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Cortical and spinal abnormalities in psychogenic dystonia
Author(s) -
Espay Alberto J.,
Morgante Francesca,
Purzner Jamie,
Gunraj Carolyn A.,
Lang Anthony E.,
Chen Robert
Publication year - 2006
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/ana.20837
Subject(s) - dystonia , psychogenic disease , neuroscience , cervical dystonia , focal dystonia , psychology , medicine , neurological disorder , silent period , central nervous system disease , transcranial magnetic stimulation , psychiatry , stimulation
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