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Arnold E. Merriam, MD
Division of Neuropsychiatry Departments of Psychiatry and Neurology Albert Einstein College of Medicine/ Montefiore Medical Center Bronx Municipal Hospital Center, Room 1022 Bronx, NY 10461

Stanley R. Kay, PhD
Schizophrenia Research Program, Bronx Psychiatric Center Department of Psychiatry Albert Einstein College of Medicine/ Montefiore Medical Center Bronx, NY 10461

Lewis A. Opler, MD, PhD; Paul M. Ramirez
Department of Psychiatry Columbia Presbyterian Medical Center New York, NY 10032

Arch Gen Psychiatry. 1989;46(8):760.

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

To the Editor.—

In their article in the September 1988 issue of the ARCHIVES, Braff and Huey¹ demonstrated that the administration to normal individuals of an agent that augments catecholaminergic transmission induced in them a susceptibility to backward masking similar to that encountered in schizophrenics. As the authors rightly point out, while their findings are compatible with the notion of hyperdopaminergia-induced information processing dysfunction in schizophrenia, the hypothesis remains open to question. We wish to propose an alternative, not necessarily biochemical, explanation of the schizophrenic backward masking vulnerability, one that is linked to prefrontal impairment.

The task utilized by Braff and Huey is fundamentally a test of proactive interference, a generic term for the negative effect exerted by a subsequently performed activity on a prior mental operation. In the case of the backward masking paradigm, this involves interference to the point of nonrecognition by a masking visual stimulus . . . [Full Text PDF of this Article]

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