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. Sensory evoked potentials have been used to study the effects of alcohol on the human central nervous system. Significant reductions in the amplitude of auditory cortical potentials are normally reported after alcohol ingestion (1). Cortical potentials elicited by visual and somatosensory stimulation have also been reported to be reduced in amplitude, although those components of the potentials which were thought to originate in the primary receiving areas in each modality remained unchanged (2). Similar results have been noted with animal subjects. Cortical potentials are generally depressed by alcohol while the amplitudes of potentials recorded from subcortical structures are unaffected (3, 4), one exception being auditory potentials from the inferior colliculus which are reduced in amplitude (4). To date no studies have been conducted to examine in humans the effects of alcohol on subcortical structures involved in sensory transmission. However, techniques have been developed for recording auditory brainstem potentials from the scalp in humans. These potentials are the presumed "far-field" re-

flection 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. The first peak in the waveform probably represents the compound action potential of the auditory nerve, and the remaining peaks have been attributed to subsequent activity in the cochlear nucleus, superior olive, lateral lemniscus, and inferior colliculus (6-8). 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 primary auditory pathway (9). In the study reported here, the analogous experiment was conducted with human subjects. Recordings were also made of the midlatency potentials (latencies between 10 and 50 msec) which are attributed to thalamic or early cortical activity (8). The subjects were six adult males, including the three authors and three laboratory personnel. All had a history of so-

Table 1. Latencies of auditory brainstem potential peaks before and after alcohol consumption. The statistical significance of the change in each peak latency is given; N.S., not significant.

Subject

Latency of peak (milliseconds after stimulus onset) V III IV VI

I

II

5 6 Mean

1.68 1.50 1.49 1.81 1.77 1.40 1.61

2.97 2.83 2.82 2.70 2.82 2.73 2.83

3.85 3.81 3.60 3.68 3.78 3.83 3.78

1 2 3 4 5 6 Mean

1.65 1.47 1.53 1.82 1.80 1.44 1.62

2.97 2.78 2.92 3.03 2.87 2.82 2.90

3.82 3.95 3.80 3.87 3.88 3.94 3.88

0.01

0.07

0.10

1 2 3 4

Before alcohol 5.10 5.18 4.84 4.90 5.04 5.11 5.05 After alcohol 5.13 5.40 5.13 5.14 5.16 5.31 5.21

VII

5.80 5.88 5.38 5.40 5.90 5.71 5.70

7.58 7.35 6.93 7.05 7.20 7.54 7.29

9.18 9.05 8.37 8.57 8.54 9.14 8.83

5.90 6.05 5.64 5.58 6.05 5.87 5.85

7.68 7.60 7.21 7.21 7.28 7.77 7.46

9.25 9.25 8.88 8.86 9.06 9.33 9.10

0.15

0.17

0.27