Category Archives: D-I

Diagnosis and Psychopathology


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


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

Mental disorders due to GMC & substance induced mental disorders

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


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


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

a.) selective attn to neg events in env

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

c.) stringent standards for self-eval

d.) insufficient self-reinforcement

e.) excessive self-punishment

Bipolar Disorder

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

Anxiety Disorders

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

Somatoform Disorders

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

Pervasive Developmental Disorders

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

Learning Disabilities

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

Attention Deficit Hyperactivity Disorder

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

Conduct Disorder

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

Feeding Disorders

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

Tic Disorders

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

Mental Retardation

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

Personality Disorders

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


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

Design and Stats


Internal validity

  • permits the conclusion that there is a causal relationship btwn IV and DV
  • extraneous Fs (that might account for IV differences, not DV)
  • threats: hx (external event), maturation (biological or psychological, e.g., fatigue, boredom, phys/intellectual dev), testing (exp with pre-test), instrumentation (change in nature of instrument), regression toward the mean (individual variation in species is limited, selection biases, differential mortality (drop-outs), experimenter bias (Rosenthal effect/Pygmalion effect, experimenter expectancy effect- beh of S changes b/c your expectancies)
    • random assignment of Ss (most powerful -minimizes this), matching Ss (ensure equivalency), blocking (studying the effects of an extraneous S characteristics- treat as IV), ANCOVA

External validity

  • generalizability of results
  • threats: interactions btwn selection and txt (txt effects don’t generalize to members of same pop), testing and txt (txt effects don’t generalize to individuals who don’t take a pre-test; see demand Cs and HE), hx and txt (txt effects don’t generalize beyond setting or time period exp done), demand Cs (cues in research setting allow Ss to guess rsch Hs), Hawthorne Effect (tendency of Ss to beh differently when they are being observed in rsch setting), order effects (repeated measures studies)
    • random S selection from pop of interest, conducting naturalistic/field research, using single or double-blind research designs, counterbalancing
    • stratified random sampling (taking a random sample from each of several subgroups of the total target population)
    • cluster sampling (unit of sampling is a naturally occurring group of individuals, rather than the individual)

Types of Designs

True experimental design

  • Ss randomly assigned to IV; permits greatest experimenter ctrl and highest internal validity

Quasi-experimental design

  • manipulated variable is studied, but Ss not randomly assigned to group (often pre-existing- pt grps), since Vs are manipulated, some experimenter ctrl

Correlational design

  • Vs not manipulated and no causal relationship btwn Vs can be assumed
  • measure the degree of relationship btwn Vs

Developmental research

  • assessing Vs as a fx of dev over time (aging on IQ scores)
  • longitudinal (pblms: high cost, attrition, practice effects; tend to under-est true age-related change b/c of attrition and practice effects), cross-sectional (cohort effects- intergenerational effects, difference might due to experience rather than age; tend to overestimate true age-related declines in performance), cross-sequential (Ss of different age grps studied over a short period of time; combines the two)

Time-Series Design

  • DV is measured several times, at regular intervals, both before and after txt is administered
  • ctrls for maturation, regression and testing; but hx (internal validity threat)

Single-Subject Designs

  • designs involving a single S (or one group txt as single S) and at least one baseline (pre-txt) phase and one txt phase, DV measured several times during both phases; simple AB (baseline-txt) design, reversal designs (txt withdrawn to determine if beh reverts to baseline levels; ABA or ABAB), multiple baseline designs (txt is sequentially admin across different beh, settings, or Ss)

Qualitative (Descriptive) Research

  • collect data in order to arrive at a theory about “how things are” (data fishing)
  • observation, interviews, surveys, case studies
  • often used in pilot studies to ID Vs and Hs for future studies

Scales of Measurement

  • nominal (unordered categories; gender)
  • ordinal (ordered/rank data; Likert scale)
  • interval (successive pnt =, but no absolute 0 pnt; IQ)
  • ratio (has absolute 0; weight, time)

Parametric Statistics

  • one-way ANOVA significant findings: population means differed

Parametrics test interval/ratio

  • assumes: normal distrib, homogeneity of variance (variance of all grps =), indep of observations
  • many parametric tests robust, esp to deviations of 1st 2, but not for multicolinearity

t-test: comparison of 2 means (Student’s t-test)

  • one sample t-test (comparing sample mean to known population mean) df=N-1
  • t-test for indep samples (compare means from 2 indep samples) df=N-2
  • t-test for correlated samples (compare means of 2 correlated samples- before/after design) df=N=1 (N is number of pairs of scores); e.g.s would be matched samples and pretest-posttest design

One-way ANOVA

  • one DV and more than 2 grps
  • yields an F value (ratio of btwn group variances-differences btwn grp means also known as txt variance; and within grp variance-differences btwn scores within each group); B variance/W variance; want B>W
  • sum of squares is measure of variability of a set of data; B df=k-1 (k is number of grps); W df=N-k (N is total number of Ss); Sum of Sq/df for each divided by each gives you F ratio
  • post-hoc tests (Tukey, Scheffe): pinpoint exact pattern of differences among the means b/c F alone doesn’t indicate exact patterns of differences among the means
  • doing multiple comparison’s increases Type I error (experimenter wise error)
  • other post-hoc tests: Neuman-Keuls test, Duncan’s multiple range test, Fischer’s Least Significant Difference Test
  • Scheffe is most conservative of all (greatest protection against Type I error; also highest Type II error rate)
  • Tukey appropriate if conducting pairwise comparisons
  • can also conduct planned pairwise or complex comparison (Hs a priori)

Factorial ANOVA

  • study involves 2/more IV and one DV
  • allows assessment of both main effects (group/IV differences; marginal means), and interaction effects (degree to how IV is different at different levels of the IVs)
  • can’t interpret main effects when interaction b/c don’t generalize to all situations (IV acts differently at different levels of another IV)


  • used to analyze data from studies with multiple DVs and at least one IV
  • can also conduct separate ANOVAs, one for each DV; but overall advantage of reducing Type I error

Nonparametric Statistics

  • nonparametrics test nominal or ordinal; distribution free tests; less powerful
  • both parametrics and nonparametrics assume samples are rep of pop


  • used to analyze nominal data (compares observed freqs of observations within nominal categories to freqs that would be expected under the null)
  • cautions in using chi-sq:
  1. all observations must be indep (no for before/after study)
  2. each observation can be classifiable into only one category/cell
  3. % of observations within categories can’t be compared (freq data required)
  • expected frequencies= (column total)(row total)/N

Mann-Whitney U

  • compare two indep grps on a DV measured with rank-ordered data
  • alternative to t-test for indep samples (if nonparametric)
  • can convert ratio/interval data to ordinal rank if assumptions of parametric tests not met

Wilcoxon Matched Pairs Test

  • compare 2 correlated gps on DV measured with rank-ordered data
  • alternative to t-test for correlated samples (if nonparametric)

Kruskal-Wallis Test

  • compares 2/more indep grps on a DV with rank-ordered data
  • alternative to one-way ANOVA (if nonparametric)

Distribution issues

  • descriptive stats describe data set
  • inferential stats makes inferences about entire pop based on sample data
  • negative skewed: most scores are high (to the right), but a few extreme low scores
    • mean is lower than the median, median lower than the mode
    • easy test; ceiling effects
  • positive skewed: most scores are low (to the left), but a few extreme high scores
    • mean is higher than the median, median higher than the mode
    • difficult test; floor effects
  • z-scores have same shape distribution as raw score distribution which it was derived
  • standard deviation most commonly used measure of variability
    • curve: 68% scores fall btwn +1 sd; 95% btwn +2; 99% +3
    • 16% >1 sd v-v; 2% >2 sd v-v
    • percentiles: 0.1% (z = -3); 2% (z = -2); 16% (z = -1); 84% (z = 1); 98% (z = 2); 99.9% (z = 3)
  • variance: average of the sq differences of each observation from the mean
  • sd: square root of the variance
  • stanine: divide the distribution into 9 = intervals, 1 lowest, 9 highest
  • % score refers to items on the test; % rank refers to other scores in the distribution
    • % ranks have a flat (rectangular) distribution- within a given range of % ranks, same number of scores- compared to normal distribution where most scores fall at ctr and few at extremes; non-linear transformation (changing to % distribution)
    • in a normal distribution,
      • z-score of 1.0 is equivalent to a % rank of 84 (top 16%) and z-score of -1.0 is equivalent to 16% (bottom 16%)
      • z-score of 2.0 = PR 98 (top 2%); -2.0 = PR 2 (bottom 2%)
    • change in raw score in middle of normal distribution results in much greater change in PR than same raw score change at the distribution’s extreme
  • homogeneity of variance: parametric tests robust to this unless unequal number of Ss in all exp groups (then Type I error increases)
  • sampling distribution of means: distrib of values of that stat, which each value computed from same-sized samples drawn with replacement from a pop
  1. has less variability than pop distrib
  2. sd is standard error of the mean
  • central limit theorem:
  1. as sample size increases, shape of sampling distrib of means approaches normal shape (even if pop distrib of scores not normally distrib)
  2. mean of sampling distrib of means is equal to mean of pop

Samples, Populations, Sampling Error

  • sample values limited b/c est of pop values
  • sample value=stat; pop value=parameter
  • sampling error always occurs in stats (b/c sample mean no always = pop mean)

Standard Error of the Mean

  • provides index of expected inaccuracy of sample mean (deviation btw est pop mean (i.e., sample mean) and true pop mean)
  • difference btwn sample mean and pop mean (e.g. of sampling error)

sd/√N sd (of pop); N (sample size)

  • decreasing SD and increasing N will result in smaller value and v-v

Statistical Decision Making

  • null H: IV has no effect on DV
  • alternative H: IV has effect on DV
  • possibilities:
  1. true null retained (correct; no difference btwn IV)
  2. true null rejected (incorrect; Type I error; at alpha- saying difference, not)
  3. false null rejected (correct; find difference that does occur)
  4. false null retained (incorrect; Type II error; beta; unknown value)
  • one-tailed H: predict the direction that means differ
  • two-tailed H: don’t predict direction
  • power: probability of rejecting null H when it’s false (probability of not making at Type II error); 1-beta (power)
    • increases by: larger N; increase alpha, 1-tailed test; greater difference btwn pop means under study
  • to determine whether or not to reject the null, you must compare stat value obtained to a critical value and dependent upon 2 Fs:
    • pre-set alpha level
    • degrees of freedom for stat test
  • if obtained value is lower than critical value, null retained


  • correlation (relationship of 2 Vs); correlation coefficient (stat index of relationship)- tells you magnitude and direction
  • use of scattergram to pictorially represent this
  • Pearson r (correlation btwn 2 continuous Vs): Pearson Product Moment (PPM)
    • Fs that can affect it: linearity (assumes linear relationship btwn 2 Vs); homoscedasticity (dispersion of scores are equally distributed); range of scores (wider the range of sample beh, more accurate est of correlation)
    • sq Pearson r: percentage of variability in one measure that is accounted for by variability in the other measure (coefficient of determination)
    • nonlinear relationship can be measured by coefficient eta.
  • point-biserial coefficient (correlates one continuous V with one dichotomous V)
  • phi coefficient (correlate 2 dichotomized Vs)
  • contingency (correlation btwn 2 nominally scaled Vs)
  • Spearman’s rho (correlate 2 rank-ordered Vs)


  • when 2 Vs correlated, construct equation to est the value of a “criterion” (outcome) V on the basis of scores on a “predictor” (input) V; multiple regression (2 or more Vs used to predict scores on one criterion)
  • assumptions: linear relationship btwn X and Y; regression line is picture of the overall relationship btwn 2 Vs
  • error score: difference btwn predicted and actual criterion score; error scores assumed to be normally distributed with mean of zero; correlation btwn error scores and actual criterion scores assumed to be zero; relationship btwn error scores and actual criterion scores must be homoscedastic
  • location of regression line determined using least sqrs criterion (line drawn at location where least amnt of error in predicting Y scores from X scores)
  • relationship btwn 2/more predictor Vs and one criterion V (multiple correlation coefficient; multiple R)
  • multiple correlation coefficient (predictive power of MR equation) is highest when predictor Vs each have high correlations with criterion but low correlations with each other; don’t want multicollinearity (when predictor Vs correlate)- doesn’t add predictive power
  • multiple correlation coefficient never lower than the highest simple correlation btwn individual predictor and criterion; it’s also possible that adding predictors can decrease multiple R due to multicollinearity
  • multiple R can never be negative (b/c of calculation procedure won’t allow it)
  • like Pearson r, multiple R can be squared (R2) called coefficient of multiple determination (proportion of variance in criterion V accounted for by combination of predictor Vs)
  • goal of stepwise regression is to come up with smallest set of predictors that maximizes predictive power (retain predictors that have high multiple correlation with criterion)

Other Correlation Techniques

  • Canonical Correlation: used to calculate relationship btwn 2/more predictors and 2/more criterion Vs
  • Discriminate Function Analysis: used when goal is to classify individuals into groups based on their scores on multiple predictors
  • Multiple Cutoff: setting a minimum cutoff score on a series of predictors; if cutoff score not achieved on even one of the predictors, person isn’t selected
  • Partial Correlation: used to assess relationship btwn 2 Vs with the effects of another V “partialled out.” (stat removed); converse to this is zero-order correlation (correlation btwn 2 Vs determine without regard for any other Vs); can have a suppressor V (suppresses relationship btwn predictor and a criterion)
  • Structural Equation Modeling: general term used for techs that involve calculating pairwise correlations btwn multiple Vs; purpose for causal modeling, testing a H that posits a causal relationship among multiple (3/more) Vs (path analysis, LISREL)
    • assumes linear relationship btwn Vs
    • path assumes one-way causal flow; LISREL one-way and/or 2-way; Path used in models that include observed Vs only; LISREL used when model specifies both latent and observed Vs
    • basic steps:
  1. specifying a structural model involving many different Vs
  2. conducting stat analysis
  3. interpreting results of analysis
  • Trend Analysis: stat tech used to examine trend of change (linear, quadratic, cubic, quartic) in DV, as opposed to whether or not DV changes at all
  • logistic regression like discriminate fx analysis b/c makes predictions about which criterion grp person belongs to; mostly used for dichotomous DV
    • differences btwn LR and DFA:
  1. DFA has 2 assumptions: multivariate normal distrib, homogeneity of variance/covariance
  2. can use nominal or continuous Vs and DFA continuous only (interval/ratio)

Advanced statistics

  • autocorrelation: correlation btwn observations at given lags (e.g., every 2nd observation); used in time-series analysis
  • Bayes’ theorem: formula for obtaining special type of conditional probability; revise conditional probabilities based on additional info

Dementia versus Depression



  • Dementia is not a separate disease entity. Instead, it is a “set of symptoms” which may be associated with many disorders.
  • “The essential feature of Dementia is impairment in short- and long-term memory, associated with impairment in abstract thinking, impaired judgment, other disturbances of higher cortical function, or personality change”
  • Dementia is not synonymous with declines in intellectual functioning which are associated with normal aging.
  • Dementia is never diagnosed unless “the disturbance is severe enough to interfere significantly with work or usual social activities or relationships with others” (1).
  • Dementia always has an underlying organic cause. Examples given in the DSM-III-R include:
    • Primary Degenerative Dementia of the Alzheimer’s Type(DAT).
    • Vascular disease (multi-infarct dementia (MID]).
    • CNS infections (viral encephalitis, AIDS, etc.)
    • Brain trauma (especially chronic subdural hematoma)
    • Toxic metabolic disorders (e.g., hypothyroidism)
    • Normal pressure hydrocephalus.
    • Neurologic-diseases (e.g., Huntington’s chorea, multiple sclerosis, Parkinson’s, etc.)


“Estimates of the prevalence of dementia among the elderly…have ranged from 1.3% to 6.2% of persons over 65 years of age for severe dementia, and from 2.6% to 15.4% for those with milder dementia…”

  • “The prevalence of dementia appears to be age associated, with a four to sevenfold increase from ages 70-79 to ages greater than 80”
  • Alzheimer’s Disease accounts for approximately 1/2 of all cases of dementia, affecting 5-6% of people above age 65


Dementia is more commonly found among the elderly, but it may occur at, any age after IQ is stable (age 3-4). Therefore, “if a four-year-old developed a chronic neurologic disorder that interfered with previously acquired functions so as to significantly lower intellectual or adaptive functioning, he would be considered to have both dementia and retardation.” (1)


The course of dementia depends on its underlying etiology; it may be progressive, remitting, or static (1).

  • Dementias which are due to brain tumors, subdural hematomas, and metabolic factors may have a gradual onset (1).
  • Primary Degenerative Dementia of -The Alzheimer Type usually involves slow deterioration over many years, continuing until death (l,2,5)
    • “The condition typically begins so insidiously that often the family is unaware that anything is wrong until a sudden disruption in routine leaves the patient disoriented, confused, and unable to deal with the unfamiliar situation. Because the early behavioral decline is so gradual and unsuspected and because most simple functions — as measured by elementary tests of language and of sensory and motor functions — remain intact in the early stages of the disease … it is difficult to date the onset of the condition with any sureness” (5).
    • Researchers at the New York University Geriatric Study and Treatment Program have outlined three phases in the progression of DAT:
      • The forgetfulness phase: increasing forgetfulness (noticed by the individual and sometimes by others close to him) and accompanying anxiety caused by the forgetfulness (2).
      • The confusion phase: “severe deficit in memory for recent events, difficulty in orientation and concentration, and subtle language deficits (e.g. word finding difficulty) despite generally intact vocabulary and syntax” (2).
      • The dementia phase: “characterized by severe disorientation, abnormalities of language, perception and praxis, and behavioral problems, including motor restlessness, wandering, and psychotic symptoms (e.g., paranoid ideation) (2).
    • Dementia resulting from a clearly defined episode of a neurologic disease (e.g., cerebral hypoxia or encephalitis) may begin quite suddenly, but then remain stationary for a long time (1).
    • In MID (multi-infarct dementia), the deficits are believed to be the result of the accumulation of abrupt vascular episodes (“strokes”). Therefore, the onset of dementia in MID is typically abrupt. There is also a stepwise course of deterioration, with further deficits being noted after each stroke. With MID, the neurological signs and symptoms are more likely to be focal; and there is a history consistent with cerebrovascular accident (CVA), and a history or presence of hypertension” (2,5).
    • “If the underlying cause can be treated (e.g., subdural hematoma), dementia can be arrested or even reversed. However, the more widespread the structural damage to the brain, the less likely clinical improvement” (l)

Memory Problems

The memory problems associated with dementia will vary depending on the severity of the dementia (1,4).

  • Mild dementia; moderate memory loss which is more marked for recent events (e.g., forgetting names, telephone numbers, directions, conversations’. and events of the day) (1).
  • Severe dementia: “only highly learned material is retained, and new information is rapidly forgotten. The person may leave a task unfinished because of forgetting to return to it after an interruption. This may cause a person to leave water running in the sink or to neglect to turn off the stove” (1).
  • Advanced stages of dementia: “memory impairment is often so severe that the person forgets the names of close relatives, his own occupation, schooling, birthday, or occasionally even his own name (1)”

Abstract Thinking Problems

Impairment in abstract thinking will result in:

  • Trouble coping with novel tasks, especially if pressed for time (1).
  • Problems with new situations or tasks that require the processing of new and complex information (1).

Personality changes

  • Alteration or accentuation of premorbid traits:
    • A previously active person may become increasingly apathetic and withdrawn from social interactions; he may be described as “not himself anymore” (1).
    • A previously neat and meticulous person may become disorganized and extremely careless about his appearance and possessions (1).
    • Others may display accentuated preexisting traits. Common changes include extreme irritability, cantankerousness, meanness, tactlessness, impulsiveness, and sexual inappropriateness (1,2).

Anxiety and depression (1).

  • These may occur as a psychological reaction to the fact that they are no longer able to function as well as they have in the past (1,4).
  • Paranoid ideation, resulting in false accusations, or verbal and physical attacks (e.g., accusing spouse of infidelity) (1).
  • Increased vulnerability to physical and psychosocial stressors (e.g., minor surgery or retirement may aggravate deficits) (1).


“While excess mortality varies with age of onset and diagnosis, overall, dementia patients have approximately one-third the life expectancy of non-demented age-matched individuals…” (2)



  • The Essential feature is a depressed mood or loss of interest or pleasure in all, or almost all, activities. Clinical depression also results in a diminished ability to think or concentrate (1).
  • Not initiated or maintained by organic factors (1).


variable … may be sudden, but usually develops over days to weeks (1).


variable … untreated, usually lasts 6 months or more, then remission of symptoms and return to previous functioning level…but chronic type can go two years (1).


Varies … but there is always some interference in social and occupational functioning (1).


“In elderly citizens who dwell in the community, the prevalence of clinical depression has been reported to be as high as 13% …. As many as 20% to 25% of elderly patients with concurrent medical illnesses are depressed” (6)

Memory & Learning Problems

Memory and learning functions are impaired in depressed patients (3,4,6).

  • Deficits are apparent in sustained attention on tasks requiring “effort.” This deficit interferes both with the reception of new information and with its initial processing (3).
  • Deficits in initial acquisition appear to be related to later recall failures. Weingartner et al (1981) demonstrated that memory deficits are not apparent when information is presented in a structured format. As the presentation structure is disrupted, however, memory problems develop (3,6).
  • Depressed patients appear to retain information once it is learned, although it is uncertain how effectively this is done (3).
  • Retrieval deficits are apparent in depressed patients. Part of this failure may be due to poor initial processing. However, “effort” may also be a factor because recognition memory is less impaired than recall memory (3).
  • As a result, some researchers speculate that depressed patients do not really suffer from a deficit in memory per se but that their memory problems stem from deficits in motivation, drive, and attention (6).

Motor Problems

  • Depressed patients demonstrate deficits on several motor performance tasks (e.g., tapping) and on skills requiring sustained effort, concentration, perceptual flexibility, abstract thinking, and performance accuracy (3,6).
  • Reaction time is longer in depressed patients (thus indicating longer times required for information processing) (3).
  • A Major Depressive Episode may involve symptoms severe enough to be mistaken for dementia: memory problems, difficulty thinking and concentrating, overall reduction in IQ; the individual also may perform poorly on mental status exam and neuropsychological testing (1).



Pseudodementia is a label given to psychiatric disorders (such as depression, schizophrenia, and hysterical disorders) which involve dementia-type symptoms and which persist if not treated (3,6).


Pseudodementia can occur in numerous disorders: hysterical disorders, schizophrenia, etc. However, major depression appears to be the most frequent cause. Numerous studies have documented the presence of cognitive deficit in depression…, and older depressed patients (also the prime -targets for dementia) may be more likely to show such deficits…” (2).


There is some disagreement as to whether or not patients who have an organic-based dementia which is not progressive should also be included in the pseudodementia grouping. The argument is that, rather than differentiating the groups on the basis of organic vs. non-organic, it would be more pragmatic to divide the groups according to favorable prognosis for treatment vs. unlikely to improve (2).

  • Some patients with “organic” findings on neuropsychological testing experienced complete remission of symptoms following treatment. Others improved but showed residual deficits (3).
  • “It may be impossible to determine where a psychiatric disorder leaves off and a neurological disorder begins. Indeed such a distinction may not be necessary as long as one establishes that the course is non-progressive. Therapeutic interventions are based on the presence of responsive target symptoms, and although a diagnosis is important, it may not be essential for initiating effective treatment measures” (3).

Problems in Differentiation

Imprecise use of the term “dementia”

  • The disagreement over whether all organic-based dementias should, in fact be called dementia, or whether those which are not progressive in nature should be termed “pseudodementia” poses problems in itself (3,5).
  • “Imprecision in using the term ‘dementia’ can confuse discussions of patients and conceptualization of their disorders” (5).

Intellectual functioning declines with normal aging

This normal decline can be mistaken for dementia. (2,4).

  • In the early stages of dementia (when symptoms are relatively mild), differentiation from the memory changes associated with normal aging is difficult or impossible (2,3).
  • “Elderly depressed patients often do not report the common symptoms of depression associated with younger adults. Their only complaint may be of memory problems” (4).
    • “The inexperienced clinician might focus only on the assessment of memory and, indeed, discern short-term memory difficulties in such an individual” (4).
    • If depression is treated, the short-term memory difficulties might also remit (4).
    • “If the clinician focuses only on the memory aspect of the assessment, it is possible to misdiagnose an elderly patient as having a progressive dementing illness when the problem is really depression. This last kind of assessment error can have a profound impact on the life of an individual so diagnosed” (4).
  • Depression is frequently accompanied by cognitive problems, especially in older persons; and, in some cases, these cognitive problems are severe enough to be labeled pseudodementia (1,2).

Overlapping signs and symptoms

  • “The signs and symptoms of neurologic disorder accompanied by dementia (e.g., Alzheimer’s, Huntington’s, and Parkinson’s disease) may have some overlap with those of depression…” (2).
    • Both interfere with social and occupational functioning.
      • To qualify as dementia, it must interfere significantly (1,2).
      • With depression, the degree of interference may be mild; or it may be so severe that the person is unable to feed or clothe himself. (1)
  • Both result in withdrawal from activities:
    • With depression, this is mainly due to loss of interest (1).
    • With dementia, it may be due to anxiety and attempts to hide deteriorating faculties as well as loss of interest resulting from depression (1).
  • Depression often occurs as a complication of dementia (2,3).
    • “Depressive reactions are often the first overt sign of something wrong in a person who is experiencing the very earliest subjective symptoms of a dementing process” (5).
    • Reifler et al (1982) diagnosed depression in 27 of 103 geriatric outpatients who conformed to the DSM-III-R diagnosis of dementia. (3)
    • Reifler found that, overall, depression decreased as the severity of the dementia increased (3).
  • “Unfortunately, we have no sound method for demarcating the boundaries between (1) intellectually intact depressed elderly individuals; (2) others who have significant affective symptoms and substantial cognitive impairment, where the intellectual deficits are reversible following vigorous therapeutic intervention; and (3) those who suffer a progressive neurological disease which manifests itself with both behavioral symptoms” (3).
  • Because the symptoms of normal aging, depression, and mild dementia are quite similar, misdiagnosis does occur when the clinician confuses signs and symptoms of dementia with those of other disorders (2).
  • “Those aspects of the clinical presentation of both an early dementing process and depression that are most likely to contribute to misdiagnosis are depressed mood or agitation; a history of psychiatric disturbance; psychomotor retardation; impaired immediate memory and learning abilities; defective attention, concentration, and tracking; impaired orientation; an overall shoddy quality to cognitive products; and listlessness with loss of interest in one’s surroundings and, often, in selfcare” (5).

Frequency of misdiagnosis:

  • Ron and colleagues (1979) conducted a 5-15 year follow-up study on 51 patients discharged from hospitals with a diagnosis of presenile dementia. All of these patients were under age 65 at time of diagnosis. The original diagnosis was confirmed in 35 cases (69%) and rejected in 16 (31%). Retrospective diagnoses of the latter group were: eight affective illnesses, one paranoid psychosis, one schizophrenic disorder, three Parkinson’s disease, two nonprogressive brain damage of uncertain etiology, and one transient acute organic reaction with marked affective symptoms (2).
  • Garcia et al (1982) conducted a “study of 100 older patients referred to a specialized outpatient dementia clinic. Twenty-six were found to be not demented. Of these, 15 were diagnosed as depressed, seven as having other miscellaneous neuropsychiatric disorders, and four as being normal. Thus, misdiagnosis of dementia appears to be common, with differentiation from depression posing the greatest difficulty” (2).

Importance of Accurate Diagnosis

  • Accurate differential diagnosis is important because many of the causes of pseudodementia are both treatable and reversible (2).
  • When uncertain, the least serious diagnosis (i.e., depression or pseudodementia) should be given, and the appropriate treatment prescribed. This prevents the patient from being dented potentially helpful treatment because the clinician has assumed the more hopeless diagnosis of dementia (1,3).

Diagnostic Tools


  • Because it is sensitive to focal lesions, CT scanning has been useful in evaluating dementia; however, its use as a diagnostic tool in helping to differentiate DAT or MID patients from normally aging or depressed older persons remains in doubt (2).
  • “Although DAT patients, as a group, show greater ventricular and sulcal enlargement than age-matched control subjects, there is considerable group overlap…” (2)


Same problem with differentiating from normal aging.

Mental Status Exams

  • “A clinical mental status examination and thorough history typically reveal the syndrome of dementia once the patient is several years into the course of a dementing illness. However, the clinician must be cautious that his expectations for cognitive functioning in the elderly are not inappropriate. Intellectual functioning, learning and memory, psychomotor speed, and sensory/perceptual functioning all show age-related changes in adulthood. Consequently, the use of mental status examination protocols with age-appropriate standardization is important” (2).
  • “The Geriatric Mental Status Interview (GMS), developed by Gurland et al, (1976), is one of the more comprehensive mental status examinations available. The GMS is a semistructured interview technique which can be administered by a trained interviewer in typically less than an hour. Between 100 and 200 questions, concerning dimensions such as cognitive functioning (including specific tests of orientation and memory), affective state, behavior symptoms, and somatic concerns are asked, resulting in ratings on 500 items …. Valid discrimination of dementia from functional psychiatric disorders (including depression) has been demonstrated for the GMS….” (2)
  • The GMS has been expanded and incorporated into the Comprehensive Assessment and Referral Evaluation (CARE), which covers psychiatric, medical, nutritional, economic, and social problems. The items of the CAPE that are most relevant to the assessment of dementia demonstrate high interrater reliability …. Two relatively short CARE scales, for assessing cognitive impairment and depression respectively, together misclassified only 2% of a sample of 107 depressed and 31 demented older persons (2)
  • The disadvantage of the GMS and the CARE are that “they are relatively lengthy to administer and require specific training. Brief, specific mental status examination protocols are available for examining patients with known or suspected dementia” (e.g., the orientation and memory examination of Blessed, Tomlinson, and Roth [1968] and the Mint-Mental State Examination of Folstein, Folstein, and McHugh [1975]) (2).
  • “An additional advantage of the very brief mental status screening instruments is that they “can be administered to more severely demented patients who may not be examinable with more complex psychometric instruments, thus allowing repeat examinations over several years of the patient’s illness …. However, these advantages also result in unacceptable high false-negative errors for patients early in the course of dementia” (2).

Dementia Rating Scales

  • These attempt to combine the brevity and ease of brief mental status screening instruments with a tool that samples a wide range of cognitive functions, using both interview question and direct performance measures. (2)
  • The Mattis Dementia Rating Scale (MDRS) is one of the more widely used dementia rating scales. “Items of the MDRS are grouped into five areas, designed to assess attention, initiation and perseveration, construction, conceptualization, and memory … Scores from all five areas are also summed to provide a general index of dementia severity…” (2).
  • “Since DAT, MID. and several other dementias progressively deteriorate, there is a need for instruments that can be repeatedly administered throughout the course of dementia …. Observation-based rating scales are a useful addition to such instruments since they typically do not necessitate patient cooperation ‘. and often provide ratings of behavioral features observed later in the course of dementia. An example of a rating scale developed specifically to evaluate various ‘stages’ throughout the course of dementia … is the Global Deterioration Scale of Primary Degenerative Dementia (GDS) … It defines seven stages in the course of dementia, with well-specified observational criteria” (2).

Comprehensive Neuropsychological Assessment

  • “While mental status examination protocols and dementia rating scales play an important role in diagnostic assessment and patient follow-up, they are often inadequate alone. Typically, they are relatively insensitive to very mild dementia, and they lack sufficient specificity to separate various disorders presenting as dementia” (2).
  • The Halstead-Reitan battery has frequently been used in the study of dementia, and normative data are available for the battery. However. the difficulty level of some of its subtests may make it most useful for milder forms of dementia (l)
  • “While there is some variability in the specific tests neuropsychologists include in a recommended battery, most agree on the need to sample a range of cognitive functions, including general intelligence, memory, attention, language, perception, and praxis” (2). (Praxis refers to the motor integrationemployed in the execution of complex learned movements.)
  • Assessment of intelligence:
    • Important because impairment in intellectual functioning is one of the defining features of dementia (2).
    • “One attempt to improve the accuracy of the WAIS in the diagnosis of dementia is to employ procedures that estimate intellectual decline.
      • Wechsler’s (1958) deterioration index uses several of the WAIS subtests showing least decline with age as indicators of premorbid levels, with other subtests, more sensitive to the effects of age, as measures of present levels. Such approaches are problematic in that they assume the manifestations of dementia to be similar to those of normal aging; and the results of validation studies employing such deterioration indices generally have not been encouraging.(2)
      • “An alternative approach is to estimate premorbid intelligence by applying an equation differentially weighting age, sex, race, years of formal education, and occupation. The application of such a formula, based upon such a regression has been supported in a recent validation study (Wilson et al, 1979). However, given the variation in IQ among people with comparable educational and occupational backgrounds, caution needs to be exercised in the clinical application of this estimation equation” (2).
      • “Abstract thinking ability is most frequently evaluated by examining WAIS Similarities and Comprehension (“proverbs” items) subtests. Other procedures for evaluating abstraction ability and cognitive flexibility, such as the Wisconsin Card Sorting Test, are available, but adequate norms for older age groups are not widely available, and its specific validity in assessing dementia remains to be empirically demonstrated” (2).
  • Memory Assessment:
    • Memory impairment is another essential feature for the diagnosis of dementia. The Wechsler Memory Scale (WMS) is the instrument most often used to assess this (2).
    • Proper interpretation depends on the application of age-appropriate norms (2).
    • Digit span, although relatively unaffected by normal aging … becomes lncreasingly impaired over time in DAT” (2).
  • Language Assessment:
    • “One dimension of verbal impairment that appears early in the course of the disease (DAT) is loss of spontaneity so that conversation always has to be initiated by someone or something else … In extreme cases, a verbally capable patient may become mute” (5).
    • “The loss of verbal spontaneity characteristic of patients with Alzheimer’s disease is typically reflected in dysfluency (i.e., difficulty in generating words). Thus verbal fluency tests are sensitive to this problem” (5)
    • On the Boston Naming Test, DAT patients make significantly more errors than age- and education matched controls (2).
    • DAT patients also make more errors on the object and body-naming portions of the Boston Diagnostic Aphasia Examination.
    • It is important to note that, although naming errors are common with DAT.. they may not occur in other types of dementia (e.g., those associated with Huntington’s and Parkinson’s diseases).
    • Both the Boston Naming Test and The Boston Diagnostic Aphasia Examination have normative data (both by age and education) for ages 25-85 (2).
  • Perceptual Assessment:
    • Perceptual deficits in dementia tend to be more frequent and apparent as the severity of the dementia increases over time (2).
    • Both the Benton Facial Recognition Test and the Benton Line Orientation Test have been shown to be valid instruments for assessing dementia. Deficits on these tests were common for dementia patients, but rare for normal controls. In addition, both of these tests have available normative data for ages 65-84 (2).
  • Constructional Ability
    • Assessed by the Block Design subtest of the WAIS-R or by various drawing tests (2).
    • “Studies have consistently demonstrated Block Design impairment, inability to copy two-dimensional geometric forms, and significantly more errors in drawing the Bender-Gestalt geometric figures” (2).

Differential Diagnosis

Identify Signs and Symptoms

“The first step in diagnosis is the identification of signs and symptoms which raise the suspicion of dementia” (2).

Does the condition have an organic basis?

  • If not, it does not meet the DSM-III-R diagnostic criteria for dementia (1).
  • If it does have an organic basis, is the disorder progressive or non-progressive? Is the underlying cause likely to improve with treatment? (2,3)


Has there been a significant deterioration of cognitive abilities which cannot be explained by normal aging, depression, etc.?

  • If the deterioration is not severe enough to significantly interfere with work, usual social activities, or relationships with others, it does not meet the DSM-III-R criteria for dementia (1).
  • Miller (1977) reviewed ten dementia studies and found that only one of these studies failed to find average IQs below the expected population mean of 100. In all of these studies which utilized controls, the dementia group always showed lower scores than the controls (2)
  • Individuals with dementia tend to have greater variability in their subtest scores than age-matched controls (2).
  • Coolidge et al found that, with early Alzheimer’s patients, “the highest scores are obtained on tests of overlearned behaviors presented in a familiar format and of immediate memory recall. Thus, Information, Vocabulary, many Comprehension and Similarities items, and Digits Forward (-Digit Span) will be performed relatively well, even long after the patient is not capable of caring for himself. The more the task, is unfamiliar, abstract, speed-dependent, and taxes the patient’s dwindled capacity for attention and learning, the more likely it is that he will do poorly: Block Design, Digit Symbol, and Digits Backward typically vie for the bottom rank among test scores” (5).
  • “A Vocabulary subtest score that is at least twice as large as the Block Design subtest score is a highly likely indicator of dementia and rarely if ever occurs among depressed patients”
  • Even so, an examination of WAIS-R score patterns or levels by themselves may not be very helpful in differentiating dementia from depressive pseudodementia. Numerous other factors need to be considered. (2)

Is there depression?

“If the symptoms suggesting a Major Depressive Episode are at least as prominent as those suggesting Dementia, it is best to diagnose Major Depressive Episode and to assume that the symptoms suggesting Dementia are secondary to the depression.” If the symptoms do not improve with treatment, then the appropriate diagnosis is dementia with depression” (1).

Duration of symptoms?

How long have the symptoms been apparent?

  • Cognitive deterioration associated with dementia typically has a slow and insidious onset; cognitive impairments accompanying depressive reactions are more likely to evolve over a much shorter period of time (5,6). The exception is dementia associated with MID, which has a sudden onset and is associated with a vascular event (e.g., stroke) (115).
  • Dementia (especially DAT) doesn’t usually come to professional attention until several years into the disorder. At this point, thorough history taking, a careful mental status exam, and knowledgeable application of psychological and neuropsychological testing instruments are reasonably successful in differentiating the demented patient from those suffering from normal aging processes, depression, etc. (2,5).
  • In depressive pseudodementia, onset can frequently be dated with some precision because of its association with some precipitating event or series of events. The presence of such an event or events, however, does not rule out the possibility of dementia because the timing of the events may be coincidental or may be the result of problems created by as-yet undiagnosed symptoms (1,5,6).

Vegatative Symptoms of Depression?

“Dementia patients are much less likely to suffer vegetative symptoms of depression such as loss of appetite, disturbed sleep, and constipation (5).


“The structure and content of speech remain essentially in tact in depression but deteriorate in dementia of Alzheimer’s type” (5).


“Depressed pseudodemented patients can learn, showing this on delayed recall and recognition memory tasks even when their immediate recall performance may have been significantly impaired” (5).

Aphasia, Apraxia, Agnosia?

“The presence of aphasias, apraxias, or agnosias clearly distinguishes an organic dementia from the pseudodementia of depression” (5).

Drawing and Construction?

“Quite early in the course of their illness, dementia patients show relatively severe impairment on drawing and constructional tasks, making virtually no appropriate response or a fragment of a response that may be distorted by perseverations despite their obvious efforts to do as asked. In contrast, the performance of depressed patients on drawing and construction tasks may be careless, shabby, or incomplete due to apathy, low energy level, and poor motivation; but, if given enough time and encouragement, they may make a recognizable and often fully accurate response” (5)


Disorientation is found with both depression and dementia. In depression, however, this disorientation in often inconsistent and may be due to an “attentional motivational deficit.” In dementia, the disorientation is more consistent and, therefore, predictable (5).


“Depressed patients are more likely to be keenly aware of their impaired cognition, making much of it: in fact, their complaints of poor memory in particular may far exceed measured impairment …. Dementia patients, in contrast, are not likely to be aware of the extent of their cognitive deficits and may even report improvement as they lose the capacity for critical self-awareness” (5).

Differential Diagnosis Table

Pseudodementia Dementia
Clinical course & History Clinical course & History
Family always aware of dysfunction & its severity Family often unaware of dysfunction & its severity
Onset can be dated with some precision Onset can be dated only within broad limits
Symptoms of short duration before medical help is sought Symptoms usually of long duration before medical help is sought
Rapid progression of symptoms after onset Slow progression of symptoms throughout course
History of previous psychiatric dysfunction common History of previous psychiatric dysfunction unusual

Source: Wells, C.E. (1979) “Pseudodementia” American Journal of Psychiatry, 136,7, Jul 1979.

Another Summary

Depressed Patients Demonstrate deficits in

  • Motor performance tasks
  • Sustained effort or concentration
  • Perceptual flexibility
  • Abstract thinking
  • Performance accuracy
  • Reaction time (and therefore, processing speed is also affected)
  • May also perform poorly on a MSE, neuropsych testing, and decreased overall IQ score


  • Label given to psychiatric disorders (e.g., depression, schizophrenia, and hysterical disorders) which cause dementia type symptoms
  • Major depression is the most frequent cause

Problems in differentiating depression vs. dementia

  • Elderly depressed patients often do not report the affective symptoms of depression; instead frequently present with complaints of memory difficulties
  • Depression often occurs as a complication of dementia


1. American Psychiatric Association. (1987). Diagnostic and statistical manual of mental disorders (third edition – revised). Washington, D.C.: Author.

2. Kaszniak, A. W. (1986). The neuropsychology of dementia. In I. Grant and K. M. Adams (Eds.), Neuropsychological assessment of neuropsychiatric disorders (pp- 172-220). NY: Oxford University Press.

3. Caine, E. D. (1986). The neuropsychology of depression: The pseudodementia syndrome. In I. Grant and K. M. Adams (Eds.) Neuropsychological assessment of neuropsychiatric disorders (pp. 221-244). NY: Oxford Press.

4. MacInnes, W. D., & Robbins, E. E. (1987). Brief neuropsychological assessment of memory. In L. C. Hartlage, M. J. Asken, & J. L. Hornsby (-Eds.). Essentials of neuropsychological assessment (pp- 175-196). NY: Sprinqer Publishing Company.

5. Lezak, M. (1985). Neuropsychological assessment. N.Y: Oxford University Press.

6. Jenike, M. (1988). Depression and other Psychiatric disorders. In M. S. Albert and M. B. Moss (Eds.), Geriatric neuropsychology (pp 115-144). NY: The Guilford Press.



  • Term has been used since 1800’s
  • Loss of function in multiple cognitive abilities
  • (According to DSM diagnosis) Does NOT imply specific underlying cause, progressive course, OR irreversibility (it can be static, progressive or remitting)
  • Distinction b/t delirium and dementia can be difficult (frequently may coexist)

Some definitions do require persistence in order to exclude acute traumatic, metabolic, or toxic disorders

DSM-IV Diagnosis requires memory impairment AND at least one kind of cognitive deficit (e.g., aphasia, apraxia, agnosia, executive function) ~ thereby distinguishing it from simple amnesia or aphasia

  • Deficit must cause problems in occupational or social functioning
  • Must be a decline from higher level of functioning
  • Not occur exclusively during delirium
  • DAT dx adds:
    • Course is characterized by gradual onset and continuing cognitive decline
    • Disturbance not better accounted for by another Axis I or medical disorder
  • Disadvantages of DSM definition
    • Excludes patients with persevered memory (e.g. Pick’s)
    • Requirement for social/occupational disability renders definition imprecise


  • Depends on etiology – but generally happens late in life
  • Uncommon in children but may occur as a result of a general medical condition


  • approximately 5% of individuals >65 are severely demented and 10-15% are mildly impaired
  • prevalence increases with age  20% or more of population are demented by age 85
  • presenile dementia – when re-examined 1-15 years later 25-57% failed to deteriorate in expected manner; believed due to unrecognized depression
  • Alzheimer’s most common, followed by vascular dementia (many patients have both)


  • detailed history – assess for inherited types of dementia
  • evaluate for depression, hysteria, or psychosis
  • explore medical history for strokes, seizures, TBI, alcohol/drug abuse, AIDS, endocrine dysfunction, vitamin deficiency (B12) and cancer
  • Neurological exam and comprehensive evaluation of cognitive skills

Cortical Dementias

Alzheimer’s Disease

(Dementia of the Alzheimer’s Type – DAT) loss of cholinergic neurons in the nucleus basalis of Meynert leading to development of senile plaques and neurofibrillary tangles

characterized by marked deficits in memory, language and perception. Can also have symptoms of depression (quite common)


  • onset – between 40 and 90 years and becomes increasingly common w/advancing age; most commonly seen after age 65
    • affects 5-10% of people over 65
  • risk factors – female, family history of down syndrome, TBI and history of thyroid disease
  • diagnosis – typically a matter of exclusion; w/c makes it a catch all for all unrecognized dementias and renders DAT a nonspecific diagnosis; definitive dx can only made on autopsy

Neuropathologic features

The primary motor, somatosensory, visual, and auditory cortices are relatively spared See Figure 19.14 on page 873 for a visual depiction.


The following areas are generally affected first (and later, more severely). Listed in decreasing order:

  • medial temporal lobes, including amygdala, hippocampal formation, and entorhinal cortex
  • basal temporal cortex extending over the lateral posterior temporal cortex, parieto-occipital cortex, and posterior cingulate gyrus
  • frontal lobes

Anatomical Changes

  • Cerebral Atrophy
  • Neuronal Loss – prominent in the nucleus basalis, septal nuclei, and nucleus of the diagonal band where cholinergic projections arise. Also present to a lesser extent in locus ceruleus (norepinephrine) and raphe nuclei (serotonin).
  • Amyloid Plaques (aka senile plaques) – insoluble protein core containing beta-amyloid and apolipoprotein E (APOE) surrounded by abnormal axons and dendrites called dystrophic neuritis.
  • Neurofibrillary Tangles – intracellular accumulations of tau proteins – prominent in the nucleus basalis, septal nuclei, and nucleus of the diagonal band where cholinergic projections arise. Also present to a lesser extent in locus ceruleus (norepinephrine) and raphe nuclei (serotonin).

Cognitive Features

  • Show more problems with short term memory and explicit vs. Implicit learning
  • Remote memory relatively preserved, but may deteriorate in later stages
  • associated w/anterograde memory loss, followed by retrograde; the first area of the brain to show pathology is the medial temporal cortex. As other areas b/c involved, (lateral temporal and frontal lobes) retrograde amnesia is observed
  • Dominant early feature is memory loss (i.e., of recent memories or new learning). Next common feature is word-finding difficulty (i.e., anomic aphasia), along with apraxia and visuospatial deficits. Behavioral difficulties typically occur later in the disease course as compared to frontotemporal dementias, and hallucination are uncommon, especially early in the disease course unlike dementia with lewy bodies. Motor disturbances are usually not present early on; other diagnoses should be considered if motor disturbances are among the early clinical signs.

Pathological Findings

  • Neuritic Plaques – found chiefly in the cerebral cortex; these plaques are nonspecific –they can be found in patients with Down’s syndrome or other forms of dementia (can also be see in a diminished number in non-Alz. patients)
  • Paired Helical filaments/neurofibrillary tangles – found in the cortex and the hippocampus (again, these are nonspecific) – there is some debate in the literature re: whether plaques or tangles are most closely related to cognitive deterioration, however, most recent findings suggest that the amount of tangles is directly correlated w/degree of cognitive deterioration
  • Granulovacular Bodies – outer membranes with small dense granules in the center – more common in Alz patients than in the general aged population; degeneration of cells, occurs especially in hippocampus

Other Neuroanatomical Correlates

  • Neocortical changes – cortical atrophy – loses as much as 1/3 of its volume as the disease progresses. This atrophy is not uniform:
    • primary sensory and motor areas are spared
    • most extensive change to parietal tertiary areas, inf. temporal cortex and limbic cortex (i.e., primarily the mesial temporal, parietal, and frontal convexity regions)
    • frontal lobes also affected but less than those listed above
    • Limbic cortex changes – the most severe degenerative changes. The Entorhinal cortex shows the most cell loss; responsible for relaying information to and from the neocortex and hippocampus. So, damage here is equivalent to loss of the hippocampal formation.
    • Cell changes – there is a dispute as to whether cell are actually lost or whether they simply shrink. The more widespread cause of cortical atrophy appears to be the loss of dendritic arborization. It should be pointed out that elderly w/o Alz. appear to increase their arborization, so this sign is not merely a development associated with aging.
    • Neurotransmitter Changes – although many studies emphasize the reduction of Ach in Alz. patients, it should be noted that in fact there are marked reductions in many transmitter systems and the patterns of loss are uneven from patient to patient. But strongest association between dementia and cell degeneration occurs with dysfunction in cholinergic neurons (hence newest interventions which focus on enhancing cholinergic function such as Tacrine)


  • Chromosome 19 – associated with late-onset AD (after age 60) – encodes APOE and has several different alleles. Presence of the E2 allele reduces the risk of developing AD, while presence of the E4 allele increases the risk (risk is increased the most with presence of E4 allele and history of head injury with LOC) – thought to play a role in modulating plaque formation and clearance
  • Chromosome 12 – associated with late-onset AD – encodes alpha2-macroglobulin (a protein). Two alleles have been identified that increase susceptibility – thought to play a role in amyloid deposition.
  • Chromosome 21 – associated with early-onset AD (as early as the 3rd and 4th decade) – mutations of the amyloid precursor protein – connection with Down’s syndrome (extra chromosome 21) whose victims develop early pathologic and clinical features of AD after age 30.
  • Chromosome 1 – also associated with early-onset AD – mutations of the presenilin 1 and presenilin 2 genes.


Tend to occur in an orderly and consistent manner

  • Stage 1 (first 1-3 years)
    • Memory – new learning defective, mildly impaired remote memory
    • Visuospatial skills – topographic disorientation, poor complex construction
    • Language – empty speech with few substantive words and paucity of ideas, anomia
    • Personality – indifference, occasional irritability
    • Motor systems – normal, including speech articulation
    • EEG – normal
    • MRI/CT – normal
  • Stage 2 (2-10 years)
    • Memory – recent and remote recall more severely impaired
    • Visuospatial skills – poor constructions, spatial disorientation; patients cannot find way about or copy constructions
    • Language – fluent aphasia, impaired comprehension, but relatively preserved repetition
    • Cognitive skills – severely impaired
    • Calculation – acalculia
    • Praxis – ideomotor apraxia
    • Personality – indifference or irritability
    • Motor system – restlessness, pacing
    • EEG – slowing of background rhythm
    • CT/MRI – normal or ventricular dilation and sulcal enlargement
    • PET/SPECT – bilateral parietal and frontal hypometabolism/hypoperfusion
  • Stage 3 (8-12 years)
    • Intellectual functions – severely impaired
    • Language – verbal output is reduced to echolalia, palilalia or mutism
    • Motor – limbs assume a rigid and flexed position
    • Sphincter control – urinary and fecal incontinence
    • CT scan – diffuse cerebral atrophy w/ventricular dilation and sulcal enlargement
    • PET/SPECT – bilateral parietal and frontal hypometabolism/hypoperfusion
    • EEG – diffusely slow
    • death often results from pneumonia or urinary tract infection w/sepsis

Possible Causes

  • Genetics – possible cause; there is an increased frequency in families who have a member with Alz., and a higher risk if family members have Down’s syndrome (perhaps caused by a gene/group of genes)
  • Trace Metals – early studies w/ animals have shown neurofibrillary degeneration similar to what is seen in Alz. when they were given aluminum salts. Also, Alz. patients have an increase of 10 – 30 times the normal concentration of aluminum in their brains. But, earlier studies of link to aluminum have not been confirmed
  • Immune Reactions – some believe that in old age the immune system loses its ability to recognize it’s own body and, therefore, develops antibodies w/c attack the brain and cause neuronal degeneration
  • Slow Viruses – some believe that it is caused by a virus w/ takes years to develop. (Creutzfeldt-Jakob’s disease appears to be caused by slow viruses w/c can be passed onto other humans and animals). Attempts to localize viruses have been unsuccessful.

Pick’s Disease

Rare disorder consisting of atrophy of frontal and temporal lobes from unknown causes

  • like DAT, it is also a cortical dementia


characterized by symptoms that are virtually indistinguishable clinically from Alz., but at autopsy the disease can be distinguished, b/c atrophy is confined to the frontal and temporal cortex, and the plaques and tangles characteristic of Alz. are not present

Differences between Pick’s and Alzheimer’s Disease

  • less memory, calculation and visuospatial impairments but
  • more extravagant personality alterations
  • both diseases produce aphasia
    • but Pick’s have a greater tendency to produce a stereotyped verbal output, repeating the same story or joke again and again
  • Kluver-Bucy symptoms; hyper oral tendencies are characteristic
  • Pick’s patients are also likely to demonstrate changes in personality and social conduct (consistent with frontal lobe deficits)
  • Normal EEG late in course of illness can also help to differentiate from Alz
  • pathologically- focal atrophy in the frontal and/or anterior temporal lobes
  • histologically – inflated neurons and neurons containing highly argyrophilic Pick bodies
  • neuronal loss and a fibrillary gliosis of the subcortical white matter
  • EEG – normal
  • On autopsy – neurofibrillary tangles and senile plaques are absent
  • NO selective involvement of a selective transmitter has been found

Diffuse Lewy Body Dementia

There is some controversy regarding how this dementia may be distinguished from Pick’s and/or Alzheimer’s dementias….

Characterized by

  • Fluctuating arousal throughout the day which leads to differences in overall cognitive functioning
  • Visual hallucination
  • Labile affect
  • Parkinsonian symptoms but symptoms of dementia more similar to DAT
  • These patients are NOT responsive to l-dopa, and are overly responsive to DA blocking agents
  • Early age of onset
  • Lewy bodies are found in the cortex rather than confined to the basal ganglia as they are in Parkinson’s patients

Creutzfeldt-Jacob’s Disease

caused by a rapidly progressive viral infection of the nervous system w/c usually leads to death w/in 6 months of onset

  • the virus is an unconventional slow virus w/c differs from conventional viral agents in its failure to stimulate an inflammatory or immune response, its invisibility to electron microscopes and its unusual resistance to traditional physical and chemical disinfection
  • has been related to sporadic, familial and transmitted causes
  • leads to generalized cortical atrophy
  • symptoms may affect fxn of the spinal cord, cerebellum, extrapyramidal system or cortex
  • as the disease progresses, the virus spreads to involve the nervous system diffusely and the patients eventually die in a vegetative state
  • myoclonus is a prominent clinical finding but may not appear until late in the course of the disease

Difference between Alzheimer’s and Pick’s

  • Course is very rapid, leading in just a few months to stupor, coma and death.
  • memory loss is prominent from the outset, but deterioration can be measured nearly day to day
  • at autopsy there is a generalized thinning of the cortex and generalized abnormalities in subcortical structures
  • may affect spinal cord, cerebellum, extrapyramidal system or cortex
  • rare disorder – occurs in 1/1,000,000
  • clinical triad – dementia, involuntary movements (especially myoclonus) and periodic EEG

bovine spongioform encephalopathy

considered a new variant of CJD – associated with mad cow disease and has an earlier age of onset

Other Prion Related Dementias

  • kuru
  • fatal familial insomnia
  • bovine spongioform encephalopathy

Other Dementias of the Frontal Lobes

  • Progressive subcortical gliosis – extensive frontotemporal atrophy (like Pick’s) but no Pick’s cells
  • Long duration of Creutzfeldt Jacob Disease
  • On autopsy 10-15% of suspected Alz. Patients end up having another variant of a degenerative dementia with frontal and anterior temporal lobe pathology

Definition of frontal lobe dementia

A degenerative condition characterized by changes in personality, breakdown in social conduct, loss of social awareness and emotional empathy, disinhibition (the major finding), impulsivity, unconcern, changes in eating conduct (hyperphagia) and stereotyped and perseverative behavior.


e.g.’s Huntington’s, Parkinson’s, Wilson’s disease and progressive supranuclear palsy

  • Dementia is present in ~ 60% of patients w/ Parkinson’s disease (and approximately 93% have some deficits on npsych testing
  • Pathologically Parkinson’s disease is characterized by loss of dopamine-containing cells in the substantia nigra

Huntington’s disease

dementia is a uniform part of the disease and may be the initial symptoms preceding the appearance of chorea or other abnormalities

  • pathologically – cellular loss in the caudate and putamen and some atrophy of the thalamus

Huntington’s Chorea

A degenerative loss of neurons in basal ganglia, frontal cortex and corpus callosum due to a genetic abnormality ~ leads to progressive intellectual deterioration and abnormal movements

  • autosomal dominant (chromosome 4); rare degenerative disorder – approximately 5/100,000
  • associated with repeats of the trinucleotide CAG (the more repeats you have, the more severe the disorder)
  • usually diagnosed in late 30’s or 40’s although has been seen as young as 4 years
  • patients known to have Huntington’s disease are impaired at a broad range of memory, perceptual, and various frontal lobes tests
  • presentation can be quite variable – with cognitive or affective symptoms seen first; however, patients with early onset (e.g., childhood) frequently demonstrate parkinsonian symptoms rather than chorea first
  • people in the at-risk groups appear to perform poorly only on the frontal lobe tests, suggesting that these tests may be useful as predictors


  • dementia (concentration/attention; executive abilities; memory – storage and retrieval)
    • has both cortical and subcortical features, but disorders which do not occur include apraxia, aphasias and agnosias (w/c do result from progressive cortical disorders)
  • choreiform movements – frequent, discrete, brisk movements; jerks of pelvis, trunk, limbs, accompanied by dystonic posturing of the extremities and trunk; face has intermittent frowns, grimaces and smirks
    • first symptom – usually a reduction of activity and restriction of interest
    • first movements usually appear w/in a year after onset of psychiatric symptoms. The involuntary movements are initially slight and consist of little more than continuos fidgeting — but increase until incessant
    • the movements never involve single muscles but include whole limbs or parts of a limb
    • they are also irregular and follow no sense of pattern
    • eventually the movements b/c controllable and affect the head, face, trunk, and limbs – impeding all voluntary movements including speech and swallowing
  • slow voluntary movements
  • impaired saccades
  • gait abnormality
  • psychiatric disturbances (in ~ 50%)
  • subtle alterations in personality, memory & motor coordination often the first symptoms
  • oculomotor disturbance
  • small percentage have parkinsonian features
  • language affected later in disease, but hard to test b/c of dysarthria in later stages
  • in absence of positive family history it is important to rule out Wilson’s disease


  • at autopsy brains are shown to show shrinkage and thinning of the cerebral cortex and the basal ganglia (in particular, the caudate) is grossly atrophied
  • MRI and CT scan often show caudate atrophy, especially in later stages – atrophy of the caudate frequently correlates with severity of the dementia
  • theory – neurotransmitters w/c normally inhibit the DA pathways (GABA and NE) die during the course of the disease creating a hyperactive DA system – w/c leads to the chorea

Parkinson’s Disease

due to the degeneration of the substantia nigra and to the loss DA w/c is produced by this nucleus; the substantia nigra is the source of DA for the basal ganglia (Parkinson’s patients show a decrease of brain DA of over 90%)

although it is a subcortical dementia, can see some cortical changes…

  • Most common extrapyramidal disorder – affects 1/100 over age 65
  • Does not appear to be inherited
  • Environmental toxins may play a role


  • Clinically diagnosable dementia occurs in approximately 20-60%
  • Bradyphrenia or mental slowing may occur early and in a large percent of clients
  • Memory problems
  • Executive problems
  • Attentional difficulties
  • Visuospatial deficits
  • No cortical disturbances like aphasia or apraxia (later stages may show naming problems
  • Depression relatively common (~30%)
  • Disorders of movement (see below)

4 Major Symptoms

(resting tremor*, cogwheel rigidity*, bradykinesia*, and disturbances of posture) each of these symptoms can affect different body parts in different combinations.

  • “classic triad of symptoms” can be divided into:
    • positive symptoms – actions w/c are not seen in normals
    • negative symptoms – inability to engage in behaviors that normals can

Positive Symptoms include

  • Tremor at rest – stop during voluntary movements or during sleep; tremors often have a “pill rolling” quality. Are frequently asymmetrical!!
  • Muscular rigidity – increased muscle tone simultaneously in both extensors and flexors – muscles allow movement for a short distance and then resist movement again (cogwheel effect)
  • Involuntary movements – may include continual changes in posture, sometimes to relieve tremor or stiffness, but often for no apparent reason – sometimes referred to as akathesia

Negative Symptoms Include

  • Disorders of posture – inability to maintain or difficulty in maintaining a part of the body in normal position (e.g., head may droop)
  • Disorders of righting – difficulty in standing from a sitting position
  • Disorders of locomotion – difficulty initiating stepping and when they do they shuffle; often once they begin to walk they take faster and faster steps and end up running (festinating gait)
  • Disturbances of Speech – difficulties in the physical production of sound
  • Akinesia – poverty or slowness of movement; may manifest itself in blankness of facial expression, lack of blinking, etc.
  • Aphagia – difficulty in chewing and swallowing

Anatomy and Treatment

  • Neuronal loss in substantia nigra, associated with Lewy bodies leading to decrease in striatal dopamine concentration
  • Neurochemical deficiencies: dopamine (especially), acetylcholine, serotonin and corticotrophin releasing features
  • Medications can help with motor symptoms, but do not improve cognitive deficits – in fact, in some patients medications can cause confusion
  • Similarly, neurosurgery will selectively help only one major physical symptom –
    • Pallidotomy can help treat the dyskinesia
    • Thallotomy helps with the tremor (“t” helps with “t”)

Other Extrapyramidal Dementias

(i.e., “Parkinson +” or “Multisystem” dementias)

Progressive supranuclear palsy (PSP)

  • in addition to parkinsonism symptoms, causes swallowing difficulties and supranuclear opthalmoplegia
  • Also known as Steele-Richardson-Olszewski syndrome
  • Due to degeneration of multiple structures including the superior colliculus, red nucleus, dentate nucleus, subthalamic nucleus and globus pallidus
  • Gaze paresis – loss of downward gaze, leads to frequent falls and ‘dirty tie’ sign
  • Axial rigidity – trunk/neck rigidity producing erect or hypererect rather than stooped posture
  • Bradykinesia
  • Pseudobulbar palsy – masked face, increased jaw and facial jerks, exaggerated palatal and pharyngeal reflexes, dysphagia, drooling, emotional lability
  • Gait disorder, falls and akinesia can also be present
  • “wide-eyed stare”

Wilson’s disease

Characterized by hepatic and CNS dysfunction due to abnormalities in copper metabolism; peak onset teens-20’s

  • Neurologic symptoms include Parkinsonian symptoms such as tremor, rigidity, dysarthria, and akinesia, as well as dystonia, “wingbeating tremor,” and ataxia
  • Psychosis, mood changes and dementia can also occur
  • Treatable if diagnosed early
  • Autosomal recessive disorder (chromosome 13)
  • Kaiser Fleischer rings are present in most cases – while it is pathognomonic it may not be seen in every patient

Hallerverorden-Spatz disease

Rare inherited and progressive illness with late childhood or early adolescent onset, characterized by dementia with spasticity and rigidity, dystonia or chorea. Caused by an accumulation of iron in the brain. There is no current cure.

Syndenham’s Chorea

Affects children between the ages of 5 and 15

  • Associated with rheumatic fever and Pandas
  • Also frequently associated with tics, tourette’s, ADHD and dystonia

Subacute Sclerosing Panencephalitis (SSPE)

  • Develops primarily in children
  • Poor school work, behavioral disturbance, restlessness, personality change —- dementia
  • Myoclonus is a characteristic symptom
  • Rarely develops in adults
  • Measles may be a cause

Shy Drager Syndrome

  • Parkinson’s symptoms + autonomic disturbance (impotence, urinary incontinence)

Olivopontocerebellar atrophy

  • Parkinson’s symptoms + ataxia – but NO rigidity or bradykinesia (DOES have tremor)

Striato-Nigral Degeneration

  • Patients become stiff and slow develop difficulty with walking and balance
  • Usually do not have a tremor, but cannot be distinguished from PD patients by a neurological exam alone
  • Do not respond to L-dopa
  • Can be distinguished from PD on autopsy because most of the damage is in the striatum rather than the substantia nigra


specific characteristics are variable, but includes psychomotor retardation and emotional lability in most cases

Second most common form of dementia following Alzheimer’s


  • abrupt onset
  • stepwise deterioration/fluctuating course
  • previous stroke or transient ischemic attacks
  • previous hypertension or other cardiovascular disease

Neurological Examination

  • focal deficits
  • pseudobulbar palsy (w/ dysarthria)
  • gait disturbance
  • psychomotor retardation

Mental Status Exam

  • dementia (cortical and/or subcortical features)
  • depression
  • emotional lability
  • relative preservation of personality

Laboratory assessment

  • focal slowing on EEG
  • infarcts usually visible on CT (but normal scan does not preclude the diagnosis )


  • discovery and treatment of underlying risk factors (e.g., emboli, hypertension, smoking, diabetes)
  • Dysarthria and aphasia may improve w/ speech and language therapy

Risk Factors

  • Hypertension, abnormal lipid levels, smoking, diabetes, and obesity
  • Patients with cerebrovascular disease may have vascular disease AND episodes of coronary insufficiency with associated systemic hypotension leading to more diffuse brain damage

Key factors to differentiate from Alzheimer’s Dementia

  • Abrupt onset
  • Stepwise deterioration
  • Focal neurological symptoms
  • Risk factors for vascular disease
  • Tend to have an earlier onset that DAT and are more common in men

Lacunar Strokes – see vascular notes Binswanger’s disease – when strokes are limited to white matter double check – notes have it both for gray and for white matter…

Other Causes of Dementia

Vasculitis Dementia

  • Caused by inflammation of the cranial arteries
  • Often associated with systemic illnesses such as giant cell arteritis and lupus

Bacterial Infections Producing Dementia

syphillic general paresis

Probably the best known example. It is currently rare;

  • typically appears 15 – 30 years after the initial infection and is characterized by progressive intellectual impairment combined in some cases w/ psychosis
  • manifests as multiple strokes and associated dementia
  • also accompanied by changes in personality
  • examination of CSF can lead to definitive dx

Lyme disease

  • symptoms include facial palsy, headaches, peripheral neuropathy, meningitis, memory difficulties, irritability, depressed mood

African trypanosomiasis

  • African sleeping sickness transmitted by the tsetse fly

Viral Infections Producing Dementia

Dementia can be caused by acute encephalitis or by affects of neurotransmitter dysfunction, demyelination, etc.

Postinfection encephalomyelitis

May be caused by measles, varicella, rubella and other viral illnesses

HIV Type 1 encephalopathy

(see it’s own section below)

Progressive multifocal leukoencephalopthy

  • due to an opportunistic infection that occurs in immunologically compromised individuals

Cruetfeldt-Jakob disease

– see own section

Dementia due to HIV Disease

Primarily subcortical dementia but with some cortical changes

  • diffuse, multifocal destruction of white matter and subcortical structures
  • characterized by forgetfulness, slowness, poor concentration, and problem solving difficulties
  • behavioral manifestations include: apathy, social withdrawal
  • may have visual hallucinations, delusions or delirium
  • tremors, impaired repetitive movement, imbalance, ataxia, hypertonia
  • FL signs
  • Affects 20-60% or AIDS patients and over 90% of patients dying with AIDS show evidence of subacute encephalitis
  • Micronodules are scattered throughout brain

Chronic Meningitis

  • may lead to dementia and can be caused by syphilis, tuberculosis, fungi or parasites.
  • In addition to intellectual deterioration, affected patients manifest cranial nerve palsies, stiff neck and headache
  • focal neurological deficits may occur and hydrocephalus may be an acute or late complication

Toxic and Metabolic Dementias

Toxic and metabolic disturbances frequently produce intellectual disturbances

  • when the mental state disturbance has an abrupt onset and a short course, an acute confusional state is diagnosed
  • if there is a gradual onset and is insidiously progressive, persisting for weeks, months or longer, the disorder is a dementia syndrome
  • adult onset biochemical disorders
    • although rare, adult onset forms of inherited metabolic dementias can occur
  • characterized into leukoencephalopathies, encephalopathies, etc.
  • metabolic disorders – can include hypoxia due to cardiopulmonary disease or failure, anemia, etc. and endocrine disease
    • most prevalent in elderly populations
    • caused by diffuse dysfunction of the brain at the molecular-chemical level
    • some can be reversible
    • can be caused by neuroleptics, antidepressants, metals, nutritional deficiencies, or over the counter medications

Endocrine Dysfunction

  • can cause cognitive impairments
  • treatable with hormone replacement
  • hyperthyroidism – anxious, restless, tachycardia, palpitations, heat intolerance
  • hypothyroidism – leads to basal ganglia calcifications…..Parkisonism-like or chorea-like symptoms

Non-Degenerative Dementias

  • may be due to vascular, viral, or bacterial causes

Dementia Pugilistica

  • syndrome usually begins with a gait disturbance and slurring dysarthria
  • gradually progresses into an extrapyramidal Parkinsonlike syndrome with evidence of both pyramidal and cerebellar dysfunction
  • seizures may occur in some patients
  • dementia appears later in course, first manifestation is usually disturbance in memory
  • psychomotor retardation is apparent
  • may be personality changes and general intellectual decline
  • psychiatric manifestations include: paranoia, euphoria and depression
  • CT may demonstrate cerebral atrophy w/ventricular enlargement
  • Autopsy may also demonstrate thinning of the corpus callosum, depigmentation of the substantia nigra and presence of neurofibrillary tangles

Hepatic dysfunction

  • Can be associated with mental impairment, probably due to elevated levels of ammonium
  • ~ 5% of patients with cirrhosis may develop encephalopathy
  • with every episode of liver failure, a static dementia syndrome may result
  • motor symptoms are frequently associated with the dementia


  • Normal pressure hydrocephalus – characterized by dementia, gait disturbance and urinary incontinence, but the clinical presentation is nonspecific (this is discussed in more detail in another section of your study notes)
  • Head trauma
  • Neoplasms
  • Cardiopulmonary dysfunction – multiple episodes of hypoxia may lead to step-wise deterioration

Characteristics of the 3 Stages of DAT and Pick’s Diseases

Stage DAT Pick’s Stage 1

Language Anomia, empty speech Anomia

Memory Defective Relatively spared

Visuospatial Skills Impaired Relatively spared

Calculation Impaired Relatively spared

Personality Indifferent Disinhibited

Motor System Normal Normal

EEG Normal Normal

CT scan Normal Normal

Stage 2

Language Fluent aphasia Aphasia, stereotyped output

Memory Severely impaired Impaired

Visuospatial ability Severely impaired Impaired

Personality Indifferent Disinhibited

Motor system Restlessness Restless stereotyped behavior

CT scan Atrophy frontal &/or temporal atrophy

Stage 3

Intellectual fxn Severely impaired Severely impaired

Language Palilailia echolalia or mutism Echolalia, mutism

Sphincter control Incontinence Incontinence

EEG Diffuse slowing Diffuse fronto- temporal slowing

CT scan Diffuse atrophy same as stage 2


  • subcortical dementia – dementias produced by diseases affecting subcortical structures; cardinal features include psychomotor retardation, poor fluid thinking, memory impairment (difficulty retrieving spontaneously, aided by cues and structure), abnormal cognition, mood disturbances and speech or motor system abnormalities
    • e.g.’s Parkinson’s disease, Huntington’s disease, Wilson’s disease, Progressive Supranuclear Palsy
    • motor impairments include: stooped/hyperextended posture, slow movements, choreotathetosis, tremor, dystonia, and dysarthria
    • causes – extrapyramidal disorders, hydrocephalus, white matter disease, and subcortical vascular disease that affects basal ganglia, thalamus and brainstem
  • cortical dementia (DAT and Pick’s) – common features include: aphasia, agnosia, apraxia, amnesia, visual-spatial deficits, persevered personality, deficits in judgement, BUT neurological exam is relatively normal as are motor fxn, gait, posture, and tones; speech also has normal volume and articulation
  • multi-infarct dementia, viral infections, trauma and chronic-toxic metabolic disorders can produce symptoms of both kinds of dementia

Comparison Table

Clinical Characteristics Cortical Dementia Subcortical Dementia
Language Aphasia early No aphasia (but anomia and comprehension deficit when severe)
Memory Recall & Recognition Impaired Recall impaired; recognition normal or better preserved than recall
Visuospatial Skills Impaired Impaired
Calculation Involved early Preserved until late
Other Intellectual fxns Acalculia, Apraxia,Agnosia Poor strategy formulation
Frontal systems Impaired to a degree consistent with other impairments Disproportionately affected
Speed of cognition Normal until late in course Slowed early
Personality Unconcerned Apathetic
Speech Normal articulation until late Dysarthric
Posture Upright Bowed or extended
Coordination Normal until late Impaired
Motor Speed Normal Slowed
Motor system Relatively spared until late Abnormal (Parkinsonism, chorea,Dystonia, etc.)
Anatomic Involvement Neocortical association areas and hippocampus Thalamus, basal ganglia,and brainstem

Classification of Major Causes of Dementias

Cortical Dementias Combined cortical & subcortical dementias
Alzheimer’s Multi-infarct dementias
Frontal Lobe Degeneration Infectious dementias
Subcortical Dementias Toxic and metabolic encephalopathies
Extrapyramidal Syndromes Endocrine disorders
Parkinson’s disease Nutritional deficiency states
Huntington’s disease Drug intoxications
Progressive supranuclear palsy Miscellaneous dementia syndromes
Wilson’s disease * posttraumatic
Spinocerebellar degenerations * postanoxic
Idiopathic basal ganglia calcifications * neoplasms
Hydrocephalus xxx
Dementia syndrome of depression Differentiate from:
White matter disease * Delirium
* MS * Depression
* HIV encephalopathy * Normal Aging
Vascular dementias

Higher Order Cerebral Function


  • Subcortical structures almost always work with association cortex
    • Consequently, lesions of subcortical structures (e.g., thalamus or basal ganglia) as well as white matter can produce deficits such as aphasia or neglect that resemble lesions of the association cortex
  • Functions of association cortex: higher-order sensory processing, motor planning, language processing/production, abstract thought, etc.
  • Historically there has been a debate between theories of brain function: localization versus networks of structures – in reality both networks and localized mechanisms participate in brain functions


Unimodal AC

  • Modality-specific (e.g., somatosensory AC, auditory AC, visual AC)
  • Receives input from primary cortices (e.g., sensory, auditory, visual) and performs higher-order sensory processing for that modality

Heteromodal AC

  • Higher order processes (prefrontal cortex, parieto-occipito-temporal junctions)
  • Bi-directional connections with AC of all modalities and limbic cortex
  • Allows integration of abstract sensory and motor information from unimodal Acs and emotional and motivational information from limbic cortex
  • Found in the frontal lobes and at the parieto-occipitotemporal junctions


  • Although each hemisphere controls simple movements of the contralateral limbs, skilled complex motor tasks for both right and left limbs are programmed mainly b the dominant (usually left) hemisphere
    • Therefore, apraxia is more commonly associated with lesions of the dominant hemisphere
  • Although each hemisphere controls attention to the contralateral environment, only the right side is significantly involved in attending to both sides
    • Therefore, neglect is more often seen in lesions of the right hemisphere (even if right dominant for language)
    • Right hemisphere specialization may therefore be even more highly conserved than left hemisphere dominance for language

Hemispheric Specialization

  • Usually present by age 3 or 4
    • Lesions before this age may lead to major reorganization of function without noticeable deficits
  • 90% of population is right handed
    • Left hemisphere is dominant for over 95% of right handers and over 60-70% of left handers
    • Persons with family history of left handedness or ambidextrousness may have more significant bilateral representation of language and may recover language more quickly than right handers


  • Language processing and related functions

Primary Auditory Cortex

  • Superior bank of Sylvian fissure in the temporal lobe
  • Perceives sound

Wernicke’s Area

  • Superior temporal gyrus/ Brodmann’s area 22
  • Site of auditory association cortex where sounds are identified and understood
  • Wernicke’s area connects with parietal and temporal lobes to help with language comprehension and lexicon (mapping sounds to meaning for both comprehension and production of meaningful language)
  • Lesions to Brodmann’s areas 22, 37 (inferior temporal language area), 39 (angular gyrus), and 40 (supramarginal gyrus) produce Wernicke’s aphasia

Primary Motor Cortex

  • The face area of the motor cortex is responsible for articulation of sounds
  • Inferior portion of the precentral gyrus

Broca’s Area

  • Inferior frontal gyrus (opercular and triangular portions)/Brodmann’s areas 44 and 45
  • Auditory AC which programs the motor sequences of sounds to produce words
  • Lesions to Brodmann’s areas 44-47, 6, and 8-10 produce Broca’s aphasia
  • Broca’s area connects with prefrontal cortex, premotor cortex, and supplementary motor cortex for higher-order motor aspects of speech formulation and planning and syntax

Arcuate Fasciculus

  • Subcortical white matter pathway that connects Broca’s and Wernicke’s areas

Other Important Issues About Language

  • Reading
    • Depends on connections involving the visual primary cortex, visual association cortex, angular gyrus (Brodmann’s area 39) and Wernicke’s area
  • Corpus Callosum
    • Allows nondominant hemisphere to participate in language by recognition and production of affective elements of speech; these connections may help nondominant hemisphere take over some language functions allowing for partial recovery


Gerstmann’s Syndrome

  • Characterized by:
    • Agraphia
    • Acalculia
    • Right-left disorientation
    • Finger agnosia
  • Any one of these deficits in isolation could be caused by lesions in a number of locations, but in combination, they are very localizing to the dominant (usually left) inferior parietal lobe in the region of the angular gyrus
  • Often associated with contralateral visual field cut, alexia, anomia, or more severe aphasia


Ideomotor Apraxia

  • Inability to formulate correct motor sequences
  • Can affect orofacial, proximal or distal movements differently
  • Not well localized but at least a third of patients with aphasia also have apraxia
  • Body part substitution (using fingers cutting as opposed to correctly holding imaginary scissors while cutting) is indicative of mild apraxia

Aphemia (verbal apraxia or foreign accent syndrome)

  • Severe apraxia of the speech articulatory apparatus
  • Characterized by effortful, poorly articulated speech; severe aphemia can produce muteness
  • Caused by a small lesion to the dominant frontal operculum restricted to Broca’s area (however, written language is intact)
  • Can occur as a developmental disorder (referred to as verbal apraxia in those cases)


Cortical Deafness

  • Awareness that a sound has occurred but cannot interpret the sound whether verbal (e.g., words) or nonverbal (e.g., phone ringing)
  • Caused by bilateral lesions of the primary auditory cortex in Heschl’s gyrus

Pure Word Deafness (aka verbal auditory agnosia)

  • Can identify nonverbal sounds but not spoken words
  • Can read and write normally and speech is usually normal although some paraphasic errors may be present acutely
  • Caused by infarct in the auditory area of the dominant hemisphere that extends to subcortical white matter, cutting off auditory input from contralateral hemisphere, as well
  • Can also be caused by bilateral lesions of superior temporal gyrus

Nonverbal Auditory Agnosia

  • Patients understand speech but not nonverbal sounds
  • Caused by lesions in the nondominant hemisphere


  • Naturally occurring lesions involving the corpus callosum primarily are rare but can be caused by MS, gliomas, metastases, lymphoma, lipona, and infarcts (especially ACA or PCA)
  • Corpus Callosotomy (surgery severing the corpus callosum) is sometimes performed in patients with refractory epilepsy in which falls are a major problem – goal is to prevent secondary generalization, not to cure the seizures.
    • Following surgery, the right hemisphere is unable to access language from the left hemisphere, which results in left hand agraphia, inability to name objects placed in left hand with eyes closed, and inability to read in left hemifield (hard to illicit with special apparatus)


  • Nondominant hemisphere is more important for attention and for generating an integrated visual-spatial gestalt


  • Global (i.e., vigilance, concentration, arousal)
  • Selective or directed (focusing attention)
    • Depends on the activating systems discussed in chapter 14 (e.g., reticular formation, diencephalic structures) and cingulate gyrus and limbic, frontal, and parietal association cortices
  • Right Hemisphere
    • More important than left hemisphere for attention mechanisms in most persons
    • Responds to stimuli on both sides whereas the left hemisphere responds to stimuli on right side only
    • Lesions of right hemisphere often lead to prominent and long-lasting deficits in attention to the contralateral side while left hemisphere lesions lead to relatively mild or undetectable neglect

Spatial Analysis and Integration

  • Parietal Association Cortex
    • Analyzes where, i.e., location and movement of visual objects in space
  • Gestalt
    • Patients with right hemisphere lesions often have difficulty appreciating the gestalt, or overall spatial arrangement, of visual information while patients with left (usually parietal) lesions tend to understand the gestalt but omit certain important details
  • Posterior parietal cortex also integrates spatial analysis incorporating visual, proprioceptive, vestibular and auditory information

Emotional or Personality Change

  • Generally associated with right parietal or frontal lobes
  • Patients may appear bland or apathetic, and in addition to hemineglect, they may display an overall decrease in the level of alertness and attention; on the other hand, irritability is common
  • Anosodiaphoria
  • When patients are aware that they have severe deficits, yet show no emotional concern or distress about it
  • Hemiasomatognosia
    • When patients deny that the neglected part of their body belongs to them
  • Contralateral Hemineglect
    • Occurs primarily with lesions of right parietal or frontal lobes, but can also occur with lesions of the cingulate gyrus, thalamus, basal ganglia or reticular formation
    • Allesthesia: When a patient erroneously reports the location of a stimulus to one side of the body as being on the other side
    • Allokinesia: When the patient inappropriately moves the normal limb when asked to move the neglected limb
    • Spatial akinesia: When movements of the limbs are worse when they are located in the neglected hemispace
  • Right-sided lesions, especially right parietal infarcts, can also cause bilateral ptosis (keeping both eyes forcibly closed) and psychotic symptoms
    • Right sided lesions can also reduce comprehension of emotional content of others’ speech (receptive aprosody) and conveying appropriate emotional expression in their own speech (expressive aprosody) can be impaired.
  • Impaired Geographic Orientation (sense of direction)
    • Caused by lesions of right parietal or right occipitotemporal cortex.
  • Déjà vu
    • Experienced more frequently by patients with right temporal seizures or lesions
  • Capgras Syndrome
    • Patients insist their family members have been replaced by identical-looking imposters – thought to be caused by right hemisphere lesions
  • Reduplicative Paramnesia
    • Patients believe a person, place, or object exists as two identical copies – seen in patients with right hemisphere lesions

Contralateral Hemineglect Syndrome

  • Usually caused by lesions to the right parietal and frontal lobes but also can be caused by lesions of cingulate gyrus, thalamus, basal ganglia, or midbrain reticular formation
  • Can be identified by 4 types of testing
    • Sensory Neglect
      • Visual, auditory, and tactile stimulation such as that done on the Sensory Perceptual Exam of HRB. Patients may exhibit allesthesia
    • Motor-Intentional Neglect
      • Notice that the patient performs fewer movements with contralateral limb using methods like tactile response test (instruct patient to move whichever limb is touched – used with patients who have trouble following commands such as “left” and “right”) or crossed response test (instruct patient to move the limb opposite of the one touched)
      • Some of these patients may exhibit spatial akinesia (tested by asking patients to cross their arms and perform movements)
      • Patients may exhibit allokinesia, which is when they move the normal limb when asked to move the neglected limb
    • Combined Sensory-Motor Neglect
      • Elicited by tests like Line Bisection and Clock Drawing
    • Conceptual Neglect
      • Neglect of internal representations of their own bodies or external world
      • Anosognosia (unawareness of deficits) is common in hemineglect syndrome and can also be seen with Wernicke’s aphasia, frontal lobe disorders, and cortical blindness
      • Less common forms of conceptual neglect are anosodiaphoria and hemiasomatognosia


  • Due to the diversity of the functions of the frontal lobes, the author discusses their functions in three broad areas:
    • Restraint
      • Inhibition of inappropriate behaviors
    • Initiative
      • Motivation to pursue positive or productive activities
    • Order
      • The capacity to correctly perform sequencing tasks

Prefrontal Cortex

  • Largest part of the frontal lobes
  • Consists of the higher-order heteromodal association cortex
  • Has connections to other cortical (i.e., parietal, occipital, and temporal ACs, limbic cortex, anterior cingulate gyrus, and orbitofrontal cortex) and subcortical (e.g., amygdala, thalamic nuclei, basal ganglia, hypothalamus, septal region, cerebellum, and midbrain) regions
    • Most connections are bi-directional
  • Also receives projections from multiple subcortical and brainstem modulatory neurotransmitter systems

Functions of Frontal Lobes

  • Working Memory and Shifting Cognitive Set
    • Functional imaging indicates dorsolateral prefrontal cortex underlies this skill
  • Learning New Material
    • Both dorsolateral prefrontal cortex and medial temporal lobes show activation on functional imaging (usually left side for verbal material and right side for nonverbal material)
  • Selective Attention
  • Decision Making
    • Frontal lobes integrate information from the limbic and heteromodal association cortex for this function


  • Utilization behavior/environmental dependency – when patients tend to respond to whatever stimuli are at hand, even when inappropriate
  • Witzelsucht: Inappropriate jocularity
  • Incontinence: Sometimes seen in frontal lobe disorders, especially those affecting the medial frontal regions
  • Patients are characteristically unconcerned about their incontinence

Dorsolateral Convexity Lesions

  • Produce apathetic, lifeless, abulic state
  • Abulia: Passive, exhibiting little spontaneous activity, markedly delayed responses, tendency to speak briefly or softly; in the extreme may be immobile, akinetic and mute, but will continue to appear awake, sitting with their eyes open

Orbitofrontal Lesions

  • Impulsive and disinhibited behavior
  • Left frontal more associated with depression and right frontal more associated with mania


  • Dorsal Pathway
    • Projects to the parieto-occipital association cortex
    • Answers the question Where? by analyzing motion and spatial relationships between objects and between the body and visual stimuli
  • Ventral Pathways
    • Projects to occipitotemporal association cortex
    • Answers the question What? By analyzing form, with specific regions identifying colors, face, letters, and other visual stimuli

Primary Visual Cortex Syndromes

  • Blindsight
    • When individuals can perform tasks without conscious visual perception (e.g., they cannot “see” a mail slot, but they can insert an envelope into the slot)
    • Some studies have shown that there may be small islands of preserved vision in the blind hemifield that may influence behavior although conscious vision is not recognized
  • Cortical Blindness (aka Anton’s syndrome)
    • Patients have complete visual loss on confrontational testing but are completely unaware of loss
    • Show a loss of blink to threat, loss of eye closure in bright light, and loss of optokinetic nystagmus. Some have blindsight, too
    • Results from bilateral lesions
  • Anosognosia for Visual Loss
    • Also seen with combined occipital and frontal lesions (results in confabulation) and combined occipital and parietal lesions (results in neglect)
  • Color Agnosia (aka color anomia)
    • Patients cannot name or point to colors presented visually despite intact perception of color (patients can match colors presented visually)
    • Caused by lesions of dominant hemisphere’s primary visual cortex and extending into corpus callosum
    • Often associated with alexia without agraphia and right hemianopia
    • Not a true anomia, b/c patient can name the color of an object if it is described verbally



  • Inability to recognize faces (including animal faces) usually from bilateral lesions especially if deficit does not resolve
  • Often associated with achromatopsia (see below) and sometimes associated with alexia and with upper quadrant or bilateral upper visual field defects


  • Like cortical blindness only for color perception – cannot name, point to, or match colors presented visually but can name appropriate color for an object described verbally
  • These patients often describe vision as shades of gray
  • Deficits can be in one quadrant, a hemifield, or the entire visual field
  • As with prosopagnosia, it is sometimes associated with alexia and with upper quadrant or bilateral upper visual field defects
  • When the whole visual field is affected, usually associated with prosopagnosia and bilateral lesions
  • Hemiachromatopsia is caused by lesions to the contralateral inferior occipitotemporal cortex


  • Objects appear unusually small (can occur in only part of the visual field)


  • Objects appear unusually large (can occur in only part of the visual field)


  • Objects have distorted shapes and sizes
  • The “Alice in Wonderland” syndrome – can be caused by migraines, infarct, hemorrhage, tumor, or other disorders of the inferior or lateral visual AC. Also occasionally seen in retinal pathology or toxic or metabolic disturbances

Visual Reorientation

  • Environment appears tilted or inverted


  • When a previously seen object reappears periodically (e.g., patient saw a plant and a few minutes later sees the plant going out of her sandwich) – can be caused by meds like Trazadone

Cerebral Diplopia (aka polyopia)

  • Patients see 2 or more images of objects – sometimes can be psychiatric in origin


  • Unnatural coloring of visual field, like gold, red, or purple – can be see with certain drugs, such as in digitalis toxicity, in which objects have a yellowish halo


Balint’s Syndrome

  • Caused by bilateral lesions and resulting in a clinical triad of symptoms
  • Simultagnosia
    • Impaired ability to perceived parts of a visual scene as a whole (can perceive only a small part of the visual field at a time and this region shifts unpredictably so they have trouble with complex scenes and identifying moving objects)
  • Optic Ataxia
    • Impaired ability to reach for or point to objects in space under visual guidance (unlike cerebellar ataxia because proprioceptive and auditory cues are intact allowing the patient to perform smooth movements back and forth to an object once it has been touched one time)
  • Ocular Apraxia
    • Difficulty directing gaze toward objects in peripheral vision through saccades (patients need to move their heads to initiate a voluntary redirection of gaze
  • Associated Deficits
    • May include inferior-quadrant visual field cuts, aphasia, or hemineglect.
  • Most Common Etiology
    • Most bilateral lesions in this brain region are caused by MCA-PCA watershed infarcts, although bilateral hemorrhage, tumors, or other lesions can produce this syndrome

Optic Allesthesia

  • False localization of objects in visual space – sometimes seen in patients with bilateral lesions that do not present with a full Balint’s syndrome

Cerebral Akinetopsia

  • An inability to perceive moving objects – sometimes seen in patients with bilateral lesions that do not present with a full Balint’s syndrome



  • Persistent ringing tone or buzzing in one or both ears, usually caused by peripheral auditory disorders affecting the tympanic membrane, middle ear ossicles, cochlea, or 8th cranial nerve

Self-Audible Bruits

  • Pulsating “whooshing” sounds that can be associated with turbulent flow in AVMs, carotid dissection, or the extracranial-to-intracranial pressure gradient produced by elevated intracranial pressure

Release Phenomenon

  • Analogous to Bonnet syndrome (visual hallucination caused by visual loss) in that patients hear elaborate auditory hallucinations (e.g., music, voices) – most often associated with sensorineural deafness but in rare cases can be caused by lesions or ischemia of the pontine tegmentum


  • A sound that is heard once is then heard repeatedly (analogous to palinopsia) – very rare

Musical Hallucinations

  • Most often caused by seizures in the nondominant hemisphere


Widespread Projection Systems

  • Important for arousal but also involved in attention
  • Upper Brainstem Projection Systems
    • Include cholinergic (pedunculopontine and laterodorsal tegmental nuclei) and noncholinergic (pontomesencephalic reticular formation, possibly glutamatergic) projections to thalamus, hypothalamus, and basal forebrain systems, which in turn, have widespread cortical projections. Also include noradrenergic (locus ceruleus and lateral tegmental area) and serotonergic (dorsal and medial raphe) systems that project to cortex and other structures and dopaminergic (substantia nigra pars reticulata, ventral tegmental area) systems project to striatum, limbic cortex, and prefrontal cortex
  • Thalamic Systems
    • Intralaminar, midline, ventral medial, and other thalamic nuclei that transfer inputs from the upper brainstem reticular formation and cholinergic nuclei to widespread areas of the cerebral cortex are involved in arousal, and the thalamic reticular nucleus is thought to play a role in gating information transfer through the thalamus because it receives inputs form the cortex, thalamus, and brainstem systems and sends inhibitory (GABAergic) projections to the thalamus (and possibly back to the brainstem)
  • Hypothalamic Systems
    • Posterior lateral hypothalamic histaminergic neurons are important for arousal – they receive inputs from basal forebrain, anterior hypothalamus, and brainstem and project widely to cortex and thalamus
  • Basal Forebrain Systems
    • Nucleus basalis, diagonal band, and medial septal cholinergic and GABAergic neurons are involved in arousal – they receive inputs from the brainstem and project to the entire cortex and thalamus

Frontal and Parietal AC

  • Communicate with each other through strong reciprocal connections
  • Lateral Parietal Cortex
    • Its location at the temporal-parietal-occipital junction makes it a perfect place of heteromodal integration in attention
  • Prefrontal Cortex
    • The region of the prefrontal eye fields is important for directed attention to the contralateral side and in the initiation of eye movements toward attended to targets – also may play a role in motor-intentional aspects of attention toward the contralateral side – crucial for sustaining attention and reducing distractibility

Anterior Cingulate Cortex and Limbic Pathways

  • The anterior cingulated is important in motivational aspects of attention and works together with amygdala, medial orbitofrontal cortex, thalamic mediodorsal nucleus, and other limbic structures to direct and sustain attention toward relevant or interesting stimuli

Tectum, Pretectal Area, and Pulvinar

  • Work with the parietotemporo-occipital cortex and frontal eye fields in directing visual attention toward relevant visual stimuli for saccadic eye movements – directed attention for other modalities (e.g., audition) may also be processed by these pathways

Basal Ganglia and Cerebellum

  • There is accumulating evidence that these areas participate in directed attention.

Awareness of Self and Environment

  • The mechanisms involved in our subjective and personal experience of awareness are unknown, but it is likely to be a combination of a network with both specialized regions of local processing and widespread regions of distributed processing
  • Because of the frequent comorbidity of hemineglect syndromes and anosognosia, it is possible that the mechanisms involved in attention play a role


Acute Delusional States (e.g., delirium, encephalopathy)

  • Typically develop over the course of days to months, have prominent attentional disturbances, tend to wax and wane over the course of hours, often have marked slowing on EEG, and are most often caused by toxic or metabolic disorders, head trauma, infection, and seizures

Chronic Mental Status Changes (i.e., dementias)

  • Usually develop over months to years, do not tend to fluctuate as rapidly (although exacerbations of function can occur in certain settings), and early in their course tend to have less prominent disturbances in attention and a relatively normal EEG
  • Static Encephalopathy
    • Another term for chronic mental status changes but usually refers to permanent nonprogressive brain damage that results from head injury, anoxia, or congenital abnormalities of brain development (e.g., mental retardation)
  • Cortical Dementias
    • Refer to dementias with prominent disturbances of language, praxis, visuospatial functions, and other typically cortical functions
  • Subcortical Dementias
    • Refers to dementia in disorders such as Huntington’s disease that do not have such prominent cortical features; however, the use of the cortical/subcortical distinction has been questioned (due to the frequency of disruption among cortical-subcortical circuits in all progressive dementias)
  • Primary Dementia
    • Typically associated with neurodegenerative conditions for which definitive treatments are unavailable
  • Secondary Dementia
    • Caused by conditions that may be reversible, such as electrolyte abnormalities (esp. of calcium, magnesium, or sodium), hepatic, renal, or pulmonary failure, hyper/hypothyroidism, vitamin B12 deficiency, chronic meningitis, lyme disease, neurosyphilis, Wilson’s disease (liver unable to excrete copper) – approximately 10% of all dementia cases
  • Sundowning
    • Cute mental status change superimposed on a dementia process
  • Cortical-Basal Ganglionic Degeneration (aka corticobasal degeneration)
    • Asymmetrical onset of a movement disorder (e.g., dystonia) accompanied by cortical features most often consisting of a marked apraxia
  • Primary Progressive Aphasia
    • Likely a family of degenerative conditions in which aphasia is the predominant symptom
  • Vascular Dementia
    • Second most common cause of dementia (10-15% of cases)
  • Binswanger’s disease
    • Diffuse subcortical infarcts often associated with chronic hypertension
  • Leukoaraiosis
    • Diffuse white matter changes often seen in older patients but not always associated with dementia
  • Cerebral Amyloid Angiopathy
    • Can cause dementia through multifocal recurrent hemorrhages, as well as through white matter ischemic disease – often familial
  • Psychiatric Pseudodementia
    • Resulting from depression or conversion disorder
  • Dementia due to Alcoholism
    • Likely multifactorial, with possible causes including thiamine deficiency, other nutritional deficiencies, multiple head injuries, and seizures
    • The jury is still out with regard to whether or not alcohol itself causes permanent cortical neuronal injury, although it likely causes cerebellar degeneration

Infections – Diseases



  • Infection within the subarachnoid space
  • Usually caused by spread of an infectious agent via the bloodstream from an infective focus elsewhere in the body
    • In neonates, 50% are from things like E coli and H influenzae
    • In children, 50% are from H influenzae
    • In adults, 30% are from S pneumoniae
  • Clinical manifestations
    • Rapid onset over several days
    • Clinical symptoms include generalized headache, fever, vomiting. Lethargy, stiff neck, and confusion.
    • Malaise and backache are common
    • Treatment is with a high-dose of intravenous antibiotics that cross the blood-brain barrier
    • Neurologic Complications
      • Seizures
      • Focal cerebral signs
      • Acute cerebral edema
      • Dysfunction of cranial nerves 3, 4, 6, & 7 in about 15% of patients
      • Hearing loss
      • Hemiparesis
      • Dysphasia and hemianopsia in 15%

Brain Abscess

  • Causes
    • Infection spread from middle ear or sinus
    • In association with congenital heart disease
    • Spread of infection from a distant site
    • Direct introduction of bacteria following penetrating head injuries
  • Cardinal symptom is a relentless and progressive headache, which is usually followed by focal neurologic manifestations
  • Fever is seen in only two thirds of patients
  • Early diagnosis is possible with CT
  • Lumbar puncture should be avoided to prevent herniation or rupture of the abscess into the ventricular system
  • Treatment with penicillin or the such may be successful such that surgery may not be necessary


  • Paretic neurosyphilis is the late complication of syphilis occurring decades after the original infection (there are other types of neurosyphilis)
  • Clinical presentation resembles meningoencephlitis
  • Early symptoms include fatigue, irritability, personality changes, forgetfulness, and tremor
  • Symptoms at late stage include impaired memory and judgment, confusion, disorientation, seizures, dysarthria, myoclonus, and poor motor control
  • Treatment with penicillin is the antibiotic of choice for all forms of neurosyphilis


  • Infection with the larval form of the porcine tapeworm
  • Humans acquire the adult tapeworm by eating uncooked pork
  • Humans also may accidentally ingest tapeworm eggs, which hatch in the small intestince, burrow into venules, and are carried to distant sites
  • The larvae are relatively large and may lodge in the subarachnoid space, ventricles, or brain tissue
  • Symptoms may not occur until 4-5 years later, when larvae die and provoke an inflammatory response
  • Cysts in the cerebrum may mimic a brain tumor
  • Cysts in the subarachnoid space may result in a chronic meningitis and arachnoiditis
  • Cysts in the ventricular system may cause obstructing hydrocephalus


  • Affects the motor unit of the peripheral nervous system
  • There are three type of bacteria-produced toxins known to affect humans
  • Clinical manifestations
    • Early symptoms include restlessness, localized stiffness and soreness, low-grade fever, and sometimes hemorrhage at the wound site.
    • Initial symptoms of generalized tetanus are nonspecific, including irritability, insomnia, and headache
    • Eventually, tonic contractures appear, secondary to the continuous activity of multiple muscle groups (early symptoms after an incubation period)
      • Nuchal rigidity
      • Lockjaw (trismus)
      • Risus sardonicus – facial expression seen as raised eyebrows and grinning distortion of the face, resulting from spasm of face muscles
      • Dysphagia
    • Treatment is best with immunization starting at newborn, and continuing every 10 years
      • Penicillin or other antibiotics are used to treat active tetnus
    • Recuperative period may be 2-4 months, and mortality is 25-75%

Viral (HIV/AIDS discussed elsewhere)


  • Referred to aseptic memingitis
  • Rarely fatal
  • Typically runs its course
  • Clinical syndrome consists of fever, headache, and other signs of meningeal irritation and a predominantly lymphocytic pleocytosis with normal CSF glucose
  • Other symptoms may include lethargy, irritability, and drowsiness. Also may see photophobia, pain with eye movements, or stiffness of the neck and spine on forward bending (meningeal irritation)
  • It’s rare to see confusion, stupor, or coma


  • Varicella-Zoster is an exclusively human herpesvirus that cause chickenpox (varicella), becomes latent in cranial nerve and dorsal-root ganglia, and frequently reactivates decades later to produce shingles (zoster) and postherpetic neuralgia
  • Associated with severe, sharp pain and characteristic rash
  • Occurs more often in immunocompromised patients or the elderly
  • Varicella occurs mostly in the spring, but zoster develops throughout the year
  • Common cranial nerve involvement are 5, 7, & 3
  • Treatment may include analgesics (e.g., acetaminophen, codeine) and antivirals (e.g., famciclovir, oral acyclovir)

Herpes simplex encephalitis

  • It’s the most common sporadic acute viral disease of the brain in the U.S.
  • It affects both sexes and all age groups in every season
  • Mortality is high (70%)
  • Survivors often have significant neuropsychiatric sequelae
  • Most greatly affects the medial temporal and frontal lobes
  • Common to see hemorrhagic necrosis, infammatory infiltrates, and cells containing intranuclear inclusions
  • Most common clinical findings are fever and alteration of consciousness
  • In majority, we see headache, personality changes, speech difficulties, and seizures
  • Mortality can be substantially reduced by early antiviral therapy (e.g., Acyclovir), although cognitive deficits are permanent


  • Acute viral disease of the central nervous system
  • Usually transmitted to humans through a wound contaminated by the saliva of a rabid animal
  • Rare airborne transmission has been noted in bat-infested caves
  • Dog and cat bites account for 90% of human rabies cases
  • The virus travels by nerve routes into the brain where it disseminates widely, then traveling to multiple organs
  • Incubation periods range from 15 days to 1 year
  • The disease begins with a prodrome of anxiety, fever, and headache, often with paresthesias at the bite site
  • 2-10 days later, we see delirium, seizures, nuchal rigidity, paralysis, and excitability
  • Stimulus-sensitive spasms of the pharynx, esophagus, or neck muscles may occur. Survival is not great at this stage
  • Treatment with vaccine, but no known effective treatment once clinical illness develops