Painful alcoholic polyneuropathy with predominant small-fiber loss and normal thiamine status

Background: Although polyneuropathy related to chronic alcoholism has been reported frequently, its clinical features and pathogenesis remain to be cl arified. Objective: To determine the clinicopathologic features and pathoge nesis of alcoholic polyneuropathy associated with pain in patients with nor mal thiamine status, particularly in comparison to beriberi neuropathy. Pat ients and methods: Clinical, electrophysiologic, and histopathologic findin gs were assessed in 18 patients with painful alcoholic polyneuropathy and n ormal thiamine status. Results: Symmetric sensory-dominant polyneuropathy p redominantly involving the lower limbs was the major clinical pattern. Pain ful sensations with or without burning quality represented the initial and major symptom. Progression of symptoms usually was gradual, continuing over months or years. Electrophysiologic and pathologic findings mainly indicat ed an axonal neuropathy. Densities of small myelinated fibers and unmyelina ted fibers were more severely reduced than the density of large myelinated fibers, except in patients with a long history of neuropathic symptoms and marked axonal sprouting. Conclusions: The clinicopathologic features of pai nful symptoms and small axon loss are distinct from those of beriberi neuro pathy. Sensory-dominant involvement with prominent neuropathic pain is char acteristic of alcoholic neuropathy when thiamine deficiency is not involved , supporting the view of direct neurotoxic effect by alcohol or its metabol ites.