Bio explanations of schizophrenia

One other biological explanation of schizophrenia involves the brain structure. According tot his explanation schizophrenia is a mental detoriation at an early age. In other words brain damage at the time or before the time of birth could be a factor in the development of schizophrenia. Schizophrenics are found to have enlarged ventricles in the brain. This is supported by Pahl, Swayze and Andreason who reviewed 50 studies and found that schizophrenics had abnormally large lateral ventricles in their brain. Further evidence of the involvement of ventricles was reported by Suddath et al who used MRI to obtain pictures of brain structure from MZ or identical twin pairs in which only 1 twin had schizophrenia. He found that the schizophrenic twin generally had more enlarged ventricles and reduced anterior hypothalamus. The differences were so large that the schizophrenic twin could be identified readily from the brain images. However a negative criticism is that the extent to which brain abnormalities in schizophrenic patients are due to genetic factors is still unclear. Although Suddath et al’s finding that there were clear differences in brain structure between schizophrenic and non schizophrenic identical twins suggests that environmental factors must be of importance. In addition other parts of the brain may also be involved. Buchsbaum used pet scans with schizophrenics and normals. The schizophrenics had lower metabolic rates than the normals in the prefrontal cortex while performing psychological tests.

A third biological explanation of schizophrenia comes from neurochemistry which involves the dopamine hypothesis. This hypothesis suggests that dopamine over activity causes schizophrenia. This hypothesis is supported by Wise and Stein who proposed that a lack of the enzyme that converts dopamine to norepinephrine cause schizophrenia. This results in too much dopamine and not enough norepinephrine. However a problem with the dopamine over activity theory is that the antipsychotic medication clozapine works by blocking norepinephrine receptors. i.e: reducing the activity of norepinephrine. If a deficit of norepinephrine were a factor in schizophrenia it would be expected that clozapine would make the symptoms worse not better. Nevertheless nueroleptic drugs that block dopamine which seem to reduce the symptoms of schizophrenia provide evidence that dopamine does play a role in schizophrenia. Although Barlow and Durrant pointed out that there are problems with the dopamine hypothesis. Firstly because nueroleptic drugs block dopamine fairly rapidly, but generally fail to reduce the symptoms of schizophrenia. This is puzzling if high levels of dopamine are responsible for maintaining the symptoms.