Brain damage in social drinkers? Reasons for caution.

Abstract

Most of our knowledge about the effects of alcohol on the CNS of humans has been derived from three basic experimental paradigms. In the first of these, the transient effects of alcohol ingestion are investigated by examining changes in information-processing ability during an episode of acute intoxication. In the second, less-commonly used paradigm, the immediate aftereffects of intoxication are determined by recording behavioral and electrophysiological changes during withdrawal from alcohol. In the third paradigm, the chronic sequelae of long-term alcohol use are assessed by examining neuropsychological and neuroradiological indices of brain damage in alcoholics who have been detoxified for several weeks. Each paradigm focuses on states that would appear to have very different biological properties (e.g., neuropsychological changes may be completely reversible in one, but not in another; evidence of cerebral atrophy may often be found in one, but not in another). Nevertheless, there are also many behavioral similarities between these states. For example, both the intoxicated college student and the detoxified chronic alcoholic use similar, inefficient strategies on verbal learning tasks and make similar types of errors.1 Perhaps because of those common features, many writers now assume that any time an individual’s score on a neuropsychological test is found to be correlated with some measure of alcohol use, that person must necesssarily have incurred measurable cerebral damage that is cumulative, most likely irreversible, and proportional to the total amount of alcohol consumed over his lifetime.