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Alcoholic Dementia

Published online by Cambridge University Press:  18 September 2015

Maurice Victor
Maurice Victor*
Affiliation:
Department of Medicine (Neurology), Dartmouth Medical School, Hanover, New Hampshire, and the Veterans Affairs Medical Center, White River Junction, Vermont
*
VA Medical Center, White River Junction, VT U.S.A. 05009
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Abstract:

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At least four distinct cerebral diseases — Wernicke-Korsakoff, Marchiafava-Bignami, pellagrous encephalopathy, and acquired hepatocerebral degeneration — have a close association with chronic alcoholism. Each is characterized by a distinctive pathologic change and a reasonably wellestablished pathogenesis; in each the role of alcohol in the causation is secondary. The question posed in this review is whether there is, in addition to the established types of dementia associated with alcoholism, a persistent dementia attributable to the direct toxic effects of alcohol on the brain — i.e., a primary alcoholic dementia. The clinical, psychologic, radiologic, and pathologic evidence bearing on this question is critically reviewed. None of the evidence permits the clear delineation of such an entity. The most serious flaw in the argument for a primary alcoholic dementia is that it lacks a distinctive, well-defined pathology, and it must remain ambiguous until such time as its morphologic basis is established.

Résumé:

RÉSUMÉ:

Au moins quatre maladies cérébrales distinctes — le Wernicke-Korsakoff, le Marchiafava-Bignami, l'encéphalopathie de la pellagre, la dégénérescence hépatocérébrale acquise — ont une association étroite avec l'alcoolisme chronique. Chacune est caractérisée par des changements anatomopathologiques distincts et une pathogenèse bien établie. Le rôle de l'acool est secondaire dans chacune. Dans cette revue, nous posons la question suivante: en plus des types de démence reconnus comme étant associés à l'alcoolisme, y a-t-il une démence persistante attribuable aux effects toxiques directs de l'alcool sur le cerveau, i.e., une démence alcoolique primaire? Nous revoyons de façon critique les données cliniques, psychologiques, radiologiques et anatomopathologiques reliées à cette question. Aucune observation ne permet de définir clairement une telle entité. La lacune la plus sérieuse vient du fait qu'il n'existe pas de lésion anatomopathologique distinctive. La situation demeurera ambiguë tant que ses assises morphologiques ne seront pas établies.

Type
Articles
Information
Canadian Journal of Neurological Sciences , Volume 21 , Issue 2 , May 1994 , pp. 88 - 99
Copyright
Copyright © Canadian Neurological Sciences Federation 1994

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