Somatosensory and brainstem auditory evoked potentials in alcoholic liver disease with and without encephalopathy.

Median somatosensory and brainstem auditory evoked potentials (SEP and BAEP) were studied in chronic alcoholics with and without complications of alcoholic liver disease. The alcoholics were divided into 4 groups: Group 1 with minimally abnormal liver function tests; Group 2 with hepatic failure; Group 3 with mild to moderate hepatic encephalopathy; and Group 4 with severe encephalopathy. A control group consisted of age-matched normal subjects. In the alcoholic groups, BAEPs showed a significant prolongation in the latencies of peaks III to VI and interpeaks I-III, III-V, and I-V. The peak latency prolongation was associated with a reduction in all peak amplitudes. In median SEPs, the cervical N13 and cortical N20 latencies were significantly delayed in the alcoholic groups. The amplitude of all cortical SEP components within 150 msec analysis time was also significantly reduced. In addition, the alcoholic groups had slowing in median nerve conduction and prolongation in central conduction time (N13 to N20 interpeak latency). In both BAEPs and SEPs, there were no differences in the peak amplitude and the peak latency among the alcoholic groups except for the late cortical SEP components which showed progressive prolongation and eventual absence from Groups 2 to 4. The present data indicate that chronic alcoholics have subclinical dysfunction in the central somatosensory and brainstem auditory pathways irrespective of the complications of alcoholic liver disease. However, the late components of the cortical SEPs can be affected in hepatic failure and hepatic encephalopathy.