The concept of alcoholic neuropathy has been obscured because of an often undetected or overestimated influence of thiamine deficiency. We describe clinicopathologic features of alcoholic neuropathy, taking the effect of thiamine status into consideration, and recent progress associated with the pathogenesis.
Clinical features of alcoholic neuropathy without thiamine deficiency are characterized by slowly progressive, sensory-dominant symptoms. Superficial sensation is predominantly impaired and painful symptoms are the major complaint. Pathologic features are characterized by small-fiber-predominant axonal loss. In contrast, the clinicopathologic features of alcoholic neuropathy with concomitant thiamine deficiency are variable, constituting a spectrum ranging from a picture of a pure form of alcoholic neuropathy to a presentation of nonalcoholic thiamine-deficiency neuropathy. One possible mediator of the direct neurotoxic effects among the metabolites of ethanol is acetaldehyde. Axonal transport and cytoskeletal properties are impaired by ethanol exposure. Protein kinase A and protein kinase C may also play a role in the pathogenesis, especially in association with painful symptoms.
Nutritional deficiency as well as the direct neurotoxic effects of ethanol or its metabolites can cause alcoholic neuropathy. Although clinicopathologic features of the pure form of alcoholic neuropathy are uniform, they show extensive variation when thiamine deficiency is present.