Chronic alcoholism and the peripheral nerves

Fifty cases of chronic alcoholism were investigated clinically and electrophysiologically. Clinically the diagnosis of polyneuropathy (PN) was established in 21 cases and mononeuropathy (MN) in 11. Eighteen cases constituted the subclinical (SC) group. With the electromyography needle applied to 371 sites in the striated muscles of the 50 cases, spontaneous denervation potentials were encountered in 27% of the PN group, 11% of the MN group and 5% of the SC group. Spontaneous denervation potentials recorded in at least 1 muscle were determined in 62% of the PN cases, 63% of the MN cases and 22% of the SC group. Maximum motor conduction velocities were measured in various peripheral nerves. Pathological slowing of conduction was found in 61% of 113 nerves in the PN group, 27% of 67 nerves in the MN group and 28% of 82 nerves of the SC group. Pathologically slow conduction in the motor nerves was encountered in 1 or more nerves in 95% of cases in the PN group, 72% of cases in the MN group and 50% of the others. Sensory action potentials were recorded from the median, ulnar and saphenous nerves. Pathological slowing of sensory conduction and alterations in the sensory action potentials were observed in 85% of 35 nerves of the PN group, 68% of 22 nerves in the MN group and 53% of 32 nerves of the others. These pathological changes in sensory conduction and sensory action potentials, determined at least in 1 nerve, were found in 90% of the PN group, 82% of the MN group and 67% of the others. The progressive increase of these electrophysiological changes is discussed, beginning with subclinical cases and extending to mononeuropathy and polyneuropathy