The purpose of this study was to determine whether meeting historical criteria for unsuspected Wernicke's encephalopathy (WE), largely under-diagnosed in vivo, explains why some alcoholics have severe neuropsychological deficits, whereas others, with a similar drinking history, exhibit preserved performance. Demographic, clinical, alcohol related, and neuropsychological measures were collected in 56 abstinent alcoholics and 38 non-alcohol-dependent volunteers. Alcoholics were classified using the clinical criteria established by Caine et al (1997) and validated in their neuropathological study of alcoholic cases. Our alcoholics who met a single criterion were considered 'at risk for WE' and those with two or more criteria with 'signs of WE'. Whole blood thiamine was also measured in 22 of the comparison group and 28 alcoholics. Of the alcoholics examined, 27% met no criteria, 57% were at risk for WE, and 16% had signs of WE. Neuropsychological performance of the alcoholic subgroups was graded, with those meeting zero criteria not differing from controls, those meeting one criterion presenting mild-to-moderate deficits on some of the functional domains, and those meeting two or more criteria having the most severe deficits on each of the domains examined. Thiamine levels were selectively related to memory performance in the alcoholics. Preclinical signs of WE can be diagnosed in vivo, enabling the identification of ostensibly 'uncomplicated' alcoholics who are at risk for neuropsychological complications. The graded effects in neuropsychological performance suggest that the presence of signs of WE explains, at least partially, the heterogeneity of alcoholism-related cognitive and motor deficits.
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http://dx.doi.org/10.1038/npp.2010.189 | DOI Listing |
BMJ Case Rep
January 2025
Department of Clinical Neurosciences, University of Cambridge, Cambridge, UK.
We present a case of a male in his early 50s assessed in the emergency department with a seemingly clear alcohol history but with classic symptoms of Wernicke's encephalopathy (WE): disorientation, gait ataxia and vertical nystagmus. He also had significant bilateral hearing loss and profound anterograde amnesia. Neuroimaging revealed hallmark signs of WE, including symmetrical T2/fluid-attenuated inversion recovery hyperintensity in the medial thalami.
View Article and Find Full Text PDFPalliat Support Care
January 2025
Department of Psycho-Oncology, Saitama Medical University International Medical Center, Saitama, Japan.
Objectives: Wernicke encephalopathy (WE) is an acute neuropsychiatric disorder caused by thiamine deficiency. The classical triad of symptoms for WE include mental status changes, ataxia, and ophthalmoplegia. In contrast, more uncommon symptoms include hallucinations.
View Article and Find Full Text PDFJ Clin Med
January 2025
Department of Emergency Medicine, Henry Ford Health, Detroit, MI 48202, USA.
: Wernicke's encephalopathy can occur in oncology patients independent of alcohol use, likely resulting from poor dietary thiamine intake. High metabolic demands, such as those in acute illnesses seen in the emergency department (ED), can exacerbate thiamine deficiency. In this study, our objective was to assess the incidence of thiamine deficiency in ED oncology patients, which could lead to Wernicke's encephalopathy or other thiamine deficiency disorders if left untreated.
View Article and Find Full Text PDFPediatr Neurol
December 2024
University of Alabama, Birmingham, Children's of Alabama, Birmingham, Alabama.
Wernicke encephalopathy is a well-described neurological complication of thiamine deficiency that is classically characterized by a triad of mental confusion, ophthalmoplegia, and gait ataxia. Although most commonly linked to alcoholism and thiamine deficiency in adults, it can present in pediatric patients. Wernicke encephalopathy presenting as dysnatremias is not well described.
View Article and Find Full Text PDFCureus
December 2024
Critical Care Medicine, Springfield Clinic, Springfield, USA.
A 27-year-old male patient with chronic alcohol use disorder was diagnosed with Marchiafava-Bignami disease (MBD) after experiencing an episode of unconsciousness. MRI scans revealed lesions in the corpus callosum and adjacent white matter. Despite prompt initiation of intensive treatment with high-dose thiamine and corticosteroids, the patient only partially recovered, remaining disoriented and exhibiting persistent neurological deficits during follow-up.
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