Contemporary histological studies have addressed two main areas. First, to clarify the frequency and nature of neurodegenerative abnormalities in schizophrenia. Second, to investigate the cellular organization (cytoarchitecture) of the cerebral cortex and other components of the limbic system (hippocampus, prefrontal cortex, and thalamus).

Neurodegeneration and schizophrenia Gliosis

The issue of gliosis (reactive astrocytosis) has been extensively investigated since an influential report (2Z> that gliosis was common in schizophrenia, especially in the diencephalon around the third ventricle. As gliosis is a sign of past inflammation (see Chapter,,2.,3;.5), this finding supported aetiopathogenic scenarios for schizophrenia involving infective, ischaemic, autoimmune, or neurodegenerative processes. However, many subsequent investigations have not found gliosis, and Bruton and colleagues^8,' found that it was only present in cases exhibiting coincidental neuropathological abnormalities, indicating that gliosis is not an intrinsic feature of schizophrenia but merely of superimposed pathological changes which occur by chance in some cases.

The gliosis issue is esoteric but has considerable implications. The gliotic response is said not to begin until the end of the second trimester in utero, and hence an absence of gliosis is taken as prima facie evidence of a disease process occurring before this time. Unfortunately, both the absence of gliosis, and its interpretation, are less clear than often assumed. First, detecting gliosis is surprisingly difficult, and it can be argued that the data do not wholly rule out its occurrence in (a subtype of) schizophrenia. Second, despite the widely cited time point at which the glial response is said to begin, the matter has not been well investigated; therefore it is prudent not to use this to time the pathology of schizophrenia with spurious accuracy. Furthermore, it is a moot point whether the subtle kinds of morphometric disturbance described in schizophrenia, whenever and however they occurred, would be sufficient to trigger detectable gliosis.

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