Dysfunction of Ib (Autogenic) spinal inhibition in patients with progressive supranuclear palsy

Authors

  • Dr. Edward J. Fine MD,

    Corresponding author
    1. Neurology Service, Department of Veterans' Affairs Medical Center, and Department of Neurology, State University of New York at Buffalo, New York
    • Neurology Service, VA Medical Center, 3495 Bailey Ave., Buffalo, NY 14215, U.S.A.
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  • Mark Hallett MD,

    1. National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland
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  • Irene Litvan MD,

    1. National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland
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  • Nancy Tresser MD,

    1. National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland
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  • David Katz MD

    1. Department of Pathology and Laboratory Medicine, Hartford Hospital, Hartford, Connecticut, U.S.A.
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Abstract

We compared the activity of Ib spinal interneurons in five patients with progressive supranuclear palsy (PSP) with six age-matched control subjects. Stimulation of the medial gastrocnemius nerve at motor threshold intensity activated Ib afferents that in turn inhibit H reflexes from the soleus muscle. Maximum inhibition occurred at interstimulus intervals of 6 and 8 ms for both control subjects and PSP patients and was significantly greater in the PSP patients. Increased Ib activity of PSP patients may be caused by loss of inhibition of Ib interneurons through degeneration of the medullary reticulospinal pathway. The corticospinal pathways, unopposed by the medullary reticulospinal tract, may excessively activate Ib internurons.

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