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Alcohol and Alcoholism Advance Access originally published online on October 23, 2007
Alcohol and Alcoholism 2008 43(2):180-186; doi:10.1093/alcalc/agm149
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Copyright © The Author 2007. Published by Oxford University Press on behalf of the Medical Council on Alcohol.

Wernicke's encephalopathy: ‘plus ca change, plus c'est la meme chose’

Allan D. Thomson1,4, Christopher C. H. Cook2, Irene Guerrini1, Donna Sheedy3, Clive Harper3 and E. Jane Marshall4,*

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 W1 T 4JF, UK
2 County Durham & Darlington Priority Services NHS Trust, Durham DH1 3RS, UK
3 Department of Pathology (D06), University of Sydney, NSW 2006, Australia
4 National Addiction Centre, Institute of Psychiatry, King's College, London, De Crespigny Park, London SE5 8AF, UK

* Author to whom correspondence should be addressed at: National Addiction Centre, Institute of Psychiatry, King's College, London, De Crespigny Park, London SE5 8AF, UK. Tel: 0044 (0) 203 228 2345; Fax: 0044 (0) 203 228 2349; E-mail: jane.marshall{at}slam.nhs.uk

Received 27 April 2007; first review notified 23 July 2007; in revised form 7 September 2007; accepted 11 September 2007


   Abstract

Aims: To develop clinical guidelines to identify individuals who misuse alcohol and are at risk of developing Wernicke's Encephalopathy (WE). Method: Non-systematic literature review of studies which includes a careful clinical record of the development of signs and symptoms of thiamine deficiency and in which the diagnosis of WE has been confirmed at autopsy. Results: The review of the clinical findings in cases of WE, diagnosed at autopsy, shows a consistent pattern of signs and symptoms. The pattern appears to be similar regardless of whether the thiamine deficiency is related to nutritional problems alone or associated with alcohol misuse. Conclusions: The assessment of the degree of thiamine deficiency and the diagnosis of WE remain a clinical evaluation, and guidelines are suggested to help the clinician. Since neurotoxicity due to the metabolism of excessive alcohol in patients with chronic and severe alcohol dependence may be an important factor in determining long-term outcome of treatment, this must form part of the overall evaluation.


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