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Neurology 2000;54:2182-2184
© 2000 American Academy of Neurology


Brief Communications

Ineffective subthalamic nucleus stimulation in levodopa-resistant postischemic parkinsonism

P. Krack, MD, P. Limousin Dowsey, MD, PhD, A. L. Benabid, MD, PhD, N. Acarin, MD, A. Benazzouz, PhD, G. Künig, MD, K. L. Leenders, MD, J. A. Obeso, MD and P. Pollak, MD

From the Department of Clinical and Biological Neurosciences (Drs. Krack, Limousin Dowsey, Benabid, Benazzouz, and Pollak), Joseph Fourier University, Grenoble, France; the Neurology Department (Dr. Krack), Christian Albrechts Universität Kiel, Germany; MRC Human Movement and Balance Unit (Dr. Limousin Dowsey), Queen Square, London, England; Paul Scherrer Institut Villigen (Drs. Künig and Leenders), Switzerland; Neurology Department (Dr. Leenders), University of Groningen, the Netherlands; Neurology Service (Dr. Acarin), Hospital Valle de Hebron, Barcelona; and the Division of Neuroscience (Dr. Obeso), Clinica Universitaria and Medical School, University of Navarra, Pamplona, Spain.

Address correspondence and reprint requests to Dr. Paul Krack, Neurology Department, University of Kiel, Niemannsweg 147, 24105 Kiel, Germany; e-mail: p.krack{at}neurologie.uni-kiel.de

The authors report a patient with postischemic parkinsonism who responded neither to levodopa nor to bilateral subthalamic nucleus (STN) stimulation. MRI revealed bilateral lesions of the substantia nigra, the striatum, the external pallidum, and part of the internal pallidum. PET showed reduced striatal dopa-decarboxylase activity, D2 receptor binding, and glucose metabolism. Perioperative microrecording showed low-frequency activity of STN cells. This case suggests that parkinsonian patients who do not have a good response to levodopa or in whom a postsynaptic dopaminergic lesion can be shown may not be good candidates for STN surgery.

Key words: Subthalamic nucleus—Deep brain stimulation—Postischemic parkinsonism.




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