Schizophrenia

Schizophrenia

Schizophrenia is a severe and disabling brain disorder characterized by abnormalities in the perception or expression of reality. It most commonly manifests as auditory hallucinations, (Szasz 1976) paranoid or bizarre delusions, or disorganized speech and thinking with significant social or occupational dysfunction. Onset of symptoms typically occurs in young adulthood,[with approximately 0.4-0.6% of the population affected. Diagnosis is based on the patient's self-reported experiences and observed behavior. No laboratory test for schizophrenia currently exists. (Walker 2004)

Increased dopamine activity in the mesolimbic pathway of the brain is consistently found in schizophrenic individuals. The mainstay of treatment is antipsychotic medication; this type of drug primarily works by suppressing dopamine activity. Dosages of antipsychotics are generally lower than in the early decades of their use. (Shaner 2004) Psychotherapy, vocational and social rehabilitation are also important. In more serious cases—where there is risk to self and others—involuntary hospitalization may be necessary, although hospital stays are less frequent and for shorter periods than they were in previous years. (Roazen 1991)

Studies using neuropsychological tests and brain imaging technologies such as fMRI and PET to examine functional differences in brain activity have shown that differences seem to most commonly occur in the frontal lobes, hippocampus, and temporal lobes. These differences have been linked to the neurocognitive deficits often associated with schizophrenia. The role of antipsychotic medication, (Noll 2006) which nearly all those studied had taken, in causing such abnormalities is unclear.

Particular focus has been placed upon the function of dopamine in the mesolimbic pathway of the brain. This focus largely resulted from the accidental finding that a drug group which blocks dopamine function, known as the phenothiazines, could reduce psychotic symptoms. (Laing 1990) It is also supported by the fact that amphetamines, which trigger the release of dopamine may exacerbate the psychotic symptoms in schizophrenia. An influential theory, known as the Dopamine hypothesis of schizophrenia, proposed that a malfunction involving dopamine pathways was the cause of (the positive symptoms of) schizophrenia. This theory is now thought to be overly simplistic as a complete explanation, partly because newer antipsychotic medication (called atypical antipsychotic medication) can be equally effective as older medication (called typical antipsychotic medication), but also affects serotonin function and may have slightly less of a dopamine blocking effect. (Keen 1999)

Interest has also focused on the neurotransmitter glutamate and the reduced function of the NMDA glutamate receptor in schizophrenia. This has largely been suggested by abnormally low levels of glutamate receptors found in postmortem brains of people previously diagnosed with schizophrenia and the discovery that the glutamate blocking drugs such as phencyclidine and ketamine can mimic the symptoms and cognitive problems associated with the condition. (Fleck 1985) The fact that reduced glutamate function is linked to poor performance on tests requiring frontal lobe and hippocampal function and that glutamate can affect dopamine function, all of which have been implicated in schizophrenia, have suggested an important mediating (and possibly causal) role of glutamate pathways in schizophrenia. Further support of this theory has come from preliminary trials suggesting ...