Neuropsych Aspects of Psychopathology


Brief History

  • Kraeplin (1919) came up with first definition (called it dementia praecox)
  • Blueler (1950) introduced the term “schizophrenia” (Bleuler’s 4 A’s: Association, Affect, Ambivalence, and Autism)
  • Schneider (1959) came up with 11 pathognomonic symptoms (Schneiderian First Rank Symptoms)
  • Crow (1980) proposed that schizophrenia be divided into 2 major syndromes (Type I and Type II)
    • Type I = domination of positive symptoms (Normal brain structure, Most intact neurocognitively, Relatively good response to treatment)
    • Type II = domination of negative symptoms (Structural brain abnormalities, Impaired cognitive functioning, Poor response to treatment)

DSM-IV criteria (briefly)

  • Characteristic Symptoms (two or more)
    • delusions
    • hallucinations
    • disorganized speech
    • grossly disorganized or catatonic behavior
    • negative symptoms
  • Social/Occupational Dysfunction
    • work
    • interpersonal relationships
    • self-care
  • Duration
    • Continuous signs of the disturbance persist for at least 6 months
    • This 6-month period must include at least 1 month of symptoms (or less, if being treated)
  • Exclusion of schizoaffective and mood disorder
  • Exclusion of substance/general medical condition
  • If there is a relationship to a pervasive developmental disorder, schizophrenia is only diagnosed if prominent delusions or hallucinations are also present for at least a month

Etiology (Biological View)

  • Genetics
    • General population is 1%
    • Identical twin = 48%
    • Offspring of two schizophrenic parents = 46%
    • Fraternal twin = 17%
    • Sibling = 9%
    • Half sibling = 6%
    • First cousin = 2%
    • Adoption studies
    • Possible defects found on several chromosomes
  • Biochemical Abnormalities
    • Dopamine Hypothesis (Too much dopamine; Neuroleptics block dopamine receptors)
    • Amphetamines prevent reuptake of dopamine, and individuals on amphetamines can display symptoms of schizophrenia
  • Abnormal Brain Structure
    • Smaller frontal lobes
    • Smaller temporal lobes (decreased amygdale, hippocampus, and parahippocampal gyrus)
    • Abnormalities in the limbic system and basal ganglia
    • Enlarged ventricles (especially in Type II)
    • Smaller amounts of cortical gray matter
    • Abnormal blood flow in certain areas of the brain (especially frontal lobes)
  • Viral Problems
    • In vitro viral exposure that is activated by changes in hormones or other viruses
    • Influenza exposure
    • Pestiviruses (found in 40% of schizophrenics)
    • Higher number of schizophrenics during the winter
    • May explain why fraternal twin has a greater chance than a sibling

Neuropsychological Functioning

  • Frontal lobe dysfunction
    • Impaired attention including problems with filtering, problems distinguishing relevant from irrelevant information, selective attention is often impaired with increased information load, sustained and focused attention abilities are often poor.
    • Problems with abstraction
    • Problem solving deficits on WCST, CST
    • Poor planning on the Clock Drawing, secondary to verbally mediated planning difficulties
  • Memory deficits
    • Impaired CVLT-II, WMS-III, BVRT
    • CVLT research shows impairment in learning, recall, and recognition measures, but equal-to-normal retention of information over the delay (i.e., normal storage)
  • Can have deficits on language tests
    • In speech disordered schizophrenics (e.g., Disorganized Type), can have impaired BNT
    • On the COWA, Schizophrenics produce more phonemic responses than category words
  • Slower reaction time to both auditory and visual signal on the RT

Bipolar Disorder

DSM-IV Criteria of mania (briefly)

  • Elevated, expansive, or irritable mood lasting at least one week
  • Three or more of the following (four if mood is only irritable)
    • Inflated self-esteem or grandiosity
    • Decreased need for sleep
    • More talkative or pressured speech
    • Flight of ideas or racing thoughts
    • Distractibility
  • Increase in goal-directed activity
    • Excessive involvement in pleasurable activities that have a high potential for painful consequences
  • Significant stress or impairment
  • All typical exclusions apply (not due to other psych, medical, substance D/O, etc.)

Bipolar I Disorder vs. Bipolar II Disorder vs. Cyclothymia (briefly)

  • Bipolar I Disorder – Presence of mania and depression
  • Bipolar II Disorder – Presence of depression and hypomania (no history of manic episodes)
  • Cyclothymia – Two years of mood cycles, but events don’t meet criteria of depression or mania (less severe with shorter swings)

Etiology (Biological Model)

  • Structural brain abnormalities (ventricular enlargement)
  • Genetic factors (possible genetic links have been found on chromosomes 11 and X
    • 40% chance for MZ twin to get it
    • 5-10% chance of a close relative to get it
    • 1% chance in the general population
  • Neurotransitters
    • High norepinephrine
    • Serotonin can be implicated (low)
  • Ion Activity
    • Improper transportation of sodium and potassium ions between the outside and the inside of the neuron’s membrane

Neuropsychological Functioning

  • General intellectual function is largely preserved in BD.
  • Impairments when present are limited to acute episodes and to performance scores.
  • Abnormalities in attention are seen in symptomatic patients and persist in remission in measures of sustained attention and inhibitory control.
  • Verbal memory may be impaired even in euthymic patients, while visual memory deficits are variable depending on the tasks used.
  • Executive functioning (planning, abstract concept formation, set shifting) are impaired in symptomatic patients, but it may be normal in fully recovered patients

Obsessive Compulsive Disorder

DSM-IV Criteria (briefly)

  • Either obsessions or compulsion
  • Insight at some point (If not, then subtype “poor insight)
  • Marked distress, time consuming (>1 hour per day), or significantly impairs functioning
  • If there is another Axis I disorder, O-C are not restricted to it
  • Not due to substance use or medical disorder

Etiology (Biological Model)

  • Structural abnormalities
    • Orbital frontal cortex
    • Caudate nucleus
    • Cingulate gyrus
  • Neurochemical: Possible down-regulation in both the number of serotonin receptors and release of serotonin

Neuropsychological Functioning

  • Investigations generally agree on localization of dysfunctional areas (e.g., prefrontal and frontal regions, limbic system, basal ganglia).
  • They disagree as to hemisphere and frontal lobe side impairment, involvement of other brain areas, pathophysiological connections, and impact of developmental phases and of concomitant cognitive and affective conditions.