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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Persistence of disturbed thalamic glucose metabolism in a case of Wernicke-Korsakoff syndrome.

We report the case of a 40-year-old alcoholic male patient, hospitalized with an acute ataxia of stance and gait, ocular muscle weakness with nystagmus and a global apathetic-confusional state. After admission, an amnestic syndrome with confabulation was also observed and diagnosis of Wernicke-Korsakoff syndrome was made. Under treatment with intravenous thiamine, the patient recovered completely from gaze weakness and ataxia, whereas a severe amnestic syndrome persisted. Fluorodeoxyglucose (FDG) positron emission tomography (PET) showed bilateral thalamic and severe bilateral temporal-parietal hypometabolism resembling a pattern typical for Alzheimer's disease. Longitudinal assessment of the alcohol-abstinent and thiamine-substituted patient revealed improvements of clinical state and neuropsychological performance that were paralleled by recovered cerebral glucose metabolism. In contrast to metabolic rates that increased between 7.1% (anterior cingulate, left) and 23.5% (parietal, left) in cortical areas during a 9-month remission period, thalamic glucose metabolism remained severely disturbed over time (change: left +0.2%, right +0.3%).[1]


  1. Persistence of disturbed thalamic glucose metabolism in a case of Wernicke-Korsakoff syndrome. Fellgiebel, A., Scheurich, A., Siessmeier, T., Schmidt, L.G., Bartenstein, P. Psychiatry research. (2003) [Pubmed]
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