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Implications of Normal Brain Development for the Pathogenesis of Schizophrenia

Samuel G. Siris, MD
Arch Gen Psychiatry. 1988;45(11):1055. doi:10.1001/archpsyc.1988.01800350089019.
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To the Editor.—  In his article, published in the July 1987 issue of the Archives, Weinberger1 presents an intriguing and heuristically rich model of hypothesized interaction between prefrontal cortical and mesolimbic dopamine systems in schizophrenia. This model is consistent with a great deal of evidence that has accumulated with regard to schizophrenia, including, crucially, the timing of its onset in terms of developmental maturation within the central nervous system. Weinberger's is the latest of a series of structural versions of the "diathesis" in the stress-diathesis model of schizophrenia.2Weinberger notes that the structural lesion in such a model does not necessarily imply the existence of a distinct, discontinuous biologic subgroup. The "schizophrenia lesion" in such a model could possibly be no more than the extreme end of a developmental spectrum with regard to the organization of a particular central nervous system functional system, such as the hypothesized abnormality


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