Abstract

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.

Highlights

  • Sensory evoked potentials have been used to study the effects of alcohol on the human central nervous system

  • Cortical potentials are generally depressed by alcohol while the amplitudes of potentials recorded from subco11ical structures are unaffected [3, 4], one exception being auditory potentials from the inferior colliculus which are reduced in amplitude [4]

  • By recording auditory brainstem potentials in rats, we have demonstrated that acute alcohol intoxication produces significant and progressive prolongations of the latencies of brainstem potential peaks; these results indicate a depressive effect of alcohol on sensory transmission within the p1imary auditory pathway [9]

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Summary

Introduction

Sensory evoked potentials have been used to study the effects of alcohol on the human central nervous system. These potentials are the presumed "far-field" reflection of neural events occurring in the primary auditory pathway [5], and consist of a series of seven positive waves of submicrovolt amplitude within the first 10 msec after a click stimulus. By recording auditory brainstem potentials in rats, we have demonstrated that acute alcohol intoxication produces significant and progressive prolongations of the latencies of brainstem potential peaks; these results indicate a depressive effect of alcohol on sensory transmission within the p1imary auditory pathway [9]. Recordings were made of the midlatency potentials (latencies between IO and 50 msec) which are attributed to thalamic or early cortical activity [8] .

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