Diagnosis and Psychopathology


  • good prognostic Fs:
    • availability of social support, good premorbid adjustment, acute onset, LOS, female, precipitating events, mood disturbances too, good interepisode fx, minimal residual sxs, normal neurological fx, family hx of Mood ds., no family hx of SZ, family hx of Mood ds
  • Brief Psychotic Disorder (Sx don’t last longer than 1 mos)
  • Schizophreniform Disorder (same as SZ but duration <6 mos)
  • individual therapy less effective than reality-adaptive support or family counseling
  • family therapy + meds most effective
  • circumstantiality less serious than loosening of associations


  • Cocaine:
    • intoxication: euphoria, IP sensitivity, talkativeness, hypervigilence, impaired judgment; tachycardia, pupillary dilation, increased BP, psychomotor agitation or retardation, nausea/vomiting
    • withdrawal: dysphoric mood, fatigue, insomnia/hypersomnia, increased appetite, vivid dreams, psychomotor retard/agitation
  • opiate addiction might have substitute for txt (methadone) or antagonist (naloxone)
  • Amphetamine user Sxs:
    • paranoid ideation, aggressive beh, anxiety, depression, wt loss
  • Barbiturate withdrawal (abrupt termination)
    • grand mal SZ (can be fatal)
    • can also see depression, agitation, REM rebound effect, physical distress (resume use)
  • most smokers quit on their own
    • strong desire, awareness of negative health consequences, social support (+ indicators)
  • substance dependence includes 3/7 sxs
  • abuse includes at least 1/4
  • alcohol intoxication sx:
    • beh signs: aggressive/sex beh, mood lability, talkativeness, impaired memory/ judgement; slurred speech, loss of coordination, nystagmus, stupor/coma
  • alcohol withdrawal sx:
    • agitated state: ANS hyperactivity, psychomotor agitation, hand tremor, insomnia, depression, seizures, nausea/vomiting, anxiety, hallucinations
  • alcohol delirium: experienced in 5% with withdrawal: have delirium tremens: hallucinations, delusions, ANS hyperactivity, agitation; often co-occur with liver failure, TBI or pneumonia
  • Korsakoff’s Syndrome: thiamine deficiency; recent memory impair, disorient to time/ place, poor insight, retrograde amnesia, confabulation
  • Marlatt and Gordon argue that due to abstinence violation effect (in relapse), feelings of guilt and depression lead to more use b/c person attributes relapse to internal (I am worthless) and stable attributions.

Mental disorders due to GMC & substance induced mental disorders

  • personality change due to GMC: labile type, disinhibited type, aggressive type, apathetic type, paranoid type, unspecified/combined type
  • for all of these, want disturbance and disease to be related through a physio mech (cause)
  • catatonic disorder due to GMC: TBI, CV disease, encephalitis, metabolic conds
  • hallucinogen persisting perception disorder: occurs when not using hallucinogens, but experience hallucinogen flashbacks
  • organically-based mood sxs: substance induced (PCP, hallucinogens), endocrine ds (hypothyroidism), carcinoma of pancreas, viral illnesses, structural disease of brain


  • Delirium
    • most common in very young (fever or med induced) or 60+ (delirium)
    • following surgery (60+ at risk)
    • pts with decreased cerebral reserve at higher risk (e.g., TBI, stroke, dementia)
    • postcardiotomy pts at increased risk
    • pts going through drug withdrawal increased risk
  • Dementia
    • always includes memory impairment
    • at least 1 more sx: aphasia, apraxia, agnosia, exec dysfx
    • more common in 85+
    • rare in children (TBI, HIV)
    • AD accounts for 50%
    • 3-4xs more likely to have affected relative than those without AD
    • VD accounts for 10-20%
    • HIV-D seen in 2/3 of all AIDS pts: 1st signs- conc loss and mild memory pblms; death in 1-6 mos after severe sxs onset


  • anaclitic depression: occurs in infants deprived of maternal attn (6-8 mos)
    • withdrawal, weepiness, insomnia, decline in health
  • dysthymia: sx last at least 2 yrs
  • MDE have at least 5 sxs
  • prediction of relapse:
    • absence of social support from family, family members who are hostile, critical or overinvolved; other mental disorders, chronic medical conditions
  • 15% MDE die from suicide
  • twice as common in F and adolescents in industrial countries
  • F risk factors: passive/dep/pessimistic personality, poverty, children
  • 50-80% experience postpartum mood swings; 10-20% severe enough for depression (last usually 2-8 weeks, up to 1 yr); onset within 4 weeks of delivery
  • double depression: MDE and dysthymia: poorer px, more severe, melancholia higher, suicide attempt higher
  • SSRIs and tricyclics-typical; MAO inhibitors for atypical depression (anxiety, hypochondria, OC); 60% efficacy with meds
  • CBT and IPT most effective therapies; CBT efficacious; but IPT + meds for more severe
  • ECT for severe endogenous forms of depression: biochem imbalances; delusions, SI- non-med responsive; right sided ECT less memory effect or disorientation
  • SAD thought due to abnormal regulation of melatonin secretions by pineal gland
  • env has greater impact on sxs during early stages of disorder
  • etiology:
    • NE or 5-HT low
    • sleep disturbances (short delay of onset of REM sleep, reduced slow-wave sleep, early morning awake)
    • hostile impulses toward others directed inward (psychoanalytic)
    • learned helplessness/hopelessness model
    • Beck’s: distortion of self, others, world
    • Wolpe’s classical conditioning model: low rate of response contingent reinforcement results in neurotic depression (1st dev anxiety then depression)
    • Bandura’s self-efficacy model
    • Rehm: deficits in self-ctr beh (created group therapy from this):

a.) selective attn to neg events in env

b.) selective attn immediate not long-range outcomes of beh

c.) stringent standards for self-eval

d.) insufficient self-reinforcement

e.) excessive self-punishment

Bipolar Disorder

  • BP1: currently in manic episode and hx of at least one other episode of mania, depression, or mixed
  • BPII: hypomanic + depression
  • manic duration (1 week+); hypomanic (4+ days)
  • 10-15% of BPI die from suicide
  • cyclothymic 2+ yrs (like dysthymia)
  • etiology:
    • NE excessive, 5-HT deficient
    • genetics: 60-65% have bio relative

Anxiety Disorders

  • PTSD vs Acute Distress Disorder (latter up to 4 weeks since event)
    • txt: crisis intervention (when applied immediately, shown to prevent dev of delayed or chronic sxs and reduce distress), CBT, B interventions (systematic desensitization); brief psychodynamic therapy (person integrate experience of trauma into overall personality structure); hypnosis and relaxation therapy (reduce motor tension and ANS arousal); antidep (imipramine)- to help with flashbacks and nightmares; short-term therapy preferred; px better if onset sooner
  • Panic Disorders:
    • etiology: dev of PA and high levels of sodium lactate; genetics
    • txt: meds (antidep- imipramine, MAOIs, Alprazolan, train not to hyperventilate)
  • Phobias:
    • etiology: Psychodynamic (unacceptable sex/aggressive impulses toward person/ object- unconsciously associated with feared objects; Freud- phobia erected as a “frontier fortification” against anxiety)
    • learned behavior- classical conditioned
    • Seligman (biology)- certain stimuli are “biologically prepared stim”- adaptive to fear them
    • txt: antidepressants (imipramine); for social phobia- MAOIs and beta blockers; flooding; meds + BT most effective for relapse
  • OCD
    • recent research suggests higher SES and IQ
    • onset earlier in boys (so B>G); adulthood, no gender differences (F peek in 20s)
    • etiology: Freud (ego and superego dev outstripped libido dev in those disposed toward obsessional neurosis (reaction formation and displacement); 2 factor theory for CBT (person 1st acquires anxiety response to previous neutral stim as result of CC then engage in compulsive rituals to avoid stim; O associated with S)
    • BT doesn’t address depressed mood, sex dysfx, family relationship pblms; bio Fs (SSRI pblms- respond to clomipramine and fluoxetine)

Somatoform Disorders

  • Conversion disorder: 1/more sx of motor/sensory dysfx
    • primary vs secondary gain (sx reduced anxiety to keep internal conflict or need out of conscious awareness; vs sx helps one avoid noxious activity or obtain otherwise unavailable support form env)
    • txt: hypnosis, narcosis (interview with drug), dramatic placebo
  • Somatization Disorder
    • 4 pain sxs, 2 GI sxs, 1 sex sx, 1 neuro sx
    • vague complaints; onset prior to age 30 (usually in teens); chronic course
    • often referred as Briquet’s syndrome
    • often see anxiety, depression, and suicide attempts (rare success)
  • Undifferentiated Somatoform Disorder
    • at least 1 physical complaint 6+ mos
  • Somatoform Disorder, NOS
    • sx duration <6 mos
  • Hypochondriasis
    • associate with “Dr. shopping,” depression, anxiety, OC sx
  • Factitious Disorder
    • need to assume sick role
    • with psych sxs vs with physical sxs (Munchausen Syndrome)
    • Factitious Disorder by proxy (Munchausen by Proxy); mom’s with this: overemphasize their roles as caretaker, deny own needs, devise indirect of getting needs met, uninvolved husbands, passive/dep kids, risk for child abuse, might be some real illness

Pervasive Developmental Disorders

  • Autism seen in 2-5 cases out of 10,000; most common of all PDDs
    • need 2 sxs from social impair; 1 from lang and 1 from stereotype/repetitive beh (total of 6); all seen before age 3
    • 75% also MR
    • genetic Fs; linked to neuro Fs: higher ANS arousal, ventricular enlargement, FL dsyfx, cerebellar underdev, abnormal brain lateralization; maternal rubella, birth complications, elevated 5-HT in brain
    • txt: meds (neuroleptics- Haloperidol- reduce aggression, emotional lability, withdrawal, stereotyped beh); Lovaas
  • Rett’s Disorder
    • dev regression seen by age 4
    • life-long communicative and beh pblms (usually)
    • decelerated head growth, loss of hand skills (replaced by stereo hand move), uncoordinated gait/trunk, severe lang impair, psychomotor retard
    • reported only in F; evidence of genetic mutation
  • Childhood Disintegration Disorder
    • like Rett’s dev stts out normal and regresses: occurs after age 2 but before age 10
    • regress in at least 2 areas: lang, social skills/adapt beh, bowel/bladder ctrl, motor
  • Asperger’s (better px than Autism, lang ok)

Learning Disabilities

  • 20-50% of LD have ADHD
  • Dyslexia:
    • surface (orthogonal) dyslexia (can read regularly spelled words, but pblms deciphering irregularly spelled words
    • deep dyslexia make “semantic paralexia” errors (producing a response that’s related to target word but meaning not visually or phonologically correct- hot for cold, arm for leg)
    • neuro and genetic Fs: neuro b/c: inattn, stm deficits, hyperactivity, L/R confusion (associated with BD)
    • can be linked to: toxin exposure, malnutrition, iron deficiency, food allergies, hemi ab, cerebellar-vestibular dysfx (ottis media with effusion)
  • stuttering note: remits on own in 60% of cases by age 16

Attention Deficit Hyperactivity Disorder

  • 3-5% of kids have; 10% show signs
  • ADHD kids perform several points lower on IQ tests and nearly all have academic pblms; IQ scores also more variable
  • 4-9 xs more common in boys
  • 50% show pblms by age 3 (hyperactive type)
  • 50% of ADHD have conduct pblms; 25% have emotional disorder, 20% LD
  • masked ADHD sxs in adults or can look like Anxiety Ds, Bipolar Ds, Major Depression, OCD, impulse ctrl ds, Substance Abuse, hyper/hypothyroidism
  • etiology:
    • bio Fs: food allergies, high lead levels, alcohol/nicotine prenatal exposure
    • preF cortex
    • genetics (57% risk if parent had it); .80 heritability
    • Barkley’s behavioral disinhibition hypothesis (lack of ability to adjust activity levels to fit requirements of different settings, rather than inattn)
  • txt:
    • CNS stimulants: higher dose reduce activity level and improve social beh; lower dose reduce activity improve attn
    • side effects: somatic sx: insomnia, decreased appetite, stomach aches; move abn: motor/vocal tics (30-70%) or unmasks TS; OC sxs: 30-50% more common with dextroamphetamine than methyphenidate; growth suppression

Conduct Disorder

  • prior age 10 (childhood onset- more aggression, violence and comorbid ADHD and substance abuse; antisocial PD); after age 10 (adolescent onset)
  • previous arrests single best predictor of recidivism rates; multiple: previous arrests, school achv, hx of drug use

Feeding Disorders

  • Rumination disorder (onset 3-12 mos); mortality rate from malnutrition- 25%

Tic Disorders

  • coprolalia (<10%)- utterance of obscene/vulgar words
  • antipsychotic meds most effective: haloperidol, pimozide; clonodine
  • age 4 (encopresis); age 5 (eneuresis); 7% boys and 3% girls (have latter); meds (antidepressant- imipramine); hypnosis, bell/pad, bladder-ctrl exercises

Mental Retardation

  • IQ<70, 2 or more impair adapt fxs, <18 yrs old
  • MR infants: respond less readily to parents and other stim, less physically and vocally active, more compliant
  • mild (50/55-70); educable; 85%; up to 6th grade level; often not dx until late childhood
  • moderate (35-55); trainable; 10%; often require guidance/minimal supervision (social/ occupational); 2nd grade level; sheltered workshops, unskilled
  • severe (25-35); 3-4%; poor motor skills, limited communicative speech; live in community or group homes or with families
  • profound (<25); 1-2%; severe limitations in motor and sensory fx; required highly structured env and constant aid/supervision
  • bio causes: 30% due change in embryonic dev (DS, FAS, etc.); env influences and other mental disorders (nutrition dep, autism, etc.) due 15-20% cases; 10% due to pregnancy/ perinatal pblms (fetal malnutrition, hypoxia, trauma); 5% hereditary Fs (Tay-Sachs, fragile X); 30-40% no clear etiology

Personality Disorders

  • disorder typically manifest in adolescence and chronic;
  • severe PD: hx of dev pblms as child (inability to cope with env stress, poor ego fx, low IQ, disorganized families)
  • genetic component esp shown for: Antisocial PD (5-10xs more prevalent in 1st degree relatives); Schizoid, Schizotypal, Paranoid (possibly Borderline with affective ds)
  • poor childhood adaptive beh better predictor of PD than ed, SES, or alcoholism
  • for Paranoid PD: supportive therapy most effective; CBT good to reduce anxiety, oversensitivity to criticism, and strengthen IP skills
  • Narcissistic PD: Kernberg said- chronically envious, protean sense of self, thwarted as child (unsympathetic/unresponsive mom), libido turned inward- grandiose self; self-importance, egocentricism, and anger is compensatory; Kohut said – arrest in dev rather than a defense; age-appropriate infantile grandiosity not neutralized by mom’s mirroring of reality
  • Borderline PD: 8-10% who attempt suicide are successful
    • ego/object relations theorists: mom withdraws her “libidinal availability”- child attempts separation-individuation producing undifferentiation btwn self- and object-world
    • defense mech: splitting, idealization, projective identification
    • Kernberg says innate bio disposition toward aggression
    • Cognitive theorists: can’t acknowledge wants and to discriminate btwn wants/ needs; anger results from notion that “others should act well toward them and that conditions of the world must be easy or it is awful”
    • evidence that 80% of BPD phys/sex abused
    • txt: CBT (decrease self-destructive beh, improve pblm-solve skills, more accurate perceptions of self, others, world); meds (neuroleptics, lithium, antidep, anxiolytics); dialectical behavioral therapy (CBT, social skills training, self-soothing exercises, group dynamics)
  • Antisocial PD:
    • etiology: genetics, XYY, lower levels of arousal and anxiety to noxious stim, low-wave activity (brain activity ab)
    • therapy: B (withdrawal of reinf for improper times and punish for antisocial beh modeling of appropriate beh; gradual fading of external rewards/reinforcers with more self-ctrl and responsibility); help with anger, impulsivity, and specific behs
  • OC PD: reaction formation d.mech


  • Minuchin believed psychosomatic families (asthma, diabetes, anorexia) more likely to be enmeshed, with highly permeable boundaries: less autonomy and more protective
    • “family lunch” family members and therapist eat meal together (dx- dysfx beh within family structure, and encourage autonomy)
  • reactive attachment disorder of infancy or early childhood: inhibited or disinhibited
  • SIDS is 1 in 500 births (7,000 per year); 1-3 mos of age
  • anorexia etiology: domineering, overinvolved, and insensitive mom, affectively uninvolved dad; psychoanalytic theory (fear of increasing sexuality and/or oral impregnation); dev theory (weight phobia or fear of growing up); poor ego dev due to poor mother-child interactions; bio theories (endocrine/hypothalamus dsyfx); genetics; media
  • eating disorders thought to be related to low serotonin (SSRI txt)
  • Bulimia side-effects: swollen glands, tooth pblms, stomach ruptures, liver damage, sore throat; 50% of overweight women engage in binge eating
    • etiology: low s-e, external locus of ctrl, fear in IP intimacy, perfectionism
    • beh sings: freq wt fluctuations, emotional instability/impulsivity, social maladjust, depression, perfectionism- for approval
    • imipramine, antidep
  • 30% of eating disordered individuals sex abused (similar to other psych disorders)
  • Gasner’s syndrome: syndrome of approximate answers: may be associated with hallucinations, disorientation, amnesia, lack of insight; falls under Dissociative Ds, NOS
  • sex sadism (pleasure in giving pain); sex masochism (pleasure in receiving)
    • covert sensitization txt for paraphilias (pair aversive stim with exciting stim- in mind); orgasmic reconditioning
  • nightmares and sleep paralysis occurs with REM; sleepwalking and night terrors (non-REM)
  • Selye’s general adaptation model (stress): alarm, resistance, exhaustion