Volume 13, Issue 4 p. 648-652
Article

Inhibition of levodopa effects by internal pallidal stimulation

Paul Krack MD

Corresponding Author

Paul Krack MD

Department of Clinical and Biological Neurosciences and INSERM U318, Joseph Fourier University of Grenoble, France

Neurologische Klinik der Christian Albrechts Universität zu Kiel, Niemannsweg 147, 24105 Kiel, GermanySearch for more papers by this author
Pierre Pollak MD

Pierre Pollak MD

Department of Clinical and Biological Neurosciences and INSERM U318, Joseph Fourier University of Grenoble, France

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Patricia Limousin MD

Patricia Limousin MD

Department of Clinical and Biological Neurosciences and INSERM U318, Joseph Fourier University of Grenoble, France

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Dominique Hoffmann MD

Dominique Hoffmann MD

Department of Clinical and Biological Neurosciences and INSERM U318, Joseph Fourier University of Grenoble, France

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Abdelhamid Benazzouz PhD

Abdelhamid Benazzouz PhD

Department of Clinical and Biological Neurosciences and INSERM U318, Joseph Fourier University of Grenoble, France

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Alim-Louis Benabid MD, PhD

Alim-Louis Benabid MD, PhD

Department of Clinical and Biological Neurosciences and INSERM U318, Joseph Fourier University of Grenoble, France

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First published: 04 November 2004
Citations: 33

A videotape accompanies this article.

Abstract

We report three patients with bilateral GPi stimulation for stage 4 Parkinson's disease (PD) with severe levodopa-induced dyskinesias (LID). In all three it was possible to completely inhibit LID using high-stimulation parameters. Parallel to complete inhibition of LID, an inhibition of the anti-akinetic effect of levodopa was observed, whereas, at the same time, rigidity was markedly improved. GPi stimulation is adaptable over time, and stimulation parameters have to be programmed according to off-and on-period motor symptoms. The main interest of stimulation is the possibility of finding a compromise between LID alleviation in on-phase without loss of the beneficial motor effects and improvement in parkinsonism in off-phase. In some patients, residual dyskinesias have to be accepted so as not to aggravate on-period motor symptoms by a presumed overinhibition of basal ganglia outflow.