Characteristics of
alcoholic neuropathy have been obscured by difficulty in isolating them from features of
thiamine-deficiency neuropathy. We assessed 64 patients with
alcoholic neuropathy including subgroups without (ALN) and with (ALN-TD) coexisting
thiamine deficiency. Thirty-two patients with nonalcoholic
thiamine-deficiency neuropathy (TDN) also were investigated for comparison. In ALN, clinical symptoms were sensory-dominant and slowly progressive, predominantly impairing superficial sensation (especially nociception) with
pain or painful burning sensation. In TDN, most cases manifested a motor-dominant and acutely progressive pattern, with impairment of both superficial and deep sensation. Small-fiber-predominant axonal loss in sural nerve specimens was characteristic of ALN, especially with a short history of neuropathy; long history was associated with regenerating small fibers. Large-fiber-predominant axonal loss predominated in TDN. Subperineurial
edema was more prominent in TDN, whereas segmental de/remyelination resulting from widening of consecutive nodes of Ranvier was more frequent in ALN. Myelin irregularity was greater in ALN. ALN-TD showed a variable mixture of these features in ALN and TDN. We concluded that pure-form of
alcoholic neuropathy (ALN) was distinct from pure-form of
thiamine-deficiency neuropathy (TDN), supporting the view that
alcoholic neuropathy can be caused by direct toxic effect of
ethanol or its metabolites. However, features of
alcoholic neuropathy is influenced by concomitant
thiamine-deficiency state, having so far caused the obscure clinicopathological entity of
alcoholic neuropathy.