Abstract

Using a range of electrophysiological techniques, it has been possible to demonstrate impaired function in smaller calibre motor fibres and in distal large cutaneous sensory nerve fibres in both alcoholic patients without neuropathy and in those alcoholics with clinical manifestations of peripheral nerve disease. Evidence of more proximal involvement of Ia sensory fibres was obtained, but in the majority of our patients, large motor fibres functioned normally. The nature of the underlying pathological process is discussed.