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Dennis E. Lee
Interdepartmental Program for Neuroscience University of California, Los Angeles Los Angeles, CA 90095

Allan J. Tobin
Los Angeles Correspondence to Life Sciences Building, University of California, Los Angeles, Los Angeles, CA 90024-1606 (Dr Tobin).

Arch Gen Psychiatry. 1995;52(4):267-268.

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

Understanding the neural substrates of schizophrenia has long been a goal of psychiatrists and neurobiologists. For the clinician, more precise understanding could translate into advances in diagnosis and treatment. For the neurobiologist, such knowledge could provide general insights into the mechanisms of higher cognitive function.

Much recent work has focused on the prefrontal cortex (PFC), especially the dorsolateral PFC (DLPFC), which roughly corresponds to Brodmann's area 9. While changes in other brain regions have been reported,^1,2 a growing body of converging evidence suggests that disruptions of the DLPFC play a particularly important role in the origins and course of the illness. Positron emission tomography studies,³ regional cerebral blood flow studies in patients performing the Wisconsin Card Sort,⁴ and cytoarchitectonic studies¹ have revealed abnormalities in the DLPFC. These studies suggest that in schizophrenics, the DLPFC is hypoactive relative to other brain regions. . . . [Full Text PDF of this Article]

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