Suppression of motor cortical excitability by electrical stimulation over the cerebellum in ataxia

Authors

  • Dr. Yoshikazu Ugawa MD,

    Corresponding author
    1. Department of Neurology, Institute for Brain Research, School of Medicine, University of Tokyo, Tokyo, Japan
    • Department of Neurology, Institute for Brain Research, School of Medicine, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113, Japan
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  • Kieko Genba-Shimizu,

    1. Department of Neurology, Institute for Brain Research, School of Medicine, University of Tokyo, Tokyo, Japan
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  • John C. Rothwell PhD,

    1. RMRC Human Movement and Balance Unit, Institute of Neurology, Queen Square, London, U.K.
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  • Makoto Iwata MD,

    1. Department of Neurology, Institute for Brain Research, School of Medicine, University of Tokyo, Tokyo, Japan
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  • Ichiro Kanazawa MD

    1. Department of Neurology, Institute for Brain Research, School of Medicine, University of Tokyo, Tokyo, Japan
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Abstract

We studied the effect of electrical stimulation over the cerebellum on electromyographic responses evoked by magnetic stimulation over the cerebral motor cortex in 14 normal volunteers and 32 patients with ataxia due to various disorders. In all the normal subjects, stimulation over the cerebellum significantly reduced the size of electromyographic response in the first dorsal interosseous muscle evoked by magnetic cortical stimulation, when the cerebellar stimulus preceded the cortical stimulus by 5, 6, and 7 msec. This suppression was absent or reduced in ataxic patients who had atrophy of the cerebellar hemispheres as demonstrated by magnetic resonance imaging and in patients with dysfunction of the cerebellothalamocortical pathway who had lesions in the superior cerebellar peduncle or in the motor thalamus. In contrast, suppression was normal in ataxic patients who had pontine lesions that affected the pontocerebellar afferent pathway to the cerebellum. Results were also normal in patients without cerebellar ataxia, such as those with Parkinson's disease, sensory ataxia, and cerebrovascular disease without ataxia. We conclude that electrical stimulation activates cerebellar structures that suppress motor cortical excitability through a cerebellothalamocortical pathway and that the afferent systems to the cerebellum make no or little contribution to the effect. The technique described here would be useful for distinguishing ataxia due to lesions of cerebellar afferent pathway from other types of cerebellar ataxia.

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