Quantitative electrophysiological study of alcoholic neuropathy.
Thirty-one chronic alcoholic patients were investigated using quantitative electrophysiological techniques. Estimates of the numbers of functioning motor units in the extensor digitorum brevis muscles and measurements of the parameters of the potentials of these units are presented along with the values for motor nerve conduction velocities in the innervating lateral popliteal nerves. Motor conduction velocities and sensory nerve action potential amplitudes were also measured in the ulnar nerves. The results and their inter-relationships lead us to conclude that the slowing of motor nerve conduction and reduction in sensory nerve action potential amplitudes in alcoholic neuropathy are a consequence of axon loss. We found no evidence of pathological slowing of conduction in surviving axons. Reinnervation by functioning motor axons is poor compared to a number of other neuropathic conditions. In our patients there was no evidence of preferential involvement of sensory axons. The results support a predominant axonal dysfunction in alcoholic neuropathy.
D000200:Action Potentials; D000437:Alcoholism / Q000150:complications / Q000503:physiopathology*; D001369:Axons / Q000502:physiology*; D004594:Electrophysiology; D005071:Evoked Potentials; D006801:Humans; D008875:Middle Aged; D009046:Motor Neurons / Q000502:physiology; D009132:Muscles / Q000294:innervation; D009416:Nerve Regeneration; D009422:Nervous System Diseases / Q000209:etiology / Q000503:physiopathology*; D009431:Neural Conduction; D011930:Reaction Time; D014459:Ulnar Nerve / Q000503:physiopathology