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Alcoholic neuropathy is clinicopathologically distinct from thiamine-deficiency neuropathy.
Ann Neurol. 2003 Jul; 54(1):19-29.AN

Abstract

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.

Authors+Show Affiliations

Department of Neurology, Nagoya University, Graduate School of Medicine, Nagoya, Japan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

12838517

Citation

Koike, Haruki, et al. "Alcoholic Neuropathy Is Clinicopathologically Distinct From Thiamine-deficiency Neuropathy." Annals of Neurology, vol. 54, no. 1, 2003, pp. 19-29.
Koike H, Iijima M, Sugiura M, et al. Alcoholic neuropathy is clinicopathologically distinct from thiamine-deficiency neuropathy. Ann Neurol. 2003;54(1):19-29.
Koike, H., Iijima, M., Sugiura, M., Mori, K., Hattori, N., Ito, H., Hirayama, M., & Sobue, G. (2003). Alcoholic neuropathy is clinicopathologically distinct from thiamine-deficiency neuropathy. Annals of Neurology, 54(1), 19-29.
Koike H, et al. Alcoholic Neuropathy Is Clinicopathologically Distinct From Thiamine-deficiency Neuropathy. Ann Neurol. 2003;54(1):19-29. PubMed PMID: 12838517.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Alcoholic neuropathy is clinicopathologically distinct from thiamine-deficiency neuropathy. AU - Koike,Haruki, AU - Iijima,Masahiro, AU - Sugiura,Makoto, AU - Mori,Keiko, AU - Hattori,Naoki, AU - Ito,Hiroki, AU - Hirayama,Masaaki, AU - Sobue,Gen, PY - 2003/7/3/pubmed PY - 2003/8/21/medline PY - 2003/7/3/entrez SP - 19 EP - 29 JF - Annals of neurology JO - Ann. Neurol. VL - 54 IS - 1 N2 - 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. SN - 0364-5134 UR - https://www.unboundmedicine.com/medline/citation/12838517/Alcoholic_neuropathy_is_clinicopathologically_distinct_from_thiamine_deficiency_neuropathy_ L2 - https://doi.org/10.1002/ana.10550 DB - PRIME DP - Unbound Medicine ER -