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Alcohol & Alcoholism Vol. 39, No. 2, pp. 150-153, 2004
Alcohol & Alcoholism Vol. 39, No. 2 © Medical Council on Alcohol 2004; all rights reserved.


CASE REPORT

INCREASED CEREBELLAR PET GLUCOSE METABOLISM CORRESPONDS TO ATAXIA IN WERNICKE–KORSAKOFF SYNDROME

Andreas Fellgiebel1,*, Thomas Siessmeier2, Georg Winterer1, Hartmut Lüddens1, Klaus Mann1, Lutz G Schmidt1 and Peter Bartenstein2

Departments of 1 Psychiatry and 2 Nuclear Medicine, University Hospital of Mainz, Mainz, Germany

* Author to whom correspondence should be addressed at: Department of Psychiatry, University of Mainz, Untere Zahlbacher Strasse 8, D-55131 Mainz, Germany. Tel.: +49 (0) 6131 172525; Fax: +49 (0) 6131 176690; E-mail: fellgiebel{at}psychiatrie.klinik.uni-mainz.de

(Received 25 July 2003; first notified 12 September 2003; in revised form 20 October 2003; accepted 20 October 2003)

Aims: To investigate a possible relationship between cerebellar glucose metabolism and recovery from ataxia in the first months of acute Wernicke–Korsakoff syndrome. Methods: Two cases of alcoholic Wernicke–Korsakoff syndrome were followed up with the clinical status and cerebral glucose metabolism over a 4- and 9-month period. Results: Initially both patients showed severe ataxia and elevated cerebellar glucose metabolism that decreased corresponding to the restitution of stance and gait. Conclusion: Increased cerebellar glucose metabolism at the onset of the illness may reflect the reorganization process of disturbed motor skills and may indicate cerebellar plasticity.


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