symptoms
diagnostic criteria
associative features
etiological features
special notes
100

dissociative disorders

types, what it is 

disorders due to separation of consciousness and/or loss of certain portions of memory

dissociative amnesia 

dissociative identity disorder 

100

dissociative amnesia 

dissociative identity disorder 

Dissociative Amnesia

loss of extensive personal information

Dissociative Identity Disorder (formerly known as multiple personality disorder)

coexistence of two or more personalities (not to be confused with schizophrenia)

expressed amnesia for the other personalities but other memory tests suggest awareness of the other personalities

alters may be very different from the original personality

transitions may be sudden

100

have the # of diagnoses of dissociative identity disorder increased or decreased over the years? 

increased- iatrogenic effect? 

100

stress? past? 

Stress – but why does stress affect some people in this way and not others?

iatrogenic

severe emotional trauma during childhood

ability to dissociate? but lack of independent verification very controversial; etiology is very unclear

100

what is dissociative fugue 

dissociative fugue is a subtype of dissociative amnesia- Definition: Dissociative fugue involves memory loss for personal autobiographical information along with unexpected travel or wandering. People may appear normal to others but are unaware of their true identity or past

200

major depressive disorder 

so many but what is loss of interest in pleasurable things called? 

-persistent sadness and/or loss of interest in previously pleasurable things (i.e. anhedonia)

weight loss or weight gain

insomnia or hypersomnia

psychomotor retardation or agitation

fatigue

feelings of worthlessness or guilt

can’t concentrate

recurrent thoughts of death

200

how many symptoms must one exhibit? 

Diagnostic criteria:

(5 or more)

200

onset? what does an earlier onset mean? how many episodes does one typically have? how long are the episodes? lifetime prevalence? cohort effect? gender?

Onset: around puberty & highest incidence around 20s (your chapter says differently – but ignore)

earlier onset = worse severity and prognosis

40-50% have recurrences: avg. of 5-6 episodes

Average duration: 6 mos.

Tends to be episodic but some have persistent depression for many years; corre. with ↑ risk of physical health problems and ↑ mortality risk

Lifetime prevalence: 13-16% (at least 40 million people in the US)

Cohort effect

But some suggest this is inflated to include normal sadness in response to severely stressful situations

women 2x greater: men

200

genetic vulnerability, interpersonal roots, stress (FOR BIPOLAR TOO) 

Genetic vulnerability

Large ↑ concordance rate for MZ twins

65-80% of variance for bipolar disorder

40% of variance for bipolar disorder

Predisposition not determination

Actual manifestation may be different among family members

Interpersonal roots

Poor social skills → punishing social experiences → worse mood/depression 

Stress: Can trigger onset of depression and bipolar. With more occurrences, stress plays less of a role


200

what are hypotheses for the gender ratio? 

genetics unlikely

tied to reproductive cycle/hormones?

greater stress & adversity (environmental factors)

rumination

300

bipolar disorder 

inflated self-esteem/grandiosity

decreased need for sleep

more talkative

flight of ideas/racing thoughts

distractibility

psychomotor agitation and/or ↑ goal-oriented behavior

excessive involvement in pleasurable activities

300

what is necessary and how many symptoms are necesary? 

at least one manic episode (persistently elevated, expansive or irritable mood, lasting at least 1 week)

(3 or more)

300

prevalence, gender ratio, onset


Prevalence: 1% of population

women: men = equitable

Onset: late teens or early 20s

300

Neurochemical and neuroanatomical factors (FOR MAJOR DEPRESSIVE DISORDER TOO) 


NE & 5-HT (but other monoamine neurotransmitters have been implicated as well)

↓ volume of hippocampus/↓ neurogenesis assoc. with depression

Stress → ↑ HPA(C) activity → ↓ neurogenesis in hippocampus? → ↓ hippocampal volume?

Hyper-reactivity of the amygdala

Hypo-reactivity of the reward system

Correlation or causal?

Cognitive factors

Learned helplessness

Reformulated learned helplessness theory – pessimistic explanatory style (esp. internal, global)

Rumination

May explain differences in gender rates

May also contribute to generalized anxiety disorder, eating disorders, substance-abuse disorders

Hindsight bias

Correlation or causal? Can it be both?

300

talk about suicide

amish too 

are you more likely to get disorder or predispositon? 


10th leading cause of death; 45,000 deaths per year

perhaps underestimation

suicide attempts (25): suicides (1)

attempts: women (3-4x): men

successful: men (4x): women

90% likely have a type of psychological disorder

50-60% may be major depressive & bipolar disorders

↑ severity of depression → ↑ chance of suicide

-amish suicide rates are very low (much lower depression rates) suggests that something is running down family that leads to depression 

-predispostion- disorders can manifest differently across generations 

400

schizophrenia (positive + negative) 

positive: delusions, hallucinations, disorganized speech or thought, grosly disorganized or catatonic behavior

negative: affective flattening, alogia, avoliution 

400

how many symptoms must one exhibit 

2 or more 

400

when males? when females? what does ealier onset mean for prognosis? lifetime prevalence? 

Males: mid-20s

Females: later 20s/early 30s, possibly also peri-menopausal age

Earlier onset → worse prognosis and ↑ risk of suicide or early death (e.g. variety of physical diseases)

Lifetime prevalence: 1% of US population


400

genetic vulnerability, neurochemical factors, structural abnormalities, neurodevelopmental hypothesis, expressed emotion, stress 

Genetic vulnerability

Concordance rate:  48% MZ twins vs. 17% DZ twins

2 parents with schizophrenia = 46% risk of schizophrenia vs. 1% risk

Low IQ corre. with increased risk

Predisposition

Neurochemical factors

DA hypothesis

Updated DA hypothesis

Dysregulation (e.g. too low in prefrontal area, too high in nucleus accumbens area)

5-HT, GABA, glutamate also implicated

Marijuana use during adolescence + genetic vulnerability may ↑ risk

Structural abnormalities

Enlarged ventricles, ↓ Volume of both gray and white matters

Synaptic pruning gone awry?

Correlation or causation?

Neurodevelopmental hypothesis

e.g. viral infection (which may lead to inflammation), malnutrition, obstetrical complications

minor physical anomalies support this theory

Q for you – if the problem is negative conditions during prenatal development, why do symptoms show up at a later age?

Expressed emotion

Affects course of disorder, after onset

Relapse 3x greater for those with schizophrenia returning to families with high expressed emotion

Stress

Can trigger first episode and subsequent episodes

400

define catatonic behavior, affective flattening, alogia, avolition,

  • Catatonic behavior → Abnormal motor activity, ranging from complete immobility and mutism to bizarre movements or postures.

  • Affective flattening → Very limited outward emotional expression (flat voice, minimal facial expressions, reduced gestures).

  • Alogia → Poverty of speech; very brief, sparse, or empty verbal responses.

  • Avolition → Severe lack of motivation, difficulty initiating or sustaining purposeful activities.

500

austism spectrum disorder 

Diagnostic criteria:

Social communication and interaction deficits in multiple contexts

Repetitive/restrictive behaviors and/or interests

500

how many don't develop speech? how do they react to change? IQ? Onset? Diagnosis age? prevalence? gender ratio? Who has more severe impairments? 

30-40%  may not develop speech; others may have unusual characteristics of speech (e.g. echolalia)

possible extreme reactions to relatively minor changes in environment

1/2 have sub-normal IQ scores

Onset: symptoms generally appear between 15-18 mos.

Diagnosis usually at a young age (e.g. before age 2-3)

Prevalence: 1.5%

80% of cases are males; females may have more severe impairments

500

genetics? brain abnormalities? mercury?

Etiology

Genetic

Brain abnormality

e.g. brain enlargement by age 2 yrs. (overgrowth in various areas of cortex), beginning possibly prenatally

Study suggesting mercury involvement has been deemed fraudulent

500

what are outcomes? 

Outcomes:

20% good (high level of independence)

31% fair (some independence but support/supervision still necessary)

48% poor (residential supervision or hospital care needed)

Increasing #s are entering college and workforce