alexa Thirty Days without a Bite: Wernicke’s Encep
ISSN: 2329-6895

Journal of Neurological Disorders
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Case Report

Thirty Days without a Bite: Wernicke’s Encephalopathy in a Patient with Paranoid Schizophrenia

Mélanie Langlois1, Marie-Claire Doré1 and Robert Laforce Jr1,2,3*
1Department of Neurological Sciences, University Hospital of Quebec, Canada
2Faculté of Medicine, Laval University, Quebec, Canada
3Clinique Interdisciplinary Memory (CIME), University Hospital of Quebec, Canada
Corresponding Author : Robert Jr Laforce
Department of Neurological Sciences
University Hospital of Quebec-Hôpital de l'Enfant-Jésus
1401 18th Street, Quebec, G1J 1Z4, Canada
Tel: (418) 649-5980
Fax: (418) 649-5981
E-mail: [email protected]
Received June 16, 2014; Accepted September 23, 2014; Published September 25, 2014
Citation: Langlois M, Doré MC, Laforce Jr R (2014) Thirty Days without a Bite: Wernicke’s Encephalopathy in a Patient with Paranoid Schizophrenia. J Neurol Disord 2:182. doi: 10.4172/2329-6895.1000182
Copyright: © 2014 Langlois M, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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Wernicke’s Encephalopathy (WE) is a preventable neurologic condition characterized by altered mental status, ophthalmoplegia, and ataxia. Although historically associated with alcoholism, a few authors have described WE in patients with non-alcohol related psychiatric disorders. We report herein the case of a 36-year-old young man with paranoid schizophrenia who was brought to hospital for confusion and difficulties with his vision. His roommate said he had gone about thirty days without eating ‘…because he was on a slimming cure’. History and physical examination suggested WE as a result of isolation and poor diet leading to nutritional deficiency. This was confirmed by brain magnetic resonance imaging showing classic thalamic, mammillary bodies and brainstem lesions. Of note, his cognitive profile was far more heterogeneous than what had classically been described in the literature and involved both cortical and subcortical pathology, generating memory but also significant executive deficits. Intravenous treatment with thiamine was given and our patient showed mild improvements in visual acuity and nystagmus. However, persistent cognitive and physical disabilities consistent with Korsakoff syndrome remained, and he now lives in a supervised home. This case illustrates the tragic consequences of nutritional deficiencies in a patient with paranoid schizophrenia. The threshold to suspect WE in schizophrenic patients should be lowered and in doubt prophylactic parenteral thiamine should be administered.

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