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Flashcards in Schizophrenia Deck (11):

Positive symptoms

distorted or excess of normal function
(abnormal beliefs not based in reality)
(the sensation of an experience that isn't actually happening)
thought disorders


Negative symptoms

deficit or decrease in normal function
flattened emotional response
poverty of speech
lack of initiative and persistence
social withdrawal


The early neurodevelopmental model:

fixed lesion from early life interacts with normal neurodevelopment later, lying dormant until the brain matures sufficiently to call into operation the damaged systems (Murray & Lewis, 1987).


The late neurodevelopmental model

schizophrenia may result from an abnormality in peri-adolescent synaptic pruning (Feinberg, 1983).


“2-hit” model

maldevelopment in schizophrenia takes place during 2 critical time points (early brain development and adolescence):
Early developmental insults may lead to dysfunction of specific neural networks that would account for premorbid signs
At adolescence, excessive synaptic pruning and loss of plasticity may account for the emergence of symptoms.


Neuropathology of schizophrenia

Ventricular enlargement
Reduced brain volume (less gray matter)
(temporal lobes, frontal lobes, subcortical structures)

Functional changes in the brains of schizophrenics
Hypofrontality during periods of high cognitive load - Increases in activity in dorsolateral prefrontal cortex seen in healthy volunteers absent in schizophrenics.


Neurocognitive Deficits in Schizophrenia

Lower IQ
Attentional deficits (e.g. Stroop Test)
Working memory deficits (e.g. Wisconsin Card Sorting Test)
Planning and information processing deficits

e.g. Stroop Test

Sensory Motor Gating deficits
-failures of information processing may be due to poor sensory motor gating
-screening out irrelevant stimuli and focusing on salient aspects of environment


Oculomotor Functions

Smooth pursuit eye movements
tracking a spot - schizophrenic movements are
not smooth (catchup saccades)
Anti-saccade task
look away from a target (do not follow it)
schizophrenics cannot suppress looking at the target


Dopamine hypothesis

1) Antipsychotics
- D2 receptor antagonists. Antipsychotic dosage
correlates with their potency as D2 receptor antagonists.
2) Drugs boosting DA function e.g. cocaine, amphetamine, L-DOPA can (in large doses) cause positive symptoms of schizophrenia (e.g. psychoses).
3) These drug-induced psychoses can be treated with the D2 antagonist antipsychotics.


Dopamine hypothesis problems

- It explains only part of schizophrenia (positive symptoms not negative symptoms)
- Anti-dopaminergic drugs usually make negative symptoms worse in patients,induce negative symptoms in healthy people.
- Atypical antipsychotic drugs e.g. Clozapine (with weaker anti-dopaminergic activity) are better anti-psychotic drugs.


The Glutamate System

- NMDA receptor antagonists e.g. PCP and Ketamine > - NMDA glutamate system hypofunctional and results in:
positive symptoms such as delusions and hallucinations
Affective, negative and cognitive symptoms
Physiological symptoms of schizophrenia
- Glutamate agonists seem to improve both positive and negative symptoms of schizophrenia
- Neurophysiological studies also suggest that hypofunction of NMDA receptors could better explain the negative, cognitive and affective symptoms of schizophrenia than the DA theory.