Citation

Nichols JM, Martin F. J. Stud. Alcohol 1996; 57(2): 125-135.

Affiliation

Department of Psychology, University of Tasmania, Hobart, Australia.

Copyright

(Copyright © 1996, Rutgers Center of Alcohol Studies)

DOI

unavailable

PMID

8683961

Abstract

OBJECTIVE: It has been suggested that alcohol-related brain impairments progress on a continuum from subtle deficits in social drinkers through to end-state Korsakoff syndrome. The aim of the present study was to investigate whether heavy levels of social drinking have an adverse effect on sober cognitive functioning in young nonalcoholic adults. METHOD: Event-related potentials (ERPs) were recorded from heavy ( > 200 gm/week) and light ( < 20 gm/week) male social drinkers under the effects of a pharmacological challenge (lorazepam-ATIVAN) and a placebo. The heavy (n = 14) and light (n = 14) social drinkers completed a free-recall task with a rare word probability of .30. RESULTS: Analysis of the P300 component of the ERP to recalled and not-recalled words found that P300 amplitude in heavy social drinkers (HSDs) was reduced following placebo compared to the light social drinkers (LSDs). Lorazepam produced a distinctive pattern of anterograde memory deficits in both groups and reduced P300 amplitude to rare words in the LSDs compared to both the placebo treatment and the HSDs. CONCLUSIONS: The differences in central nervous system functioning evident between HSDs and LSDs were reflected in ERP deviations in both the presence and absence of lorazepam. Even though no definite statements can be made because of the small sample size, the results appear to indicate that HSDs have an impairment in their information-processing ability in the absence of an acute inhibitory agent (e.g., alcohol or a benzodiazepine) as well as a differential response to the depressant effects of lorazepam.

Language: en