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Painful alcoholic polyneuropathy with predominant small-fiber loss and normal thiamine status.
Neurology. 2001 Jun 26; 56(12):1727-32.Neur

Abstract

BACKGROUND

Although polyneuropathy related to chronic alcoholism has been reported frequently, its clinical features and pathogenesis remain to be clarified.

OBJECTIVE

To determine the clinicopathologic features and pathogenesis of alcoholic polyneuropathy associated with pain in patients with normal thiamine status, particularly in comparison to beriberi neuropathy.

PATIENTS AND METHODS

Clinical, electrophysiologic, and histopathologic findings were assessed in 18 patients with painful alcoholic polyneuropathy and normal thiamine status.

RESULTS

Symmetric sensory-dominant polyneuropathy predominantly involving the lower limbs was the major clinical pattern. Painful sensations with or without burning quality represented the initial and major symptom. Progression of symptoms usually was gradual, continuing over months or years. Electrophysiologic and pathologic findings mainly indicated an axonal neuropathy. Densities of small myelinated fibers and unmyelinated fibers were more severely reduced than the density of large myelinated fibers, except in patients with a long history of neuropathic symptoms and marked axonal sprouting.

CONCLUSIONS

The clinicopathologic features of painful symptoms and small axon loss are distinct from those of beriberi neuropathy. Sensory-dominant involvement with prominent neuropathic pain is characteristic of alcoholic neuropathy when thiamine deficiency is not involved, supporting the view of direct neurotoxic effect by alcohol or its metabolites.

Authors+Show Affiliations

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

Pub Type(s)

Journal Article

Language

eng

PubMed ID

11425941

Citation

Koike, H, et al. "Painful Alcoholic Polyneuropathy With Predominant Small-fiber Loss and Normal Thiamine Status." Neurology, vol. 56, no. 12, 2001, pp. 1727-32.
Koike H, Mori K, Misu K, et al. Painful alcoholic polyneuropathy with predominant small-fiber loss and normal thiamine status. Neurology. 2001;56(12):1727-32.
Koike, H., Mori, K., Misu, K., Hattori, N., Ito, H., Hirayama, M., & Sobue, G. (2001). Painful alcoholic polyneuropathy with predominant small-fiber loss and normal thiamine status. Neurology, 56(12), 1727-32.
Koike H, et al. Painful Alcoholic Polyneuropathy With Predominant Small-fiber Loss and Normal Thiamine Status. Neurology. 2001 Jun 26;56(12):1727-32. PubMed PMID: 11425941.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Painful alcoholic polyneuropathy with predominant small-fiber loss and normal thiamine status. AU - Koike,H, AU - Mori,K, AU - Misu,K, AU - Hattori,N, AU - Ito,H, AU - Hirayama,M, AU - Sobue,G, PY - 2001/6/27/pubmed PY - 2001/8/3/medline PY - 2001/6/27/entrez SP - 1727 EP - 32 JF - Neurology JO - Neurology VL - 56 IS - 12 N2 - BACKGROUND: Although polyneuropathy related to chronic alcoholism has been reported frequently, its clinical features and pathogenesis remain to be clarified. OBJECTIVE: To determine the clinicopathologic features and pathogenesis of alcoholic polyneuropathy associated with pain in patients with normal thiamine status, particularly in comparison to beriberi neuropathy. PATIENTS AND METHODS: Clinical, electrophysiologic, and histopathologic findings were assessed in 18 patients with painful alcoholic polyneuropathy and normal thiamine status. RESULTS: Symmetric sensory-dominant polyneuropathy predominantly involving the lower limbs was the major clinical pattern. Painful sensations with or without burning quality represented the initial and major symptom. Progression of symptoms usually was gradual, continuing over months or years. Electrophysiologic and pathologic findings mainly indicated an axonal neuropathy. Densities of small myelinated fibers and unmyelinated fibers were more severely reduced than the density of large myelinated fibers, except in patients with a long history of neuropathic symptoms and marked axonal sprouting. CONCLUSIONS: The clinicopathologic features of painful symptoms and small axon loss are distinct from those of beriberi neuropathy. Sensory-dominant involvement with prominent neuropathic pain is characteristic of alcoholic neuropathy when thiamine deficiency is not involved, supporting the view of direct neurotoxic effect by alcohol or its metabolites. SN - 0028-3878 UR - https://www.unboundmedicine.com/medline/citation/11425941/Painful_alcoholic_polyneuropathy_with_predominant_small_fiber_loss_and_normal_thiamine_status_ L2 - http://www.neurology.org/cgi/pmidlookup?view=long&pmid=11425941 DB - PRIME DP - Unbound Medicine ER -