 Transference: from Freudian psych; when person respons to someone or some situation as

they were person or situation from past; strong, emo’al & unconscious; it’s why we like or
dislike some ppl on sight
 Introjection: absorbing behaviors of others & acting they have, on to another person;
unconscious imitation, how we gather pieces of what we construct as our self from world
around us
 Blocking: transient inability to rmr
 Denial: refusal to accept some objective reality; ie. after fighting w/husband, say you never
fight w/him
 Displacement: expressing feeling/rxn that belongs to 1 person to someone diff; ie. if woman
was angry at her husband & yelled at group members instead
 Isolation of affect: separation of feeling from fact; reality is recog’d but expected emo’al rxn
is missing; ie. if woman recounts argument w/husband to support group in bland, matter of
fact tones
 Projection: seeing thoughts, feelings & ideas part of oneself as really pt another person; ie.
angry w/someone but see them as angry with you
 Reaction formation: global attitude reversal; love becomes hate, joy becomes sadness
 Regression: return to earlier lvl of func’ing & coping, when adult responds in child-like
manner; ie. woman giigles like little girl whenever husband pays attention to her
 Splitting: rendering world into simple polar opp’s; extreme eval’s
 Sublimation: getting gratification from unacceptable impulse by channeling it in socially
acceptable direction
 Undoing: fixing, repairing & making things better again; can cause many compulsive
behaviors & superstitions; ie. saying prayer every time you’re angry w/someone

Personality disorders:
 Paranoid PD: ideas of reference, overly suspicious, emo’ally restricted (don’t become too
close to anyone; NO TRUST = stuck in oral phase; need therapy for intimacy & trust; can take
meds (benzodiazepines for anxiety & agitation; antipsychotics if severe; sometimes won’t take
meds b/c won’t see anything wrong w/themselves)
 Schizoid PD: cold & aloof, reserved & uninvolved, self-absorbed, A-SOCIAL! (don’t hurt others,
just enjoy own company) will NEVER SAY THEY’RE LONELY; can take meds (low dose
antipsychotics);
 Schizotypal PD: magical thinking & superstitious (think they can tell future) but still in touch
w/reality* – ODD thinking, behavior & comm; at risk of suicide (w/trust & intimacy issues); can
take meds (antipsychotics esp. Haldol)
 Antisocial PD: conmen (manipulative & proud of it), disregard for others, violate other’s
rights, lack of remorse/empathy, poor impulse control, poor attention, sensation seeking, low
resp to threat of pain, difficulty stopping in face of failure; no func’ing super ego nor ego;
50/50 genetic/env’al; mostly males; therapeutic issues strong confrontation, neurological work
& residential treatment
o insula: awareness of body states, pain perception = hence HIGHER PAIN THRESHOLD
o post cingulate: emo’al memory, emotion processing = hence DON’T RMR PAST exp’s
emotions
o temporal pole: integration of emotion & perception, social processing
o amygdala: evaluating sensory stimuli & emo’al resp’s; ESP FEAR* = don’t learn from
punishment & no depth of emotion
o orbitofrontal cortex: learning from rewards & punishments, behavioral flexibility,
impulse control, emo’al & social decision making = DON’T LEARN FROM PUNISHMENT
o ant cingulate: empathy, affect, decision making, cognitive control
o Lack serotonin or DA – happy/sensation hormone missing
 Borderline PD: CRISIS ADDICT*; mood swings, impulsive, self destructive, identity diffusion
(don’t know who they are), similar to APD but mostly females; therapeutic issues is
countertransference is problem; volatile in moods & rel’nships; distraught at ending of 3-mo
rel’nship, convinced despite short duration that marriage was in offing & sees all rel’nships as
intrinsically ‘stormy’; mood changes quickly as she first describes sister in glowing terms then
derides her for interference; emo’al volatility, shifting opinions & unstable rel’nships
o 10% commit suicide – manipulative suicide that goes; ie. Woman takes lot of pills to get
husband’s attention
o 40-70% exp’d childhood sex abuse; grew up in chaotic’s so didn’t exp love; when exp’ing
loving situations, don’t know how to handle situation  feel odd in smooth situations
o borderline b/c border btwn PD & psychosis so both can lose touch w/reality; will be lonely
o use splitting defense mechanism; very severe = lose touch w/reality
o AMYGDALA WORKING AT FULL SPEED = always looking out for those scary/crisis situations
o ant cingulate – no empathy & identity confusion
o Downreg’d intraparietal sulcus 1st rxn to look twds disgusting/disturbing situations which
most would try to avoid
o superior temporal gyrus – don’t think situation thru, solve it like knee-jerk reflex; hyper-
reflexive
o ant insula – trust; don’t understand what socially awkward is so they have boundary
issues; grab someone’s lipstick & use it b/c don’t think its abnormal
o no depressive phases (DD: bipolar disorder)
o Tx: antipsychotics for anxiety & their defense mechanism to help them
 Histrionic PD: attention seeking; physically & provocatively; superficial & need for assurance;
talk in exaggerate adjective (splitting), very dramatic; demanding, don’t have ego, very low
superego & low self-esteem; dramatic entrance; need to be center of attention for reassurance
(type of rxn formation); lack deep feelings; problem in phallic stage; use suppression when
everything’s gone wrong  will think about it tmr
 Narcissistic PD: sense of self importance, feel entitled, ambitious, exploitative, fragile self-
esteem; surround self w/large entourage b/c need to remind themselves how great they are;
can take meds (Lithium/Eskalith) for mood swings, antidepressants for depression or rejection)
 Avoidant PD: shy & socially w/drawn, introverted w/inferiority complex, timid (afraid of
rejection, can’t ask someone on date), WILL ADMIT they’re lonely & want friends but too afraid
o Tx: develop rapport, provide power, permission & protection, & social skills &
assertiveness training
 Dependent PD: follows, need others to tell them what to do; submissive, dependent (can’t
make own decision/indecisive), possibly learned helplessness; dx when over 18 & when
interfering w/real world
o Therapeutic issues: insight oriented therapy & assertiveness training
o Careful when prescribing meds
 Obsessive-compulsive PD: rigid & formal, lack spontaneity & anxious if not in control, like
rules & reg’s, designed to keep anxiety down & so no one can tell them they’re wrong; dislike
change
o Tx: nondirective therapy & group therapy
o Medications: clonazepam (Klonopin) & Benzodiazepines w/anticonvulsant properties
o Don’t do rituals like OCD; but like to keep control of situations to reduce anxiety
 PD NED (not elsewhere defined):
o Mixed personality disorder: exhibiting sx of >1 PD w/personality traits that go together &
cluster of traits dysfunc’al in person
 Ie. Passive aggressive PD:
o Passive-aggressive personality disorder

4 stages of human sexual response cycle:
1. Desire phase: psych’al motivations to have sex, drives & personality; after school age &
puberty
a. behavioral & physio’al component – androgen required, parading, what’s sexy? Social
signals
b. falling in love – pair bonding & tie signs (signs 2 ppl are tied together ie. Wedding ring,
feeding each other, touching)
c. on latency stage  kids do things together, then separate boys & girls, all this to avoid
incest taboo
2. Excitement phase:
a. Females: can be long; engorgement of blood in surface of skin, so feel warm & see
flushing, breasts become engorged & nipples engorged w/blood & get erect & sensitive 
labia & 1st 3rd vaginal wall get sensitive (that’s only pt that feels contact so size doesn’t
matter)  labia changes color (purple) b/c of vasocongestion  transudate starts to
lubricate vaginal wall  where older women who’ve reached menopause start having
problems b/c don’t make enough transudate
b. Males: engorgement of penis w/blood in corpus cavernosum & spongiosum keeps urethra
open & nipples get engorged/more sensitive, penis more sensitive, testicles engorged,
start to move from normal position & retract up into body cavity  start making pre
ejaculate that lubricates possesses no semen but does have sperm
3. Platue: then flattens out;
4. Orgasm phase: sharp peak;
a. Females: repetitive m contraction (includes uterus & suspensory organs of reproductive
system)  best for pregnancy  when orgasm, mouth of cervix dips down into pool where
arrow is  if women is having trouble getting pregnant, becomes imp for her to have
orgasm after man ejaculates to suck sperm thru uterus); missionary pos best way to get
sperm closer to cervix
b. Males: rhythmic m contraction; ejaculation (ejection of seminal fluids & sperm)
i. Blue balls: males not able to ejaculate, penis stays engorged w/blood
5. Resolution phase
a. General relaxation & m relaxation
b. Males: Refractory to orgasm; one shot pistol; time when male can’t have another orgasm
(shorter in younger males (15 mins), longer in older…
c. Females: no refractory period; machine gun (have multiple orgasms)
d. Return to baseline physiological state

 Sexual response reflex: S2, 3, 4 keep penis off floor (point & shoot); works even during
spinal cord injury if above S2 (however, mental stimulation & manual stimulation not possible)
o S2-4: shooting: ejaculation symp’s à pudendal
o P for pointing; pelvic splanchic

Sexual Disorders/dysfunc’s: inhibition of 1 or + of psychophysio’al phases; organic etiology noted
 Hypoactive sexual desire disorder: frequency of coitus (sex); overt cause of lack of
desire; more in females; psych’al phase
 (Phobic) Sexual aversion disorder: aversion to genital sexual contact, repugnance twd sex,
phobic resp to sexual activity  due to –ve exp’s, maybe rape or abuse, more of anxiety based
disorder
 Male sexual arousal disorders: inhibition during sexual activity à inability to attain or
maintain erection to satisfy partner
o Primary: never got erection, harder to treat cause pt doesn’t know what to work twds
o Secondary: acquired, had b4, now can’t
o Selective impotence: erection in some situations but not others ie. Virgin & whore
syndrome
 Stamp test: biological if failed, psych’al if passes aka if broken
 Female arousal disorder: dysfunc in excitement phase (can’t get excited) want sex but
don’t have same sexual activity; vaginal lubrication; ie. Post menopause; exp painful
intercourse
Orgasmic disorders
 Women’s orgasmic disorder (anorgasmia): despite rep’t of high sexual
arousal/excitement there’s lack of ORGASM, diminished intensity of orgasmic sensations or
delay of orgasm; 22-28% prevalence
 Male orgasmic disorder (delayed ejaculation in DSM V): delay in or absence of orgasm
following normal sexual excitement; retarded
o Retarded ejaculation: no orgasm even tho there’s stimulation or delayed; biological or
psych’al
o Retrograde ejaculation: ejaculate directed into bladder – only biological
 Premature ejaculation: more in males; ejaculate before entering or after
o Biological factors: chronic prostatitis, diabetes mellitus, hyperthyroidism
o Psych’al factors: more likely to produce primary PM, > common in college pop
(overconscious to satisfy partner), score higher on MF scale in MMPI (men more feminine
side)
 Use off label:

Genito-Pelvic Pain/Penetration Disorder (DSM V) /Sexual Pain Disorder (DSM IV)
 Dyspareunia: sexual intercourse so painful they don’t want to do it anymore
 Vaginismus: clamping down of m’s in vaginal wall so cannot penetrate thru it
 Aversion disorder:
 Sexual disorder NED:

Sex therapy:
- medical eval
- sx relief
- psychotherapy – can be ind, marital, group, behavior (systemic desensitization, deep m
relaxation, assertiveness training), hypnotherapy
- prescribed sexual exp’s – refer pt to sex therapist

 Sensate focus: sensory awareness (focus on sensations) primarily massages  nongenital
massage 1st so no pressure to perform, just feeling skin on skin contact, tell them they don’t
have to have sex so pressure is off  over time after nongenital, give genital massage  but
again, not massage that leads to sexual intercourse; focused in what feels good & not physical
aspect in body; premature ejac tx
 Semen’s technique: “start-stop” technique for erectile dysfunc; man lays back while woman
gives him erection again & again; male in inf pos so woman gets more control of her body so
she can stop b4 he ejaculates; then go side to side  then male in sup pos so he understands
its something that can be replicated in any pos over & over again, he can get erection any
time he wants to  works well unless there’s some sort of pathophysiology
 Squeeze technique: for premature ejaculation, vaginismus; manual stimulation for retarded
ejaculation & anorgasmia; biofeedback; squeeze base of glans stops sensation of wanting to
ejaculate to delay gratification let guy enjoy sensation and prolong this as long as possible to
unlearn what he learned as young boy

….

Psychotherapy: btwn mental health practitioner & client to treat sx of mental disorder,
psychosocial stress, rel’nship problems, & difficulties in coping in social env

 Cognitive therapy (RET): focus on changing –ve thoughts & beliefs to eliminate maladaptive
behaviors (&  vulnerability to depression); detect unrealistic, self-defeating & irrational
thoughts; develop alternative rational beliefs; based on Skinner (& Albert Ellis)
o Rational emotive therapy:
o Elli’s Approach: our emotions are result of our cognitions, ABC (activating event  belief
 consequences)
o Beck’s Approach

Behavioral therapies: encourage appropriate behavior & changing malaptive 1’s thru learning
& apply conditioning principles
- Classical conditioning techniques:
o Systemic desensitization: treat phobias, pair relaxed states w/increasingly fearful
stimuli
o Aversive conditioning/therapy: repeatedly pairing problematic behavior w/aversive
stimuli (ex. Drug causing nausea, esp used for alcoholism)
- Social skills training (assertiveness training)
o Modeling (derived from social learning theory)
o Behavioral reversal
- Operant conditioning techniques
o Extinction: remove stimulus that makes behavior less likely in future; ie. ignoring child
having temper tantrums (so tantrums stop)
o Fading: gradually removing operative ingredient producing behavior but in way that keeps
behavior; thus behavior is still maintained unlike extinction; ie. gradually replacing
addictive pain medication w/amts of placebo (so pt still rep’ts pain relief)
o Punishment
o Token economy
o Flooding: last resort
- Family system therapy: resolve problems dev’d in fam setting to improve fam
rel’nships/comm; prefer to speak to whole fam together

 Positive reinforcement:
 Negative reinforcement:
 Secondary reinforcement:

3 factors at work in all types of psychotherapy – supportive rel’nship, opportunity to open &
reason for hope

Effective of psychotherapies:
- avg psychotherapy client shows more improvement than 80% of those in no-tx control group

Sleep stages of sleep cycle:
Awake: low voltage & high frequency
NREM: synchronized & idling; w/age
- Stage 1: low voltage & mixed frequency; 1-7 mins; m tone; N1
- Stage 2: sleep spindles & K complexes; light sleep; 45% sleep; sleep talking & teeth
grinding/bruxism; N2
 N3 = stage 3 + 4; sleep walking (w/in 1st 3 hrs of sleep); 25% of sleep; w/age; deep or slow
wave
- Stage 3: mostly slow waves; <50% delta waves; <3 rate & respiration; hard to awake,
lower frequency & waves
- Stage 4: slow waves (larger amplitude), slightly m tone, intact reflex; >50% delta waves;
night terrors
REM: low voltage, mixed frequency + /saccadic/rapid eye movement & m atonia; 3-5 ~90-120
min total; ‘paradoxical’; each 10-20 min & thru out night; paralyzed during dream sleep (via
pons  inhibit motor neurons, most ppl have 2 hrs of dreams); most in 2nd ½ of night (Vs. 1st ½ of
night more delta sleep); not synchronized; pulse, BP & resp; poikilothermic (unreg’d) temp;
w/age
 Myotonic jerk: feeling like falling when going into sleep & wake up suddenly
 Night terrors: sleep walking in stage 4
 EEG: electroencephalogram; measures brain wave activities during sleep
 Sleep paralysis: when person wakes up & can’t move (feeling something heavy pushing on
chest); something ppl w/narcolepsy exp; paralysis upon awakening, lasting sec’s to mins

4 NT’s rel’d to sleep:
1. ACh – sleep efficiency & REM sleep
2. 5-HT – sleep efficiency & delta sleep
3. DA: sleep efficiency
4. NE: sleep efficiency & REM sleep

 Sleep latency: from turning lights off to stage II sleep; in narcoleptics
 REM latency: from onset of sleep & first REM period

Sleep-wake disorders:
 Insomnia disorder: persistent difficulty falling asleep or staying asleep; sx, NOT dis; 20-40%
pop; difficulty falling asleep, maintaining sleep for at least 3 mo’s (+3 nights/week)
o Tx’d by deconditioning (sleep in other bed) massage, meditation, sex (for short term use
meds)
o Therapy: benzodiazepines (antidepressants – valium), sleep meds; diet supplements,
melatonin, antihistamines & neuroleptics (antipsychotics – very strong)
o Early/Initial (can’t fall asleep; sleep onset)
o Middle (keep waking up; can’t stay asleep; sleep maintenance)
o Late (waking up too early & can’t get back to bed); depression worsens
 Hypersomnolence disorder: excessive daytime sleepiness (EDS) or sleep; opp of insomnia!
Must be 3X/week for 3 mo’s; causes include – narcolepsy, sleep deprivation or stimulant
w/drawal; Tx: stimulants (amph) or sometimes SSRI’s
o Self rept’d excessive sleepiness despite main sleep period last at least 7 hrs, w/1 of
following –
 Recurrent periods of sleep or lapses into sleep w/in same day
 Prolonged main sleep episode of >9 hrs/day that’s non restorative
 Difficulty being fully awake after abrupt awakening
 Klein-Levin syndrome: “sleeping beauty”; recurring periods of excessive sleepiness &
eating; feel tired, go to bed for 24 hrsor+, only get up to use bathroom & eat & get ‘spacey’;
episodes can last days, mo’s & yrs can pass btwn episodes; exhibit hyperphagia & less often
hypersexuality
 Narcolepsy: sleep latency; recurrent periods of irrepressible need to sleep, lapsing into
sleep or napping occurring in same day (3X/week for 3 mo’s)
o Long term- cataplexy & tongue sticking out
o also exhibit: sleep paralysis (60%), hypnagogic hallucinations, automatic behavior,
nighttime sleep disruption & social complications
 Hypnagogic hallucinations: intense, vivid dreamlike exp’s that occur just b4 falling
asleep
 Automatic behavior: 80% pt’s; episodes of semi-purposeful activity often nonsensical
(like putting clothes in oven or partially preparing a meal)
 Hypnopompic hallucinations: similar to hypnagogic but occur when waking up
 Tx: no ‘cure’; sx can be managed (scheduled naps, &/or stimulants or anti-
depressants); orexin blockers shown good initial results
o Presence of at least 1 of following –
 Cataplexy episodes, for those w/long standing narcolepsy; triggered by strong emo’al
stimuli; ie. laughter, excitement, anger, sex & can last 20sec-20min; sudden loss of m
tone that could involve 1 or all m’s
 Spontaneous grimaces: jaw-opening episodes w/tongue thrusting or global
hypotonia (w/in 6 months of onset of narcolepsy)
o Cause  pt’s don’t produce hypocretin/orexin in hypothalamus  might be auto-immune
problem
o So problematic tx: orexin blockers show good initial results for treating narcolepsy; helps
more release
 Breathing-rel’d sleep disorders –
o Obstructive sleep apnea hypopnea: excessive relaxation of pharyngeal m’s causes
snoring or restriction/collapse of upper airway; interferes w/stage 3 & 4 causing daytime
sleepiness; +snoring most common type; 8:1 ratio M to F; can get respiratory acidosis
o Central sleep apnea: 5or+ central sleep apneas/hr; presents in 2 ways –
 Repeated episodes of apneas & hypoapneas during sleep caused by variable
respiratory effort, but w/out evidence of airway obstruction
 Cheyne-Stokes breathing pattern causing repeated episodes of apneas & hypo-
apneas – seen in terminally ill pt’s, periods of no breathing & then start breathing;
mammillary & brain damage
o Obesity hypoventilation syndrome (‘pickwickian’): obese ind’s failure to breath
rapidly/deeply enough; cessation of breathing during sleep causing repeated awakenings,
leading to EDS; also get breathing problems when awake  causing hypercapnea (blood
CO2)
 Circadian rhythm sleep-wake disorders –
o DSPS (delayed sleep phase syndrome): late sleep onset, late awakening, normal amt
sleep once asleep
o ASPS (advanced sleep phase syndrome): early sleep onset (6-9 pm) w/early wakeup
(3-5am); rel’d w/depression
o Jet lag
o Shift work: working overnight
 Parasomnias: all abnormal things that can happen to ppl while they sleep
o REM sleep behavior disorder: acting out dreams, grunting thrashing, occurs during REM
sleep, usually in men 60 yrs &+; lack atonia or sleep paralysis in REM sleep; treated
w/clonazepam (benzodiazepine); pathway of pons don’t work properly & somatic motor
neurons NOT inhibited
o Nightmare disorder: repeated awakenings due to extreme nightmares w/detailed recall
o Restless leg syndrome: unpleasant sensations in legs, most common in ½ area; occurs
when ind lies down or sits for extended periods; feel ‘uncontrollable’ urge to move or
massage affected area
o Non-REM movement sleep arousal:
o Disorders
 Sleepwalking/somnambulism: occurs during non-REM (stage ¾) sleep usually only
in kids;
 Sleep terrors: during stage ¾ sleep; non specific feelings of terrors during 1 st 1/3 of
night’s sleep
o Periodic limb movement syndrome (nocturnal myoclonus): stereotyped contractions
of leg m’s (extension of toes, flexion of ankle & knee); may not be aware of movements
but may complain of insomnia; partner will definitely know ;)
o Bruxism: teeth grinding, usually stage 2 sleep; tx is mouth guard; treat anxiety
o Jactatio capitis nocturnis: sleep rel’d head banging; rhythmic head & maybe body
rocking
o Sleep talking (somniloquy): ranges from mumbling to complicated
dialogues/conversations; most common in males & children; can be due to many factors
(stress, depression, sleep deprivation) & does seem to run in fam’s; short duration; not
product of conscious or rational mind & thus inadmissible in court; lighter stage of sleep =
more intelligible the conversation can be
 Assessed by severity (1) mild (>1X/week), (2) moderate (several times/week) & (3)
severe (nightly, major problem for partner)
 Duration: acute (<1 month), subacute (1 month to 1 yr) & chronic (>1 yr)
o Sexsomnia: sexual episodes during NREM sleep; pt rmr’s little or nothing of event; used in
several cases (successfully) as rape defense
o Exploding head syndrome: person wakes up in night thinking they head really loud
noise (explosion, gunshot, or screams); not painful, may be caused by small temporal lobe
seizures
o Fatal familial insomnia: AD (50% chance of inheritance); VERY rare (40-50 fam’s
worldwide), onset at midlife; sleepless nights until coma & death (5-10 months after
onset); prion disease
 Dreams: not only in REM sleep; in REM are ‘abstract & surreal’ VS. NREM dreams (less
frequent) are ‘purposeful & lucid’ but don’t forget night terrors; 2 theories to why we dream –
o Psychoanalytic theory: dreams represent unconscious desires & thoughts, based on
aggressive & sexual instincts repressed from conscious awareness; anything tunnelly
represented sex/female; & pointy represented phallic stage
o Activation-synthesis theory: results from brain activation during REM sleep;
unconscious pt of brain is busy processing unconscious rel’d memory

2. Neurocognitive Disorders
 Delirium (acute confusional state): rapid short term confusion & changes in cognition; ex.
Terminal care; abnormal EEG; 70%+ of older person’s in intensive care; disturbance in
attention & awareness that develop over short period of time; diff DSM criteria for diff causes
(medical condition, substance abuse, multiple causes (ie. Head trauma & kidney disease),
delirium NOS (ie. Sleep deprivation); Often preceded by prodromal sx (restless, fearful,
something is off); sx last as long as causative factors exist (<1 week) & resolve w/days-week
or 2 after causative factors removed; events occurring during delirium often poorly recalled
later; Tx: removing underlying cause (medical condition, drug use); Delirium onset fast, lasts
hrs to weeks, speech incoherent, recent memory poor, disorg’d thoughts, delusions &
hallucinations may be present; Presents in 3 ways –
 Hyperactive: rapid onset of severe confusion & disorientation w/fluctuating intensity
 Hypoactive: sudden w/drawal from interax’n w/outside world
 Mixed: alternate btwn hyperactive & hypoactive
o >50% cases hospitalized pt’s (esp ICU) – appear out of touch w/surroundings &
spontaneously producing evidence of his confusion & disorientation by muttering,
rambling, shouting (often offensively & continuously) w/evidence of delusion &
hallucination & often w/so much associated motor activity that physical exhaustion
overcomes him
o dx must be made against prev baseline mental activity; ie. Long term schizophrenic would
show potential delirium sx but won’t be necessarily delirious b/c delirium must have
organic cause (disease, drug)
o most cases ACh in pathway from reticular formation to thalamus & tectum (dorsal
tegmental pathway) (many delirium-inducing factors cause ACh)
o Antilirium prescribed in cases of anticholinergic toxicity
 Dementia: severe impairment in memory, judgment, orientation & cognition; many types;
either major or minor disorders (NCD); seen in 15% ind’s >85 yrs; normal EEG; most common
cause is Alzheimer’s & 2nd is vascular dis; declining mental abilities esp memory; chronic
condition w/slower onset than delirium
o Major NCD: evidence of sig cognitive decline from previous lvl of performance in 1or+
cognitive domains (memory, executive func, language); interferes w/capacity for
independence; derived from pt, knowledgeable informant, or clinician or standardized
testing; correspond to conditions listed in DSM-IV-R as dementias
 Alzheimer’s: MC form of dementia; neurofibrillary tangles inside neurons, plaques
outside; beha’al changes b4 cognitive decline; IQ declines w/progression of dis;
insidious onset & gradual progression of impairment; 65% of dementias, women> men;
age onset in 8th-9th dec (70s/80s), early onset forms in 5th-6th dec;
 Peanut butter test: pt closes eyes, occludes 1 nostril (tests olfactory n), PB
moved up twds nose until person can smell it; ‘normal’ ind has symmetric detection
(can smell PB at same distance for both nostrils) but ALZ pt’s have L side less
sensitive than R, upto 10 cm difference

gyri shrunk, dark spaces = CSF
 Frontotemporal dis (Pick’s): sx onset similar to ALZ but learning & memory
minimally affected; only see atrophy of frontal & temporal lobes; see behavioral
disinhibition, apathy, loss of sympathy/empathy, perseveration, stereotyped behaviors,
decline in executive func &/or decline in language ability
 LBD (Lewy body dis): may have delusions & hallucinations (ex. +ve psychotic sx);
similar to PD w/PD-like sx; other sx & time course differentiate LBD from PD; can also
show ALZ-like cognitive impairments due to loss of cholinergic neurons
 If dementia of same onset or w/in yr of motor sx = LBD
 Lewy bodies found cortically
 PD (Parkinson’s dis): can go yrs w/out showing altered cognitive func; same as
above except for onset; HYPOKINETIC (diff from Huntington’s)
 Both have motor/kinetic problems, slowness of movement, difficulty in
initiating movements, ex. May also have REM behavior disorder
   if dementia onset more than yr after motor sx = PD W/DEMENTIA
 Lewy bodies in basal ganglia (structures that plan movements)
 Vascular dis: memory loss & cognitive impairment due to cumulative small strokes;
2nd most common cause of dementia; sudden onset of cognitive dysfunc; stepwise loss
of some func w/each infarct; focal neurological sx (ie. Gait); 15% of dementias, onset
earlier than ALZ, men> women

white spots = edema = stroke = vascular disease
 traumatic brain injury: brain damage due to injury; onset after whatever age you hit
your head really hard
 substance/medication use, HIV infection, prion disease,
Huntington’s dis: also can have motor problems, but hyperkinetic (too much
movement); onset age is 30-40s; cognitive problems often precede motor problems
 another medical condition or multiple etiologies
o Mild NCD: does not interfere w/independence; not dementias; pt has some cognitive
decline but it doesn’t interfere w/capacity for independence; need more strategies &
compensatory mechanisms, ex. Grocery list even though only 3 items needed from store);
DSM V criteria same as for Major NCD, except use of phrase ‘mild cognitive decline’ instead
of ‘sig’ cognitive decline; list is same as Major NCD but at earlier stages where difficulties
are managable
 Amnesia: memory impairment & forgetfulness; accompanies delirium & NCD’s

 Pseudodementia (mild cognitive impairment): depression in elderly misdx’d/mimics as
dementia; memory problems less severe than ALZ, IQ not affected; elderly don’t have minor
forgetfulness that doesn’t mean early ALZ onset…otherwise ½ of us would be in trouble
 Aphasia: loss of ability to produce or understand language
 Apraxia: inability to make certain movements, despite healthy body; ie. pick up phone & talk
w/out dialing
 Agnosia: problems recognizing familiar persons & objects, even though senses func’ing
o Tactile agnosia: put something in hand but cannot recognize by feel of it
 Executive dysfunc: inability to plan, organize or reason

Memory & Amnesia; diff types of memory dysfunc –
 explicit/declarative: knowledge of factors & what they mean; used ‘consciously’; ie.
personal; affected in pathology
 implicit/non-declarative: involves info about how to perform something; used
‘unconsciously’; rarely affected in amnesic states; how you do automatic ax’ns (ie. Tying
shoes)

Memory types:
- Working memory: seconds
- Short term memory: minutes
o Short term & working tested for by: Spell word backwards, serial 7’s, object recall
(immediate & 5 min later)
- Long term memory: years
Memory deficits:
- Anterograde amnesia: can’t form new long-term memories (pt HM, Clive); causes include
encephalitis, meningitis & surgery
- Retrograde amnesia: can’t recall past memories or identity; causes included getting bonked
on head
- Global amnesia: both of above
- Getting bonked on head could cause any or all of above
- Post traumatic amnesia: due to blow to head; results in varying degrees of memory dfx,
from transient loss of most recent events to preceding slide; prognosis relates to extent of
trauma or damage; no cause; ie. Wandering around central park, unsure confused, goes home
& rmr’s everything & is fine; thus, unexpected period of memory loss
- Transient global amnesia: transient condition resolving in <24 hrs; cannot form new recent
memories but sense of identity intact; common in middle age to elderly; good prognosis
- Blackout phenomenon: partial loss of anterograde memories due to excessive alcohol
consumption; can’t recall events from intoxicated period; good prognosis b/c only things
forgotten are during drinking
- Korsakoff’s syndrome: persistent memory loss, but w/interesting condition of confabulation
(2 types):
o ‘provoked’ momentary: likely ‘normal’ resp to faulty memory, ie. Pt’s asked to recall
story about woman whose purse was stolen rmr it was ‘women was thief’
o ‘spontaneous’ fantastic: bizarre, delusional memories or beliefs, usually firmly believed

Psychologically rel’d memory deficits:
- Dissociative amnesia/psychogenic amnesia: inability to recall imp autobiographical info,
of traumatic or stressful nature, inconsistent w/ordinary forgetting; consists of localized or
selective amnesia for specific event(s); or generalized amnesia for identity & life hx; presents –
o Localized amnesia: cant recall events in circumscribed period of time (child abuse yrs,
military service)
o Selective amnesia: ind can recall some but not all events during circumscribed period of
time
o Generalized amnesia: complete loss of memory for 1’s life hx; can include loss of
personal identity
 2 types of dissociative amnesias:
1. Global transient (fugue state): stress or depression induced loss of identity, lasting
hrs to days; very rare, good prognosis, ex. Yrs of abuse
a. Dissociative fugue (fugue state): apparently purposeful travel or bewildered
wandering associated w/amnesia for identity or other imp autobiographical info;
when person suddenly leaves & creates new identity elsewhere, often ‘going back to
age’ b4 traumatic or stressful life events occurred that precipitated fugue; very rare
2. Situation specific: memory loss of particularly stressful event (war, rape); prognosis
more variable & often requires long term therapy
Ex: Agatha Christie: famous author (Hercule Poirot, Miss Marple, Murder on Orient Express); in
1926, her husband requested a divorce; Christie disappeared; 11 days later, after a massive
search, she was found in a hotel room across country, registered as Mrs. Teresa Neele
- 50-75% depressed pt’s exp impaired concentration & forgetfulness
- sleep deprivation may also contribute to memory problems
- dietary issues (thiamine def) can be underlying cause
- seizure disorders often have associated memory losses/impairments
Characteristics Delirium Dementia Amnesic Disorders

Hallmark Impaired Loss of memory & intellectual Loss of Memory
Consciousness abilities
Etiology CNS dis, trauma or Tangles & fibrils; Vascular; CNS dis, Thiamine def; temporal lobe
infection; Systemic trauma or infection trauma, infection or vascular
dis; High fever; S/A or dis
w/drawal
Occurrence >common in children Elderly Associated with Hx of EtOH
& elderly abuse
Associated Acute medical illness No medical illness Same as dementia
Physical Findings ANS dysfunction Little autonomic dysfunction
Abnormal EEG Normal EEG
Associated Impaired Normal consciousness Normal consciousness
Psychological consciousness No psychotic sx No Sx early; depression later
findings Illusions/hallucinations Depressed mood Confabulation
Anxiety & Agitation
Sun downing
Course Quick onset; Acute Slow, Insidious Develops slowly
Fluctuating course w/ Progressive Progressive downhill course
lucid periods Chronic
Tx and Px Remove underlying No effective tx; rarely reversible Same as dementia
Medical disorder; Rx to treat Sx
reorient Structured env
ACHe inhibitors for Alzh
3. Schizophrenia & Other psychotic disorders:
 Schizophrenia: sx begin in adolescence, then prodromal phase brought on major changes
(starting college), then psychotic sx; subsequently undergo series of recoveries & relapses
 Prodromal phase: social activities, new/changing interests in religion, occult,
philosophy (seeking answers b/c thinking diff’ly)
 Active phase: ie. Psychotic episode
 Residual phase: period btwn psychotic episodes, usually –ve sx
o requires 2 of following of Criterion A – (+1 of 1st 3 sx)
 Delusions
 Hallucinations
 Disorg’d speech
 Grossly disorg’d or catatonic behavior
 –ve sx (flattened affect, alogia, avolution, anhedonia)
 alogia: complete lack of speech
 avolution: lack of desire to pursue meaningful goals
 anhedonia: inability to exp pleasure
o Criterion B: social/occupa’al dysfunc; impaired func’ing thru out active phase of illness
o Criterion C: duration must be of 6 mo’s
o Criterion D: no dx of schizoaffective disorder or mood disorder
o Criterion E: not due to drugs or medical condition
*Note: not split personality, dangerous, retarded, unstable &/or wild
- 5-10 yrs after initial hospitalization, only 10-20% considered to have had ‘good outcome’
- 60% or + remain sig’ly impaired for remainder of life
- only 20-30% of schizophrenics lead ‘normal’ lives
- 1% lifetime prevalence, 50% don’t get treated, equal male/sex ratio but males affected
earlier, winter births more affected; more likely to become drug users (risk taking behaviors,
judgment is impaired, & ind isolated)
- 40-60% get re-admittance to hospital w/in 2 yrs of 1st episode; schizo’s occupy 50% of
psychiatric beds
- 50% concordance w/MZ twins of schizo pt
- Dad’s >60 more likely to produce children w/schizo
- 50% schizo’s attempt suicide
- Comorbidity w/
1. Varied neuro’al signs (motor disorders, tic, hypertonicity, lack coordination, fine motor
skill problems)
2. Higher blinking rate (due to DA)
3. Lack of prosody (pitch movements & tone; could involve non-dominant parietal lobe)
4. # of conditions/diseases associated –
a. Obesity (higher avg BMI)
b. Diabetes, COPD, <3 dis’s (b/c higher smoking rate)
c. HIV (d risk behavior)
Theories:
 Emil Kraepalin: ‘dementia precox’ (precox = early onset); ‘paranoia’ identifies separate
group charac’d by persistent persecutory delusions
 Eugene Bleuler: ‘schizophrenia’ (schizo=schism) b/c felt it represented breaks btwn thought
& reality

- +ve sx: sx in schizo’s but not in ‘normal’ pop; ie. hallucinations, delusions, racing thoughts
- -ve sx: traits/charac’s in normal person’s but lacking in schizo’s; indicating lack of something/
missing; apathy (blunted affect), lack of emotion/desire, poor or non-existent social func’ing
- cognitive: disorg’d thoughts, difficulty concentrating or following instructions & memory
problems; may be apparent in both +ve or –ve categories
 Illusions: misperception of real stimuli (for a second, I thought tree was alien)
 Delusion: false belief not shared by culture (aliens secretly running USA)
 Hallucination: sensory impression or activation w/out actual stimuli (aliens talking to me all
the time); 75% hallucinations in schizo are auditory
 5 substypes of schizophrenia – paranoid, disorg’d, catatonic, undifferentiated, or residual;
ELIMINATED due to poor validity, reliability
 Physiology/pathology of schizophrenia:
- DA system over activity; drugs that DA (AMPH) cause schizo-like sx & anti-psychotic drugs
are D2R antagonists; excess DA correlates w/+ve sx
o Haldol (haloperidol): long-time anti-psychotic/neuroleptic D2 antagonist; ‘typical’
antipsychotic; inhibits DA
- 5-HT (Serotonin): excess seen w/+ve & -ve sx
o clozapine ‘atypical’ antipsychotic b/c interacts w/both 5-HT & DA
- GABA: interacts w/both 5-HT & DA systems; works w/antiseizure meds (GABA meds) major
inhibitory NT
- Glutamate: phencyclidine (GLU antagonist) can induce schizophrenia-like condition (ie. Angel
dust – same side efx of excess glutamate – super symp system kicking in!)
- ACh: nicotinic receptors (do schizo’s self medicate by smoking? Also b/c bored)
- Deficits in smooth pursuit eye movements following moving finger, 80% show saccadic
eye movements (whereas N show activity in prefrontal cortex when faced w/cognitive task,
schizo’s show activity)
- Hypofrontality: activity in frontal lobes
- ventricle size
- size of limbic structures (emo’al circuitry)
- Progressive loss of corticol gray matter in chronic schizo pt’s (pathology MORE
PINK, LESS BLUE!)
- no single sign/sx pathognomonic for schizo & sx can change over time so pt hx imp!
o Pathognomonic: sign unique to 1 dis
o Premorbid: preceding dis’s (weeks b4)
o Prodromal: early, nonspecific sx(s) indicating start of dis’s; YRS b4
- Premorbid/prodromal signs & sx: tricky b/c some aspects of pt’s hx would be similar – ie.
Introverted in teens, no or new friends, no girl/boy friend; problem that early signs recalled
after schizo dx’d aka hindsight 20/20/ “Monday morning quarterback”
- Mental status
o Generally variable so can’t be summarized; more specific
o Hallucinations: auditory common, visual may also occur; other sensory hallucinations may
suggest medical/neurological condition
 Cenesthetic type: altered states of body organs (ie. My brain is on fire)
o Violence/suicide/homicide: violence common among untx’d, suicide leading COD among
untx’d but homicide not rel’d
o Orientation & memory frequently intact
o Judgment/insight: don’t do well recognizing they have condition; so poor tx compliance &
meds common
Tx:
- Pharmacoptherapy (antipsychotic drugs) good but not sufficient
- Therapies/interventions can help to  degree of recovery
- Single approaches do not generally work well (schizo complicated!)
2 categories of Treatment drugs:
1. Typical/conventional DA drugs: effective for treating +ve sx but not so for –ve sx
a. Chlorpromazine (thorazine)
b. Haloperidol (Haldol)
c. Perphenazine (Etrafon, Trilafon)
d. Fluphenazine (Prolixin)
2. Atypical: preferred for initial tx over typicals, but more expensive & side efx (weight gain)
a. Clozapine (Clozaril) – very effective for tx resistant schizo’s but serious side efx
(agranulocytosis & myocarditis so more prone to infections)
b. Risperidone (Risperdal) – MC
c. Olanzapine (Zyprexia)
 Side efx of antipsychotic drugs: EPS (extrapyramidal side efx) & movement disorders (Tardive
dyskinesia)

Differential dx’s – (don’t mix up w/schizophrenia!) slide 20
 Medical & Neurological –
 Drugs: cocaine, AMPH-induced psychosis, PCP (angel dust), alcohol or barbiturate w/drawal
 Dis’s: HIV, encephalitis, Huntington’s, Wilson’s, Wernicke-Korsakoff; if causes brain
damage/dysfunc, could result in sx similar to schizo
 Psychiatric –
 Malingering (pretending to get out court)
 Schizophreniform disorder: very similar to schizo except –
o Sx >1 mo but <6 mo’s
o long term prognosis good; life time prevalence ~0.1%
o pt’s have more affective sx (ie. Mania) so condition may be more similar to mood disorder
o course: can have >1+ episode; ~70% go on to develop schizo
o Tx: same as schizophrenia;
 Schizoaffective disorder: schizo & manic or depressive syndrome; features of both schizo &
affective (mood) disorders; prevalence ~<1%; difficult to estimate course or prognosis b/c of
difficulty in dx’ing; rmr also get hallcuinations, delusions; dx via DSM V:
o Uninterrupted period of illness during when there’s major mood episode (major depression
or manic), concurrent w/criterion A for schizophrenia
o Delusions or hallucinations for 2or+ weeks in absence of major mood episode
o sx that meet criteria for major mood episode present for majority of duration of illness
 Delusional disorder: delusions w/out other schizo sx for at least 1 mo!*; criterion A for schizo
not met (Hallucinations might occur, but rel’d to delusional theme, ie. Person thinks they’re
infested w/insects (delusion) & think they can feel them moving inside them (hallucination)
o aside from delusional aspects, func’ing not markedly impaired & behavior not odd/bizarre
o can be mood congruent (manic w/delusions of grandiosity) OR mood incongruent
(someone depressed who has delusions of grandiosity)
o not listed as specific types of delusional disorders, but still delusions:
 of being controlled: feelings, thoughts, ax’ns are under someone else’s control
 thought broadcasting/insertion: thoughts being broadcast out loud or inserted into pt’s
mind
 of reference: idea events/things in person’s immediate vicinity have some sort of
unusual sig
o Types of delusional disorders:
 Bizarre: totally implausible phenomenon (Aliens stole my internal organs)
 Non-bizarre: believable delusions (can happen in real life), ie. Police got my apartment
under surveillance
 Jealous/Orthello syndrome: believe partner cheating on them; can be very sudden
onset w/no prior psychiatric hx; > common in men; potentially dangerous
 Erotomanic: false belief someone imp in love w/them; show ‘paradoxical conduct’ ie.
Any denials or –ve rxns from ‘love’ are interpreted as +ve; often lonely, unattractive
woman in low lvl job
 Grandiose: delusion of inflated worth, power, knowledge; megalomania
 Persecutory: belief of being attacked, cheated, harassed, harmed. sometimes become
obsessed w/pursuing litigation against their supposed harassers
 Somatic: delusion pertaining to appearance or func’ing of body
 Ex. Delusional parisitosis: convinced their body is infested w/parasites
 Mixed type: when no 1 delusional theme predominates*; thus more than 1 theme
 Unspecified type: when dominant delusional belief cannot be clearly determined in
specific types
 Psychotic disorder NOS:
 Brief psychotic disorder: >day but less than month; pt’s show full remission; more common
in younger (20-30s; esp 30) than older; abrupt onset; follows major life stressors; avg age
onset mild 30s
 ‘Folie a Deux’/Shared psychotic disorder: couples/pairs that go & kill ppl; ‘madness
shared by 2’; 1 partner dominant, influences other (more naïve/gullible/less intelligent/low self
esteem) to join in on fun; 1 person begins to believe/share another person’s delusion; know
each other for long &/or live together
 Randy & Evi Quaid: ‘escaped’ to Canada from Hollywood to avoid Hollywood Starwhackers that
were killing celebrities
 Shanita Cunningham & Erica butts in 2011: Both sentence to life in prison b/c spent 2 weeks
beating, whipping & hitting Butts’ 3 yr old goddaughter until she died; both were in rel’nship
(common in this condition)
 Catatonia: not dx of own, in several disorders, presence of 3or+ of 12 psychomotor features
w/another mental disorder; marked psychomotor disturbance seen w/motor activity,
engagement during interview or PE or excessive/peculiar motor activity; can range from
marked unresponsiveness to marked agitation
o Criterion A sx for Catatonia:
1. Stupor (no psychomotor activity)
2. Catalepsy (passive induction of posture held against gravity); imagine m rigidity of
gradual onset to pt person is immobile in bed & thought dead, then buried
a. Edgar Allen Poe featured catalepsy in 3 stories: premature bural, fall of house of
Usher & Berenice
3. Waxy flexibility (resistance to pos’ing): also in video, when pt’s were posed by others
4. Mutism (no verbal resp)
5. Negativism (no resp to instructions)
6. Posturing (maintaining postures against gravity): like in video, pt holds odd posture for
long lengths of time, but obviously not dead
7. Mannerism (odd caricature of normal ax’ns)
8. Stereotypy (repetitive movements)
9. Agitation (not influenced by external stimuli)
10. Grimacing
11. Echolalia (mimicking another’s speech)
12. Echopraxia (mimicking another’s ax’ns)
 Autoscopic: pt sees ‘phantom’ of themselves, colorless & transparent; very rare
 Postpartum psychosis: occurs soon after birth; to mother, not baby; many drugs can also
cause psychosis (ie. Amphetamines, cocaine, PCP)
 Bouffee Delirante: brief psychosis w/good prognosis (kind of btwn psychotic disorder &
schizophreniform disorder)
 Oneiroid: dream like state when pt exists almost exclusively in their hallucinatory state, not
well oriented to time & place, seem very confused
 Simple deteriorative disorder (simple schizophrenia): gradual loss of drive & ambition,
social w/drawal; not ‘heavily’ psychotic & hallucinations/delusions not persistent
 Deficit schizophrenia: long lasting –ve sx (blunted affected, poverty of speech, social drive
& interax’ns)
o Early/late onset: early in children, late starting over age 45; sx, prognosis, progression
for early onset similar to dx of adult schizophrenia
Culture-Bound syndromes: only w/in certain culture/region; no physio’al/biochem’al evidence
(ie. Not Kuru)
 Amok (Malaysia): only in men; perceived slight or insult results in violent or homicidal
outburst; period of brooding follows
 Dhat (India): severe hypochondriacal & anxiety concerns associated w/discharge of semen &
white urine
 Piblokto (Inuit/Eskimo’s): extreme excitement for 30 min then seizures, coma up to 12 hrs
then become VERY violent
 Ghost sickness (native American tribes): preoccupation w/death & deceased; bad
dreams, fainting, hallucinations, fear, poor diet & feelings of suffocation
 Rootwork/hoodoo (African-American or Caucasians in southern US/Carribean): not
voodoo, based in pt on components of Christianity; putting curses on ppl
 Brain Fag (West Africa): old term for mental exhaustion; most in male students, sx vague
somatic concerns, depression. ‘fag’ pt comes from ‘fatigue’
 Jumping Frenchman of Maine (rare; French Canadian lumberjacks): exaggerated
startle resp; may jump, hit, yell more than normal ppl; also show echolalila & echopraxia
 Koro (Asia/southeast Asia): intense fear 1’s genitalia’s shrinking; more prevalent in men
who cheat, visit prostitutes. (ie. Guilt)

4. Depression & Mood Disorders:
- Depression & elation normal human emotions  become ‘disorder’ when exist for too long or
extreme; aka…
- Mood disorders: primary disturbance in internal emo’al state, causing distress & problems in
func’ing
 Depression (unipolar disorder): 10% M, 20% F; F>M; mean onset age: 40; Only
depression = unipolar depression or major depressive disorder; Person w/depression
may show occasional manic sx (see Criteria A for mania later) but if NO dx of mania (or
hypomania) ever made, REMAIN dx’d w/major depressive disorder; 60% depressed pt’s
have suicidal ideation (15% depressed pt’s die by suicide); CF’s: Depressed mood, low
self-esteem, loss enjoyment of pleasurable activities (anhedonia), ‘worthless, hopeless,
loser, useless’; 80% w/insomnia; low serotonin*; 90% w/anxiety
o ‘Masked’ depression: ~50% not aware OR deny having depression; often see
doctor for vague physical sx & sometimes misdx’d as hypochondriac but will
show other sx inconsistent w/hypochondriasis (ie. Weight loss)
o DD: hypothyroidism, hypogonadism, metabolism disturbances, infection, age-
rel’d (Alzheimer’s), adverse rxns to meds, alcohol abuse, Lyme dis, Wilson’s,
Huntington’s, Parkinson’s, stroke, hyperthyroidism, pancreas cancer, MS  THUS,
~1/3 w/serious medical condition exp depression!
 Course/prognosis: 50% show depression sx b4 major ‘episode’ identified
o Untx’d episode 6-13 mo’s
o Tx’d episode: 3 mo’s
o Early drug cessation: recurrence of sx
o 5-10% exp manic episode(s)
o chronic pt’s tend to relapse
 Bipolar disorder: 1% for both sexes; F = M; mean onset age 30; must have manic &
depressive episodes; Mania more likely in men but women have higher rate of
occurring manic episodes
 Hypomania: episode of mania that doesn’t meet full DSM-IV-R criteria for manic
episode; less <week of sx
 Higher risk for both if fam hx present but bipolar more among single & divorced
 no correl’n w/ethnicity, edu, marital status or income
 Cyclothymia: less severe form of bipolar disorder
o Depression rel’d mood disorders include –
 Major depressive disorder: highest lifetime prevalence 17% of any psychiatric
disorder
 DSM V Criteria for Major depressive episode:
A. Major depressive episode must last at least 2 weeks & have 5or+ of following sx:
(1)depressed mood most of day, ~every day
(2)markedly diminished interest in all/~all, activities most of days, ~every day
(3)sig weight loss when not dieting, or weight gain (>5% change in body weight
in <mo)
(4)insomnia or hypersomnia (sleeping too much)
(5)psychomotor agitation or retardation
(6)fatigue or loss of energy
(7)feelings of worthlessness or excessive guilt
(8)diminished ability to think or concentrate
(9)recurrent thoughts of death/suicidal ideation; *For 4-9 add ‘nearly every day’
B. Sx cause clinically sig distress or impairment of func’ing (social)
C. Sx not due to medical condition
D. Sx not better explained by another condition
E. Never been manic or hypomanic episode
 Major depressive disorder, single episode (criteria as described earlier)
 Major depressive disorder, recurrent (episodes separated by at least 2 mo’s)
Subtypes/specifiers of major depressive pt’s:
 W/anxious distress: presence of 2or+ sx during period of depression –
1. feeling keyed up or tense
2. feeling unusually restless
3. difficulty concentrating b/c of worry
4. fear something awful may happen
5. feeling person might lose control
 W/mixed features: presence of 3 of manic/hypomanic sx during depression –
1. elevated, expansive mood
2. inflated self esteem or grandiosity
3. more talkative than usual
4. flight of ideas (or racing thoughts)
5.  in energy or goal-directed activity
6. excessive involvement in ‘risky’ activities
7. need for sleep
 minimum amt of hyperactivity (infrequent)
 W/melancholic features: 1 of these sx during depression – (1) loss pleasure in
most or all activities OR (2) failure of reactivity to pleasurable stimuli; & 3 of
following –
1. quality of depressed mood charac’d by profound despondency (empty mood)
2. worsening of sx in morning hrs
3. early morning waking
4. psychomotor agitation or retardation
5. excessive weight loss
6. excessive guilt
 W/atypical features (paradoxical anhedonia): must have mood reactivity
(mood improves in resp to something good & 2 or+ of –
1. sig weight gain (appetite) ”reverse vegetative signs” – crave carbs, might
involve thyroid dysreg; high in women [*vegetative signs are insomnia & not
eating]
2. hypersomnia
3. leaden paralysis (sensation of heaviness in limbs)
4. sig social impairment due to hypersensitivity to perceived interpersonal rejection
 MAO-I’s more effective than SSRI’s or TCA’s
 W/Catatonia: rare & severe form major depression w/motor behavior disturbances,
mute & almost stuporous, & either remains immobile or exhibits purposeless or
even bizarre movements
 W/peripartum onset: intense, sustained & sometimes disabling depression exp’d
by women after giving birth
 W/seasonal pattern, ie. SAD (seasonal affective disorder): depressive sx during
winter mo’s – ^ sleep, ^ appetite, esp for carbs, energy, morning sickness,
difficulty waking up; caused by abnormal melatonin metabolism; < common in
summer; sx similar to major depression but can be melancholic OR atypical
o Tx: sunlamps (but cancer causing!), melatonin tablets may or may not help,
SSRI’s (antidepressants); -ve air ionization, tanning (more affordable!)
o DSM V Criteria:
1. Depressive episodes must occur at particular time of yr
2. Remissions or mania/hypomania at charac time of yr
3. patterns must’ve lasted 2 yrs w/no nonseasonal major depressive episodes
during same period
4. These seasonal depressive episodes outnumber other depressive episodes
thru pt’s life
 Drugs for tx’ing depression interact w/NE, 5-HT & sometimes DA (all in depression
 Tricyclic antidepressants: 1st in 1950s now largely replaced by SSRI’s; still for pt’s
not responsive to SSRI’s
 SSRI’s: ‘go-to’ guys; inhibit uptake of 5-HT to prolong 5-HT activity in synapse
 MAO inhibitors: block degradation of transmitters thus prolonging their ax’n
 Pathophys of depression:
 PET scan w/abnormally high glucose metabolism in amygdala (big area for emotions
& +)
 Smaller hippocampus & atrophies greater as depression continues
 High circulating GC lvls
 thyroid issues: 5-10% w/circulating TSH or release TSH in resp to TRH admin; OR
20-30% w/blunted TSH resp to TRH (less TSH!)
 HPA activity in 40-60% depressed pt’s (elevated stress hormones – cortisol &
adrenaline!)
o Dexamethasone (Decadron) suppression test: give DEX, HPA activity for 24 hrs;
non-suppression correlates w/depression
o DEX normally suppresses stress hormones, doesn’t in depressed
 CSF somatostatin (GHIH) in mania & in depression. What does somatostatin do?
Inhibit?
 Genetics & Psychosocial factors & Learned helplessness
 Genetics: if 1 parent w/mood disorder, kid 10-25% chance of developing; if both
parents, 20-50%
 Twin studies suggest genetics acc’t for 50-70% of etiology of mood disorders
 Psychosocial factors: stressful life events precede 1st appearance of mood disorder,
not subsequent episodes; but how much life stress contributes to dev’t is unclear
o Life event most often associated w/depression in losing parent b4 age 11
 Learned helplessness: mental state in which organism forced to endure aversive
stimuli becomes unable/unwilling to avoid subsequent encounters w/those stimuli,
even if escapable, presumably b/c learned they cannot control situation; idea
depression results from perceived lack of control over situation(s); Ex. Dogs prev’ly
exposed to inescapable shock had difficulty learning to avoid escapable shock in
new situation; Always explains why we love underdog “Our greatest heroes/heroines
are ones we perceive as never giving up, always figuring out new strategy, beating
odds; learned helplessness is antithesis of this”
 Persistent depressive disorder: dysthymia (low-moderate depression) or chronic
major depressive disorder – these of diff severities; less severe form of major
depression; chronic low grade depression, often say they’ve been like this for yrs
 DSM V criteria –
A. Depressed mood for most of day, for more days than not, indicated either by
subjective acc’t or observation by others, for at least 2 yrs; (in kids or adolescents,
mood can be irritable & less than 1 yr duration)
B. Presence, while depressed, of 2 or + of 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
 Vascular depression: prefrontal lobe damage due to ischemic events resulting in age
rel’d depression often unresponsive to anti-depressants; repetitive transcranial
magnetic stimuli (rTMS) been effective treating vascular depression & also been used
for Parkinson’s, tinnitus, dystonia, etc.
 Recurrent brief depressive disorder: recurring, brief (<2 weeks) episodes of
depressed that meet all criteria of major depressive disorder; MC amongst young
adults; depressive periods must last 2 days to 2 weeks & occur 1x/month for 12 mo’s,
not relating to menstrual cycle; no major depressive, manic or hypomanic episodes
during that time
 Premenstrual dysphoric disorder (PMDD): super PMS; mood, behavior & physical
sx occurring at specific time during menstrual cycle; 5% of women; subsequent greater
risk for postpartum depression; Mood lability (crying spells, verbal outbursts,
tantrums); Dx in majority of menstrual cycles, at least 5 sx must be present in final
week b4 onset of menses, start to improve w/in few days of onset menses, & become
minimal or absent in week postmenses; Sx: marked affective lability (mood swings),
marked irritability or anger, marked anxiety/tension, marked depression or feelings of
hopelessness (& other sx of depression, insomnia)
 Post partum depression: afx women most (can also affect men) after childbirth; now
grouped as ‘major depressive disorder w/peripartum onset’; why? B/c ~50% depressive
episodes begin during pregnancy, just not after
 Postpartum blues (‘baby blues’): onset w/in few days of birth, sx duration ~2
weeks; upto 1/3 or ½ women exp this
 Major depressive episode: starting w/1 month of delivery, can last yr, 5-10% women
 Brief psychotic disorder w/postpartum onset: psychotic sx, w/in 2-3 weeks
after birth lasting up to?
 Disruptive mood regulation disorder: chronic, severe, persistent irritability that
alternates btwn temper outbursts & chronic, irritable mood, in children up to 18 yrs;
outbursts must occur at least 3x/week, for 1 yr, in > 1 location; irritable mood must be
most of time (most days, most of day)
 Substance/medication induced depression: major depressive disorder sx but
associated w/ingestion, injection, or inhalation of substance (medication, drug of
abuse); depressive sx present beyond expected length of physiological efx, intoxication
or w/drawal period
 Hysteroid dysphoria: ex. Girl gets asked by amazing guy, laughs & doesn’t respond
properly but then when alone regrets it & eats tub of ice-cream; reverse vegetative
signs along w/ -
1. ‘Giddy resp’s to romantic opportunities & strong dysphoria
(angry/depressive/suicidal) resp to romantic disappointment’
2. Impaired anticipatory pleasure
3. Craving for chocolate & sweets
 Depression due to medical condition
 Other types of depression
 Suicide & depression:
- depressed person’s at risk for suicide; >90% suicides had been dx’d w/depression or other
mental disorder
- factors risk of suicide in depressed pt’s: prev attempt, >45 y/o, alcohol dependence, hx of
violent behavior, & male
- men 4X likely to commit suicide, but women 3-4X more likely than men to attempt it
- firearms MC method (M=F) but pills most likely method for attempting in women
- 25% suicides in >65 yrs; 80% suicides saw their physician in preceding 6 mo’s (50%or+ in last
1 mo)
- in tx, suicide attemps often occur at pt begins to feel better (ie. Have enough energy to do it)
- dentistry : highest suicide rate of any profession

 Bipolar disorder: pt’s w/both manic & depressive episodes or just manic episodes
 Mania: distinct period of abnrormally & persistently , expansive or irritable mood lasting at
least 1 week, or less if hospitalization is required (DSM V Criterion A)
B. During period of mood disturbance, 3 or + following -
1. Inflated self-esteem or grandiosity
2. need for sleep
3. More talkative than usual
4. Flight of ideas
5. Distractibility (distinguishing factor from depression w/mixed features)
6. Psychomotor agitation or  in goal-directed activity
7. Excessive involvement in pleasurable activities having potential –ve outcomes
 Hypomanic episode, DSM V Criteria:
A. distinctive period of persistently elevated expansive or irritable mood, lasting thru out at
least 4 days, that’s clearly diff from usual nondepressed mood
B. same as for manic episode
C. episode associated w/unequivocal change in func’ing uncharac of person when not
symptomatic
D. disturbance in mood & change in func’ing observable by others
E. episode not severe enough to cause marked impairment in social or occupa’al func’ing or to
necessitate hospitalization & there are no psychotic features
F. same as for manic
o Bipolar rel’d mood disorders include –
 Bipolar I: criteria for manic episode must be met & manic episode may have been
preceded by & followed by hypoamic or major depressive episodes; vast majority of
persons who meet criteria for manic episode also exp major depressive episodes; also,
hypomanic episodes may be present but are not diagnostic requirement
 ¾ male & 2/3 of female pt’s start w/depression
 10% pt’s exp only manic episodes
 90% of pt’s w/single manic episode will have another
 Poorer prognosis than major depressive disorder
 Bipolar II: criteria for hypomanic episode, & major depressive episode must be met;
can’t dx Bipolar II if person has had full manic episode
 Onset age little later than Bipolar I; may actually have more episodes than Bipolar I
 Some bipolar pt’s exp ‘mixed affective episodes’ when sx of both mania & depression
co-exist; may have suicidal thoughts but be extremely energized
 Cyclothymic Disorder (cyclothymia/Bipolar III): chronic, fluctuating mood disturbance
w/ numerous periods of hypomanic sx & periods of depressive sx distinct from each
other; equal in M=F; esp pessimistic; if 1 twin has it, other twin has 60% chance of
developing; DSM V criteria –
 for at least 2 yrs, many periods w/hypomanic sx that don’t meet criteria for
hypomanic episode, & numerous periods w/depressive sx that don’t meet criteria
for major depressive episode; duration is 1 yr for children & adolescents
 during 2 yr period, hypomanic & depressive sx present for at least ½ time, & hasn’t
been w/out sx for >2 mo’s at time
 criterion for major depressive or manic episode have never been met; remainder
similar to Criterion for Bipolar (no other physio’al condition)
 Substance/med-induced bipolar: sx of bipolar but due to ingestion, injection or
inhalation of substance (meds, drug of abuse); sx beyond expected length of physio’al
efx, intoxication or w/drawal period (same idea for substance/medication induced
depression)
 Bipolar due to medical condition

 Pathophysiology of Bipolar Disorder:
- MRI studies  frontal lobe size/activity, in bipolar (could be due to poor connection to limbic
structures (mood)
- Na/K pump also involved; cyclical changes w/too much activity occurs (mania) or not enough
(depression)
- DA lvls in manic episodes

 Treatment for bipolar disorders:
- Hospitalization if required (ie. Manic episode)
- Pharmacology for initial treatment
o Lithium: effective mood stabilizer around a long time, side efx include tremor, weight
gain, GI uses; periodic blood testes required for potential liver or thyroid issues
o Anticonvulsants may help in some cases such as valproic acid (Depakene)
o Antidepressants may work (although might trigger manic episodes, & loss of libido as
side efx)
- Continued (maintenance) treatment to manage condition
- Substance abuse treatment (if necessary)
- Surgical & Other options for psychiatric disorders:
o OCD: stereotactic ablation of ant cingulum has been effective for drug-resistant OCD
o Depression: Vagal n stimulation NE & 5-HT, may be effective for depression
o OCD & depression in PD pt’s may be relieved by Deep Brain Stimulation
- Electro-convulsive therapy: fast, effective & ‘safe’ w/long hx of use in depression
o 25-60 sec of current results in generalized seizures; pt is pre-medicated w/anesthetic & m
relaxant; typical course is 5-10 treatments over 2-3 weeks
5. Anxiety Disorders
 Normal anxiety: ‘vague’ discomfort associated w/meeting new ppl, going to new job, etc.
o Freud: anxiety signals presence of danger in unconsciousness
o Behavioral: usual conditioned response deal
o Higher prevalence of anxiety disorders in women, overall prevalence w/higher SES
o Pathophysiology:
 ANS: some anxiety pt’s show symp tone
 NT’s: NE, 5-HT, GABA (anxiolytics act on these)
 Hypothalamic: overproduction of cortisol associated w/PTSD & maybe panic disorder
 Person’s w/panic disorder or social phobia often have alcohol or drug (benzodiazepine
ie. Valium) issues (~50%); this dependence eventually exacerbate & prolong anxiety
 Panic disorder: acute intense attack of anxiety coupled w/feelings of impeding doom; attacks
can range from several times/day-yr; often associated w/agoraphobia & other phobic anxiety
disorders; Tx w/SSRI’s & MAO-I’s
 LSA (limited sx attack): milder, 4 sx or less (see upcoming slide of sx)
 Panic disorder pt’s usually have both full panic attacks, as well as LSA; >90% of panic disorder
pt’s have another psychiatric disorder; >80% have agoraphobia; DSM V criteria:
A. Recurrent unexpected panic attacks: abrupt surge of intense fear/discomfort that reaches
peak w/in mins & during when 4or+ of following sx occur –
1. Palpitations, pounding or accelerated <3 rate
2. Sweating
3. Trembling or shaking
4. Sensation of SOB (shortness of breath) or smothering
5. Feeling of choking
6. Chest pain or discomfort
7. Nausea or abdominal distress
8. Feeling dizzy or faint
9. Chills or hot flushes
10. Parasthesias
11. Derealization or depersonalization
12. Fear of losing control or going crazy
13. Fear of dying
B. At least 1 of attacks followed by 1 month (or +) of 1 or both of following consequences:
1. persistent control/worry about additional panic attacks or their consequences
2. sig maladaptive change in behavior relating to attacks
C. Note: said ‘unexpected’ in criteria for panic disorder  thus no obv cue/trigger VS.
expected panic attack w/obvious cue (ie. About to fly, or public speak); these attacks not
considered mental disorder of own
D. CF’s: in PANIC DISORDER, 1st panic attack usually not preceded by specific event (ie.
Stress, sex, excitement); rapid onset of sx w/in 10 mins w/overall episode 20-30 min; often
have serious concerns about <3 attacks (panic + chest pain)
E. Course & Prognosis: late adolescence onset; ~35% end up sx free, 50% w/manageable sx,
15-20% still have sig sx
 Agoraphobia: fear/anxiety associated w/open/public spaces from which escape may be
difficult; develops as result of panic disorder, person terrified to think they might have attack
in exposed env; CF’s: almost always want to be accompanied by fam member/friend when
going anywhere; extreme cases don’t leave home, most cases follow onset of panic disorder,
prognosis poorer if not preceded by panic disorder
o DSM V criteria:
A. Marked fear/anxiety about 2or+ of following 5 situations
1. Using public transportation
2. Being in open places
3. Being in enclosed spaces
4. Standing in line or being in crowd
5. Being outside of home alone
B. Ind fears/avoids these situations b/c thoughts that escape may be difficult or help
might not be there if develop panic-like sx or other incapacitating/embarrassing sx
 Social Phobia/Social anxiety disorder: strong persistent fear of being judged by others or
embarrassed; could be anything (ie. Not wanting to eat in front of someone, or use public
restroom), ie. Even shy bladder; Onset ~13 yrs age; CF’s onset in late childhood or early
adolescence; DSM V criteria:
A. Marked fear/anxiety about 1 or + social situations when ind exposed to possible
scrutiny by others
B. Fears they’ll act in way or show anxiety sx that’ll be –vely evaluated
C. Social situations almost always provoke fear/anxiety
 Specific phobia: 2X> in women, except for fear of blood, injection or injury (equally likely), in
US from 5-10 25% pop
o broad categories (in order of prevalence)–
 Animal type
 Natural env type (storms, heights, water)
 Blood/injection/injury type
 Situational type (airplanes, elevators)
 Other type (clowns, vomiting)
o DSM V Criteria Specific Phobia:
A. Marked fear/anxiety about specific object/situation (ie. Flying, heights, animals,
seeing blood)
B. Phobic object/situation almost always provokes immediate fear or anxiety
C. Phobic object/situation actively avoided or endured w/intense fear/anxiety
D. Fear/anxiety out of proportion to actual danger
E. Fear persistent, typically lasting 6 mo’s or +
o Adults recognize fear is irrational (children may not)
o Blood/injection injury type also followed by bradycardia (<12 breaths/min) & hypotension
(<60 beats/min)
o Ex’s:
 Acrophobia: heights
 Tomophobia: surgical operations (tomo = slicing/cutting)
 Hydrophobia: water
 Pantophobia: everything
 Tetraphobia: # 4; big in pts of Asia & Southeast Asia; very superstitious about #4; in
many languages in these areas, word for ‘4’ sounds very similar to word death
 Coulrophobia: clowns
 Sinophobia: Asians (specifically sino = chinese)
 Aeronausiphobia: vomiting due to air sickness
 Mysophobia: dirt & germs
 Allodoxaphobia: opinions
 Xenophobia: strangers
 Zoophobia: animals
 Agoraphobia: sexual abuse
 Caligynephobia: beautiful women
 Bromidrophobia: body odors
 Nosocomephobia: hospitals
o Clinical features: animal type most common in children; situational type most common in
elderly adults
 Generalized anxiety disorder: long-term condition that cause ind to feel anxious about
wider range of situations & concerns, not just 1 specific event; feel anxious most days & have
difficulty rmr’ing last time they felt relaxed; physical sx include fatigue, headaches, m tension
& aches, difficulty swallowing, trembling, twitching, irritability, sweating, nausea,
lightheadedness, frequent bathroom trips, feeling out of breath & hot flashes; DSM V criteria

A. Excessive anxiety & worry (apprehensive expectation), occurring more days than not for at
least 6 months, about # of events/activities (ie. Work or school performance)
B. Ind’s find it hard to control worry
C. Anxiety & worry associated w/3 or + of following 6 sx: restlessness or feeling on edge,
being easily fatigued, difficulty concentrating, irritability, m tension, sleep disturbances
o clinical pic: intensity, duration & frequency of anxiety out of proportion to actual
likelihood or impact of anticipated events, always freaked out, uptight & need to ‘relax’
 Substance-Induced anxiety disorder: due to either recreational/prescription drugs (ie.
sympathomimetics – amphetamines, cocaine, caffeine, CNS stimulants causing anxiety
disorder sx; or 5-HT drugs like LSD & MDMA; dx if sx occur during use (intoxication) or
w/drawal (up to 1 mo after cessation of use)
o Further categorized depending on prominent features, ie. Panic attacks, OCD, generalized
anxiety, etc.
o Tx: focuses on stopping substance abuse, DUH

 TX for anxiety: pharmacology & other therapies range from helpful to very imp
- CBT (cognitive behavioral therapy): very effective in treating GAD; focus on helping pt
identify unhelpful/unrealistic, beliefs & behavior patterns; usually precedes medication
- Pharmacological treatment: involves benzodiazepines (best for anxiety, panic disorders
(also w/alcohol w/drawal, convulsions) that  affinity for GABA-A receptor for GABA (make it
easy for receptor to open up for GABA); 2 types –
o Fast acting: used for insomnia
 Diazepam (valium): for anxiety & insomnia
 Triazolam (halcion): for insomnia
o Slow/longer acting: used for anxiety
 Alprazolam (Xanax) for panic disorders & anxiety
 Lorazepam (Ativan) for anxiety & alcohol rel’d seizures
 Chlordiazepoxide (Librium): for alcohol detox
o Benzo’s not used for longer than 4 weeks (tolerance, dependence, efficacy)
o SSRI’s effective for long term (paroxetine, ex. Paxil) aka antidepressants
o Buspirone: (5-HT1A agonist) anxiolytic (thus not for insomnia); effectively treats anxiety,
little abuse potential & no tolerance; best for long term tx
 OCD: dx’d by presence of obsessions, compulsions or both*; (most have both & will see
physician rather than psychiatrist); usually sudden onset, following stressful life event
o Obsession: recurrent & persistent, intrusive thought, feeling, idea or sensation/urges or
images; ind tries to ignore/neutralize these thoughts w/some other thought/ax’n
o Compulsion: conscious, standardized, recurrent behavior; repetitive behaviors
o Equal in men/women but in adolescence, more prevalent in boys; +more common in
single ppl
o 2/3 of OCDers exp major depressive disorder
o may recognize their behaviors/beliefs not true (understand behavior is irritational & ego-
dystonic) VS some completely convinced their beliefs are 100% true & their behaviors
necessary to deal w/it
o Pathophys: 5-HT systems likely rel’d as 5-HT drugs most effective; imaging studies
suggest abnormalities in frontal lobe (higher thought), basal ganglia (planning of motor
movements) & cingulate gyrus
 DA & 5-HT result in alterations in basal ganglia func
o Sx patterns:
 Contamination: dirt, dust, feces, germs, wash/rub skin off hands in worst cases; MC*
 Pathological doubt: doubt then compulsion of checking (lock doors, etc.) 2nd MC
 Intrusive thoughts: obsessional thoughts w/out compulsion, sexual or aggressive in
nature & reprehensible to pt; ie. Killing spouse for no reason
 Symmetry: need for symmetry/precision; takes hrs to do anything
 Other sx patterns: religion obsessions, hoarding, nail biting, etc.
o 1/3 pt’s sig’ly improve over time, 1/3-½ moderate improvement, remainder stay same or
get worse
o Tx for OCD: SSRI’s to start; best w/clonaapramine
 Exposure & ritual prevention (ERP): specific CBT just for OCD; gradually learning
to tolerate or accept anxiety associated w/not performing behavior
 Ex: touching Q-tip that touched Q-tip that touched slightly dirty surface (exposure),
but not washing hands afterwards (ritual)
 Pharmacological tx: SSRI’s & TCA’s (esp clomipramine)
 CBT & other therapies usually more effective, drugs also may take several weeks
to show efx.
o OCD rel’d disorders that DSM V grouped:
 Hoarding/disposophobia: persistent difficulty discarding or parting w/possessions
regardless of their actual value, results in accumulated possessions that
congest/clutter active living areas; pt may or may not realize their hoarding is
problematic
 Trichotillomania: (1) recurring pulling out of 1’s hair resulting in hair loss & (2)
repeated attempts to /stop hair pulling; MC in scalp, eyelids, eyebrows
 Excoriation: Skin picking disorder of (1) recurrent skin picking causing skin lesions &
(2) repeated attempts to stop skin picking; MC sites are face, arms & hands, but can
happen anywhere or in multiple locations
 Body dysmorphic disorder (in dissociative lecture)
Trauma & Stressor rel’d disorders:
 PTSD (post traumatic stress disorder): in civil war (Soldier’s <3), 1st world war (shell
shock), 2nd world war (combat neurosis), Vietnam (PTSD), Gulf war (Gulf war syndrome); sx
last >1 mo & sig’ly afx social, fam & other life areas; onset w/in 3 months of event, but can be
yrs b4 full sx criteria met; DSM V criteria –
A. exposure to actual or threatened death, serious injury, or sexual violation in 1or+ ways:
1) directly exp’ing event
2) witnessing events as they occur to others
3) learning traumatic events happened to friend or fam member
B. Presence of 1or+ of these intrusion sx w/traumatic events, beginning after events occurred:
1. recurrent, involuntary & intrusive or distressing memories of events
2. recurrent distressing dreams
3. disassociative rxns (ie. Flashbacks) – ie. Reliving exp
4. 4/5. Intense or prolonged psych’al or physio’al distress at exposure to cues resembling
event
o Ex. Preston, 19, deafness, but when he hears ‘bomb’ goes for cover & after goes back to
normal
 ASD (Acute stress disorder): lesser version of PTSD; dev’t of charac sx lasting 3 days to 1
mo after exposure to 1or+ traumatic events –
A. Criteria A same as PTSD
B. Result of exposure results in sx in following areas/sx from following categories:
1. Intrusion sx (recurring dreams, memories)
2. –ve mood
3. avoidance sx
4. arousal sx (sleep problems, concentration issues)
o 50% pt’s go on to develop PTSD
o high comorbidity in PTSD w/other psychiatric conditions (depression, etc.) but not as bad
w/ASD
 Adjustment disorder: not really anxiety disorder but included to distinguish from PTSD &
ASD; emo’al & beha’al rxn that develops w/in 3 mo’s of life stress & lasts <6 mo’s; life stress is
‘serious’ ie. Divorce, moving, etc. but not life threatening; sx: anxiety, depression, conduct
problems.
o Thus WHEN ADJUSTMENT period is over, ADJUSTMENT disorder should be gone
 Disinhibited social engagement disorder: kids interact w/strangers same way they’d
interact w/parents/ parental figures; don’t discriminate btwn parents & strangers; caused by
severe neglect at young age, b4 age 2; DSM V criteria –
A. pattern of behavior where kid actively approaches & interacts w/unfamiliar adults &
exhibits 2or+ of:
1. reduced/absent reticence (reluctance) interacting w/unfamiliar adults; not uncomfortable
2. overly familiar verbal or physical behavior
3. diminished/absent ‘checking back’ w/adult caregiver after venturing away, even in
unfamiliar env’s
4. willingness to go off w/unfamiliar adult w/minimal or no hesitation
B. Kids exp’s pattern of extremes of insufficient care as evidenced by 1 or + of:
1. social neglect or deprivation
2. repeated changes of primary caregivers
3. rearing in unusual settings that limit opportunities for attachments
6. Somatic Sx, Dissociative, Factitious Disorders pt.1
 Dissociative disorders:
o Dissociative Amnesia: most lose autobiographical memory (sense of self & personal
memory); & loss of semantic (& procedural memory less common); charac’d by –
A. inability to recall imp personal info, usually of traumatic or stressful nature,
inconsistent w/ordinary forgetfulness; may have ‘w/dissociative fugue’ as specifier
(in NCD lecture)
B. loss of retrograde (past memories) & anterograde (formation of new memories)
o Depersonalization/derealization disorder: (A). presence of persistent or recurrent
exp’s of depersonalization, derealization or both & (B) reality testing remains intact
 Depersonalization: exp’s of unreality, detachment, or being outside observer
w/respect to 1’s thoughts, feelings, axns; (perceptual alterations, distorted sense of
time, unreal or absent self, emo’al/ physical numbing)
 Derealization: exp’s of unreality or detachment w/respect to surroundings
(persons/objects exp’d as unreal, dreamlike, foggy or lifeless)
 may perceive bodily changes, duality of self as observer & actor, being cut off from
others, & from 1’s own emotions
 Difficulty in expressing their feelings
 50% of pt’s rep’t histories of sig trauma or life threatening exp
o Dissociative identity disorder/multiple personality disorder: master pt*; strongly
linked to severe exp’s of childhood trauma, esp maltreatment; lots of debates if it really
exists; charac’d by –
A. Disruption of identity w/2or+ distinc t personality states (described in some cultures
as possessed); each w/own relatively enduring pattern of perceiving, relating to &
thinking about env & self
B. Recurring gaps in recall or every day events, imp personal info &/or traumatic events
 Ganser Syndrome (b4 Factitious, now dissociative; nonsense syndrome/prison
psychosis): nonsense answers to ques or doing things incorrectly; sx – confusion, stress,
echolalia (meaningless repetition), echopraxia (repetition or mimicking another’s axn),
‘clouding’ of consciousness, hallucinations; may also have other dissociative sx (amnesia
issues, fugue, conversion disorder type sx’s); due to extreme stress; very rare
 Factitious disorders (now called Factitious disorder imposed on Oneself/Munchausen’s or …
Imposed on Another (Munchausen’s by Proxy): falsifying medical/psych’al signs/sx in 1self or
others associated w/identified deception
o Munchausen’s syndrome: predominantly physical signs & sx; pt fakes illness to gain
attention/sympathy from physicians
o Munchausen by proxy: deliberately causing injury or illness to another, usually child, to
gain attention;
 Odd but sad observation: this is increasing problem in pet comm; aka ppl hurting their
dog/cat or giving them wrong or bad meds to elicit sympathy from vet, fam or friends
o Person make take drugs, inject/swallow bacteria, add contaminates to urine; typically have
long but inconsistent medical hx’s, many surgical scars, lots of doc/hospital visits,
extensive knowledge of medical terminology & func’s, & reluctance to involve fam
members or prior health care providers
 Malingering: intentional production of false/grossly exaggerated sx for external incentives ie.
Avoiding work, avoiding military duty, evading criminal prosecution or obtaining drugs;
motives include – financial gain (fraud), avoiding school, work, military service or exams,
getting drugs, hoping to get lesser criminal charges or sympathy or attention but not in same
way as Munchausen’s
o This is court-martial offense in US (& most other armed forces)
 Fun Summary: If they’re doing it, but they don’t know why then it’s Munchausen’s syndrome.
If they’re doing it to someone else & they don’t know why then it’s Munchausen’s by proxy. If
they think they’re going to die & you can’t persuade them otherwise then it’s hypochondriasis.
If they’re not doing it, but they feel unwell but pretty vague about it then they’re somatizing.
If they’re doing it, they know why & they want money for it then they’re malingering.

B4 /Final Exam Behavioral Disorders
6. Somatic Sx, Dissociative, Factitious Disorders pt.2
 Somatic sx & rel’d disorders: group of illnesses w/bodily signs & sx as major component
 Somatic sx disorder: incorporates hypochondriasis & pain disorder (so nobody is
‘hypochondriac’ anymore); charac’d by –
(A) 1or+ somatic sx distressing or resulting in sig disruption of daily life
(B) excessive thoughts, feeling or behaviors rel’d to somatic sx or w/health concerns as at
least 1 of:
1. Disproportionate & persistent thoughts about seriousness of 1’s sx
2. Persistently high anxiety about health or sx
3. Excessive time & energy devoted to these sx or health concerns
o 5-20X more common in women
o inversely rel’d to social status & often occurs w/low income & little edu
o 2/3 of pt’s have other psychiatric sx thus prognosis generally poor
o pt’s think they’ve just been ‘sickly’ all their lives w/some of more common complaints:
nausea, vomiting, dysphagia, dyspnea (SOB), limbs pain, menstrual complications &
pregnancy & amnesia
o if sx predominantly or only involve pain, dx supplemented w/”PREDOMINANT PAIN”
(eliminates ‘pain disorder’ as separate disorder)
 Illness Anxiety disorder: charac’d by
A. Preoccupation w/having or acquiring serious illness
B. Somatic sx not present, or, if present, only mild
o High anxiety of health, easily alarmed about health status & performs excessive health
behaviors
o no medical condition acc’ting for ind’s concerns
o Anxiety not alleviated by medical reassurance, -ve tests or benign course
 Conversion disorder (func’al neurological sx disorder): ‘hysteria’ (Greek; =uterus;
believed hysteria caused by uterus wandering around body); triggered by conflicts/stressors;
SX: – blindness (optokinetic resp intact in blind pt’s*), paralysis (glove anesthesia), mutism or
seizures; DSM V – (A) 1or+ sx of altered voluntary motor or sensory func, (B) BUT CF’s show
incompatibility btwn sx & recog’d neurological/medical conditions; more prevalent in women,
esp girls; & in low income, living in rural areas; onset btwn 10-35 y/o; men w/this frequently
served in military
o ‘La Belle Indifference’: often accompanied w/conversion disorder; manifestation of
‘isolation of affect’ in which reality is accepted but w/out expected human emo’al resp to it;
ex. Someone sitting there mute but not least concerned they can’t speak anymore
o Hysterical/Bizarre Gait: no obv organic basis, produced unconsciously by person
w/conversion disorder or deliberately by malingerer; may mimic organic impairment, but
more bizarre quality w/key elements missing, ie. leg paralysis w/normal reflexes & motor
strength
o Glove anesthesia: numbness of hands stops at wrists; optokinetic resp still intact in
‘blind’ conversion disorder pt’s; note: invariably conversion sx, distribution of sensory n
fibers allowing no possible neurological cause of sx b/c n that supplies hand also supplies
lower arm)
 Medical students dis: medical students who perceive themselves or others as exp’ing dis
sx(s) they’re studying; type of hypochondriasis or simply nosophobia (fear of contracting dis)
 Body dysmorphic disorder: M=F equally likely; charac’d by – (A) preoccupation w/1or+
perceived dfx/flaws in physical appearance not observable/slight to others; (B) at some point,
perform repetitive behaviors, comparing their appearance in resp to appearance concerns;
often associated w/eating disorder (anorexia nervosa); complain of several specific features or
single or vague feature or general appearance; suicidal ideation rate ~80%  HIGHER THAN
DEPRESSION; areas of highest concern: skin (75% pt’s rep’t concerns about skin); hair, weight,
nose (50%); interestingly, body pts such as hands, genitals, feet, buttocks of MINIMAL concern
(6-12%); often make many visits to dermatologists or plastic surgeons b4 accepting
psychiatric help; CBT & antidepressants can be effective alone, but best when done together;
Tx: Wellbutrin (buproprion): atypical antidepressant (DA/NE reuptake inhibitor) often w/SSRI
 Bigorexia (BDD w/m dysphorphia or Adonis complex): males feel they’re puny & thus
work excessively; never feel big enough, …esp males (‘reverse anorexia nervosa’) onset ~19
yrs; person already ‘muscular’ by others view; often depression & serotonin may be involved
 Mass hysteria/mass psychogenic illness: conversion disorder affecting group of persons
w/rapid onset & escalation; ex. Episode of House MD, passengers on plane become convinced
they all have meningitis; House tricks them w/non-meningitis sx so suddenly all get as well

B4. 1) Feeding & Eating Disorders (can overlap, dx can change over time, ie “not unusual for
person w/eating disorder to ‘move thru’ various dx’s as their behavior & beliefs change over
time”)
 Pica Disorder: (1) persistent eating of nonnutritive, nonfood substances over period of 1
month (2) inappropriate to dev’t; childhood onset MC (sometimes adolescence & adulthood);
more in kids w/intellectual disability; can cause poisoning, toxicity, infections & malnutrition
 Rumination Disorder: repeated regurgitation of food over period of at least 1 month (may
be re-swallowed, re-chewed or spit out); not attributable to rel’d GI or other medical condition;
more in kids/infants, but can occur in adults; NOT purging (in bulimia) b/c regurgitation is
effortless, no physical discomfort of vomiting; often w/in 30 sec’s-1 hr after meal
 Avoid/restrictive food intake disorder: avoiding/restricting food intake leading to 1or+ of –
o Weight loss
o Nutritional def’s
o Dependence on enteral feeding or oral nutritional supplements
o Marked interference w/psychosocial func’ing
 Anorexia nervosa: extreme low body weight, distorted body image & obsessive fear of
weight gain; primarily afx young females (90%); *anorexia & anorexia nervosa (disorder) NOT
interchangeable terms; afx 0.5% pop, 2% adolescent females; HIGHEST mortality rate for any
psychiatric illness; causes are combo of social, bio’al & psycho’al factors (how much each
contributes unclear) –
o Biological cause
 Genetic component – yes. 50% of variance
 Nutritional issues – deficient zinc, tyrosine, tryptophan or B1; ‘malnutrition induced
malnutrition’
 Neural/Physio’al? yes but unclear – serotonin may be involved & hypothalamic dysreg
o Social factors: ‘promotion of thinness’ b/c western civilization emphasizes on being thin;
lots of debate on how much this contributes; those exp’ing child sexual abuse more likely
to become anorexic
o Psychosocial factors: low self-esteem, overestimation of body size & lack of
‘overconfidence bias’, tend to be perfectionists (often have OCD, believe control of food =
control of life), distortion of body image
o DSM V Criteria –
1. restriction of energy intake relative to requirements, leading to sig’ly low body weight
in context of age, sex, dev’al trajectory & physical health; (weight less than minimally
normal or, for kids or adolescents, less than that minimally expected)
2. intense fear of gaining weight/getting fat, or persistent behavior that interferes
w/weight, even though underweight
3. disturbance in way in which 1’s body or shape is exp’d, undue influence of body weight
or shape on self-evaluation, or persistent lack of recognition of seriousness of current
low body weight
o specify if – (both of EQUAL prevalence; both excessively diet & exhibit ‘hypergymnasia’
(over-exercising))
 restricting (w/out purging): during last 3 months hasn’t engaged in recurrent
episodes of binge eating or purging; weight loss thru dieting, fasting &/or excessive
exercise
 binge eating/purging: during last 3 months, engaged in recurrent binge
eating/purging
 binge eating: consuming large quantities of high calorie food
 purging: vomiting or excessive use (or misuse) of laxatives, enemas, diuretics, etc.
to rid of stuff!
o Maintain low body weight via voluntary starvation, vomiting, excessive exercise, diet pills,
drugs
o Anorexia: ‘loss of appetite’ that’s misleading as appetite usually fine at onset of disease
o Physical sx – extreme weight loss, stunted growth, amenorrhea, libido, bradycardia,
hypotension, thinning hair, growth of lanugo* hair (hair on fetus), WBC count, immune
system, pallid complexion, sunken eyes, headaches, easily bruised, poor circulation (& +)
o Psychology of Anorexia Nervosa –
 Distortion of body image – just not seeing themselves as they really are
 Additionally perfectionists, often w/OCD, believe control of food = control of life; 40-80%
depressed
o Tx’s: weight gain (treat as outpt but can also be involuntarily under mental health laws (if
exist), psychotherapy, fam therapy (effective w/adolescents), drug therapy (not so
successful; zinc may help)
o Wannarexia: ‘anorexic yearing’; crave/want to be anorexic; may have nonspecific eating
disorder (ED-NOS) but diff from anorexics b/c satisfied/pleased w/their weight loss;
anorexics don’t like wannarexics
o Pro-ana: promoting anorexia & bulimia (‘pro-mia’) as normal, ie. not psychiatric illness nor
desirable; increasing presence online over last 20 yrs; ie. Pro-ana websites w/’thinspiration’
(pics, vids); lots of controversy here)
 Bulimia: recurrent binge eating followed by purging; onset ~adolescence, esp F’s; harder to
dx than anorexia as bulimics usually maintain normal body weight; 2 types –
1. Purging: binge eating & purging; 90% of bulimics; exercise 2ndary to purging behaviors
2. Non-purging: binge eating w/excessive exercise or dieting, but no vomiting, etc
o Causes include –
 lack of control over their lives, low self-esteem (like other eating disorders)
 Higher prevalence amongst Caucasians
 Higher correl’n w/lifestyles emphasizing thinness & body image (athletes, actors,
models, etc.)
o Physical sx – chronic gastric reflux, dehydration, cavities, esophagitis (inflamed
esophagus), pancreatitis, perimolysis (loss of tooth enamel), peptic ulcers, hypokalimea
(blood K+ lvls), mouth & throat lacerations, electrolyte imbalance (potentially affecting
<3), swollen salivary glands, bloating, abdominal pains, constipation, drug-rel’d (addiction,
seizures, mood changes)
o DSM V criteria –
A. recurrent episodes of binge eating charac’d by both of following –
1. eating in discrete period of time, food amt >avg portions under similar
circumstances
2. sense lack of control over eating in episode (feeling cannot stop/control what/how
much to eat)
B. recurrent inappropriate compensatory behavior to prevent weight gain, ie. vomiting,
laxatives, emetics, diuretics, or other meds, fasting, excessive exercise
C. sx occur at least 1X/week on avg & persist for at least 3 mo’s (episodes may
occur from several X/day to several X/week)
D. self-evaluation unduly influenced by body shape & weight
E. disturbance doesn’t occur exclusively during episodes of anorexia?
o Tx & prognosis: (lack of consistent effectiveness however seen in all of below)
 Drug approaches – TCA’s, SSRI’s, MAO-I’s, seizure meds, addiction meds
(naloxone/naltrexone)
 Behavioral therapy
*How to tell Anorexia & Bulimia apart – anorexia more in teenagers, noticeable weight loss &
missed menstrual cycles VS. Bulimia in women in ~20s, maintain healthy weight &
binging/purging
 BED (Binge eating disorder): consuming large amt’s of food in short time(<2 hrs);
causes similar to other disorder (low self esteem, etc.); MC eating disorder; DSM V criteria –
A. recurrent episodes of binge eating charac’d by both
1. eating in discrete time period, food amt >avg in similar circumstances
2. sense lack of control over eating during episode (feeling cannot stop/control what/how
much to eat)
B. binge eating episodes associated w/3 or + of eating…:
1. much more rapidly
2. until feeling uncomfortably full
3. large amt’s of food when not hungry
4. alone b/c of being embarrassed by how much 1 is eating
5. feeling disgusted w/self, depressed or very guilty after overeating
C. Marked distress regarding binge eating
D. Binge eating occurs, on avg, at least 1X/day/week for 3 mo’s
E. not associated w/regular use of inappropriate compensatory behaviors (purging, fasting,
excessive exercise) & doesn’t occur ONLY during course of anorexia nervosa or bulimia

 BMI (body weight): person’s mass (kg/lbs) divided by (their body height (m or
inches))^squared; normal 33”, overweight 45”, 60” obese
- +40 = severely obese
- 40-49.9 = morbidly obese
- +50 = super obese
- race changes #’s  Obesity in Japan when BMI >25 but in China when BMI >28
 Body fat %age: total body fat as % of body weight; hard to measure BMI or body fat % in
obese persons
 Overweight: BMI of >25 kg/m2 & 45”
 Obesity: accumulated body fat to point of–ve impact on health; BMI of >30 kg/m2 & 60”
waist; not ‘psychiatric illness’ in DSM-IV-R; causes include –
o Most cases b/c combo of overeating (diet) & lack physical exercise (sedentary lifestyle – ie.
Driving everywhere, drive thru’s everywhere)
o Few result from genetic, medical or psychiatric causes (+more)
 Lack of sleep
 Endocrine disruptors (foods that interfere w/lipid metabolism)
 variability in ambient temp
 smoking (when trying to quit, appetite s)
 Pregnancy at later age
 use of certain meds/drugs cause sig weight gain
 Ex: some ambien users exp night eating make & consume sizable meals while
asleep
 Ex: Lithium (bipolar), amitriptyline (TCA) & clozapine (schizo)
 Genetics & other factors – disposition varies w/ethnicity (6-85%) *thrifty gene
hypothesis; kids of obese parents far more likely to become obese; certain genetic
conditions have obesity as sx –
 Assortative mating (heavy dates heavy)
 Prader-Willi syndrome: very rare, w/polyphagia, food preoccupation, shortness &
LD’s
 Bardet-Biedl syndrome: ciliopathic disorder w/obesity, retardation, hypogonadism
& retinitis pigmentosa
 MOMO syndrome: extremely rare, only 4 cases currently worldwide; w/macrosomia
(big birth weight), obesity, macrocephaly & ocular problems
 Medical factors: Hypothyroidism, GH (growth hormone) def, Cushing’s dis
(overproduced cortisol)
Impact on health (prone to many health risks & conditions): DM type II, BP/cholesterol,
obstructive sleep apnea, OA, CVD, fatty liver dis, thrombosis, hernias & migraines
Tx’s:
o Diet & exercise (DUH!)
o Medications:
 Orlistat (Xenical): reduces intestinal fat absorption
 Not in slides but in pdf:
 Sibutramine (Meridia): inhibits NT inactivation in NA
 Ribonabant (Acomplia): blocks cannabinoid receptors in EUROPE only
 Belviq: appetite
 Phentermine (Adipex): appetite* (short term, use only weeks)
 Qsymia: appetite
Other interesting facts/stats:
o Most cases, weight loss due to commercial dieting/weight loss programs regained w/in 5
yrs
o Bariatic (weight loss) surgery initially effective but not so helpful in long term
 Cachexia: ‘wasting syndrome’ weight loss (& m atrophy, fatigue, weakness, loss of appetite)
in ind’s not trying to lose weight; cannot be reserved nutritionally; rel’d w/dis processes
(cancer, infection)

Neurodev’al/Neurological Disorders
 ADHD: attention deficit disorder (ADD; DSM III) or Attention deficit hyperactive disorder
(ADHD; revised name from DSM IV-R & DSM V); 5% of kids, esp boys, 10:1 M/F ratio;
>common in 1st born males; lowest prevalence in CA, highest in Alabama; West to East in
US; child onset ~<12 y/o (<7 in DSM IV); 50-70% continue sx as adults; most adults w/ADHD
have had it since childhood, but may go undx’d; other conditions mimicking ADHD sx in adults
include depression, OCD, hypothyroidism, anxiety; in category of Disruptive behavior disorders
(w/ODD & conduct disorder) – charac’d by inappropriate behaviors that cause problems in
social rel’nships & school performance; DSM-V: kids age onset b4 12 y/o w/ at least 6 sx for 6
mo’s; adults need 5 for either type of ADHD; 3 types:
1) predominantly hyperactive-impulsive type
 Hyperactivity components often–
1. fidgets w/hands or feet or squirms in seat
2. gets up from seat when staying seated is expected
3. runs about or climbs when & where not appropriate
4. has trouble playing or enjoying leisure activities quietly
5. “on the go” or acts as if “driven by motor”
6. talks excessively
 Impulsivity components often –
1. blurts out answers b4 ques have been finished
2. has trouble waiting 1’s turn
3. interrupts or intrudes on others (ie. Butts into convos or games)
2) predominantly inattentive type often –
1. fails to give close attention to details or makes careless mistakes in schoolwork,
work, or other activities
2. has difficulty sustaining attention in tasks or play activities
3. doesn’t seem to listen when spoken to directly
4. doesn’t follow thru on instructions & fails to finish schoolwork, chores or duties in
workplace
5. has difficulty organizing tasks & activities
6. avoids engaging in tasks that need sustained mental effort (ie. Schoolwork)
7. loses things needed for tasks & activities
8. easily distracted by extraneous stimuli
9. forgetful in daily activities
3) combined type; DSM V dx’s this w/ 6/9 sx from both inattentive & hyperactive type;
child’s behavior (hyperactivity) must occur in at least 2 diff settings, ie. Class,
playground, home, social or community; if only 1 location, suggests problem may not
be ADHD
o Causes include –
 DA/NE involvement as stimulants (Amph) affect these transmitters
 May be localized to frontal lobe; ADHD kids show volume of frontal cortex, esp L
prefrontal cortex & yet evidence also shows faster dev’t of motor areas
o PET scan: see brain activity, orange areas = less DA transporters in reward pathways
of ADHD’ers

o EEG’s show differences too –

higher theta waves in ADHD’ers = should be in sleep
o EEG: females ADHD – theta waves, males ADHD –alpha waves
o Genetic or social/env’al factors contributing to ADHD:
 Correl’n w/prenatal smoking & alcohol consumption (then again Mom could smoke &
drink b/c has ADHD)
 Pesticide exposure may  risk
 Violence/child abuse as always
 Internationally adopted children show higher risk for ADHD & OCD
o Sig’ly comorbid w/ADHD – very high CD (26%) & ODD (35%), anxiety (29%), depression
(30%)
o Hunter Farmer theory of ADHD: back in days of yore, ADHD type ppl better at hunting,
scavenging, moving around, while non-ADHD ppl stayed at home & cook & make better
spears & such
o Tx for ADHD:
 Pharmacological: mostly stimulant drugs (Ritalin, Concerta, Adderall, Dexedrine); adults
may start w/Prozac (Fluoxetine); but variable side efx common & minor; appetite may
inhibit growth & lead to failure to gain weight
 Video games? System hooks up w/playstation. ADHD kids ‘zone out’ during games,
w/this system, game stops if kid ZONES out.
 Therapy: various effective forms but most effective in fam* therapy
 Nutritional: no consistent links btwn diet & ADHD (ie. Sugar) but 1 British study showed
correl’n btwn certain food additives & ADHD; foods w/any of these now required to have
labels saying so
 Alternative: biofeedback, neurobiofeedback?

LEARNING DISORDERS
 Specific learning disorder: LD’s/differences/disorders; afx how person understands, rmr’s &
responds to new info; not usually recog’d until child starts school; have difficulty w/ -
 Listening or paying attention
 Speaking
 Reading, writing & arithmetic (3 R’s)
 Reasoning
 Specific learning disorder
o Not all learning disorder kids have low intelligence; main issue is w/processing info; sub
classified by type of processing deficit or specific difficulty arising from it; 4 stages of info
processing –
1. input: difficulties w/visual, audio, tactile perceptions
2. integration: not telling story in correct sequence, or see ‘big picture’
3. storage: memory problems (short term)
4. output: problems w/motor or verbal expression of info i.e. talking, writing, drawing,
fine & gross motor skills
o DSM V criteria: difficulty learning or using academic skills, w/at least 1 of these sx for at
least 6 mo’s, despite provision of interventions that target those difficulties:
 Inaccurate or slow reading
 lack of comprehension of what’s read
 poor spelling, difficulties w/writing
 problems w/# of comprehension
 calculation
 & mathematical reasoning
 Affected academic skills substantially & quantifiably below expected for ind’s
chronological age
 further classified by problem area (reading, writing, math) & by severity (mild,
moderate, severe)
Other learning disorders –
 Nonverbal LD (NVLD): lack coordination (often L side), social inadequences, balance
problems, math difficulties; usually do quite well in verbal areas (eloquent, large vocab); very
similar to High func’ing autism
o Dyspraxia: born w/difficulties w/motor skills (simple like combing hair or complex like
teeth brushing); can affect speech; component of NVLD* (if not born w/it, called apraxia*
due to stroke/injury)
 Auditory processing disorder (APD): ‘hearing’ fine but central processing affected; trouble
separating multiple sounds (like speech vs. A/C or vacuum cleaner); afx ind intermittently (not
constantly); often leads to dyslexia, often misdx’d as ADHD or Autism; pt’s prefer written
comm, oral instructions 1 at time & ask ppl to speak slowly; often accused of not listening &
say ‘huh’ a lot; M:F ratio 2:1 or 3:1; up to ~20% adults have some degree of it; may have hx of
otitis media
 Dyslexia Types: (dev’al reading* disorder)
o Surface: can read known words but not irregular words (ie. M, you, said, what, country,
colonel)
o Phonological: read regular & irregular words but have difficulty w/non-words &
w/sounding out words
o Double deficit: slow naming speed; occurs w/phonological dyslexia
 imaging studies: pt’s have over-dev’d speech production area but underdev’d speech
comprehension area
1. Broca’s area impaired? Motor production of language; over dev’d speech production area
2. Wernicker’s area – under dev’d comprehension area
3. Visual association cortex
4. Maybe cerebellar issue as well  cerebellum very imp for ‘automatic’ learnt behaviors
(habits, reflexes); could also apply to learn behaviors rel’d to reading; rel’nships btwn
syllables, ie. How to ‘read’ a sentence
a. Articulation problems can also contribute to dyslexia (harder to spell it right if it doesn’t
sound right)
 language type afx dyslexics  fewer dyslexics in languages that ‘make sense’ meaning
better orthographics (ie. Italian vs. English)
 Controversy: Is it really a disorder? Makes parents feel better to call it ‘condition’
 Reading not a ‘natural act’ only encouraged widespread in past 100 yrs
 School, parents actually to blame
o Causes/risk factors for LD:
 Genetics?
 OBVS prenatal (mom smoking, drugs) or post natal (injury, malnutrition, anoxia)
complications
 Poverty: some evidence that kids who read less w/less resources at greater risk for LD’s
by school age
 APD may have hx of otitis media
 Gender issues – when eval’d by teachers, LD >in boys (75%) vs girls; but some studies
find equal
o Dx of Learning Disorder
 Parents often notice ‘something wrong’ b4 school age, but problems MORE seen when
school starts
 ‘proper’ identification would come from school, clinical & neuropsychologists
 if child’s ‘cognitive abilities’ much higher than academic performances, child would likely
be dx’d w/LD
o ‘Discrepancy’ Model – sig difference btwn their IQ & academic performance; criticized
b/c may not be accurate & not great at predicting how tx will go (low IQ kids w/low
performance benefit as much from tx as ‘LD’ kids)
o Resp to intervention (RTI): early screening program for all to ID those ‘at risk’; problem
is program needs to be big, impressive & comprehensive (hard to do); too large of sample
size
o Tx strategies focus on: (for this lifelong disorder)
1. compensating/accommodating disability
2. specialized instruction to help w/weak areas
3. practice
 Comm disorders: speech & language disorders w/problems in language, speech & comm;
much overlap w/other areas (autism, LD’s, dyslexia, dyscalculia); types –
o Language incompetence: (comm disorders can affect any/all of these) –
 Phonology: production of word sounds (to make word sound 1 has to imitate it)
 Grammar: org’ing words in sentence to make sense
 Semantics: org’ing concepts
 Pragmatics: use of language & ‘rules’ of conversation (like when to pause)
o Language disorder: (DSM V dx) persistent difficulties in acquisition & use of language
across modalities (spoken, written, sign language, other) including –vocab, lmtd sentence
structure, impairments in discourse, language abilities below those expected at that age &
sx onset during early dev’al period; combines expressive language disorder &
receptor expressive language disorder from DSM IV-R
 Expressive ability: production of vocal, gestural or verbal signs
 Receptive ability: receiving & comprehending language msgs
 +ve Fam hx frequent & kids w/predominantly receptive problems have worse prognosis
o Speech sound/Phonological disorder: (DSM V dx) persistent difficulty w/speech sound
production that interferes w/speech intelligibility or prevents verbal comm of msgs;
occurs during early dev’al period & not better explained by general medical conditions;
omission or distortions of sounds, atypical pronunciation; sounds like they’re at younger
age; can be determined in pt by checking articulation (ie. Age 3 can articulate m, n, ng, b,
p, h, t, k, d)
o Child-onset fluency disorder (aka STUTTERING): speech prolonged by involuntary
repetitions & prolongation of sounds; DSM V dx – disturbances in N fluency & time
patterning of speech inappropriate for ind’s age & language skills, persist over time, by
frequent & marked occurrences of 1(or+) of –
+Disturbances cause anxiety about speaking, lmtd effective comm, social participation,
academic performance
1. sound & syllable repetition
2. sound prolongations of consonants & vowels
3. broken words
4. audible or silent blocking (filled or unfilled pauses in speech)
5. circumlocution (use many words to say something, going around in circle ie. Ba..Ba…
Ba..(forget Banana, I’ll just fruit)
6. words made w/excess of physical tension
7. monosyllabic whole word repetitions (ie. I..I..I see you)
o Social (pragmatic) comm disorder: (DSM V dx) persistent difficulties in social use of
verbal & nonverbal comm as manifested by all these –
 Note: while onset of sx must be in early dev’al period, condition might not be noticed
until social comm demands exceed ind’s lmtd capabilities
1. deficits in using comm for social purposes (even saying hello) in manner appropriate
for social content
2. impairment of ability to change comm (from classroom to playground)
3. difficulty following rules for conversation & story telling
4. difficulties understanding what’s not explicitly stated (ie. Making inferences)
o Other comm disorders:
 Cluttering: fluency problem (rapid speech, poor syntax, erratic rhythm); & may
sometimes have following speech patterns:
 Spoonerisms: “Is it kisstomary to cuss the bride” instead of ‘customary to kiss the
bride’
 Freudian slips (parapraxis): “Sure, I’d love to go to breast” instead of ‘Sure, I’d
love to go brunch’
 Dysnomia: super ‘tip of tongue’ (unable to recall & spell words correctly)
 ASD (Autism spectrum disorders): DSM V – neuro’al disorders; 4M = F; 80% have IQ <70
(but highly variable); linked to chr15; some have Savant skills/syndrome (unusual intellectual
abilities – calculation skills, incredible memory; replacing older & nicer terms of idiot Savant –
not very common ~1/10) sx–
(1) much delayed or sig lack of social & language skills
(2) problems comm’ing w/others & understanding language
(3) ignore or fail to understand facial expressions
(4) eye contact in social situations (DON’T like to make eye contact, b/c don’t understand
facial expression, ie. Someone smiling back, don’t get it)
 DSM V criteria for ASD:
A. Qualitative impairment in comm social interax’n via deficits in –
1. social-emo’al reciprocity
2. non-verbal comm behaviors
3. developing, maintaining & understanding rel’nships (w/all!)
B. Restricted/repetitive stereotyped patterns of behaviors, interests & activities (RRB’s):
1. stereotyped or repetitive motor movements
2. Insistence on sameness (ie. Walk & twitch hands for 5 mins b4 leaving room every
morning), DON’T LIKE CHANGE!
3. highly restricted, fixated interests abnormal in intensity/focus
4. hyper or hyporeactivity to sensory input
o If no RRB’s present, dx would be social comm disorder
o Sx NOT better acc’td by another condition, esp intellectual disability (ie. MR) or social
comm disorder
o Sx must manifest in early dev’al period THUS, Parent should be concerned if –
 No babbling by 12 mo’s
 No gesturing (pointing, waving goodbye) by 12 mo’s
 No single words by 16 mo’s
 No 2-word spontaneous phrases (other instances of echolalia) by 24 mo’s; any loss of
any language or social skills, at any age
o Cause of ASD’s –
 Genetics play role, MZ concordance greater than DZ concordance
 Alteration of brain dev’t soon after birth
 Usual env’al factors contribute (toxins, dis, PCB’s, diet, alcohol, smoking)
 Failure of apoptosis
 Pre- or peri-natal injury or dis
o Neurology of ASD’s – many theories (poor connections, too many of 1 type of neuron
somewhere) most interesting is mirror neuron system theory of autism: mirror
neurons fire when person acts & when person observes same ax’n performed by another;
may be differences in mirror neuron areas in pt’s; ie. Watching someone tie shoe lace helps
us learn how to do it (observational learning) OR brain fires off when someone smiles, get
reward, smile back; ASD pt’s lack this & thus hard to learn how to do things correctly
(hence, corrections in learning impaired)
 ASD includes following 3 disorders –
1. Asperger’s Syndrome (high func’ing autism): language & cognitive dev’t mostly
unaffected (diff from other ASD’s); note pt’s often w/intense interest or preoccupation w/
‘obscure’ objects ie. Collection of vegetable-shaped staplers or 1950s era Italian sports
cars; N cognitive dev’t & minimal or no delays in language dev’t either
 Def conversational language skills & often see physical clumsiness (guy trying to shave
in vid)
2. CDD (Childhood disintegrative disorder): N dev’t until age 3-4, then severe loss of
social, comm & other skills in few mo’s; b4 age 10)
3. PDD NOS (Pervasive dev’al disorder): used to be MC ASD form! Not good for NOS
category; Ex. Late onset, 10 y/o, except ASD’s now defined as started under 12 (not 7) so
PDD-NOS taken under ASD umbrella
4. Autism
 TX for ASD’s –
o Ind’d tx’s best approach w/to lessen associated deficits & fam distress, QoL & func’al
independence, structured teaching, speech, social & fam therapies & acquiring lvl of
self-care
o Educational interventions: better to do something vs nothing, unclear as to what works
best w/who
o Medical management: antidepressants, stimulants, anti-psychotics, anti-convulsants (for
sx, ie. seizures)
o Alternative: diets, chelation therapy; clear benefits from these have yet to be established
o Interesting therapy  ASD pt’s have strong preferences for Thomas over other characters
b/c they’re like drawn to lines, wheels & spinning wheels; Thomas & friends have bold
obvious colors; so short easy stories, exaggerated facial expressions, predictable
characters HELP!
 Other childhood disorders:
o Rett syndrome: decelerated head growth (microcephaly), small hands & feet (from 5
mo’s-4 yrs altho most occurrences 6-18 mo’s); cognitive impairments & social difficulties;
80% w/seizures; scoliosis, growth problems, difficulty walking, stereotyped movements
(hand wringing) & GI disorders associated sx; due to genetic mutation: 95% sporadic (ie.
not inherited); germline mutations also occur; almost exclusive to females; males rarely
survive to term (die in utero); dev’al progress stops & regression occurs (prev’ly acquired
skills lost)***
o Separation Anxiety disorder/‘school phobia’: child w/overwhelming fear of losing
major attachment figure (parent, esp mom); complains of physical sx to avoid going to
school; have parent accompany to school, gradually time spent there each day; these
kids at greater risk for adult anxiety disorders, esp agoraphobia
o Selective mutism: rare, speak in some social situations but not others (ie. at home but
not school); more in girls, must be distinguished from normal shyness & actual
speech/language disorders
o Tic disorders:
 Tic: sudden, rapid, recurrent, non-rhythmic motor movement or vocalization
 Tourette’s disorder: vocal & motor tics (MUST HAVE BOTH) for 1 yr’s duration; onset
must be <18 yrs old; 3X more prevalent in males; copralalia (swearing) in only ~15%
 Persistent (chronic) motor/vocal tic disorder: motor or vocal tics, but not both
o Motor disorders:
 Dev’al coordination disorder: coordinated motor skills sig’ly below lvl expected for
that age; clumsiness, slow & inaccurate movements
 Stereotypic movement disorder: repetitive, seemingly driven & apparently
purposeless motor behavior (even to pt of self-injury) ex. Hand waving, body rocking,
head banging, self hitting)

Epidemiology
 Epidemics: greater # of cases of a dis than expected; spread thru out a pop
 Endemic: constant presence of dis in particular locality, region or ppl
 Pandemics: epidemic that spreads thru human pop’s across a large region (for ex. a
continent) or even worldwide

 Descriptive Epi: examining natural hx & distribution of a dis in a pop; observing its
distribution in terms of time, place & person (triad***); includes case rep’ts, case series, cross
sectional studies
 Triad of analytic Epi: host factors, env, and agent (all influence each other)
 Cumulative incidence/incidence rate: proportion of ppl who become dis’d during specified
period of time; = new cases occurring in given period / pop @risk during same time period

 Cohort study classifies ppl based on some risk factor ie. smoking vs nonsmoking, & follows
them fwd in time to assess differential incidence rates btwn 2 groups - unchosen by
researcher. No interventions. outcome analyzed is incidence of dis for ex.
 Clinical trial/exp’al study: participants assigned to 1 of 2 groups/interventions; ie. study on
their own or participate in study groups
 Case study: description of single pt telling their hx, sx, & prognosis (if known).
 Case control study: pt’s w/certain dx compared w/ppl w/out that dx; compare by looking
retrospectively for presence or absence of any identifiable risk factors
 Community trial: exp’al study where intervention is assessed in milieu of community; goal of
this study is to assess whether some specific intervention will work in uncontrolled
circumstances of real world
 Collaborative study: one in which multiple investigations at diff geographic locations work
together & pool their data for analysis
 Crossover study: every study participant gets med being tested at some point during study
period; at start of this double-blinded study, 1 group of subjects get medication while other
group gets placebo; then at some predetermined point, crossover occurs; now placebo group
gets medication & med group gets switched to placebo; so all participants get whatever
benefit medication provides & comparision btwn pt on & not of medication is possible at every
point in time of the study*
 Cross-sectional study: researchers assess who has or doesn’t have given dis & what
features are associated w/ppl who do have dis; look at subjects at single point in time

Ethics