 110 blank squares, each paired with a random symbol.
The patient then writes as many numbers under the correct symbol as possible
within a 90-second time span. The DSM test also includes a verbally presented
component, which allows a comparison between the accuracy and speed of
written and oral responses. The test requires sustained attention, visual search,
visual sequencing, and learning ability. DSM test performance is sensitive to
the effects of central nervous system dysfunction and appears to be related to
real-world functioning. 44
Tests of Motor Coordination

and strength
Finger-Tapping Test
The Finger-Tapping Test, also known as the Finger Oscillation Test, is a frequently used measure of upper extremity motor speed. The test includes a
number of tapping trials by the index finger of each hand using a mechanical
or electrical recording tapping device. A number of reports suggest an average
for normal subjects of approximately 55 taps with the dominant hand during
a lO-second trial and approximately 10% fewer with the nondominant hand.
The test is somewhat sensitive to anterior brain dysfunction in general and,
more specifically, to lesions in the area of the contralateral motor strip.
Grooved Pegboard
The Grooved Pegboard 29 is a very useful measure of upper extremity speed,
combined with manipulatory dexterity. Patients must rapidly place ridged
pegs in a board containing a series of randomly grooved holes, using first the
179
dominant hand alone and then the nondominant hand alone. Because of the
presence of randomly positioned slots, the test is more complex and accordingly more sensitive than most pegboards. It is a good tool to objectify more
subtle motor deficits and to assess improvements in hand coordination following stroke or trauma. A wide range of standardized norms, as well as mean
scores from various clinical samples, are available to aid in the interpretation
of the test results.
Hand Dynamometer (Grip strength)

The use of a mechanical hand dynamometer to assess grip strength over several (usually five) trials with the right and left hands allows the accurate
quantification of a common motor component of the standard neurologic
examination. Reductions in strength bilaterally when compared with the expected levels for age and sex, as well as disproportionate discrepancies between hands, may indicate brain dysfunction, particularly when peripheral
factors are ruled out.
Tests of Academic Achievement

Wide-Range Achievement TestThird Edition
The Wide-Range Achievement Test-Third Edition (WRAT_III)49 is probably
the most frequently used objective screening test of achievement, owing partly
to its brevity. It assesses performance in reading recognition (reading isolated
words graduated in difficulty), spelling to dictation (using words ranging
from kindergarten to high-school level), and computational arithmetic (ranging from simple counting to addition, subtraction, division, multiplication,
and algebraic formulas). Norms allow comparison of the individual patient's
performance with normal samples ranging from 5 to 75 years of age and
educational levels from preschool to grade 12. 8
Woodcock-Johnson
psychoeducational Battery-Revised:
Tests of Achievement
The Woodcock-Johnson Psychoeducational Battery-Revised: Tests of
Achievement (WJ-R-Ach)50 represents a wide-age-range measure of academic
achievement in the basic areas of reading, mathematics, and written language,
as well as in elementary science, social studies, and humanities. Neuropsychological studies usually focus on the three basic areas. A major advantage
of this battery is the incorporation of supplemental sub tests that allow the
evaluation of specific deficits within the basic areas. The WJ-R-Ach is well
180
developed psychometrically and is also well standardized; it offers a more

comprehensive measure of academic functioning than most of the commonly
used screening tests and is useful when evaluating patients with primary
learning disorders or acquired academic deficits.
Personality Tests
Minnesota Multiphasic Personality
InventorY-2
The recently revised Minnesota Multiphasic Personality Inventory-2
(MMPI_2)16 continues to be the most commonly used standardized test of
emotional status in both psychiatric and neurologic patients. By comparing
each patient's performance with those of normal individuals, the MMPI-2
measures emotional status in the areas of hypochondriasis (physical concern),
depression, hysteria (reduced ability to cope and tendency to channel emotional stress into somatic outlets), personality disorder (or chronicity),
masculinity-femininity of interests, paranoia, psychasthenia (anxiety and
obsessive-compulsive traits), schizophrenia (or cognitive confusion), hypomania (agitation), and social introversion. In addition to the 10 basic clinical
scales, the MMPI-2 provides 15 new content scales, offering a much more
comprehensive description of the patient's emotional functioning.
At our current state of knowledge and experience with this technique,
the MMPI-2 is considered more appropriate for assessing normal individuals
and psychiatric patients than for brain-damaged patients. However, the literature pertaining to the use of the MMPI with brain-damaged patients is
expanding; the reviews by Lezak28 and Spreen and Strauss44 are good introductions. See also Algano and colleagues 1 for a recent study of MMPI use in
investigating the emotional changes that occur after closed-head injury. Despite some contention regarding the nature of interpretations of MMPI abnormalities within the context of neurologic disease, it continues to be most
useful in describing emotional functioning in neurologic patients, rather than
in establishing a psychiatric diagnosis in accordance with the Diagnostic and
Statistical Manual of Mental Disorders-Fourth Edition (DSM-IV).
other personality Instruments

A variety of self-reporting scales of anxiety, depression, physical symptoms,
more specific neurobehavioral symptoms, pain and its social ramifications,
and social adjustment are available for use with patients who are capable of
responding validly either in written form or during an interview. Such tests
can be useful for assessing the patient's subjective perception of emotional
and social well-being, as well as for research purposes. See Lezak28 and Spreen
and Strauss44 for more information regarding these instruments.
181
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intelligence of the WAIS-R. J Consult Clin Psycho I 52:885, 1984.
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1946.
4. Benton, AL, deS Hamsher, K and Silven, AB: Multilingual Aphasia Examination, ed 3. AJA
Associates, Iowa City, 1983.
5. Benton, AL, et al: Contributions to Neuropsychological Assessment: A Clinical Manual. Oxford University Press, New York, 1994.
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Resources, Odessa, FL, 1987.
8. Delise, DC, et al: California Verbal Learning Test. Psychological Corporation, San Antonio,
1987.
9. Dunn, LM and Dunn, LM: Peabody Picture Vocabulary Test, ed 3. American Guidance Service, Circle Pines, MN, 1997.
10. Golden, CL Purisch, AD, and Hammeke, TA: Luria Nebraska Neuropsychological Battery:
Forms I and II. Western Psychological Services, Los Angeles, 1986.
11. Goldstein, G and Incagnoli, TM: Contemporary Approaches to Neuropsychological Assessment. Plenum Press, New York, 1998.
12. Goodglass, H and Kaplan, E: The Assessment of Aphasia and Related Disorders. Lea {Ix
13. Graham, FK and Kendall, BS: Memory-for-Designs Test: Revised General Manual. Percept
Mot Skills (Suppl 2-VIII)11:147, 1960.
14. Grant, DA and Berg, EA: Wisconsin Card Sorting Test. Psychologic Corporation, San Antonio,
1993.
15. Halstead, W: Brain and Intelligence: A Qualitative Study of the Frontal Lobes. University of
Chicago Press, Chicago, 1947.
16. Hathaway, SR et al: Minnesota Multiphasic Personality Inventory-2: Manual for Administration and Scoring. University of Minnesota Press, Minneapolis, 1989.
17. Heaton, RK: Wisconsin Card Sorting Test Manual. Psychological Assessment Resources,
Odessa, FL, 1981.
18. Heaton, RK, Grant, I, and Matthews, CG: Comprehensive Norms for an Expanded
Halstead-Reitan Battery. Psychological Assessment Resources, Odessa, FL, 1991.
19. Holland, AL: Communicative Abilities in Daily Living. University Park Press, Baltimore,
1980.
20. Hooper, HE: The Hooper Visual Organization Test. Western Psychological Services, Los Angeles, 1958.
21. Jarvis, PE and Barth, IT: The Halstead-Reitan Neuropsychological Battery: A Guide to Interpretation and Clinical Applications. Psychological Assessment Resources, Odessa, FL, 1994.
22. Kaplan, E: WAIS-R as a Neuropsychological Instrument. Psychological Corporation, San Antonio, 1991.
23. Kaplan, E, Goodglass, H, and Weintraub, S: Boston Naming Test. Lea {Ix Febiger, Philadelphia,
1983.
24. Kertesz, A: Aphasia and Related Disorders: Taxonomy, Localization, and Recovery. Grune {Ix
Stratton, New York 1982.
25. Koppitz, EM: The Bender Gestalt Test for Young Children. Grune {Ix Stratton, New York
1963.
26. Krull, KR, Scott, JG, and Sherer, M: Estimation of premorbid intelligence from combined
performance and demographic variables. The Clinical Neuropsychologist 9:83, 1995.
27. Lees-Hailey, PR, et al: Forensic neuropsychological test usage: An empirical survey. Archives
of Clinical Neuropsychology 11:45, 1995.
28. Lezak, MD: Neuropsychologic Assessment, ed 3. Oxford University Press, New York 1995.
29. Matthews, CG and Klove, H: Instruction Manual for the Adult Neuropsychology Test Battery.
University of Wisconsin Medical SchooL Madison, WI, 1964.
30. Mesulam, M-M: Principles of Behavioral Neurology: Tests of Directed Attention and Memory.
FA Davis, Philadelphia, 1985.
182
31. Psychological Corporation: Paced Auditory Serial Addition Test. Psychological Corporation,
San Antonio, 1994.
32. Raven, JC: Guide to the Standard Progressive Matrices. Psychological Corporation, San Antonio, 1977.
33. Raven, JC: Guide to Using the Coloured Progressive Matrices. Psychological Corporation,
San Antonio, 1977.
34. Raven, JC: The Advanced Progressive Matrices. Psychological Corporation, San Antonio,
1977.
35. Reitan, RM and Wolfson, D: The Halstead-Reitan Neuropsychological Test Battery: Theory
and Clinical Interpretation, ed 2. Neuropsychology Press, Tucson, AZ, 1993.
36. Roman, DD, et al: Extended norms for the Paced Serial Addition Test. The Clinical Neuropsychologist 5:33, 1991.
37. Russell, EW, Neuringer, C, and Goldstein, G: Assessment of Brain Damage: A Neuropsychological Key Approach. Wiley-Interscience, New York, 1970.
38. Ryan, JJ and Paolo, AM: A screening procedure for estimating premorbid intelligence in the
elderly. Clin Neuropsychol 6:53, 1992.
39. Sbordone, RJ and Long, CJ (Eds): Ecological Validity of Neuropsychological Testing. GR
Press/St Lucie Press, Delray Beach, FL, 1996.
40. Schmidt, M: Manual for the Rey Auditory Verbal Learning Test. Western Psychological Services, Los Angeles, 1997.
41. Sivan, AB: Benton Visual Retention Test, ed 5. Psychological Corporation, San Antonio, 1992.
42. Smith, A: Symbol Digit Modalities Test. Western Psychological Services, Los Angeles, 1991.
43. Spreen, 0 and Benton, AL: Neurosensory Center Comprehensive Examination for Aphasia.
University of Victoria Neuropsychology Laboratory, Victoria, Be, 1977.
44. Spreen, 0 and Strauss, E: A Compendium of Neuropsychological Tests, ed 2. Oxford University Press, New York, 1998.
45. Wechsler, D: Wechsler Memory Scale-Revised (WMS-R). Psychological Corporation, San
Antonio, 1987.
46. Wechsler, D: Wechsler Memory Scale-Third Edition (WMS-III). Psychological Corporation,
San Antonio, 1997.
47. Wechsler, D: Wechsler Adult Intelligence Scale-Third Edition (WA1S-III). Psychological Corporation' San Antonio, 1997.
48. Williams, MJ: Memory Assessment Scales (MAS). Psychological Assessment Resources.
Odessa, FL, 1991.
49. Wilkinson, GS: The Wide Range Achievement Test-Third Edition. Jastak Associates, Wilmington, DE, 1993.
50. Woodcock, RW and Mather, N: Woodcock-Johnson Tests of Achievement. DLM Teaching
Resources, Allen, TX, 1989.
MENTAL STATUS
EXAMINATION
RECORDING FORM
PATIENT INFORMATION
Patient name:
Address:
Date:
Case #:
Phone:
Date of birth:
Age:
Education:
Highest level:
Failures or honors:
Handedness:
Patient:
Occupation:
Medical diagnosis:
Onset and nature:
Hospital #:
Place of birth:
Sex:
Age at completion:
Family:
Hemiplegia:
(Circle)
None
Recovered
Right
Left
Hemianopia:
(Circle)
None
Recovered
Right
Left
Neurosurgical information:
183
184
Electroencephalograph (EEG) focus:
MRI,
cr scan, brain scan, angiogram, and so forth:
(Starred items should be used with all patients.)

*1. Behavioral Observations
*A. History of behavior change, memory difficulties, bizarre behavior,
change in work habits, and the like:
* B. Physical Appearance:
*C. Emotional Status (e.g., confusion, depression, anxiety, lability):
D. Frontal Lobe Test Results (see related cortical functions):
*E. Denial or Neglect:
*11. Level of Consciousness
*A. Rate: Alert _ _ Lethargic _ _ Stupor _ _ Coma _ _

*B. Describe stimulus necessary to arouse patient, and record patient's
response:
*111. Attention
*A. Observation of patient during examination:

*B. Digit repetition: Repeat digits at a rate of one per second.
Item
3-7
2-4-9
8-5-2-7
2-9-6-8-3
5-7-1-9-4-6
8-1-5-9-3-6-2
3-9-8-2-5-1-4-7
7-2-8-5-4-6-7-3-9
Check If Correct
MENTAL STATUS EXAMINATION RECORDING FORM
185
C. Vigilance: Repeat letters at a rate of one per second. Tell patient to

indicate by tapping the table whenever he or she hears the letter
/lA."
LTPEAOAI CTDALAA
ANI A BF SAMRZEOAD
PAKL AUCJ T OEABAA
ZY KMUS AHE VAARAT
1. Errors of omission:
2. Errors of commission:
D. Unilateral inattention:
*IV. Language
*A. Spontaneous speech:
*1. Describe, including fluency, articulation, and presence of
paraphasias:
2. Verbal fluency: Total animals:
Total words:
*B. Comprehension:
*l. Patient's response to pointing commands:
Ask patient to point to one, two, three, then four room objects or body parts in sequence. Record adequacy of
performance.
*2. Patient's response to yes-no questions:

(e.g., "Is it raining today?" or "Is Grant still president?")
*C. Repetition:
Tell the patient to repeat each of the following:
Item
1. Ball
2. Help
3. Airplane
4. Hospital
5. Mississippi River
6. The little boy went home.
7. We all went over there together.
Check If Correct
186
Item
8. The old car wouldn't start on Tuesday
morning.
9. The short fat boy dropped the china vase.
10. Each fight readied the boxer for the
championship bout.
Check If Correct
*D. Naming and Word Finding:

Tell the patient to name the following simple colors and objects:
Item
1. Colors
a. Red
b. Blue
c. Yellow
d. Pink
e. Purple
2. Body parts
a. Eye
b. Leg
c. Teeth
d. Thumb
e. Knuckles
3. Clothing and room objects
a. Door
b. Watch
c. Shoe
d. Shirt
e. Ceiling
4. Parts of objects
a. Watch stem (winder)
b. Coat lapel
c. Watch crystal
d. Sale of shoe
e. Buckle of belt
Check If Correct
E. Reading:
Describe level of adequacy (words, sentences, paragraphs) and
note types of errors:
187
F. Writing:
Describe level of adequacy and note types of errors:
G. Spelling:
Describe performance to dictation and note errors:
*v.
Memory
Most of the following memory tasks evaluate verbal memory. In patients with language disturbance (aphasia), the visual memory tests
must be used.
*A. Immediate Recall (short-term memory):

Refer to Digit Repetition in Section III.
*B. Orientation:
Check If Correct
* 1. Person
a. Name
b.Age
c. Birth date
*2. Place
a. Location (at present)
b. City location
c. Home address
*3. Time
a. Date
b. Day of the week
c. Time of day
d. Season of the year
e. Duration of time with
examiner
C. Remote Memory:
Check If Correct
or Adequate
* 1. Personal Information
a. Where were you born?
b. School information
c. Vocational history
d. Family information
188
Check If Correct
or Adequate
*2. Historic Facts
a. Four US presidents during
your lifetime
b. Last war
*D. New-Learning Ability:
1. Four Unrelated Words: Tell the patient, "1 am going to tell you
four words, which I want you to remember." Have the patient

repeat the four words after they are initially presented and
then say that you will ask him or her to remember the words
later. Continue with the examination, and at intervals of 5,
la, and 30 minutes, ask the patient to recall the words. Use
categoric ("one word is a color") or phonemic ("one word
begins with B") cues if he or she is unable to recall the word
spontaneously on any trial. Record the type and amount of
cuing necessary. Three alternate sets of words are provided.
5 min
10 min
30 min
a. Brown (Fun) (Grape)

b. Honesty (Loyalty) (Happiness)
c. Tulip (Carrot) (Stocking)
d. Eyedropper (Ankle) (Toothbrush)
Describe type of cues used if necessary:
2. Verbal Story for Immediate Recall:

Tell the patient, "1 am going to read you a short story, which
I want you to remember. Listen closely to what I read because I will ask you to tell me the story when I finish." Read
the story slowly and carefully, but without pausing at the
slash marks. After completing the paragraph, tell the patient
to retell the story as accurately as possible. Record the number of correct memories (information within the slashes)
and describe confabulation if it is present.
It was July / and the Rogers / had packed up / their four children
/ in the station wagon / and were off / on vacation.
They were taking / their yearly trip / to the beach / at Gulf Shores.
This year / they were making / a special/one-day stop / at the
Aquarium / in New Orleans.
After a long day's drive / they arrived / at the motel/only to
discover / that in their excitement / they had left / the twins /
and their suitcases / in the front yard.
189
a. Number of correct memories:

b. Describe confabulation if present:
3. Visual Memory (hidden objects):

Tell the patient that you are going to hide some objects
around the office, desk, or bed and that you want him or
her to remember where they are. Hide four or five common
objects (e.g., keys, pen, reflex hammer) in various areas in
the patient's sight. After a delay of several minutes, ask the
patient to find the objects. Ask patient to name those items
he or she is unable to find.
a. Number of hidden objects found: _ __
b. Number of hidden objects named but not found:
c. Number of locations indicated but objects not
named: _ __
4. Paired Associated Learning:
Tell the patient that you are going to read a list of words
two at a time. The patient will be expected to remember the
words that go together (e.g., big-little). When he or she is
clear as to the directions, read the first list of words at the
rate of one pair per second. After reading the first list, test
for recall by presenting the first recall list. Give the first word
of a pair and ask for the word that went with it. Correct
incorrect responses and proceed to the next pair. After the
first recall has been completed, allow a lO-second delay and
continue with the second presentation and recall lists.
PRESENTATION LISTS
a. House- Income
b. Weather-Box
c. Book-Page
d. High-Low
a. Weather-Box
b. High-Low
c. House-Income
d. Book-Page
RECALL LISTS
a. House _ __
b. High
c. Weather _ __
d.Book _ __
a. High
b.House _ __
c. Book _ __
d. Weather _ __
1. Number of easy paired associates recalled:

2. Number of difficult paired associates recalled:
190
*VI. Constructional Ability
*A. Reproduction drawings:

Ask the patient to copy the following drawings in the space
provided.
Item
1. Vertical diamond
2. Two-dimensional cross
3. Three-dimensional cube
4. Three-dimensional pipe
5. Triangle within a triangle
191
Score
Total score: _ _ _ __
*B. Drawings to Command:

Tell the patient to draw the following pictures in the space
provided.
Clock with all numbers
Set dock for 2:30 or 5 to 3.
192
Daisy in flowerpot
House in perspective
Item
1. Clock
2. Daisy in flowerpot
3. House in perspective
Total score:
Score
193
C. Block Designs:
(See stimulus cards)

Item
1. Design
2. Design
3. Design
4. Design
Score
1
2
3
4
Total score:
Describe types of errors:
*VII. Higher Cognitive Functions

A. Fund of Information:
Item
1. How many weeks are in a year?
2. Why do people have lungs?
3. Name four US Presidents since
Check If Correct
1940.
4. Where is Denmark?
5. How far is it from New York to
Los Angeles?
6. Why are light colored clothes
7.
8.
9.
10.
cooler in the summer than dark

colored clothes?
What is the capital of Spain?
What causes rust?
Who wrote the Odyssey?
What is the Acropolis?
Total score:
*B. Calculations:
Describe the patient's adequacy in performance and types of errors
made on the following types of calculations:
1. Verbal rote examples:
a. Addition
b. Subtraction
c. Multiplication
d. Division
(4 + 6)
(8 - 5)
(2 X 8)
(56 -7- 8)
194
2. Verbal complex examples:

a.
b.
c.
d.
Addition
Subtraction
Multiplication
Division
(14+17)
(43 - 38)
(21 X 5)
(128 -;-
8)
*3. Written complex examples:

a. Addition
108
+ 79
b. Subtraction
-
c. Multiplication
605
86
108
X 36
d. Division
43)s59
* C. Proverb Interpretation:
Tell the patient to explain the following sayings. Record the
answers.
Item
3. A drowning man will clutch at a

straw.
Score
195
4. A golden hammer can break down an

iron door.
5. The hot coal burns; the cold one

blackens.
Total score:
Total concrete responses:
* D. Similarities
Item
1. Turnip .................................. Cauliflower
2. Car ............................................. Airplane
3. Desk ......................................... Bookcase
4. Poem ............................................. Novel
5. Horse ............................................. Apple
Score
Total score:
Total concrete responses:
VIII. Related Cortical Functions

A. Ideomotor Apraxia:
Describe the adequacy of the patient's performance in carrying out

motor acts to command using buccofacial, limb, and whole body
commands. Indicate if imitation or use of the real object was necessary to facilitate performance.
Item
1. Blowout a match.
2. Drink through a straw.
3. Lick crumbs off your lips.
4. Comb your hair.
5. Flip a coin.
Score
E. Ideational Apraxia:
Describe the adequacy of the patient's performance on the following complex motor tasks:
1. Letter-envelope-stamp
2. Candle-halder-match
3. Toothpaste-toothbrush
196
C. Psychomotor speed (if indicated):
Ask patient to write the letters of the alphabet in

capitals.
Time in
Seconds
D. Right-Left Disorientation:
Item
1. Identification on self
a. Show me your right foot
b. Show me your left hand
2. Crossed commands on self
a. With your right hand touch your left
shoulder.
b. With your left hand touch your right
ear.
3. Identification on examiner
a. Point to my left knee.
b. Point to my right elbow.
4. Crossed commands on examiner
a. With your right hand point to my left
eye.
b. With your left hand point to my left
foot.
Check If Correct
Describe nature and degree of errors made:
E. Finger Agnosia:
Describe the adequacy of the patient's nonverbal and verbal
performance.
F. Gerstmann's Syndrome:
Describe the nature and degree of impairment in the following
areas if present in the patient:
1.
2.
3.
4.
Finger agnosia:
Right-left disorientation:
Dysgraphia:
Dyscakulia:
197
G. Visual Agnosia:
Describe any deficits in visual identification of objects, naming of
objects whose use can be demonstrated, color naming, and facial
recognition:
H. Astereognosis:
Describe deficits:
Left hand
Right hand _ _ _ __
I. Geographic Disorientation:
1. Describe evidence of disorientation obtained from history:
2. Map localization:
Describe patient's ability to localize well-known cities on a map:
3. Orientation of self in hospital:
Describe patient's ability to orient self within the hospital

environment:
* J. Denial and Neglect:

If present, describe patient's response.
l. Does patient frankly deny his illness?
2. Is there evidence of unilateral neglect?
(e.g., shaving one side of face, dressing one
arm, and so on)
3. Is there evidence of unilateral neglect on
drawings? (e.g., absence of numbers on one
side of dock or absence of one side of
picture)
Yes
No
198
K. Frontal Lobe Tests:
1. Drawings:
Tell the patient to copy and continue the following sequence.
Record evidence of perservation or loss of sequence.
2. Alternating hand sequences:

This is a motor alternation task that uses both hands. Initially,
the patient places both hands on the desk, one in a fist and
one with the fingers extended palm down. Tell the patient to
alternate the position of the two hands rapidly (simultaneously extending the fingers of one hand while making a fist
with the other). Record if the patient is unable to maintain
the alternating sequence.
SUMMARY OF FINDINGS
1. Describe major areas of impairment:
2. Tentative neurobehavioral diagnosis:
3. Tentative localization:
4. Tentative clinical diagnosis:
5. Proposed management plans:
INDEX
Page numbers followed by f indicate figures; those followed by t indicate tables.
Up:' random letter test, in attention
evaluation, 42-45, 170
Abnormal posturing, in preliminary
assessment, 11
Abstract thinking, in Alzheimer's disease, 148,
150t-152t
in higher cognitive functions, 117,

122-128, 124t
tests used to evaluate, 174-175

Academic achievement tests, 179 -180
Acalculia, 128
Acquired immunodeficiency syndrome,
dementia in, 137, 153
Acute confusional state See also Delirium
defined, 13
examination summary in, 153
Addition, in higher cognitive function testing,
119-120, 193-194
Agnosia, color, 141
finger, 138-139, 196
tactile, 141-142
visual, 140-141, 197
Agraphia, clinical features of, 68, 69[
defined,48
diagnosis of, 56
AIDS, dementia in, 137, 153
Akinetic mutism, apathetic, 35-36
defined, 35-36
diagnostic features of, 37t
Alertness, in akinetic mutism, 35-36
defined, 29-30
Alexia, clinical features of, 66-68, 67[
defined,48
Alternating motor patterns test, in frontal
lobe syndrome, 18-19
Alternating sequences test, in frontal lobe
syndrome, 18, 19[-201, 198
Alzheimer's disease, clinical features of, 147

aphasia as, 65
apraxia as, 13 7
depression and anxiety as, 4
inattention as, 44-45
memory deficits as, 79-80, 81t, 86-87, 89
constructional ability in, lIlt, 113
delirium versus, 15[
higher cognitive function in, 118t,
118-119, 124, 128
mental status examination summary in,
147 -148, 149t-152t
Ambidexterity, in language evaluation, 49
Amnesia, causes of, 86-87
defined, 76
Anarithmetria, 128
Animal-Naming Test, in language evaluation,
51-52,172
Anomia, defined, 54
Anomic aphasia, clinical features of, 63-64
evaluation of, 54-55, 55t
Anosognosia, 21
Anterior corpus callosum, in apraxia, 134, 134[
Anterior language area, in aphasia, 57 -58, 58[
Anterograde amnesia, causes of, 86-87
defined, 76
Anton's syndrome, 21
Anxiety, attention and, 45
in dementia, 162
memory deficits in, 74, 89
Apallic state, defined, 36
Apathetic akinetic mutism, defined, 35-36, 37t
Apathy, in frontal lobe syndrome, 16
in inattention, 44
in preliminary assessment, depression
versus, 23 - 25
199
200
INDEX
Aphasia, 57-65
acalculia in, 128
in Alzheimer's disease, 65
anomic, 63-64
Broca's, 59
clinical features of, 57-58, 58f
conduction, 61f, 61-62
course of, 57
crossed, 65
defined,48
global, 58-59
in language evaluation, 49-50
in left-handed persons, 64
memory testing in, 88
mental status examination indicated in,
2-3, 5
progressive, 65
psychiatric referral in, 162
subcortical, 64
tests used to evaluate, 172
transcortical, 62, 63f
Wernicke's, 59-60
Aphasic acalculia, 128
Aphasic speech, types of, 50
Aphonia, 71
Apperceptive visual agnosia, 140
Apraxia, buccofacial, 66, 131-132
constructional, 94
defined, 48, 94, 130
ideational, 135-137, 195
in dementia, 71
ideomotor, 131-135, 133f-134f, 195
language and, 132-135
limb, 131-132
verbal, 135
of whole body movements, 131-132
Arcuate fasciculus, in conduction aphasia,
61f, 61-62
Arithmetic, in higher cognitive functions,
127-128
testing of, 119-120, 121f, 122, 122t
Arousal, defined, 29
Articulation disturbances, 66
Associative visual agnosia, 140-141
Astereognosis, 141-142, 197
Attention, 40-45
anatomy and clinical implications of,
43-45
defined,40
evaluation of, 41-43
in higher cognitive functions, 116
neuropsychological tests of, 170
recording form for, 184-185
Behavioral disorders, after head injury,

18
depressive, 23-25
in frontal lobe syndrome, 16

3-6
in preliminary assessment, 9
Behavioral observations, in Alzheimer's
disease, 148
in preliminary assessment, 10-26
apathy versus depression in, 23-25
delirium in, 13-15, 14t, 15f
dementia versus depression in, 25-26,
26t
denial and neglect in, 21-22, 22f
frontal lobe syndrome in, 15-20,
19f-20f
mood in, 11-12
physical appearance in, 10-11
recording form for, 184
Bender Gestalt Test, of constructional ability,
177
Benton Visual Retention Test, 174
of constructional ability, 177
Best motor response, in Glasgow Coma Scale,
32t-33t
Best verbal response, in Glasgow Coma Scale,
32t-33t
Bilateral simultaneous stimulation test, in
attention evaluation, 42-43
Birth and developmental history, in
preliminary assessment, 9
Bizarre language output, clinical features of,
68-71
Blindness, denial of, 21
Block test, of constructional ability, cube
construction in, 96f, 98f, 101f, lIlt
design in, 105, 108, 109f-11Of, lIlt, 193
Boston Diagnostic Aphasia Examination,
172
Boston Naming Test, 171-172
Brain, aphasia and, 57-58, 58f
in apraxia, 132-135, 133f-134f
attention and, 43-45
consciousness and, anatomy in, 34
injury in, 34-36
in higher cognitive functions, 127-128
lesions of, attention and, 44
2
psychiatric symptoms of, 7-8
memory and, 85-86
in visual-motor integration, 112-113
Brain stem, consciousness and injury of,
34-36
Brain tumors, mental status examination
indicated in, 2
Broca's aphasia, clinical features of, 59
Broca's area, in aphasia, 58, 58f
Brodmann's area 44, in aphasia, 57, 58f
Buccofacial apraxia, 131-132
clinical features of, 66
INDEX
Calculations, in Alzheimer's disease, 148,

15lt-152t
in higher cognitive functions, 127-128
testing of, ll9-120, 121f, 122, 122t
California Auditory Verbal Learning Test,
173-174
Category Test, of abstract thinking, 167,
174-175
Cerebral dominance, in apraxia, 132-135,
133[-134[
in language disorders, 56-57
handedness and, 48-49
Cerebrovascular accidents, mental status
examination indicated in, 2
Children, constructional ability in, ll4
Christensen's adaptation of Luria's
techniques, in neuropsychological
testing, 167-168
Clinical syndromes See also specific
syndromes
Clock draWing test, of constructional ability,
97, 104, 105f, 108f, lllt
Closing in, in constructional ability tests, 98[
Clouding of consciousness, defined, 13
in differential diagnosis of delirium, 13
Clumsiness, in apraxia, 130
Cognitive change, subcortical, 137
Cognitive function disorders, apraxia as,
130-137, 133[-134[ See also Apraxia
astereognosis as, 141-142
finger agnosia as, 138-139
geographic disorientation as, 142-143
Gerstmann's syndrome as, 140
in organic brain syndromes, 8
in psychiatric illness, 8
right-left disorientation as, 137-138
subcortical cognitive change as, 137
visual agnosia as, 140-141
Cognitive functions, disorders related to,
130-144 See also Cognitive function
disorders
higher, ll7 -129 See also Higher cognitive
functions
tests of, 168-169
Cognitive rehabilitation, 163
Color agnosia, defined, 141
Coma, defined, 30
Glasgow Scale of, 32t-33t, 34
Coma vigil, defined, 36
Communication Abilities in Daily Living Test,
172
Comorbidity, in preliminary assessment, 8
Comprehension, in language evaluation,
52-53
201
Computed tomography, in suspected brain

lesions, 3
Concussion, amnesia after, 87
Conduction aphasia, clinical features of, 61 f,
61-62
Confabulation, 21
Consciousness, clouding of, defined, 13
in delirium, 13
defined,29
levels of, 29-38 See also Level of
consciousness
Constructional ability, 93 -ll4
in Alzheimer's disease, 148, 150t, 152t
anatomy of, ll2
clinical implications of, ll2-ll4
defined, 93
results of evaluation of, 109, lIlt, 112
tests of, 94-97, 96[-103f, 104, 105[-llOf,
108, 177 See also specific tests
Content of consciousness, defined, 29
Controlled Oral Word-Association Test, 172
Conversion disorder, defined, 38
Corpus callosum, in apraxia, 134, 134[
Cortex, in higher cognitive functions, 127
Cortical blindness, denial of, 21
Cortical dysfunction, constructional ability in,
ll2-ll4
in delirium, 14
Cross, in constructional ability tests, 96f, 98f,
100f, lllt
Crossed aphasia, clinical features of, 65
Cube test, of constructional ability, 96f, 98f,
101[, lllt
Data recording and interpretation, of
examination results, 153-155
Deafness, pure word, 65-66
Delirium, bizarre language output in, 70
as cause of inattention, 44-45
constructional ability in, ll4
medical causes of, 13-14
in preliminary assessment, 13-15, 14t, 15!
scale for assessing, 13-14, 14t, 15!
Dementia, Alzheimer type senile See
Alzheimer's disease
anxiety and depression in, 162
apraxia in, 137
bizarre language output in, 70
constructional ability in, lllt, 113 -ll4
depression versus, 4
memory testing and, 74, 89
higher cognitive function in, 1I8t,
ll8-ll9, 124, 128
memory deficits in, 74, 86-87, 89
immediate recall testing and, 85
202
INDEX
Dementia, Alzheimer type senile-Continued

mental status examination summary in,
147-148, 149t-152t, 153
in preliminary assessment, delirium versus,
14, 15f
depression versus, 25-26, 26t
prevalence of, 2
pseudodementia versus, 26, 26t
psychiatric referral in, 162
subcorticaL 13 7
Dementia of depression, defined, 27
Denial of illness, in preliminary assessment,
21-22

Depression, attention and, 45
criteria for diagnosing, 23-25
in dementia, 162
dementia versus, memory testing and, 74,
89
memory deficits in, 74, 89

in preliminary assessment, apathy versus,
23-25
dementia versus, 25-26, 26t

as symptom of brain disease, 3-4
Depressive dementia, defined, 27
Developmental aphasia, defined, 48
Diagnosis, examination data in, 154
Diagnostic and Statistical Manual of Mental
Disorders, organic brain syndromes
categorized in, 1
Diamond, in constructional ability tests, 96f,
99f, 111t
Digit repetition test, in attention evaluation,
41-42, 170
of immediate recall, 77, 85

Digit Symbol Modalities Test, of visual motor
sequencing, 178
Disconnection syndromes, conduction
aphasia as, 62
Disinhibition, in frontal lobe syndrome,
16-17
Disorientation, geographic, 142-143, 197

right-left, 137-138
Dissociative state, memory deficits in, 90
Distractibility, defined, 40
postencephalitic, 44
Division, in higher cognitive function tests,
193-194
Dominant hemisphere lesions, examination

summary in, 153
Double simultaneous stimulation test, in
attention evaluation, 42-43
Drawing ability See Constructional ability
Drawings to command test, of constructional
ability, 97,104, 105f-108f, 11It
Dress, in preliminary assessment, 11

Dynamometer, hand, 179
Dysarthria, clinical features of, 66
defined, 47
Dyscalculia, 127-128
in Gerstmann's syndrome, 140
Dysfluency, clinical features of, 66
Dysgraphia, in Gerstrnann's syndrome, 140
Dyspraxia, sympathetic, 134
Dysprosody, defined, 47-48
Dysthymia, criteria for diagnosing, 25
in preliminary assessment, apathy versus,
23-25
Echolalia, in transcortical aphasia, 62

Economo's disease, 44
Educational level, in higher cognitive
function testing, 118, 124, 126
in preliminary assessment, 8, 10
Elderly patients, depression versus dementia
in, 25-26
Elective mutism, 71
Emotional status, defined, 11
memory and, 74, 89
Encephalitis, brain lesions mistaken for, 3
Encephalitis epidemic of 1918 to 1921, 44
Encephalopathy, amnesia from, 86
toxic-metabolic, 13 See also Delirium
Euphoria, in frontal lobe syndrome, 16
Expressive aphasia, defined, 58
Extinction, in attention evaluation, 43
Eye movement, in akinetic mutism, 35-36
Eye opening, in Glasgow Coma Scale,
32t-33t
Face-Hand Test, in attention evaluation, 43
Family history, in preliminary assessment,
10
FAS Test, in language evaluation, 51-52

Finger agnosia, 138-139, 196
in Gerstmann's syndrome, 140, 196
Finger-Tapping Test, of motor coordination
and strength, 167, 178
Fixed battery testing in neuropsychology,
comprehensive, 167-168
flexible versus, 167
tests used in, 168-180
Flexible battery testing in neuropsychology,
fixed versus, 167
Flowerpot drawing test, of constructional
ability, 97, 104, 106f, llIt
INDEX
Fluency, verbal, in language evaluation,

51-52
tests of, 172
Fluent aphasic speech, defined, 50

Forensic neuropsychology, 159
Four Unrelated Words Test, of memory,
80-81, 8lt, 90
Frontal lobe, in higher cognitive functions,
127
memory and, 86
Frontal lobe syndrome, alternating motor
patterns test in, 18-19
case histories of, 16-17
differential diagnosis of, l7-18
in preliminary assessment, 15-20, 19f-20f
visual pattern completion test in, 18,
19f-20f
Fugue state, memory deficits in, 90
Functional memory disturbances, clinical
implications of, 89-90
Fund of information test, of higher cognitive
functions, 117-119, 118t
Ganser's syndrome, clinical features of, 90
Geographic disorientation, 142-143, 197
Geriatric medicine, neuropsychological
evaluation in, 158
Gerstrnann's syndrome, 140, 196
dyscalculia in, 128
Glasgow Coma Scale, 32t-33t, 34
Global amnesia, transient, 87-88
Global aphasia, clinical features of, 58-59
Grasp reflexes, in apraxia, 130
Grip strength, in motor coordination and
strength testing, 179
Grooved Pegboard, in motor coordination
and strength testing, 178-179
Habits of dress, in preliminary assessment, 11
Hallucinations, illnesses associated with, 15
Halstead-Reitan battery, in
neuropsychological testing, 166-167
Hand dynamometer, in motor coordination
and strength testing, 179
Hand position test, in frontal lobe syndrome,
18-19, 198
Handedness, cerebral dominance and, 56-57

Head injury, amnesia after, 87
behavioral disorders after, 18
consciousness disturbances after, 34-36,
38
Glasgow Coma Scale in, 34
203
mental status examination indicated in, 2,

5-6
neuropsychological evaluation in, 158-159

Hemiparesis, denial of, 21
Higher cognitive functions, 117-129
anatomy of, 127-128
clinical implications of, 128
calculations in, 119-120, 121f, 122, 122t
fund of information test in, 117-119,
118t
insight and judgment testing in,
126-127
proverb interpretation in, 122-125, 124t

verbal similarities test in, 125-126
Historic events, in memory testing, 77-79
History, in attention evaluation, 41
in geographic disorientation, 142
in preliminary assessment, 7 -1 0
outline in, 9-10
Hooper Visual Organization Test, of
constructional ability, 177
Hospital orientation, in geographic
disorientation, 143, 197
House in perspective drawing test, of
constructional ability, 97, 104, 107/,
lIlt

Hyperactivity, postencephalitic, 44
Hypothalamus, consciousness and injury of,
35
Hysterical comalike state, defined, 38

Ideational apraxia, 135-137
in dementia, 71
Ideomotor apraxia, clinical implications of,
132-135, 133f-134f
Immediate recall, clinical implications of,
84-85
defined, 75
evaluation of, 77
Impairment, constructional, 94 See also
Constructional ability
Implicit memory, defined, 80
Inappropriate behavior, in frontal lobe
syndrome, 16-17
Inattention, defined, 40
in immediate recall testing, 85
as neglect syndrome, 21-22
unilateral, 42-43
Incidental memory, defined, 75
204
INDEX
Indifference, in inattention, 44-45

Infarcts, in transcortical aphasia, 62, 63[
Infections, brain lesions mistaken for, 3
Information fund, in higher cognitive
functions, 117
Insight, defined, 126
testing of, 126-127
Intellectual functioning, tests of premorbid,
169-170
Intelligence See also Higher cognitive

functions
constructional ability and, 114
memory testing and, 88
Wechsler test of, 168-169
Intelligence quotients, 169
Irritability, in akinetic mutism, 36
in frontal lobe syndrome, 16-17

terminology in, 47-48
Left hemisphere lesions, inattention in, 45
Left-handedness, aphasia in, 64
cerebral dominance and, 56-57
in language evaluation, 49
Lethargy, defined, 30
patients' responses in, 31t, 32
Letter and symbol cancellation tasks, in
attention testing, 170
Level of consciousness, 29-38
in Alzheimer's disease, 147-148
anatomy and clinical implications of,
34-38, 37t
categories of, 29
in dementia, 147-148
terminology and evaluation of, 29-34,
31t-33t
Jargonaphasia, defined, 50
Judgment, defined, 126
testing of, 126-127
Knowledge fund, in higher cognitive
functions, 117
Kohs blocks, 104
Korsakoff's syndrome, amnesia in, 86-87
Language, 47- 72
in Alzheimer's disease, 148, 149t, 152t
clinical implications of, 56-71
in agraphia, 68, 69[
in alexia, 57! 66-68
in aphasia, 57-65 See also Aphasia
in apraxia, 132-135
articulation disturbances, 66
cerebral dominance, 56-57
in nonorganic speech and language
disorders, 71
in psychotic language, 69-71
in pure word deafness, 65-66
comprehension in, 52-53
handedness in, 48-49
naming and word finding in, 54-55, 55t
protocol for, 4
reading in, 55-56
repetition in, 53-54
spelling in, 56
spontaneous speech in, 49-51
verbal fluency in, 51-52
writing in, 56
nonorganic disorders of, 71
Limb apraxia, 131-132

Limbic system, attention and, 43-44
memory and, 85-88
Limb-kinetic apraxia, defined, 130-131
Literal paraphasia, defined, 50
Litigation, neuropsychological evaluation and,
159
Localization on map test, in geographic

disorientation, 142-143, 197
Localized amnesia, 90
Locked-in syndrome, defined, 36
Luria-Nebraska battery, in neuropsychological
testing, 167-168
Luria's investigation, in neuropsychological
testing, 167-168
Magnetic resonance imaging, in suspected
brain lesions, 3
Malingering, memory deficits in, 90
Map localization test, in geographic
disorientation, 142-143, 197
Mathematics, in higher cognitive functions,
127-128
testing of, 119-120, 121! 122, 122t

Maturation, constructional ability and, 114
Medication, memory testing and, 88
Memory, 74-91
in Alzheimer's disease, 148, 149t-150t, 152t
clinical implications of, 85-90
in functional disturbances, 89-90
immediate recall, 84-85
recent, 85-89
remote, 89
defined, 75
immediate recall, 77
INDEX
new-learning ability, 79-84, 8lt-82t

patient factors in, 77
recent, 78
remote, 78-79
stages of, 75
terminology of, 75-76
tests used in, 172 -1 74
types of questions in, 76-77
Memory Assessment Scales, 173
Memory deficits, mental status examination
indicated in, 2
Memory for Designs Test, 174
Mental functioning, assessment of premorbid,
8
in delirium, 14-15
Mental status examination, indications for,
2-4
overview of, 1-6

protocol for, 4-6
summary of, 146-155
in acute confusional state, 153
in AlDS dementia, 153
in Alzheimer's disease, 147-148,
149t-152t
data interpretation in, 153-155

in dominant hemisphere lesions, 153
Midbrain lesions, symptoms of, 34-36
Minnesota Multiphasic Personality Inventory,
180
Mood, attention and, 45

defined, 11
in depressive disorders, 23-25
Motor activity, in preliminary assessment, 11
Motor area, in apraxia, 133, 133f
Motor commands, in comprehension
evaluation, 53
Motor coordination and strength, tests of,
178-179
Motor function, in apraxia, 130-135 See also

Apraxia
Motor planning defect, apraxia as, 130
Motor response, in Glasgow Coma Scale,
205
Neglect, in preliminary assessment, 21-22,
22f

Neologisms, in psychotic language, 70
Neologistic paraphasia, defined, 50
Neurobehavioral disorders, defined, 1
Neurologic diseases, memory deficits in,
74
Neuropsychology, assessment methods in,

166-180
abstraction and higher cognitive function

tests in, 174-175
academic achievement tests in, 179-180
attention and vigilance tests in, 170
cognitive functioning tests in, 168-169
comprehensive fixed battery, 167-168
constructional ability tests in, 177
fixed battery versus flexible, 166-167
language functioning tests in, 171-172
Luria's, 168
memory tests in, 172-174
motor coordination and strength tests in,
178-179
personality tests in, 180

premorbid intellectual functioning
measures in, 169-170
sensory-perceptual functioning tests in,
175-176
visual motor sequencing tests in, 177-178

evaluation by, 157 -160
contributions of, 159-160
purpose of, 158
referral to, 158-159
forensic, 159
training required in, 157
Neurosensory Center Comprehensive
Examination for Aphasia, 172
Neurosis, speech disorders in, 71
New-learning ability, evaluation of, 79-84
Nondominant hemisphere lesions,
examination summary in, 153
in neglect syndrome, 23
Nonfluent aphasic speech, defined, 50
32t-33t
Multilingual Aphasia Examination, 172

Multiple infarct dementia, constructional
ability in, 113-114
Multiplication, in higher cognitive function
testing, 119-120, 1211, 193-194
Mutism, akinetic, 35-36, 37t
elective, 71
Naming, in anomic aphasia, 63-64
in language evaluation, 54-55, 55t
Obtundation, defined, 30
patients' responses in, 32
Organic brain syndromes, abstract thinking
impairment in, 128
defined, 1
prevalence of, 1-2
psychiatric illness in, 161-162
psychiatric illness versus, 3-4, 7-8
Organic driveness, postencephalitic, 44
Orientation, clinical implications of, 85-89
evaluation of, 78
recording form for, 187, 197
206
INDEX
Paced auditory serial addition test, 170-171

Paired associate learning, recording form for,
189
testing o 83-84
Paramnesia, 21
Paraphasia, defined, 50
Parietal lobe, in acalculia, 128
in geographic disorientation, 143
in visual-motor integration, 112-113
Patient information, recording form for, 183
Peabody Picture Vocabulary Test, 171
Perseveration, in constructional ability tests,
98f
in inattention, 44-45
Persistent vegetative state, diagnostic features
of, 37t
Persistent vegetative states, defined, 35-36
Personal cleanliness, in preliminary
assessment, 11
Personality tests, 180
Phonemic paraphasia, defined, 50
Physical appearance, in preliminary
assessment, 10-11
Pick's disease, symptoms o 17
Pipe, in constructional ability tests, 96f 102f
lIlt

Posterior language area, in agraphia, 68, 69f
in aphasia, 57, 58f
Posttraumatic stress disorder, memory deficits
in, 90
Praxis, constructional See Constructional
ability
defined, 93
Premorbid intellectual functioning,
neuropsychological tests o
169-170
Premorbid mental functioning, assessment o
8
Prognosis, neuropsychological evaluation and,
160
Progressive aphasia, clinical features o 65
Prosopagnosia, defined, 141
Proverb interpretation test, in Alzheimer's
disease, 148, 151t-152t
of higher cognitive functions, 122 -125,
124t

Pseudodementia, defined, 8, 26
dementia versus, 26, 26t
depression in, 4
Psychiatric illness, memory deficits in, 74
2-3
in organic brain syndromes, 161-162
organic illness versus, 3-4, 15
in preliminary assessment, 9
Psychiatry, referral to, 161-162
Psychogenic amnesia, 90
defined, 76
Psychogenic unresponsiveness, defined, 38
Psychotic language, clinical features o 68 - 71
Psychotropic drugs, memory testing and, 88
Pure word deafness, 65-66
Rancho Los Amigos Scale, 34
Raven's Progressive Matrices, in abstract .
thinking evaluation, 175
in constructional ability evaluation, 177
Reading. disorders o 48, 55-56, 66-68, 67f
Recall. as component of memory, 75
Recent memory, clinical implications of.
85-89
defined, 75
evaluation of, 78
Receptive aphasia, defined, 58
Reduplication of body parts, 21
Referrals, to cognitive rehabilitation, 163
to neuropsychology, 158-159
to psychiatry, 161-162
to social work 163
to speech pathology, 161
Rehabilitation, cognitive, 163
neuropsychological evaluation for, 158
Rancho Los Amigos Scale in, 34
Remote memory, clinical implications of, 89
defined,75
Repetition, in conduction aphasia, 61
Reproduction drawings, in constructional
ability tests, 95-97, 96f 98f-103f
Retrieval of information, as component of
memory, 75
Retrograde amnesia, causes of. 86-87
defined, 76
Rey Auditory Verbal Learning Test, 173-174
Right hemisphere lesions, inattention in, 45
Right-handedness, cerebral dominance and,
56-57
Right-left disorientation, 137-138, 196
in Gerstmann's syndrome, 140, 196
Rotation, in constructional ability tests, 98f
Schizophrenia, abstract thinking impairment
in, 128
bizarre language output in, 68-70
cognitive dysfunction in, 8
delirium versus, 15
head injuries in, 162
INDEX
Seashore Rhythm Test, of sensory-perceptual

functioning, 167, 175-176
Semantic paraphasia, defined, 50
Semicoma, defined, 30
Senile dementia Alzheimer type See
Alzheimer's disease
Sensory input, as component of memory,
75
Sensory-perceptual functioning, tests of,
175-176
Septal rage, defined, 36
Short-term memory, clinical implications of,
84-85
defined,75
evaluation of, 77
Similarities test, in Alzheimer's disease, 148,
15lt-152t
of higher cognitive functions, 125-126

Sleep, as testing factor, 38
Social awareness, in higher cognitive
functions, 117, 126-127
Social inappropriateness, in frontal lobe
syndrome, 16-17
Social work, 163
Somatoform disorder, defined, 38
Somatoform disorders, psychiatric referral in,
162
Somnolence, defined, 30
Speech, aphasic, 50-51 See also Aphasia
disorders of, nonorganic, 71
speech pathology in, 160
spontaneous, in language evaluation,
49-50
Speech pathology, referral to, 161
Speech Sounds Perception Test, 167, 176
Spelling, in language evaluation, 56
Spontaneous speech, in language evaluation,
49-50
Stereognosis, defined, 141
Storage of information, as component of
memory, 75
Stupor, defined, 30
patients' responses in, 3lt, 32
Subcortical aphasia, clinical features of, 64
Subcortical cognitive change, 137
Subtraction, in higher cognitive function
testing, 119-120, 121f 193-194
Sustained attention, evaluation of, 42
Sympathetic dyspraxia, defined, 134
Tactile agnosia, 141-142
Tactile perception testing, 176
Tactual Performance Test, 167
Temporal lobes, in amnesia, 86-87
Thalamus, consciousness and injury of, 35
207
Thinking, abstract See also Abstract thinking

in higher cognitive functions, 117,
122-128, 124t
Three-dimensional block, in constructional

ability tests, 96f 98/, 101f lIlt
Three-dimensional pipe, in constructional
ability tests, 96f 102f lIlt
Token Test, 171
Trail-Making Test, of visual motor
sequencing, 177 -178
Transcortical aphasia, clinical features of, 62,
63/
Transient global amnesia, 87-88
Trauma, amnesia after, 87
behavioral disorders after, 18
mental status examination indicated in, 2,
5-6
neuropsychological evaluation in, 158-159
Triangles within a triangle, in constructional
ability tests, 96f 103f lIlt
Tumors, mental status examination indicated
in, 2
Two-dimensional cross, in constructional
ability tests, 96/, 98f 100f lIlt
Unilateral inattention, evaluation of, 42-43
Unresponsiveness, psychogenic, 38
Vascular accidents, mental status examination
indicated in, 2
Vascular disorders, neglect syndrome in, 23
symptoms of brain, 35-36
Vegetative states, persistent, 35-36, 37t
Verbal apraxia, defined, 48, 135
Verbal fluency, in language evaluation, 51-52
tests of, 172
Verbal paraphasia, defined, 50
Verbal response, in Glasgow Coma Scale,
32t-33t
Verbal similarities test, in Alzheimer's disease,

148, 15lt-152t
of higher cognitive functions, 125-126

Verbal story recall, in memory testing, 81 t,
81-82
Vertical diamond, in constructional ability
tests, 96f 99f lIlt
Vigilance, defined, 40
neuropsychological tests of, 170
Visual agnosia, 140-141, 197
Visual cortex, in alexia, 67, 67/
Visual memory, recording form for, 189
testing of, 83
208
INDEX
Visual motor sequencing, tests of, 177-178

Visual pattern completion test, in frontal lobe
syndrome, 18, 19f-20f, 198
Visual perception testing, 176
Visuoconstructive ability See Constructional
ability
Wada test, of cerebral dominance, 57
Wechsler Adult Intelligence Scale, 167-169
Wechsler Memory Scale, 172-173
Wernicke's aphasia, clinical features of, 59-60
Wernicke's area, in aphasia, 57
Western Aphasia Battery, 172
Whole body movement apraxia, 131-132

Wide-Range Achievement Test, 179
Wisconsin Card-Sorting Test, of abstract
thinking, 175
Woodcock-Johnson Psychoeducational
Battery, academic achievement
measured by, 179 -180
Word finding, in language evaluation, 54-55,
55t
Word recall, in memory testing, 80-81, 81t
Writing, disorders of, 48, 68, 69f
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THE MENTAL STATUS

F. William Black, PhD

Foreword by Norman Geschwind

F. A. DAVIS COMPANY. Philadelphia

1915 Arch Street

THE MENTAL STATUS EXAMINATION IN NEUROLOGY

THE MENTAL STATUS EXAMINATION IN NEUROLOGY

THE MENTAL STATUS EXAMINATION: A RATIONALE

HISTORY AND BEHAVIORAL OBSERVATIONS ........................................ 7

LEVELS OF CONSCIOUSNESS ............................................................... 29

CONSTRUCTIONAL ABILITY ................................................................. 93

HICHER COCNITIVE FUNCTIONS ........................................................ 116

RELATED COCNITIVE FUNCTIONS ................................. 130

SUMMARY OF EXAMINATION ........................................................... 146

FURTHER EVALUATIONS ................................................................... 157

STANDARD NEUROPSYCHOLOCICAL ASSESSMENT

MENTAL STATUS EXAMINATION RECORDINC FORM ............. 183

THE MENTAL STATUS

THE MENTAL STATUS EXAMINATION IN NEUROLOGY

WHEN SHOULD A MENTAL STATUS EXAMINATION

Known Brain Lesions

THE MENTAL STATUS EXAMINATION: A RATIONALE AND OVERVIEW

suspected Brain Lesions

THE MENTAL STATUS EXAMINATION IN NEUROLOGY

Although the differentiation between psychiatric and organic disease is

vague Behavioral Complaints

HOW SHOULD A MENTAL STATUS

THE MENTAL STATUS EXAMINATION: A RATIONALE AND OVERVIEW

formed in a haphazard manner, without regard for the hierarchic nature of

THE MENTAL STATUS EXAMINATION IN NEUROLOGY

Most sections of the mental status examination involve the evaluation of

THE MENTAL STATUS EXAMINATION IN NEUROLOGY

HISTORY AND BEHAVIORAL OBSERVATIONS

1. Description of present illness

THE MENTAL STATUS EXAMINATION IN NEUROLOGY

6. Educational and vocational history

HISTORY AND BEHAVIORAL OBSERVATIONS

Mood and General Emotional status

THE MENTAL STATUS EXAMINATION IN NEUROLOGY

HISTORY AND BEHAVIORAL OBSERVATIONS

marily involve disturbances in mood, personality, and emotional reaction

Acute Confusional state (Delirium)

THE MENTAL STATUS EXAMINATION IN NEUROLOGY

3 is normal; 0 is grossly abnormal.

HISTORY AND BEHAVIORAL OBSERVATIONS

Frontal Lobe Syndrome

THE MENTAL STATUS EXAMINATION IN NEUROLOGY

HISTORY AND BEHAVIORAL OBSERVATIONS

The next case demonstrates the disinhibition, social inappropriateness,

If the behavioral manifestations of the frontal lobe syndrome are present,

THE MENTAL STATUS EXAMINATION IN NEUROLOGY

Alternating Sequences-Visual Pattern

Present the patient with the visual patterns from Figure

stimulus figure and then to continue the alternating sequence. If necessary,

Alternating Motor Patterns Test

HISTORY AND BEHAVIORAL OBSERVATIONS

FIG U R E 2 - 2. Test items for the Visual Pattern Completion Test.

perform the task until told to stop. Performance for 15 to 20 seconds

THE MENTAL STATUS EXAMINATION IN NEUROLOGY

FIG U R E 2 - 3. Common errors in the Visual Pattern Completion Test.