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Alcohol and Alcoholism Advance Access published online on December 29, 2005
Alcohol and Alcoholism, doi:10.1093/alcalc/agh249
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© The Author 2005. Published by Oxford University Press on behalf of the Medical Council on Alcohol. All rights reserved
Received December 21, 2004
Revised November 1, 2005
Accepted November 2, 2005

Article

THE NATURAL HISTORY AND PATHOPHYSIOLOGY OF WERNICKE'S ENCEPHALOPATHY AND KORSAKOFF'S PSYCHOSIS

ALLAN D. THOMSON 1 and E. JANE MARSHALL 2 *

1 Molecular Psychiatry Laboratory, Windeyer Institute of Medical Science, Department of Mental Health Sciences, Royal Free and University College London Medical School, 46 Cleveland Street, London WIT 4JF; Kent Institute of Medicine and Health Science, University of Kent at Canterbury
2 National Addiction Centre, Box 048, Institute of Psychiatry, Kings College London, De Crespigny Park, London SE58AF, UK

* To whom correspondence should be addressed.
E. JANE MARSHALL, E-mail: jane.marshall{at}iop.kcl.ac.uk


  Abstract

Aims: To identify the early clinical indications of thiamine deficiency and to understand the factors involved in the development of the amnesic state in alcohol-dependent individuals with thiamine deficiency. It is hoped that this will highlight the need for clinicians to treat alcohol-dependent patients prophylactically with parenteral thiamine and thus prevent the development of Korsakoff's Psychosis (KP). Method: We have reviewed the natural history and pathophysiology of Wernicke's Encephalopathy (WE) in both human and animal studies together with any contributory factors that may predispose the individual to thiamine deficiency. A further understanding of these problems is provided by recent studies into the metabolic consequences of thiamine deficiency and alcohol misuse. Conclusions: Where WE is due to thiamine deficiency alone (i.e. in the absence of alcohol misuse) KP rarely supervenes following thiamine replacement therapy. Successful treatment or prophylaxis of WE in alcohol dependence probably depends on a number of inter-related issues and is not simply a matter of early and adequate thiamine treatment. If sufficient alcohol-related neurotoxicity has occurred by the time of diagnosis, then this may be the more important or limiting factor with respect to the long-term outcome. This possible obstacle to complete recovery should not prevent every attempt being made to provide the patient with optimum brain thiamine replacement.


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