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Cortical and spinal abnormalities in psychogenic dystonia

Authors

  • Alberto J. Espay MD,

    1. Toronto Western Research Institute, University of Toronto, Toronto, Ontario, Canada
    2. Department of Medicine, Division of Neurology, University of Toronto, Toronto, Ontario, Canada
    3. The Neuroscience Institute, Department of Neurology, Movement Disorders Center, University of Cincinnati, Cincinnati, OH
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  • Francesca Morgante MD,

    1. Toronto Western Research Institute, University of Toronto, Toronto, Ontario, Canada
    2. Department of Medicine, Division of Neurology, University of Toronto, Toronto, Ontario, Canada
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  • Jamie Purzner HBSc,

    1. Toronto Western Research Institute, University of Toronto, Toronto, Ontario, Canada
    2. Department of Medicine, Division of Neurology, University of Toronto, Toronto, Ontario, Canada
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  • Carolyn A. Gunraj MHSc,

    1. Toronto Western Research Institute, University of Toronto, Toronto, Ontario, Canada
    2. Department of Medicine, Division of Neurology, University of Toronto, Toronto, Ontario, Canada
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  • Anthony E. Lang MD, FRCPC,

    1. Toronto Western Research Institute, University of Toronto, Toronto, Ontario, Canada
    2. Department of Medicine, Division of Neurology, University of Toronto, Toronto, Ontario, Canada
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  • Robert Chen MBBChir, MSc, FRCPC

    Corresponding author
    1. Toronto Western Research Institute, University of Toronto, Toronto, Ontario, Canada
    2. Department of Medicine, Division of Neurology, University of Toronto, Toronto, Ontario, Canada
    • 7MC-411, Toronto Western Hospital, 399 Bathurst Street, Toronto, Ontario M5T 2S8, Canada
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Abstract

Objective

The pathophysiology of psychogenic dystonia has not been examined, but a growing body of literature suggests that abnormal sensory input from repetitive movements can lead to plastic cortical changes. Reduced cortical and spinal inhibition is well documented in organic dystonia. We tested the hypothesis that aberrant sensory input associated with abnormal posture may cause similar abnormalities by testing patients with psychogenic dystonia.

Methods

We assessed cortical and spinal inhibitory circuits and cortical activity associated with voluntary movement in 10 patients with clinically definite psychogenic dystonia, 8 patients with organic dystonia, and 12 age-matched healthy control subjects.

Results

Three measures of cortical inhibition, resting short- and long-interval intracortical inhibition and cortical silent period, were reduced in both psychogenic dystonia and organic dystonia. Cutaneous silent period mediated by spinal circuitries was increased in psychogenic and organic dystonia. Forearm spinal reciprocal inhibition was reduced in psychogenic dystonia.

Interpretation

Psychogenic and organic dystonia share similar physiological abnormalities. Previous findings of abnormal cortical and spinal excitability in organic dystonia may, in part, be a consequence rather than a cause of dystonia. Alternatively, these findings may represent endophenotypic abnormalities that predispose to both types of dystonia. Ann Neurol 2006;59:825–834

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