{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,19]],"date-time":"2026-10-19T23:22:58Z","timestamp":1792452178633,"version":"4.5.0"},"reference-count":54,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2006,4,21]],"date-time":"2006-04-21T00:00:00Z","timestamp":1145577600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Annals of Neurology"],"published-print":{"date-parts":[[2006,5]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Objective<\/jats:title><jats:p>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.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>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\u2010matched healthy control subjects.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Three measures of cortical inhibition, resting short\u2010 and long\u2010interval 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.<\/jats:p><\/jats:sec><jats:sec><jats:title>Interpretation<\/jats:title><jats:p>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. 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