Schizophrenia Flashcards
schizophrenia
splitting of the mind
split cognitive perceptions → decline in functional/cognitive abilities = chronic course of deterioration; permanent + pervasive deficits
difficulties with complex decision making; abstraction
primary symptoms
most functionally limiting
ambivalence - paralyzed by indecision
loosening of associations - jumps between ideas
incongruous affect - lack of display of emotions
autism - response to internal stimuli
secondary features
positive and negative symptoms
positive symptoms
things that are there that aren’t normally
hallucinations
delusions
disorganized speech
disorganized behaviour
hallucinations
a perception in the absence of stimulus while conscious
auditory hallucinations are most common in schizophrenia
visual hallucinations are most common caused by substance use
delusions
fixed false belief not aligned with culture
- bizare: impossible
- non-bizarre: possible
paranoid (persecutory) - danger
grandiose - special
nihilistic - dead
reference - meaning
erotomanic - love
somatic - illness
negative symptoms
deficits → more functional impairment + harder to treat
apathy, anhedonia, amotivation, alogia, poor social function
cognitive symptoms
changes and impairment
originally = dementia praecox → cognitive dysfunction
can’t identify primary emotions → aspect + intonation
wisconsin card sorting - can’t abstract rule/changes
clinical course
chronic illness
age of onset: M=15-25; F=25-35
→ first presentation; usually prior history of prodromal syndrome
residual symptoms after treatment
best predictor of future function is level of function after first episode
males have worse prognosis
prodromal phase
lower intensity/non-specific symptoms
attenuated symptoms
anxiety; disturbances in sleep, mood
functional decline
~1 year before psychosis
epidemiology
1:1 sex ratio
1 in 10 000 per year
risk factors
family history
urban birth
1st generation immigrant
winter birth
infection/malnutrition
older paternal age
ultra high risk penotype
family history of psychosis + 1 of:
- positive symptoms
- brief psychotic symptoms
- functional decline
→ 50% diagnosed in 1 year
show executive dysfunction, working memory problems
brain scan similarities
genetics
22q11 deletion - Velocardiofacial syndrome
up to 4000 genes associated - development or dopamine/glutamate pathways
COMT, neuroregulin 1, dysbindin
neurodevelopmental theory
predisposition to schizophrenia based on abnormal neural development in childhood and adolescence
triggered by stress
brain changes
increased ventricular size
temporal lobe asymmetry
loss of frontal grey matter
cannabis
cannabis can precipitate psychosis in individuals with COMT polymorphism → genetic risk factor
COMT - dopamine metabolism
other substances
amphetamines - long term effects on basal ganglia - positive symptoms
cocaine - some positive symptoms
PCP
phencyclidine
PCP
best substance model of schizophrenia
best mimic
causes hallucinations, delusions, and negative symptoms
dopamine hypothesis
excess dopamine = positive symptoms
deficit of dopamine = negative symptoms
dopamine-targeting substances induce similar symptoms
anti-psychotics are D2 antagonists
PET scan shows increased dopamine activity
glutamate hypothesis
deficit in temporal and striatal regions
NMDA antagonists (ketamine) induce psychotic symptoms
explanation for negative symptoms
associated with cholinergic deficits, serotonergic deficits - prefrontal cortex
decreased dopamine
PET scan shows decreased metabolism
treatments
biological - antipsychotics, ECT
psychosocial - cognitive and family interventions
support and assistance
antipsychotics
dopamine antagonists
first generation - typical
potency
high binding affinity to D2
block dopamine in ventral striatum, basal ganglia
= lots of side effects
second generation - atypical
less D2 binding
also D4 binding and 5-HT binding
better for negative symptoms, less side effects
