Academic journal article Hong Kong Journal of Psychiatry

The Neurobiology of Schizophrenia: A Mini-Review

Academic journal article Hong Kong Journal of Psychiatry

The Neurobiology of Schizophrenia: A Mini-Review

Article excerpt


Some recent advances in schizophrenic research are summarized. The theories on the pathogenesis of schizophrenia are discussed

Key words: schizophrenia, neurobiology


In this decade of the brain advances on the neurobiology of schizophrenia have been going on rapidly. Since my last review 6 years ago (Lo, 1991) we have seen new developments in Various aspects of schizophrenic research. In this mini review I Shall concentrate on four recent themes that have been at the Centre of efforts to understand this disease: the neuropathology Of schizophrenia, functional imaging in psychiatric applications, The etiological theories of schizopherenia and the novel Antipsychotics in the treatment and understanding of the Underlying mechanisms.


Johnston's discovery (Johnston, 1976) on ventricular enlargement remains the most consistent finding in schizophrenia. Other findings are more controversial. (Chua & McKenna, 1995; Deakin, 1996)

Recent postmodern studies point to the limbic system as one major focus of pathology. Reduced volume of hippocampus, amygdale and parahippocampal gyru are found, as wlel as left temporal horn enlargement. It may be related to reduced cell number or cellsize in hippocampus/parahippocampal gyrus/entorhinal cortex. White matter in hippocampal/parahippocampal gyrus is also reduced. The cytoarchitecture is disturbed, there being increased vertical axon numbers and deficits in small interneurones n the cingulated gyrus and abnormal cell arrangements in the hippocampus or entorhinal cortex. (Falkai & Bogerts, 1995)

In the cortex, contradictory results are reported in whether there is reduction of cortical volume. There appears to be shape abnormalities in the corpus callosum in that the sex difference in aaanterior and posterior callosal thickness in normal controls seem to be reversed in schizophrenics, and the mean curvature in corpus callosum is more marked in schizophrenia, with the corpus callosum being thicker in female and thinner in male.

In the basal ganglia, it is reported that caudate volume might increase under the influence of continuous neuroleptic treatment. In the thalamus, there is volume and cell number reductionsin the medio-dorsal nucleus of the thalamus, or smaller whole thalamic volume. In the brain stem, a reduced nigral volume, and a trend for reduced locus coeruleus volume are taken as an indication of a dopaminergic/noradrenergic underactivity.

Although postmordern studies give equivocal results in the brain size and weight, the majority of CT and MRI studies dismiss the idea of reduced brain size in schizophrenia.


What are the mechanisms underlying the neuropathological Changes? Recent findings favour of static, non-progressive subtle Brain abnormalities resulting from disturbed prenatal brain Development.


Astrocytes show change sin response to almost every type of o-injury or disease in the CNS. The capacity of astrocytes to react with proliferation and hypertrophy develops during the last trimester of gestation. The majority of studies involving glial cell counts, neuron-glial ratios and glial cell nuclei volumes found no difference in temporo-limbic structures, thalamus and cingulated gyrus. Most studies dismiss a chronic progressive disease, but support the idea of a static lesion occurring prior to the 20th week of gestation.


The cytoarchitectural abnormalities, cellular disarray, lower neuronal density, smaller cellsize etc., recently described in different limbic structures, prefrontal and temporal cortex of schizophrenics are very subtle and will easily be missed using classical neuropathological methods. It is likely that the usbtle differences are due to disturbances in the late migration or final differentiation of neurons that takes place in the second and third trimester of pregnancy. …

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