Auditory brain stem potentials were recorded from unrestrained rats and from cats paralyzed with Flaxedil, before and after ingestion of intoxicating dosages of alcohol. The acute effect of alcohol was a cumulative increase in the central conduction times of successive brain stem potential peaks. Statistically significant latency changes were found for peaks attributed to neural structures as far peripherally as the medulla. This depressive influence of alcohol on sensory transmission was independent of variations in stimulus intensity and body temperature.

Auditory brain stem responses (ABRs) were obtained from 66 chronic alcoholic patients. Forty-one percent of the patients had abnormal ABR indicated by prolonged interwave intervals. The incidence of brain stem abnormalities was related to age, the type and number of alcoholic neurological complications, and cerebral atrophy in computerized tomographic (CT) scan. There was a progressive increase in the incidence of abnormal ABRs with age and the number of alcoholic neurological diseases. Among the neurological complications of alcoholism, patients with cerebellar degeneration had the highest incidence of abnormal ABRs (83%). There was a high correlation between cerebral atrophy in CT scan and abnormal ABRs. The data suggest that laboratory methods such as the ABR and CT scan are useful in evaluating the extent of CNS abnormalities in alcoholic patients.

Auditory brain stem evoked responses were in unrestrained rats during periods of acute and chronic alcohol intoxication, alcohol withdrawal, and recovery. Acute alcohol administration altered the auditory brain stem potentials by a prolongation of both peak latency and central conduction time, beginning with early peaks. Similar but lesser effects affecting only the latter peaks were observed during chronic alcohol intoxication. By contrast, alcohol withdrawal resulted in a decrease in the peak latencies of auditory brain stem potentials and a facilitation of central conduction time. Recovery of the auditory brain stem potentials to the normal form required at least three to four weeks. The present study provides the first quantitative data, to our knowledge, on manifestations of alcohol tolerance and withdrawal.

Auditory brainstem potentials were recorded from human subjects before and after an intoxicating dose of alcohol. Following alcohol ingestion there were significant, progressive increases in the latencies of brainstem potential peaks III through VII. No changes in peak amplitudes were found. The results indicate that alcohol has a depressive effect on neural transmission within the primary auditory brainstem pathway.