{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,13]],"date-time":"2026-10-13T13:41:42Z","timestamp":1791898902177,"version":"4.3.4"},"reference-count":49,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2003,5,14]],"date-time":"2003-05-14T00:00:00Z","timestamp":1052870400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Annals of Neurology"],"published-print":{"date-parts":[[2003,7]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Characteristics of alcoholic neuropathy have been obscured by difficulty in isolating them from features of thiamine\u2010deficiency neuropathy. We assessed 64 patients with alcoholic neuropathy including subgroups without (ALN) and with (ALN\u2010TD) coexisting thiamine deficiency. Thirty\u2010two patients with nonalcoholic thiamine\u2010deficiency neuropathy (TDN) also were investigated for comparison. In ALN, clinical symptoms were sensory\u2010dominant and slowly progressive, predominantly impairing superficial sensation (especially nociception) with pain or painful burning sensation. In TDN, most cases manifested a motor\u2010dominant and acutely progressive pattern, with impairment of both superficial and deep sensation. Small\u2010fiber\u2010predominant 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\u2010fiber\u2010predominant 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\u2010TD showed a variable mixture of these features in ALN and TDN. We concluded that pure\u2010form of alcoholic neuropathy (ALN) was distinct from pure\u2010form of thiamine\u2010deficiency 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\u2010deficiency state, having so far caused the obscure clinicopathological entity of alcoholic neuropathy. Ann Neurol 2003<\/jats:p>","DOI":"10.1002\/ana.10550","type":"journal-article","created":{"date-parts":[[2003,6,27]],"date-time":"2003-06-27T10:01:20Z","timestamp":1056708080000},"page":"19-29","source":"Crossref","is-referenced-by-count":208,"title":["Alcoholic neuropathy is clinicopathologically distinct from thiamine\u2010deficiency 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