Variable patchy gliosis and neuronal loss have been reported to occur in the schizophrenic brain, but such changes would not appear to be specific to the disease. It has been suggested that these changes are a manifestation of an inflammatory reaction, possibly due to a virus infection; cytomegalovirus has been specifically implicated. However, there would now appear to be little support for the virus hypothesis of schizophrenia. More recently, detailed analysis of the neuronal architecture of the hippocampal and cortical regions of the schizophrenic brain suggests that a region of the parahippocampal gyrus is abnormal, possibly due to a disturbance of
FUNDAMENTALS OF PSYCHOPHARMACOLOGY Table 11.1 Histological findings in schizophrenia
Weight of evidence
Lack of neurodegenerative lesions (e.g. Alzheimer changes) Lack of gliosis
Smaller cortical and hippocampal pyramidal neurons
Decreased cortical and hippocampal synaptic markers
Decreased dendritic spine density
Loss of neurons from dorsal thalamus
Abnormalities of white matter neurons
Entorhinal cortex dysplasia
Disarray of hippocampal neuron orientation
Loss of hippocampal or cortical neurons
0: no good evidence; +/-: equivocal data: + to +++++: increasing amounts of supportive data.
neuronal migration in a late phase of cortical development. Varying degrees of pyramidal cell disorientation in the hippocampus and reduced parahippocampal width suggest structural abnormalities in the basal cortical regions of the temporal lobe. A summary of the histological changes reported to occur in the brains of schizophrenic patients is given in Tabel 11.1.
Computed axial tomography (CAT) scan studies of the brains of schizophrenics have led to a renewed interest in the possibility that neuronal loss is causally connected with the disease. Most studies have implied that the ventricular size is increased, particularly in older patients, such structural changes being associated with neuropsychological impairment and negative symptoms of the disease, but not all investigators have found such correlations. Other CAT studies have shown that in right-handed patients there may be a lesion of the left hemisphere which correlates with the degree of psychological defect and with the occurrence of delusions. PET studies also suggest that the rate of glucose utilization by the left pre-frontal cortical lobe is slightly diminished in the schizophrenic patient. It is of interest that neurochemical studies of transmitters and their synthesizing enzymes also show asymmetry, with a higher concentration of dopamine and a higher activity of choline acetyltransferase in the left basal ganglia of the normal brain. The concentration of dopamine would appear to be greater in the left amygdala of the schizophrenic brain. A summary of the risk factors for schizophrenia is shown in Table 11.2.
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