Inhibition of levodopa effects by internal pallidal stimulation

Authors

  • Paul Krack MD,

    Corresponding author
    1. 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, Germany
    Search for more papers by this author
  • Pierre Pollak MD,

    1. Department of Clinical and Biological Neurosciences and INSERM U318, Joseph Fourier University of Grenoble, France
    Search for more papers by this author
  • Patricia Limousin MD,

    1. Department of Clinical and Biological Neurosciences and INSERM U318, Joseph Fourier University of Grenoble, France
    Search for more papers by this author
  • Dominique Hoffmann MD,

    1. Department of Clinical and Biological Neurosciences and INSERM U318, Joseph Fourier University of Grenoble, France
    Search for more papers by this author
  • Abdelhamid Benazzouz PhD,

    1. Department of Clinical and Biological Neurosciences and INSERM U318, Joseph Fourier University of Grenoble, France
    Search for more papers by this author
  • Alim-Louis Benabid MD, PhD

    1. Department of Clinical and Biological Neurosciences and INSERM U318, Joseph Fourier University of Grenoble, France
    Search for more papers by this author

  • 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.

Ancillary