Neurocognitive Deficits in Alcoholics and Social Drinkers: A Continuum?

Authors

  • Oscar A. Parsons

    Corresponding author
    1. Oklahoma Center for Alcohol and Drug-Related Studies, Department of Psychiatry and Behavioral Sciences, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma.
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  • The research reported in this paper was supported in part by Grants RO1 AA3032, RO1 AA04164, and RO1 AA06135 from the National Institute on Alcohol Abuse and Alcoholism to the author.

  • This paper was presented by the author as the recipient of the “Distinguished Research Award” at the 1997 annual meeting of the Research Society on Alcoholism in San Francisco.

Reprints requests: Oscar A. Parsons, Ph.D., Center for Alcohol and Drug-Related Studies, 800 NE 15th Street, Suite 410, Oklahoma City, OK 73104.

Abstract

Our research program has investigated neurocognitive deficits in sober alcoholics for several decades. We have shown that both male and female adult alcoholics – compared with peer nonalcoholic controls – have deficits on tests of learning, memory, abstracting, problem-solving, perceptual analysis and synthesis, speed of information processing, and efficiency. The deficits are equivalent to those found in patients with known brain dysfunction of a mild to moderate nature. Attempts to identify factors other than alcoholism to account for these differences have been unsuccessful. The deficits appear to remit slowly over 4 to 5 years. Relapse of recovering alcoholics is predicted by behavioral (e.g., depressive symptoms and neurocognitive performance) and biological measures (e.g., event-related potentials) obtained at the end of treatment. Results of recent studies support the hypothesis of a continuum of neurocognitive deficits ranging from the severe deficits found in Korsakoff patients to moderate deficits found in alcoholics and moderate to mild deficits in heavy social drinkers (more than 21 drinks/week). Individual differences in the presence and magnitude of neurocognitive deficits in social drinkers and alcoholics are hypothesized to be due, in part, to individual differences in vulnerability of the brain to alcohol or its metabolites' toxic effects.

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