The effects of alcoholism on auditory evoked potentials during sleep

Abstract

Normal aging is associated with a reduction in the probability that an auditory stimulus will evoke a K-complex during sleep. Additional concomitants of aging are a reduction in the amplitude of the K-complex-related N550, an augmentation of the P2 component and the appearance of a long-lasting positivity (LLP) in the auditory evoked potential. Normal aging is also associated with a dramatic reduction in slow wave sleep (SWS) and a reduction in the volume of cortical gray matter, particularly in the frontal and prefrontal regions of the brain. As in aging, alcoholism is associated with reductions in both cortical gray matter and SWS. It can, therefore, be hypothesized that alcoholics would show similar evoked potential changes to those seen in aging. To test this hypothesis, we studied seven middle-aged abstinent long-term alcoholics and eight age-matched normal controls. Each subject spent one night in the laboratory. Electroencephalogram (EEG) was recorded from six midline scalp sites and auditory stimuli were presented during stage 2 non-rapid eye movement sleep. N550 amplitude in the K-complex average was lower in the alcoholics as compared with controls as was the likelihood of K-complex production. No differences were noted in either amplitude or latency of the P2 or N350 components, and both groups displayed a prominent LLP potential. The pattern of reduced K-complex production and N550 amplitude in alcoholics as compared with age-matched controls is consistent with an hypothesized association between atrophy of the frontal lobes and reductions in SWS and K-complexes. The finding also suggests that the evoked K-complex may be a relatively simple measure of the effect of alcoholism on EEG during sleep.