Schizophrenia (7)

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Neural: Functional magnetic resonance imaging and other brain imaging technologies allow for the study of differences in brain activity among people diagnosed with schizophrenia.
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.[75] These differences have been linked to the neurocognitive deficits often associated with schizophrenia.[76] The role of antipsychotic medication, which nearly all those studied had taken, in causing such abnormalities is also unclear.[77]

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. 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.[78]

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[79] and the discovery that the glutamate blocking drugs such as phencyclidine and ketamine can mimic the symptoms and cognitive problems associated with the condition.[80] 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.[81] Further support of this theory has come from preliminary trials suggesting the efficacy of co-agonists at the NMDA receptor complex in reducing some of the positive symptoms of schizophrenia.[82]

There have also been findings of differences in the size and structure of certain brain areas in schizophrenia, starting with the discovery of ventricular enlargement in those for whom negative symptoms were most prominent.[83] However, this has not proven particularly reliable on the level of the individual person, with considerable variation between patients. More recent studies have shown various differences in brain structure between people with and without diagnoses of schizophrenia.[84] However, as with earlier studies, many of these differences are only reliably detected when comparing groups of people, and are unlikely to predict any differences in brain structure of an individual person with schizophrenia.

Treatment and services
Molecule of chlorpromazine, which revolutionized treatment of schizophrenia in the 1950s. The concept of a cure as such remains controversial, as there is no consensus on the definition, although some criteria for the remission of symptoms have recently been suggested.[85] The effectiveness of schizophrenia treatment is often assessed ...To be continued