Psychopathology Flashcards
Schizophreniform disorder
Symptoms of schizophrenia that last less than 6 months
Brain anatomy studies of autism-spectrum disorders have consistently found
Increased brain volume, increased level of serotonin plasma, delayed maturation of the frontal lobes, enlargement of lateral ventricles, cerebellar abnormalities
Most effective treatment for schizophrenia
Family therapy + meds
Executive functioning deficits in autism spectrum disorders
Deficits in mental flexibility & planning, switching & strategy use, but no inhibition
Attention functioning in autism-spectrum disorders
Able to sustain attention, but may require environmental supports of self-selected activity or strong incentives Display delayed orienting of attention Inconsistent findings in ability to shift attention
What are the 4 neurofunctional impairments of autism proposed by Waterhouse et al.?
- Canalesthesia - fragmented processing of incoming information from the different sensory modalities 2. Impaired affective assignment 3. Asociality 4. Extended selective attention
Following Crow’s schema (1980), name the symptoms, NP profile, prognosis in Type I schizophrenia
Positive symptoms predominate; essentially normal brain structure; most are fairly intact neurocognitively, relatively good response to treatment
Good prognostic indicators for schizophrenia
Availability of social support, good premorbid adjustment, acute onset, LOS, female, precipitation events, mood disturbances to, good inter-episode functioning, minimal residual symptoms, normal neurological functioning, family hx of mood disorders, no family hx of schizophrenia
Memory functioning in autism-spectrum disorders
Verbal memory tends to be poor, visuospatial memory tends to be intact with the exception of faces & social scenes Source memory is impaired, but may be dependent on type of context info that is to be remembered Working memory findings are mixed Episodic memory is impaired, but may be motivationally dependent
Suggested etiologies of ADHD
Food allergies, high lead levels, ETOH/nicotine prenatal exposure, prefrontal cortex, genetics
Somatization disorder
4 pain symptoms, 2 GI, 1 sex, 1 neuro; vague complaints; onset prior to age 30; often see anxiety, depression, suicide
Side effects of CNS stimulants
Insomnia, decreased appetite, stomachaches Motor/vocal tics (30-70%) or unmasks TS OC symptoms Growth suppression
Diagnostic criteria for manic episode
Elevated, expansive, irritable mood last at least one week 3+: inflated self-esteem/grandiosity, decreased need for sleep, more talkative or pressured speech, flight of ideas or racing thoughts, distractibility, increase in goal-directed activity, sig. stress or impairment
Brief psychotic disorder
Symptoms don’t last longer than 1 month
Diagnostic criteria for schizophrenia
2+ characteristic symptoms: delusions, hallucinations, disorganized speech, grossly disorganized or catatonic behavior, negative symptoms Persist for at least 6 mos Social/occupational dysfx
One theory posits that the underlying cause of schizophrenia is excessive stimulation of what type of synapses?
Dopamine
Capgrass syndrome
Delusional belief that a person has been replaced by an imposter Associated with nondominant parietal lobe lesions
Fregoli syndrome
Belief that the same person know to the pt is able to disguise or change him/herself into other people that the pt meets Seen in schizophrenia & damage to R frontal or L temporoparietal areas
Structural abnormalities in OCD
Orbital frontal cortex, caudate nucleus, cingulate gyrus
Which is considered more significant prognostically in schizophrenia: loosening of associations or circumstantiality?
Loosening of associations
Reduplicative paramnesia
Believe that the place or location has been duplicated Assoc. w/ bifrontal lesions, often w/ more diffuse RH damage
4 principle components of emotion
Physiology - CNS & ANS activity & resulting changes in neurohormonal & visceral activity Distinctive motor behavior - facial expression, tone of voice, posture Self-reported cognition - cognitive processes inferred from self-reported rankings Unconscious behavior - cognitive processes that influence bx of which we are not aware
Conversion disorder
1+ symptoms of motor/sensory dysfx without any underlying organic pathology
NP functioning in bipolar disorder
Abnormalities in attention seen in symptomatic pts & persist in remission in measures of sustained attention & inhibitory control Verbal memory may be impaired even in euthymic pts, visual memory deficits are variable Exec fx impaired in symptomatic pts, may be normal in fully-recovered pts
Rett’s disorder
-Developmental regression seen by age 4 -Life-long communicative & bx problems -Decelerated head growth, loss of hand skills (replaced by stereotypical hand movements), unccordinated gait/trunk, severe lang impairment, psychomotor retardation -Reported only in females
Biological model of bipolar disorder
Structural brain abnormalities, genetic factors, high NE, low serotonin, improper transportation of sodium & potassium ions b/t the outside & inside of neuron’s membrane
Barkley’s 3-tiered model of ADHD
1) behavioral inhibition 2) working memory, internalization of speech, regulation of arousal & emotions, reconsitution 3) Motor control, organization, & flexibility
Rehm’s model of depression
Deficits in self-centered behavior Selective attention to negative events in environment, selective attention to immediate not long-range outcomes of bx, stringent standards for self-evaluation, insufficient self-reinforcement, excessive self-punishment
Medical causes of catatonic disorder include
TBI, cerebrovascular disease, encephalitis, metabolic conditions
Following Crow’s schema (1980), name the symptoms, NP profile, prognosis in Type II schizophrenia
Negative symptoms predominate, structure brain abnormalities, impaired cognitive functions, poor treatment response
Personality change due to general medical condition
Labile type, disinhibited type, aggressive type, apathetic type, paranoid type, unspecified
Abnormal brain structures in patients with schizophrenia
Smaller frontal lobes, smaller temporal lobes, abnormalities in limbic system & BG, enlarged ventricles, smaller amounts of cortical gray matter, abnormal blood flow in certain areas (esp. frontal lobes)
Wolpe’s classical conditioning model of depression
Low rate of response contingent reinforcement results in neurotic depression
Functional imaging studies of autism spectrum disorders have shown
Hypoactivity in amygdala in processing of social stimuli, of facial processing area of fusiform gyrus, medial & dorsolateral prefrontal cortex Activiation of language areas, but less coordinated in their activity
Neuropsychological functioning in autism
Poor verbal abilities, abstraction, receptive language worse than expressive
NP functioning in schizophrenia
Poor frontal lobe functioning, memory deficits, slower reaction time; cognitive deficits may pre-date onset of obvious symptoms & diagnosis of illness
Origins of organically-based mood symptoms
Substances (e.g., PCP, hallucinogens), endocrine disorders (hypothyroidism), carcinoma of pancreas, viral illnesses, structural disease of brain
