Psych 130- Exam 2 Study Guide

Lecture Notes:

Lecture 13: ✅
Depressive Disorders:

Prevalence of depressive disorders:

- 20% of the population experiences depression
- MDD most common (16% ‘common cold of mental illness’)
- Persistent depressive disorder is new, so we don’t know, but an equivalent DSM IV
disorder is rare (2.5%)
- Prevalence varies across cultures
- 2:1 females : males

Etiology of Depression:
1. Diathesis / stress (most critically)
2. Predisposition (genes / neurobiology / cognitive style)
3. Triggering stressor

Gene / environment interaction:

- Caspi et al. 2003: in short allele (5HTT genotype) carriers, childhood maltreatment
increased likelihood of MDD, but the same isn’t true for long (l/l) allele carriers.

Commonalities & Comorbidity with Anxiety:

- High comorbidity, esp with GAD, PTSD
- Elevated neuroticism scores in both DD and AD (common genetic factor?)

Cognitive Theories:
1. Aaron Beck (1967) — Negative Triad Theory
a. Depression is caused by maladaptive thought processes.
i. Negative triad: negative views of self, world, and future
ii. Acquired as a result of negative experiences in childhood which led to
negative schemata which, when reactivated by related events, leads to
negative cognitive biases.
iii. Negative experiences -> negative triad -> negative schemata -> negative
cognitive biases (-> negative triad…) = depression

b. Cognitive errors (reinforce negative schemata)

i. Arbitrary interference: conclusion is drawn in the absence of sufficient
evidence
ii. Selective abstraction: conclusion is drawn on the basis of just one
element in a situation
 iii. Overgeneralization: conclusion is drawn on the basis of a single, trivial
event

c. Evidence for theory:

i. Depressed people:
1. Do show cognitive biases
2. Cognitive biases decrease significantly after treatment
3. Have negative automatic thoughts
4. Recall more negative information
5. Recall their own errors more than their correct answers

d. Evidence against theory:

i. Depressed people are more accurate in estimating likelihood of success
(non-depressed people overly optimistic)
ii. Negative thoughts are correlated with, but do not necessarily cause,
depression
1. Depression could cause negative thoughts
2. Longitudinal studies needed to demonstrate causality

2. Seligman (1974) — Helplessness, Hopelessness, and Attributional Style

a. Learned helplessness:
i. Uncontrollable aversive events -> sense of helplessness -> depression
b. Problem: not everyone who experiences an aversive event experiences
helplessness

3. Abramson, Teasdale, and Seligman (1978) — Attribution Theory

a. Negative events can be explained (‘attributed’) in different ways
i. Global vs specific
ii. Stable vs unstable
iii. Internal vs external factors
b. The pathological combination -> depression
c. Attributional reformulation:
i. Aversive events -> attribution to global and stable factors -> sense of
helplessness; no response available to alter the situation -> depression

d. Evidence for theory:

i. Internal, global, stable attributional style found in depressed people more
often than in controls
ii. Attributional style changes after treatment
iii. Cognitive therapy: attempts to change the person’s attributional style /
interpretations drawn
 e. Some studies suggest that Attributional Style is not a reliable predictor of MDD
onset.

4. Abramson et al. (1989) — Hopelessness Theory

a. Hopelessness:
i. Aversive events -> attribution to global and stable factors; or other
cognitive factor -> sense of hopelessness; no response available to alter
the situation and an expectation that desirable outcomes will not occur ->
depression
b. Theory allows the possibility that there are other routes to depression!

c. Empirical Evidence:
i. Metalsky et al (1993):
1. Students taking Intro to Psychology completed the ‘Attributional
Style’ questionnaire and other questionnaires assessing grade
aspirations, self esteem, hopelessness, and depressive
symptomatology
2. They were then given a test, and the students whose grades were
below expectations AND who attributed this to global and stable
factors experienced more hopelessness and depressive
symptomatology
3. This was ONLY true for students with low self esteem

Cognitive Biases in depression:

- Some shared with anxiety
- Judgement biases (future likelihood of negative events)
- Interpretive biases (die/dye, for example)
- Unique to depression:
- Memory recall: more negative, less positive

- Major Depressive Disorder (MDD)

- Psychological symptoms, biological symptoms, behavioral symptoms (some
overlap)
- Sad mood or loss of pleasure in usual activities + 4 additional symptoms of
following:
- Difficulties in sleeping
- Change in appetite or weight loss
- Loss of energy
- Agitation or psychomotor retardation
- Feelings of worthlessness or excessive guilt
- Difficulty concentrating, thinking, or making decisions
- Recurrent thoughts of suicide or death
 - Symptoms are present nearly every day, most of day, for 2+ weeks
- Symptoms are distinct and more severe than normative response to significant
loss
- Episodic disorder (symptoms tend to be present for a period of time and then
clear)
- Untreated episodes can last 5 months + and subclinical symptoms can last years
- Episodes are recurrent
- 66% of people who experience one episode will have a second, and from there
every new episode will increase the risk of another episode. Average number is 4

Neurobiology:
- Current thinking is that individuals with MDD may have less sensitive serotonin receptors
- They may also have altered dopamine receptor function
- Dopamine thought to play a key role in brain reward system
- Dysfunction of the DA system might account for deficits in pleasure, motivation,
energy in MDD (Treadway & Zald, 2011)
- MDD is associated with:
- Increased amygdala activity to negative stimuli (e.g. negative words or faces) —
Siegle et al 2002, 2007
- Decreased dorsolateral prefrontal cortical activity when doing cognitive tasks,
regulating response to emotional stimuli
- Also, decreased hippocampal activity.

- Persistent Depressive Disorder

- Depressed mood most of the day for more than half the time for 2 years + 2 other
symptoms:
- Poor appetite, overeating
- Sleeping too much/little
- Low energy
- Low self-esteem
- Trouble concentrating/making decisions
- Hopelessness
- Symptoms do not clear for more than 2 months at a time
- Bipolar disorders are not present
-

Lecture 14:

Treatments for MDD:

1. Pharmacological treatments
a. Tricyclic antidepressants (discussed below)
b. MAO inhibitors
i. The monoamine hypothesis:
 1. Depletion in the levels of monoamine neurotransmitters (serotonin,
norepinephrine/adrenaline, and/or dopamine) underlies
depression
2. 1950s: accidental discovery that MAOIs (TB) and tricyclics
(imipramine — sedative) had side effects of improving patients’
mood; thus these drugs were introduced as the first real
treatments for depression in the 1950s.
3. 1990s saw success of SSRIs

c. SSRIs (selective serotonin reuptake inhibitors)

i. 5HT-transporter re-absorbs any excess serotonin in the synaptic cleft;
SSRIs inhibit the activity of 5HT-transporters
ii. Pharmacological treatment of choice!
iii. Better than placebo?
iv. Side effects: suicide/ mania

Problems with Pharmacotherapy:

- Side effects
- Compliance necessary
- Low response rates versus placebo
- 50% of patients who recover through medication relapse within 2 years (Angst 1988) and
patients must be maintained on meds for more than 6 months

2. Electroconvulsive therapy
a. Reserved for:
i. Severe depression with high risk of suicide
ii. Depression with psychotic features
iii. Treatment non-responders
b. Induces brain seizures by passing electrical current through the skull
c. Side effects:
i. Memory loss
ii. Long term effects… associated with deficits in cognitive functioning 6
months after treatment (Sackeim, Prudic, Fuller, et al., 2007)
3. Psychotherapy
a. Cognitive Behavioral Therapy (CBT)
i. Cognitive therapy:
1. Aims to alter maladaptive thought patterns
2. To identify and challenge negative automatic thoughts; behavioral
tests ‘to disconfirm negative beliefs’; other behavioral components
to increase positive experiences
ii. Behavioral activation
iii. Process:
1. precisely identify the belief/thought/process
 2. Brainstorm ideas for an experiment to test the thought/belief (very
specific)
3. Make predictions about the outcome & devise a method to record
the outcome
4. Anticipate problems and brainstorm solutions
5. Conduct the experiment
6. Review the experiment and draw conclusions

b. Interpersonal (IPT)
i. Focuses on identifying and resolving current interpersonal problems (role
transitions, interpersonal conflicts, bereavement, interpersonal isolation)
c. Psychodynamic

Do drugs beat psychotherapy or vice versa?

● NIMH Treatment of Depression Collaborative Research Program (Elkin et al., 1985)
○ 240 patients with MDD randomly allocated to
■ Cognitive therapy vs interpersonal therapy vs tricyclic medication
(imipramine) vs placebo for 16 weeks
● Medication more effective than psychotherapy early in the
treatment
● With less severe MDD, placebo as effective as all other treatments
● With more severe MDD, imipramine more effective than all other
treatments, IPT but not CT better than placebo
● Only 20-30% symptom free 18 months later
○ Note: these analyses don’t take into account 33% medication groups dropped out
before completing treatment. Also there’s the issue that different sites had
different levels of expertise in the CT treatment provided

Lecture 15:

Bipolar Disorders:
1. Bipolar I
a. Diagnostic criteria:
i. At least one manic episode
ii. Not better explained by schizophrenia or related (schizophrenia spectrum)
disorder during lifetime
b. Most also experience depressive episodes— 50% experience 4+ episodes

2. Bipolar II
a. Must have experience at least one major depressive episode and one episode
HYPOmania (current or past)

Mania vs Hypomania:
 Manic episode: Hypomanic episode:

● Elevated, expansive, or irritable mood ● Elevated, expansive, or irritable mood

most of the day, every day most of the day, every day
● Abnormally increased activity or ● Abnormally increased activity or
energy energy
● PLUS increase from baseline in 3 of ● PLUS increase from baseline in 3 of
the following (4 if mood is irritable) the following (4 if mood is irritable)
○ Psychomotor agitation or ○ Psychomotor agitation or
increase in goal-oriented increase in goal-oriented
behavior behavior
○ Usual talkativeness ○ Usual talkativeness
○ Flights of ideas; racing ○ Flights of ideas; racing
thoughts thoughts
○ Reduced need for sleep ○ Reduced need for sleep
○ Grandiosity or inflated self ○ Grandiosity or inflated self
esteem esteem
○ Easily distractible ○ Easily distractible
○ Excessive involvement in ○ Excessive involvement in
activities with probable activities with probable
negative consequences negative consequences
● Symptoms for 1 week or more, OR ● Symptoms for 4 or more days
require hospitalization ● Change in function (& mood)
● Symptoms cause functional observable to others but
impairment or require hospitalization impairment not marked and
or psychotic features are present hospitalization not required. No
psychotic symptoms.

3. Cyclothymic disorder (cyclothymia)

a. Milder symptoms, chronic mood disorder
b. Symptoms present for at least 2 years
c. Periods of hypomania and depression
d. Differs from bipolar II in that periods of depressive symptomatology do not meet
criteria for major depressive disorder
e. Symptoms do not clear for more than 2 months at a time
f. Symptoms cause significant distress or functional impairment

Epidemiology:
● Prevalence rates lower than MDD:
○ 0.6 - 1% for Bipolar I
○ 0.4 - 2% for Bipolar II
○ ~4% for cyclothymic disorder
● Average age of onset in late teens/ 20s
 ● No gender differences in prevalence, but more depressive symptoms in women
● Comorbid with anxiety disorders (66%) and substance abuse (more than 33%)

Consequences:
- Distress / functional impairment:
- 33% unemployed one year after hospitalization (Harrow et al., 1990)
- Unemployed ~ 25% of the time
- 25% BP I and 20% BP II report history of suicide attempts (Merikangas et al.,
2011)
- Actual suicide rates high (Angst et al., 2002)
- High risk for other medical conditions (2x as likely to die from medical illness in a
given year, (Osby et al., 2001)) — heart disease, thyroid disease, diabetes,
obesity

Genetics:
- Among the most heritable of disorders:
- 85% heritability estimate (McGuffin et al., 2003)
- 93% (Kieseppa er al., 2004)
- Little success in identifying the specific genes — many non replications
- Why? It’s likely a polygenic disorder, gene x gene and gene x environment
interactions

- Neurotransmission
- Dopamine important in process reward (nucleus accumbens and frontal cortex)
- Nucleus accumbens activity increased in mania, elevated reward sensitivity
reported in BP
- Serotonin — processing threat (amygdala)
- DA and 5HT modulation of frontal function also influences impulsivity
- Original models
- Depression: low levels of norepinephrine, dopamine, and serotonin
- Mania: high levels of NE, dopamine, low levels of serotonin
- New models
- Focus on sensitivity of postsynaptic receptors
- In bipolar disorders, Increased sensitivity of dopamine receptors (Anand
et al. 2000), and decreased of serotonin receptors
- Also decreased sensitivity of serotonin receptors as in MDD, suggest that
less sensitive serotonin receptors → stronger response to serotonin levels
being lowered
- Evidence
- Drugs that increase dopamine levels trigger manic symptoms in indiv. w/
BP
- Relatives of patients with BP show stronger mood changes to tryptophan
depletion relative to controls
 - Alteration of serotonin receptors and dopamine receptors lead to bipolar
symptoms developing risk taking, sensation seeking, changes in energy,
motivation
- Triggers / predictors of episodes
- Depressive episodes - negative life events (and poor social support)
- Manic episodes - sleep disturbance
- Sleep loss high correlated with daily manic symptoms, most common
prodrome of mania, induced sleep deprivation triggers hypomania or
mania in proportion of patients
- Can follow life events, positive life events - goa
- Treatment
- Pharmacology
- Lithium - mood stabilizer mainly reduces mania
- 80% of bipolar patients experience at least some benefit
- Few experience full remission of symptomatology
- 40% lithium relapsed within 1 year, 60% on placebo
- Lithium toxicity risk of serious fatal side effects - careful monitoring via
blood tests
- Continuous treatment for life recommended
- Antipsychotics may be given as immediate calming effects
- Depression often still experiences not clear if antidepressant is beneficial
for indivs. On lithium and may trigger manic symptomatology, best
practice unclear
- Psychological
- As supplement to drugs
- Psychoeducational
- Teaches about symptoms, course, triggers, treatment
- Helps compliance up to 50% do not take meds regularly
- Family focused therapy
- Educate family, enhance communication, developing problem
solving skills
- CT - useful supplement to meds to relieve depressive symptoms
- Ethical Issues
- BP associated with high rates of suicide
- Civil commitment
- a person can be committed to psych hospital against will if judged to be
mentall ill and danger to self (suicidal or unable to provide basic needs of
food, clothing, shelter) or others
- Formal by court at request of police/family/friend
- Informal by hospital board
- Least restrictive alternative should be provided, outpatient commitment like
halfway house, supervised setting
- Right to refuse treatment unless pose clear and imminent threat
- Right to treatment like psychotherapy
 - Informed consent

Lecture 16: Schizophrenia

1. Symptoms
a. At least one of the first three
i. Delusions
ii. Hallucinations
iii. Disorganized speech (first three important)
iv. Grossly disorganized or catatonic behavior
v. Negative symptoms
b. 2 or more symptoms 1 month ++
i. Avolition
ii. Asociality
iii. Alogia
iv. Flat affect
v. Anhedonia
c. Functioning in one or more major areas has dropped markedly below time of
onset or (for childhood onset) has not reached expected levels
d. Signs of disturbance for at least 6 months, may include periods of
prodromal/residual symptoms, can be only negative symptoms or only 2+
symptoms from A in an attenuated form (odd beliefs, unusual perceptual
experiences)
e. Other diagnoses/effects of drugs or medical condition ruled out
f. Positive symptoms
i. Delusions - firmly held beliefs, contrary to reality, resistant to
disconfirming evidence
1. Persecutory delusions, can be paranoid, grandiose, lack of insight
ii. Hallucinations - sensory experiences in the absence of sensory
stimulation
1. auditory hallucinations - voices, usually critical or debate in third
person
g. Negative symptoms
i. Avolition - lack of interest and drive
ii. Flat affect - show little or no affect in face or voice
h. Other symptoms
i. Disorganized speech
1. Incoherence
2. Inability to organize thoughts and ideas
3. Loose association (derailment) rambles, difficulty sticking to one
topic
ii. Disorganized behavior
1. Odd or peculiar behavior
2. Silliness, agitation, unusual dress
 iii. Catatonic behavior
1. Motor abnormalities, repetitive behaviors, complex gestures,
increased activity, excitable wild flailing of limbs
2. Catatonic immobility - maintain unusual posture for long time
2. Differential diagnosis
a. Schizophreniform Disorder symptom duration >1 mth, <6 mth
b. Brief Psychotic Disorder - 1 day to 1 mth, 1+ delusions, hallucinations,
disorganized speech, disorganized or catatonic behavior
c. Schizoaffective disorder - concurrent major depressive or manic episode and
mood symptoms present for majority of periods with active phase symptoms
d. Major Depressive or BPD w/ psychotic or catatonic features -
delusions/hallucinations occur exclusively during major depressive or manic
episode
e. Delusional disorder - 1+ delusion for 1 month ++, but lack second symptom
3. Consequences of Schizophrenia
a. Disorder impacts families and friends
i. Difficult to life with someone who experiences delusions, hallucinations,
and paranoia
ii. Social skills deficits common, isolation, few social contacts
b. Employability - unemployed and homelessness
c. Substance abuse and suicide rates high
4. Etiology
a. Lifetime prevalence ~1%
b. Occurs equally in men and women
c. Onset typically late adolescence or early adulthood, men diagnosed at slightly
earlier age
d. Diagnosed more frequently in African americans - may reflect diagnostician bias
5. Heritability - how much explained by genetic factors passed down
a. Identical twin - high chance (44%), non identical twins also chance (12%)
6. Genetics
a. Unlikely a single gene, polygenic disorder
b. Linkage studies findings are inconsistent
c. Long history of failure to replicate
d. Led to ‘candidate gene intermediate phenotype’ approach
i. Study polymorphisms (loci) that impact on neural mechanisms that
appear to be disrupted in schizophrenia
ii. E.g. prefrontal function might be disrupted by schizophrenia, frontal
function modulated by dopamine, but still fail to replicate
e. Genome-wide association studies identified 3 copy no. variant deletions linked to
schizophrenia. Rare → idea genetic vulnerability to schiz. may involve many rare
mutations
7. Brain structure
a. Contradictory findings
b. Consistent finding = enlarged ventricles (atrophy/loss of brain cells)
 c. Structural abnormalities in subcortical temporal-limbic areas (hippocampus &
basal ganglia & PFC & temporal cortex)
d. Evidence
i. Enlarged ventricles (Nopulos et al 1997)
ii. Not seen in MZ twin w/o schiz. , may not be genetic (McNeil et al. 2000)
iii. Reduction in cortical gray matter in temporal & frontal regions (Gur et al.,
2000)
iv. Reduced vol. In basal ganglia (caudate nucleus) and limbic structures
(Velakoulis et al., 1999)
v. fMRI reveals impoverished PFC recruitment in patients w/ schiz. while
performing executive tasks (Barch et al., 2001)
8. Expressed emotion (EE)
a. family environment can impact likelihood of relapse vs sustained recovery
b. Interpersonal communication
c. High EE measured by low warmth, high over-involvement, high hostility
d. Relapse rates higher in high EE families - vicious circle of disordered thoughts
and critical comments

1. Dopamine theory
a. Schiz. may result from excess dopamine activity
b. Antipsychotic drugs
i. can produce parkinsonian type side effects as parkinsonism known to be
caused partially by low levels of dopamine
ii. Block post synaptic receptors (D2 receptors)
iii. Antidote to amphetamine psychosis
c. Amphetamine psychosis
i. Release catecholamines (norepinephrine and dopamine) into synaptic
cleft, prevent inactivation, induce paranoia, exacerbate schiz. Symptoms
2. Seeman et al., 1976
a. Across range of antipsychotic, daily clinical dosage is inversely related to drugs
effectiveness at blocking D2 receptors
b. However, the major metabolite of dopamine is homovanillic acid are not elevated
in schiz.
c. Increased no. of dopamine receptors in patients w/ schiz, revealed by
post-mortem and PET scans
e. Not linked to excess dopamine activity but to increased number or oversensitivity
of dopamine receptors
f. Only account for positive and disorganized symptoms, antipsychotics have little
to no effect on negative symptoms
3. Dopamine hypothesis revised (level of stimulation, dopamine activity imbalance)
a. Excessive subcortical (mesolimbic dopamine) → D2 over-stimulation → positive
symptoms
b. insufficient dopamine in FC → D1 under-stimulation → negative symptoms
c. A and B reciprocal relationship, B release of inhibitory control towards A
 4. Problems of theory
a. Antipsychotics
i. block dopamine receptors rapidly yet symptoms only reduce gradually
ii. reduce dopamine levels to below normal
iii. Implicate serotonin as well as dopamine, block serotonin and dopamine
receptors
iv. Street drug PCP can cause psychosis, interferes with glutamate receptors
v. Very complex neurochemistry of schiz. besides just dopamine

1. Pharmacological treatment
a. 1st generation antipsychotic (phenothiazines)
i. Block dopamine D2 receptors, tranquilizing effects
ii. Improve positive and disorganization but not negative symptoms
iii. Unwanted side effects
1. parkinsonian symptoms
2. Dyskinesia (involuntary movements)
3. Neuroleptic malignant syndrome (1%)
4. Severe muscular rigidity, heart rate increase, coma
b. 2nd generation drugs
i. May improve positive and disorganization, as well as negative and
cognitive symptoms better
ii. Better compliance, less side effects
iii. Clozapine
1. risk/side effects ~1% - affects immune system, increase risk of
infection, induce seizures
2. Psychotherapy
a. Addition to drugs
b. Educational approaches
i. Family therapy to reduce EE (understand disorder, improve
communication, avoidance of blame)
ii. Include educating patient and family about importance of taking
medication
iii. Social skills training
3. CBT
a. Randomized trials suggest CBT can help reduce hallucinations and delusions
i. Evaluate evidence for delusions
ii. Highlight inconsistent features
iii. Develop alternative perspectives
iv. Conduct behavioral experiments

Lecture 17: Personality Disorders

Personality Disorders:
1. Enduring Problems of Personality Disorders (PDs):
a. Having a stable & positive identity
b. Sustaining close & constructive relationships
c. Moderately Heritable:
i. ~Ranging from 0.55 to 0.77
d. Prevalence estimates ranging from 10-15%
2. Challenges: Reliability? Validity?
a. Research shows that PDs are unstable over time
i. Low test-retest stability
b. PDs have high comorbidity - with other PDs (as much as 50%) and other DSM
disorders
c.
3. Antisocial Personality Disorder:
a. DSM tries to classify antisocial behavior in terms of a psychiatric disorder
i. Disorders of Childhood & Adolescence ‘disruptive behavior disorders’
1. Oppositional Defiant Disorder (ODD)
2. Conduct Disorder (CD)
ii. Disorders of Adulthood
1. Antisocial Personality Disorder (ASPD)
b. Etiology of Antisocial Personality Disorder
i. DSM-V
1. A pervasive pattern of disregard for & violation of the rights of
others that happens since age 15
2. At least 18 years old
a. The ONLY personality disorder with this required criteria!
3. Evidence of CD before the age of 15
ii. And 3 or more of:
1. Failure to conform to social norms or lawful behaviors that are
grounds for arrest
2. Irritability & aggressiveness, shown by repeated physical fights or
assaults
3. Consistent irresponsibility; failure to maintain work behavior or
honor financial obligations
4. Impulsivity or failure to plan ahead
5. Deceitfulness; repeated lying, using aliases, or conning others for
pleasure or profit
6. Lack of regard for personal or other’s safety
7. Lack of remorse; being indifferent to or rationalizing having hurt,
mistreated, or stolen from another person
4. Psychopathy:
a. NOT a DSM diagnostic category
b. Poverty of emotions (Positive and Negative ones)
c. Lack of shame or guilt
d. Positive emotions are an act, even though they are convincing
 e.Superficially charming
f.Manipulates others for personal gain
g.Lack of anxiety
h.Cruel behavior
i.Antisocial behavior may be impulsive, and may done for the thrill of it
“Psychopathy” as a concept discussed in Hervey Cleckley’s classic book
The mask of sanity (1977)
No age requirement, also gender bias (more in males), more ‘internal’
differences (i.e. thoughts, feelings, motives - not just about behavior)
5. Hare’s Psychopathy Checklist (1990)
a. Identify two main clusters:
i. Emotional Detachment
1. Selfish, remorseless, inflated self-esteem, exploitation of others
ii. Anti-social lifestyle
1. Impulsive & Irresponsible
iii. Only about 20% of people with APD score high on this Hare Checklist
(Rutherford et al, 1999)
iv. 80% of convicted criminals meet the criteria for APD but only about
15-20% meet the criteria for psychopathy (Hart & Hare, 1989)
6. The Making of a Psychopath?
a. Fathers of psychopaths are also likely to be antisocial
b. Lack of family’s affection & severe parental rejection is seen as casual
c. Early abuse or parental loss linked to the development of psychopathy
d. Inconsistent discipline by parents - cause or effect?
7. Learning Theory of Psychopathy:
a. Psychopaths have no anxiety/no conditioned (learnt) fear responses
b. No “brakes” on hurting others or breaking the law
c. Unresponsive to punishment for antisocial behavior; it does not lead to strong
emotions/anxiety.

Borderline Personality Disorder (BPD):

1. Interpersonal, Emotional, and Identity Deficits
a. “I hate you, don’t leave me…”
b. “I don’t know who I am. My identity changes with every situation.”
c. “Physical pain is the only way to stop the unbearable emotional pain.”
2. BPD DSM-V Criteria
Presence of 5+ of the following signs of instability in relationships, self-image,
and impulsivity from early adulthood across many contexts:
a. Frantic efforts to avoid abandonment
b. Unstable interpersonal relationships in which others are either idealized or
devalued
c. Unstable sense of self
d. Self-damaging, impulsive behaviors in at least 2 areas, such as spending, sex,
substance abuse, reckless driving, and binge eating
 e. Recurrent suicidal behavior, gestures, or self-injurious behavior
f. Marked mood reactivity
g. Chronic feelings of emptiness
h. Recurrent bouts of intense or uncontrolled anger
i. During stress, tendency, to experience transient paranoid thoughts or dissociative
symptoms
3. Prevalence:
a. 1.2-6% of general population
b. 10% of people who meet BPD criteria commit suicide (50x the rate of general
population)
4. Treatment:
a. Dialectical Behavior Therapy (DBT):
i. Comprehensive, flexible, principle-based, time-limited
ii. Draws a lot from CBT & BT
iii. Designed for those with BPD & chronic suicidality but it’s been used with
people with emotion regulation deficits.
iv. Overall Goal: To build a life worth living
b. Components of DBT:
i. Skills training group
ii. Skills training
1. Mindfulness
2. Distress tolerance
3. Emotion regulation
4. Interpersonal effectiveness
iii. Individual psychotherapy
iv. Telephone skills coaching
v. Consultation team
5. Biosocial Theory of BPD:
a. Proposed by Marsha Linehan (Linehan, 1993)
b. Primarily a disorder of pervasive emotion dysregulation
i. Heightened emotional sensitivity
ii. Inability to regulate intense emotional responses
iii. Slow return to baseline
c. Bio-Aspect:
i. Biological factors including genetic, neurochemical, neuroanatomical
factors contribute to emotion sensitivity.
1. Recently updated to include a recognition of the role of early
impulsivity
d. Social-Aspect:
i. Invalidating early environments impede the development of effective
interpersonal and emotional regulation skills.
1. Updated model emphasizes reciprocal effects of biological
vulnerabilities and environment in shaping BPD (Crowell,
Beauchaine, & Linehan, 2009)
 6. BPD: Empirical Findings
a. Genetic: Heritability is approximately 0.67
b. Neurochemical: Disruption in serotonergic function
i. Potential role of dopamine & vasopressin, MAO, acetylcholine, and
norepinephrine
c. Neuroanatomical/Functional: Evidence of insufficient frontal control over
hyper-responsive limbic regions (e.g., amygdala)
d. Environmental
i. Higher rates of disrupted attachment with primary caregiver in people with
BPD → Cause or effect?
ii. Higher rates of history of abuse in individuals with BPD
1. Most studies retrospective
2. Not necessary or sufficient for development of BPD
iii. More prospective studies to determine a causal role of invalidating
environments in BPD

Lecture 18: Childhood disorders

1. Externalizing disorders
a. Characteristics by outward-directed behaviors
b. Noncompliance, aggressiveness, overactivity, impulsiveness
c. Includes attention-deficit/.hyperactivity disorder, conduct disorder, and
oppositional defiant
d. More common in boys
2. Internalizing disorders
a. Characterized by inward focused behaviors - depression, anxiety, social
withdrawal
b. Includes childhood anxiety and mood disorders
c. More common in girls

ADHD
1. Diagnosis
a. Inattentive cluster - 6+ inattention for 6+ months to a maladaptive degree and
greater than given person’s development level expectation (e.g. easily
distracted, forgetful in daily activity, not listening well, etc.)
b. Hyperactivity-impulsivity disorder - 6+ hyperactivity-impulsivity for 6+ months to a
maladaptive degree and greater than given person’s development level
expectation (e.g. fidgeting, running around inappropriately, restlessness,
interrupting, incessant talking, etc.)
c. Symptoms before age 12 i and/or ii
d. Present in 2+ settings
e. Clear functional impairment
f. 17+ 5 symptoms from i and/or ii
2. Specifiers
 a. Predominantly inattentive presentation
b. Predominantly hyperactive-impulsive presentation
c. Combined presentation both criteria met 6+ months
3. In partial remission: full criteria previously met, w/in last 6 months full criteria not met but
symptoms still impair functioning
4. Current severity: mild (symptoms needed to meet diagnosis only or few in excess, no
more than minor impairment in functioning), moderate, severe(many symptoms in
excess, marked impairment)
5. Prevalence
a. 3 to 11% worldwide
b. Potential over diagnosis
c. More common in boys than girls
d. Symptoms persist beyond childhood
6. Comorbidity
a. ~75% have co-morbid psychiatric disorder
b. Substantial co-occurence of ADHD and conduct disorder
c. Outcomes significantly worse for these indiv. (increased likelihood of substance
abuse, poorer academic performance, more interpersonal issues)
d. Hyperactive symptoms predict subsequent substance use, even after controlling
for symptoms of conduct disorders, both in girls and boys
e. ~30% have co-morbid internalizing disorder (childhood anxiety, depression,)
7. Girls
a. Viewed more negatively by peers than girls without ADHD
b. More likely to be anxious or depressed
c. Exhibited neuropsychological executive function deficits
d. More likely to have symptoms of eating disorder and substance abuse by
adolescence
8. Etiology of ADHD
a. Behavioral genetics
i. Currently heritability estimates ~70% to 80%
ii. Early studies suggested that ADHD aggregates in families
iii. 4 to 8 fold increase in risk for ADHD among first degree relative of male
ADHD probands
iv. 76% of variance is explained by genetic factors
v. Degree of relationship between proband and relative affects probability of
ADHD diagnosis
vi. Thapar 1999: 75+ variance genetic factors, 0-6% variance due to shared
environment, 9-20% variance due to unique environment
b. Molecular genetics
i. Prominent role for gene influencing function of dopamine system
ii. Transporter gene DAT1 (influence reuptake mechanism) and receptor
genes DRD4, DRD5 (efficacy of DA receptors on post-synaptic
membrane) associated with ADHD
iii. Likely to be polygenic disorder (influence by multiple genes)
 iv. May interact with environmental factors
v. PFC and caudate nucleus (controlling voluntary movement) volume
reductions - children with ADHD perform worse on tasks of frontal
function (PFC governs attention, response inhibition, impulse control)
c. Environmental factors
i. Low birth weight
ii. Food colorings
iii. Maternal smoking
iv. Negative family interactions (possibly maintain/exacerbate role)
9. Treatment
a. Stimulant medications
i. impact neurotransmission
ii. Ritalin, adderall, concerta, strattera
b. 75% children
i. Reduce disruptive behavior
ii. Improve interactions with parents, teachers, peers
iii. Improve goal-directed behavior and concentration
iv. Reduce aggression, impulsivity
v. Side effects - loss of appetite, weight, sleep problems
c. Psychological treatment
i. Parental training
ii. Change in classroom management
d. Behavior monitoring and reinforcement or appropriate behavior
i. Based on operant conditioning principles, positive reinforcement
engagement in desired behaviors
e. Supportive classroom environment
i. Brief assignments, immediate feedback, task-focused style, breaks for
exercise
10. Multimodal Treatment of children with ADHD (MTA) study
a. 6 sites over 14 months with 600 kids
b. Compared community based (standard) care with
i. Medication along
ii. Behavioral treatment alone
iii. Combined medication plus behavioral treatment
c. Findings
i. Combined treatment worked best compared to community based care
ii. Held across 14 months
iii. At 3, 6, and 8 yrs, no differential effects of treatment type

Conduct disorder
1. Diagnosis
a. Repetitive and persistent behavior pattern that violates basic rights of others or
conventional social norms as manifested by presence of 3+ of following in 12
months, and at least one in the previous 6 months
 i. Aggression to people and animals (bullying, initiating fights)
ii. Destruction of property (vandalism)
iii. Deceitfulness or theft (shoplifting)
iv. Serious violation of rules (running away from home overnight)
b. Significant impairment in social, academic, or occupational functioning
c. If over 18 criteria not met for antisocial personality behavior
d. Onset: before 10 in childhood, adolescence or unspecified
e. Limited prosocial emotions 2+ of:
i. Lack or remorse or guilt
ii. callous/lack of empathy
iii. Unconcerned about performance/blames others
iv. shallow/deficient affect
f. Children w/ CD and high levels of callous and unemotional traits have more
problems with symptoms, peers, and family than children with low levels of traits,
related to distinct etiologies
g. Current symptom severity: mild, moderate, severe
2. Prevalence
a. Rate of 6-10% found in school age children
b. More common in boys
3. Co-morbidity
a. Risk for depression & anxiety also elevated and substance abuse
b. Prognosis is worse for childhood onset
i. Indivs. will go on to show Antisocial behavior disorder as adults, CD
linked to poorer educational outcome, increased in substance use, violent
behavior, psychopathology
4. Subtypes (Moffitt 1993)
a. Pattern 1
i. seen by age 3, continues into adulthood (DSM V childhood onset)
ii. more common in boys
iii. Neuropsychological deficits and family psychopathology linked to pattern
1 and holds cross cultures
b. Pattern 2
i. limited to adolescence
ii. May be distinct due to gap between adolescent’s maturation and
opportunities for adult responsibilities/behaviors
c. Follow up study results suggest pattern 2 conduct issues may continue into
adulthood (adolescent onset)
5. Etiology of CD
a. Genetics
i. Findings from behavioral genetics studies (like twin studies) are mixed
ii. Early onset subtype may be more heritable (Taylor et al., 2000)
iii. Also argument we need to look at particular symptoms not overall
diagnosis (aggression vs property destruction or stealing)
iv. Serotonin receptor implicated in impulsive aggression
 1. 5 HT agonists have anti-aggressive effects
v. Monoamine oxidase A (MAO-A) point mutation linked with reactive
aggression
b. Gene x environment interactions
i. Caspie et al 2002
1. Interaction between MAO-A genotype and early maltreatment
2. Those with low activity of MAO-A were more likely to be
diagnosed with CD, even more so when childhood maltreatment is
severe
c. Environmental influences
i. Parental discipline - lack of monitoring
ii. Peer influences associated with CD
1. Rejection by peers
2. Affiliation with deviant peers (reinforcing behavior, modeling,
contagion)
iii. Sociocultural influences
6. Diminished emotional responsivity hypothesis
a. CD associated with reduced emotional responsivity
b. Acts of violence are less aversive and more palatable
c. CD associated with structural alterations in brain regions used to generate
emotional response
d. fMRI studies needed
e. Herpertz et al., 2005
i. CD boys show reduced psychophysiological responses to images from
IAPS regardless of valence
7. Treatment
a. Family interventions
i. Parental management training (operant based)
ii. Shows decreased in antisocial and aggressive behavior
b. Multisystemic treatment
i. Targets multiple factors (family, school, peers)
ii. Incorporates multiple therapeutic strategies, taking into account individual
and family strengths and social context for conduct problems, conducted
in ecologically valid everyday life settings

Lecture 19: Autism

1. Diagnosis
a. Early diagnostic confusion - equated with schiz., seen as language disorder
b. Early symptomatology - onset at birth of infancy, triad of impairments
c. Combined multiple diagnosis into Autism spectrum disorder
i. Autistic, asperger’s, pervasive development, childhood disintegrative
ii. Could lead to more stigmatization of people formally diagnosed with
asperger’s but also more access to services
 d. Persistent deficits in social communication and interaction across multiple
contexts
i. Deficits in social-emotional reciprocity
ii. Deficits in nonverbal communicative behaviors used for social interaction
iii. Deficits in developing, maintaining, and understanding relationships
e. Restricted repetitive patterns of behavior interests or activities
i. Hypo and hyper reactivity to sensory input or unusual interest
ii. Fixation in abnormal interests intensely or focus
f. Symptoms present early in developmental period
g. Cause clinically significant impairment in functioning
2. Specifiers
a. Severe vs marked vs noticeable
b. Deficits in verbal and nonverbal social communications
c. Extreme difficulty coping with change, restricted behavior
d. w/ or w/o : Intellectual or language impairment, catatonia,
medical/genetic/environmental/neurodevelopmental/mental/behavioral factors
3. Comorbidity
a. IQ less than 70 common
i. Poor related to language, abstract thinking, symbolism, or sequential logic
4. Prevalence
a. 1 out of 68 children, 5:1 boy:girl
b. Found in all SES, ethnic, and racial groups
5. Prognosis
a. Children with higher IQs who learn to speak before 6 have best outcomes
6. Etiology
a. Behavioral genetics
i. 47 to 90% concordance for MZ twins, 0 to 20% for DZ twins, heritability
~.80
ii. Shared environment also important
b. Molecular studies
i. Nothing definitive linkage studies, OT, AVPR genes, or deletion of
chromosome 16
c. Neurobiological factors
i. Brain size
1. Although normal size at birth, brains of indivs. with autism are
larger than normal
2. Pruning of neurons may not be occurring
ii. Overgrown areas include frontal, temporal, cerebellar, linked with
language, social, and emotional functions
iii. Abnormally size amygdalae
7. Treatment
a. Psychological treatments more promising than drugs
b. Medication used to treat problem behaviors
i. Haloperidol (haldol)
 1. Antipsychotic
2. Reduces aggression and stereotyped motor behavior
3. Does not improve language and interpersonal relationships
c. Earlier treatment associated with better outcomes
d. Intensive behavioral treatment
i. Operant conditioning, reinforcements, achieve desired behaviors
e. Joint attention intervention and symbolic play used to improve attention and
expressive skills
f. Parent education Family therapy

Psychological theories
1. Affective disorder theory
a. Hobson (1993)
i. Social deficits derive from inability to respond to other’s emotions
b. Evidence
i. Empathy deficits (yirmiya et al., 1992)
ii. Indivs. w/ ASD pay attention to different parts of faces than do people w/o
autism; focus on mouth, neglect eye region (may be due to difficulty in
perceiving emotion in other people)
iii. HOWEVER emotion recognition deficits are not specific to autism and
evidence for them in autism is mixed
iv. Ashwin et al 2006 Social neurosci
1. Autism < control for all aspects, fear, disgust, angry, sad, surprise,
2. More so for fear, disgust, and angry
3. Could be that it is just harder to distinguish between thhem
v. Indivs. w/ ASD do not activate normal face processing neural circuitry
(regions) when viewing faces, impaired normal recognition, using other
compensatory mechanisms
1. Fusiform face area - face
2. Amygdala - facial expression
3. Superior temporal sulcus - facial expression
c. Pierce et al. 2001
i. Showed participants faces and controlled shapes
ii. Those without autism using FFA, STS, amygdala
iii. Those with autism using different neural systems to identify faces
d. Indiv. w/o ASD constantly trying to read people’s expressions, w/ ASD can't
understand expressions so unable to utilize proper neural regions
2. ‘Theory of mind’ deficit (mindblindness)
a. Ability to understand other people’s wants and needs different to ours
b. Crucial for understanding and successfully engage in social interaction
c. Develop around 3 to 5
d. Children w ASD unable to achieve developmental milestone
e. Baron-Cohen et al., 1985
 i. inability to attribute mental states (beliefs, desires, knowledge, intentions,
emotions) to others
ii. Inability to make sense and predict actions of others
iii. Evidence
1. Seeing leads to knowing test (1994)
a. One touch, one sees, who knows what is in the box
2. False belief test (1985)
a. A put marble in basket, B move A marble from basket to
box, where will A look for marble
3. Pragmatics beliefs
f. Castelli et al., 2002
i. STS and MPFC activated known to be critical in social cognition
ii. Not activated in indivs. w/ ASD when looking at the social brain video
3. Weak central coherence theory
a. Frith (1989)
i. Inability to see the whole, not just the parts
b. Evidence
i. Navon test (Mottron and Belville, 1993, Rinehard et al 2000)
ii. Those w/ ASD can't see things as a whole but see in parts
iii. A made up of letter H, more interference for those w/ ASD

Lecture 20:

Information about the final paper. Not relevant here!

Lecture 21: Eating Disorders I ✅

Eating Disorders in DSM V:

● Anorexia Nervosa
○ Restriction of energy intake relative to requirements leading to significantly low
body weight
○ Intense fear of gaining weight or becoming fat or persistent behavior that
interferes with weight gain
○ Distorted perception of body weight or shape, undue influence of body weight or
shape on self-evaluation or lack of recognition of seriousness of current low
weight
○ SPECIFIERS:
■ Restricting subtype (dieting / fasting / excessive exercise )
■ Binge- eating / purging subtype (can be just purging)
■ Partial remission — weight gained but 1 of other criteria still met
■ Full remission
■ Severity: mild BMI <= 17 ; extreme BMI < 15
○ Personality:
 ■ Perfectionism has been found to predict onset of AN
● Also been found to remain high even after successful treatment
● Mothers of girls with anorexia also score higher on measures of
perfectionism1
○ Prevalence:
■ Found in many cultures
■ Rarer in Hispanic women (not well studied); less body dissatisfaction in
African American women
■ 1% lifetime prevalence in general population
■ Typical onset adolescence
■ Women 10 x more likely to develop disorder, but increasing prevalence in
men
■ Often comorbid with depression, OCD, phobias, panic, alcoholism &
personality disorders
○ Etiology:
■ Predisposed by genetic predisposition & societal pressures
■ Precipitating factors/ triggers: life stress; puberty; dieting episode
■ Prognosis: 50-70% eventually recover (6-7 years, relapse common),
death rates 10 times higher than in general population due to physical
complications and suicide.
■ Mortality rates 3-5% (women)
■ Sociocultural factors:
● Societal emphasis on thinness
● Unrealistic media portrayals
● Body dissatisfaction and preoccupation with thinness
● Webgroups (proana)
○ Physical and cognitive effects:
■ Low blood pressure, heart rate decrease, kidney & gastrointestinal
problems, loss of bone mass, hair loss, depletion of potassium & sodium
levels
■ Lanugo (soft, downy body hair)
■ Lack of libido, tiredness, weakness
■ Slowed information processing, disrupted executive functioning, impaired
short term memory, preoccupation with food
○ Genetics:
■ Family and twin studies support genetic link— first degree relatives 10
times as likely to have anorexia nervosa
■ Higher MZ than DZ concordance rates
■ Non-shared environment also appears important
○ Neurobiology:
■ Serotonin promotes satiety

1
 ■ Some evidence for altered serotonergic function in AN but not clear if
cause/effect
■ Endogenous opioids: substances produced by the body that can reduce
pain sensations, enhance mood, and suppress appetite
■ Opioids are released during starvation and have been hypothesized to
play a role in eating disorders
■ Starvation among people with anorexia may increase the levels of
endogenous opioids, resulting in a positively reinforcing positive mood
state (Marrazzi & Luby, 1986)
■ Excessive exercise seen among some people with eating disorders may
increase opioids and thus be reinforcing
○ Neuroimaging:
■ (Foerde, Steinglass, et al., 2015): eating habits may be important in
anorexia— dieting or restrictive eating may become habitual, and these
habits may themselves become rewarding
○ Cognitive Theories:
■ People with eating disorders may have maladaptive schemata that narrow
their attention towards thoughts and images related to weight, body
shape, and food (Fairburn, Shafran, & Cooper, 1999)
■ Many people who develop anorexia symptoms report that the onset
followed a period of weight loss and dieting
■ Behaviors that achieve or maintain thinness are negatively reinforced by
the reduction of anxiety about gaining weight as well as positively
reinforced by comments from others
■ Dieting and weight loss may also be positively reinforced by the sense of
mastery or self-control they create (Fairburn et al., 1999; Garner,
Vitousek, & Pike, 1997)
○ Role of Family Environment:
■ Not widely supported.
■ Psychodynamic view:
● Overly controlling parent? -> dieting as a means to gain control
and identity (Baruch, 1980)
■ Dysfunctional family structure? -> not well tested
● Conflict may be consequence not cause of family member’s
anorexia
○ Treatment:
■ Phase 1: weight restoration
● May require hospitalization
■ Phase 2: weight maintenance
● A challenge; CBT can help reduce relapse.
● Supportive psychotherapy + education can be just as effective
● Family therapy— helping parents restore child, building up family
functioning = some indication lower levels of remission than
individual therapy
Lecture 22: Bulimia Nervosa & Binge Eating Disorder ✅
Eating disorders in DSM V continued:

● Bulimia Nervosa
○ Uncontrollable eating binges followed by compensatory behavior to prevent
weight gain
○ DSM V criteria:
■ Recurrent episodes of binge-eating
● An excessive amount of food consumed in under 2 hours
● A feeling of loss of control over eating as if one cannot stop
■ Recurrent compensatory behavior to prevent weight gain
● Purging (vomiting), fasting, excessive exercise, use of laxatives
and/or diuretics
■ Body shape and weight are extremely important for self-evaluation
■ The binge-eating and compensatory behaviors both occur, on average, at
least once a week for three months
○ Recurrent episodes of binge-eating:
■ Typical food choices:
● Cakes, cookies, ice cream— easily consumed high calorie foods
■ Avoiding a craved food can later increase likelihood of binge
■ Shame & remorse often follow
○ Severity ratings:
■ Number of compensatory behaviors
● Mild: 1-3 per week
● Moderate : 4-7
● Severe: 8-13
● Extreme: 14+
○ Bulimia (with purging) vs Anorexia with binge-eating-purging:
■ Extreme weight loss in anorexia
■ At or above normal weight in bulimia
○ Prevalence:
■ Onset late adolescence or early adulthood
■ 90% women
■ 1-2% prevalence among women
■ Typically overweight that led to dieting
■ Comorbid with depression, PDs, anxiety, substance abuse, conduct
disorder
■ Not clear if any specific temporal order
■ Suicide attempts and completions higher than in general population but
much lower than in anorexia nervosa
○ Physical changes:
■ Menstrual irregularities
 ■ Potassium depletion from purging
■ Laxative use depleted electrolytes, which can cause cardiac irregularities
■ Loss of dental enamel from stomach acids in vomit
■ Mortality rate up to 4%
○ Prognosis:
■ ~75% recover
■ 10-20% remain fully symptomatic
■ Early intervention linked to improved outcomes
■ Poorer prognosis when depression and substance abuse are comorbid or
more severe symptomatology

● Binge Eating Disorder

○ `DSM V criteria:
■ Recurrent episodes of binge eating; on average, at least once a week for
three months
■ Lack of control experiences during episodes
■ Binge eating episodes include at least three of the following:
● Eating more rapidly than normal
● Eating until uncomfortably full
● Eating large amounts when not hungry
● Eating alone due to embarrassment about large food quantities
● Feeling disgusted, guilty, or depressed post binge
■ No compensatory behavior is present
○ Severity:
■ Mild: 1-3 binges
■ Moderate 4-7
■ Severe 8- 13
■ Extreme 14+
○ Details:
■ Associated with obesity and history of dieting
● Typically body mass index > 30
■ Not all obese people meet criteria
● Must report binge eating episodes and a feeling of loss of control
over eating
■ Risk factors:
● Childhood obesity, early childhood weight loss attempts, bullying,
low self-concept, depression, and childhood physical or sexual
abuse
■ Equally prevalent in Euro African, Asian, and Hispanic Americans
■ Lasts on average 14 years, ~60% recover
○ Physical changes:
■ Problems associated with obesity
● Increased risk of type II diabetes
● Cardiovascular disease
 ● Physical ailments (joint/muscle pain)
■ Problems independent of obesity
● Sleep problems
● anxiety/depression
● Irritable bowel syndrome
● Early menstruation in female sex
○ Etiology:
■ Societal influences — emphasis on thinness
■ 20% of college females engage in some form of binge eating and purging
■ Body dissatisfaction and preoccupation with thinness (culturally
influenced)
■ Genetic influences: first degree relatives 4 times as likely to have BN (was
10 times for AN)
■ Altered serotonergic function proposed (may explain comorbidity with
depression) — SSRIs can reduce binge eating and purging and comorbid
symptoms of depression
○ Cognitive behavioral perspective:
■ Low self-esteem
■ Self-worth strongly influenced by weight
■ Rigid restrictive eating triggers lapses which can become binges
● Many off limit foods
■ Stress, negative affect helps trigger binges
■ Disgust with oneself and fear of gaining weight lead to compensatory
behaviors
● e.g. vomiting, laxative use
■ Self-esteem further lowered (vicious cycle)
○ Cognitive behavioral therapy goals:
■ Establish normal eating patterns
■ Cognitive aspect:
● To question societal standards for attractiveness, challenge
irrational beliefs, stop all-or-none thinking, identify triggers
■ Behavioral aspect:
● Exposure: patients practice eating small amounts of forbidden
foods
● Relaxation: used to control the urge to vomit

Prevention of eating disorders:

- Psychoeducational approaches
- Educate early about the dangers of eating disorders
- De-emphasize sociocultural influences
- Risk-factor approach:
- Healthy weight intervention to develop healthy weight and exercise programs

Midterm 2 Review Lecture:

Psychological theories of ASD:
- Affective disorder theory
- Affective disorder theory
- ‘Theory of mind’ deficit (mindblindness)
- ‘Theory of mind’ deficit (mindblindness)
- The weak central coherence theory
- Weak central coherence theory

Eating Disorders:
- Cognitive formulation of bulimia nervosa

- Relationship to ideas of negative schema and cognitive errors in depression

- Compare to Beck’s cognitive model of depression (dysfunctional assumptions/
schema -> negative life events -> negative automatic thoughts about the self the
world and the future (negative cognitive triad) -> more dysfunctional
assumptions/ schema etc)

Depression and treatment:

- Cognitive formulation (lecture 13)
- Effectiveness of drug or cognitive treatments
- DeRubeis et al. 2005: both pharmacotherapy and CT treatments outperformed
placebo
- Hollon et al 2005: CT > drug followed by placebo. Maintained drug inbetween

Differential Diagnosis:

Discussion Notes:

Discussion 7:
Discussion 8:

Discussion 9:

Discussion 10:

Discussion 11:

Key Studies:

Abramson, Teasdale, and Seligman (1978): discussed in lecture 13

-Attribution theory: negative events can be explained (‘attributed’) in different ways:
-Global* vs. specific
-Stable* vs. unstable
-Internal* vs. external factors
-Global, stable, internal* (e.g., I am stupid)
• Specific, stable, internal (e.g. I'm useless at maths)
• Global, unstable, internal (e.g. I was tired)
• Specific, unstable, internal (e.g. I was bored with maths
• Global, stable, external (e.g. All tests are unfair)
• Specific, stable, external (e.g. This maths test was unfair)
• Global, unstable, external (e.g. It was Friday 13th)
• Specific, unstable, external (.e.g I was sitting in row 13)
-Evidence:
-Internal, global, stable attributional style found in depressed people
more often than in controls
-Attributional style changes after treatment
-Cognitive therapy: attempts to change the person's attributional
style / interpretations Drawn
-BUT – some studies suggest Attributional Style not reliable
predictor of MDD onset

Pierce et al. (2001): discussed in lecture 19

Baron-Cohen, Leslie, and Frith (1985): discussed in lecture 19

Fairburn (1997): discussed in a lecture for anorexia nervosa here is the link: (Fairburn, Shafran, & Cooper…

1. Cognitive behavioral Formulation of BN (Fairburn 1997)

a. Core low self-esteem (unconditional and pervasive negative view of self-worth)
→ overevaluation of shape and weight and control; dieting to feel better about
self → food intake is restricted too severely → diet is broken → binge →
 compensatory behaviors to reduce fear of weight gain → overgeneralization lead
to low self esteem cycle

Journal Articles:

DeRubeis et al. (2005)

■ Looked at immediate post treatment response, after eight weeks, drug
treatment and cbt were equally great, then compared again at sixteen
weeks, again were equally good
■ Placebo trials run then dropped at 8 weeks due to ethical
■ Remission tests by vanderbilt, drugs did better than therapy--- experience
of therapy and quality important

Hollon et al. (2005)

a. Broad focus: relapse prevention
b. Objective: to determine whether CT has enduring effect ( after discontinuing ) / to
compare this effect against the effect produced by continued ADM
c. Methods: 104 patients, three conditions. Continued ADM, withdrawn to placebo,
CT all discontinued.
d. Results: main effect of treatment type: cognitive therapy has an enduring effect
beyond medical treatment ( as effective as keeping patient on medications)
e. Conclusion: CT is as effective as keeping patients on medications

Example questions:
Is there evidence for genetic factors influencing this disorder?

How much of the variance in population diagnosis is due to heritability (know if it is low (<=20),
middling or high (e.g. 80%+)

Is there evidence for environment shared with other family members or

unique environment playing a role?
What might these environmental factors be?
Are there triggers that tend to precede disorder onset?

Is disruption to a particular neurotransmitter associated with this disorder?

Or altered function of particular brain areas? If so which?

Are there alterations in cognition or cognitive biases linked to this disorder? What?

How is this disorder typically treated? How successful is this treatment?