Cortical and spinal abnormalities in psychogenic dystonia
Article first published online: 21 APR 2006
Copyright © 2006 American Neurological Association
Annals of Neurology
Volume 59, Issue 5, pages 825–834, May 2006
How to Cite
Espay, A. J., Morgante, F., Purzner, J., Gunraj, C. A., Lang, A. E. and Chen, R. (2006), Cortical and spinal abnormalities in psychogenic dystonia. Ann Neurol., 59: 825–834. doi: 10.1002/ana.20837
- Issue published online: 21 APR 2006
- Article first published online: 21 APR 2006
- Manuscript Accepted: 17 FEB 2006
- Manuscript Revised: 28 JAN 2006
- Manuscript Received: 29 SEP 2005
- Dystonia Medical Research Foundation through the Sam and Fran Belzberg and Dennis and Barbara Kessler Research Fellowship
- Canadian Institutes of Health Research. Grant Numbers: MOP 15128, MOP62917
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.
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.
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.
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