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 Volume 59, Number 10, November 26, 2002
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Neurology 2002;59:1625-1627
© 2002 American Academy of Neurology
Brief Communications

SCA-2 presenting as parkinsonism in an Alberta family

Clinical, genetic, and PET findings

S. Furtado, MD PhD, FRCPC, M. Farrer, PhD, Y. Tsuboi, MD PhD, M. L. Klimek, RN MA, R. de la Fuente-Fernández, MD, J. Hussey, BSc, P. Lockhart, PhD, D. B. Calne, DM FRCPC, O. Suchowersky, MD FRCPC, A. J. Stoessl, MD FRCPC and Z. K. Wszolek, MD

From the Movement Disorder Clinic (Drs. Furtado, Suchowersky, and M. Klimek), Department of Clinical Neurosciences, University of Calgary, Alberta, Canada; Mayo Clinic Jacksonville (Drs. Farrer, Tsuboi, Lockhart, Wszolek, and J. Hussey), FL; and Pacific Parkinson’s Research Centre (Drs. de la Fuente-Fernández, Calne, and Stoessl), University of British Columbia, Vancouver, Canada.

Address correspondence and reprint requests to Dr. Z.K. Wszolek, Mayo Clinic Jacksonville, 4500 San Pablo Road, Jacksonville, FL 32224; e-mail: Wszolek.Zbigniew{at}mayo.edu

The authors describe an Alberta family with levodopa-responsive parkinsonism without cerebellar abnormalities. Genetic testing showed expanded repeats for SCA-2; other mutations for parkinsonism were excluded. The expanded allele shows interruption of the CAG repeat with CAA. PET in two affected members showed reduced fluorodopa uptake in striatum and normal raclopride binding. Families with autosomal dominant, levodopa-responsive parkinsonism should be tested for the SCA-2 mutation.




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