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Schizophrenia - Coggle Diagram

- - - - Due to absence of glial cells, the abnormality is unlikely to have been caused by degeneration.
      - Likely caused by development abnormality.
  - - - Selection of wrong neurones to survive in foetal brain
      - Neuronal migration to wrong area
      - Neuronal innervation of wrong targets
    - - Disease progression is consistent with progressing degeneration, not a completely formed pathological process.
      - Antipsychotic treatment loses effectiveness over time as patients become less responsive to them.
    - - One psychotic episode damages brain to increase chance for another more severe one.
  - - - Dopmaine theory: Increased dopamine function in mesolimibic pathway is associated with schizophrenia
        
        For
        
        Because agonists like amphetamine induce schizophrenia like psychosis
        
        Increase dopamine release
        
        Prevent dopamine reuptake
        
        Inhibit monoamine oxidase B from breaking down dopamine into dopac
        
        Dopamine antagonist used for pharmacological treatment of schizophrenia
        
        Against
        
        Pure antagonists ineffective against negative symptoms
        
        Dopaminergic antagonists target D2 receptors in basal ganglia, thus inhibiting of output from temporal lobe which is responsible for positive symptoms
        
        Dopaminergic antagonists target D1 receptors in frontal lobe which exacerbate negative symptoms
        
        Unclear if the increase in dopamine function are effect of disease or long term antagonist drug treatment.
        
        Amphetamine only cause positive symptoms, not cognitive or negative symptoms
      - Serotonin theory: schizophrenia linked to increased serotonin function
        
        LSD
        
        Cause hallucinations but is partial serotonin agonist.
      - Glutamate theory
        
        Phencyclidine
        
        Antagonist of NDMA at glutamate receptors
        
        The drug action likely to be same in both healthy people and schizophrenic patients
        
        Similar drug, ketamine also exacerbate schizophrenic symptoms similar to phencyclidine despite being used on schizophrenic patients.
        
        Replicates all 3 type of symptoms in healthy people [negative, positive, cognitive]
        
        Other evidence
        
        Reduced glutamate levels in CFS of schizophrenic patients
        
        Decreased cortical gulatmate post mortem
        
        Increased cortical glutamate receptors post mortem
        
        Increased binding to glutamate receptors in cortex, basal ganglia and hippocampal formation
        
        Decreased glutamate uptake sites in cingulate cortex
        
        Studies fail to show significant changes
- - - - Abnormal perceptions
        
        Auditory hallucinations
      - Abnormal ideas
        
        persecution delusions
        
        grandiose delusions
        
        hypochondriacal delusions about not being mentally ill
      - Thought disorder
        
        believing thoughts are inserted into mind
        
        Derailment - no logical cohesion of thoughts
      - Likely caused by impaired functions in temporal lobes
        
        Schizophreniacs with positive symptoms show deficits in tasks requiring temporal lobe activation e.g. latent inhibition, kamin blocking
        
        People with temporal lobe damage exhibit positive symptoms
    - - Emotional disorder
      - abnormal posture
      - Likely caused by impaired function in prefrontal cortex
        
        Schizophrenics show deficit on tasks requiring prefrontal cortex. e.g. Wisconsin card sort test
        
        People with frontal lobe damage show behaviours resembling negative symptoms