ABSTRACT We describe the clinicopathologic features of neuropathies associated with thiamine deficiency and chronic alcoholism, considering the effect of alcohol consumption and thiamine deficiency¸ respectively. In thiamine-deficiency neuropathy without alcohol consumption, clinical symptoms were variable but mainly motor-dominant with acute progression and sensory impairment of both superficial and deep sensation. Pathologically, predominant loss of large-fiber axons was characteristic. Major causes of thiamine deficiency were dietary imbalance, chronic alcoholism, and gastrectomy. On the other hand, in alcoholic neuropathy without thiamine deficiency, neuropathic features were sensory-dominant and slowly progressive, with impairment of superficial sensation mainly, and nociception in particular. Pathologic features were characterized predominantly by small fiber axonal loss. Alcoholic neuropathy can be caused by nutritional deficiency, including thiamine deficiency, as well as a result of the direct neurotoxic effects of ethanol and its metabolites. In addition, because alcoholic beverages contain different congeners that may also be bioactive, consuming different kinds of beverages may have different effects on the peripheral nervous system. Thus, regional drinking habits and genetic background also may influence the features of alcoholic neuropathy. The mechanism of the direct neurotoxic effect of ethanol has not yet been clarified. Since alcoholic neuropathy in Asian patients with hypoactive ALDH2 is related to more conspicuous electrophysiologic abnormalities, acetaldehyde may play a role. Axonal transport is impaired by ethanol exposure, which may be related to axonal degeneration. Protein kinases A and C (PKA and PKC) also may play a role in alcoholic neuropathy, especially in association with painful symptoms.
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