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Godfrey D. Pearlson, MD; Thomas E. Schlaepfer, MD
The Johns Hopkins Medical Institutions Division of Psychiatric Neuroimaging Department of Psychiatry and Behavioral Sciences 600 N Wolfe St Meyer 3-166 Baltimore, MD 21287-7362

Arch Gen Psychiatry. 1997;54(2):189.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

Sex differences in schizophrenia, including variation in clinical symptoms, onset age, risk factors, response to treatment, and putative biological risk markers, are widely recognized to exist, yet are hard to explain by any pathogenetic mechanism.^1,2 In his discussion of Olney and Farber's N-methyl-D-aspartate receptor hypothesis, Crow³ compares various (eg, neurohumoral, anatomical, physiological) theories of the pathogenesis of schizophrenia. He further examines these theories for their ability to explain various known features of the disorder, eg, clinical symptoms, brain changes, and epidemiological characteristics. Among these epidemiological features, he includes the sex differences discussed earlier. He recognizes only 2 hypotheses, the corpus callosum change model and the abnormal language lateralization model, as being able to account successfully for sex differences in schizophrenia.

Of the theories he compares, Crow expresses the opinion that the heteromodal association cortex model only "doubtfully explains" such sex differences. We be lieve that in fact . . . [Full Text PDF of this Article]

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