Cortical and spinal abnormalities in psychogenic dystonia

AJ Espay, F Morgante, J Purzner… - Annals of Neurology …, 2006 - Wiley Online Library
Annals of Neurology: Official Journal of the American Neurological …, 2006Wiley Online Library
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 …
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
Wiley Online Library
以上显示的是最相近的搜索结果。 查看全部搜索结果