Funding agencies: This study was supported (in part or in full) by the National Center for Research Resources and the National Center for Advancing Translational Sciences of the National Institutes of Health through Grant Number KL2 TR000089 and Grant Number UL1 TR000041. The project was also supported through NIH/NINDS Intramural Funds. The content is solely the responsibility of the authors and does not necessarily represent the official views of the NIH.
Abnormal dorsal premotor–motor inhibition in writer's cramp
Version of Record online: 7 APR 2014
© 2014 International Parkinson and Movement Disorder Society
Volume 29, Issue 6, pages 797–803, May 2014
How to Cite
Pirio Richardson, S., Beck, S., Bliem, B. and Hallett, M. (2014), Abnormal dorsal premotor–motor inhibition in writer's cramp. Mov. Disord., 29: 797–803. doi: 10.1002/mds.25878
Relevant conflicts of interest/financial disclosures: Nothing to report.
Full financial disclosures and author roles may be found in the online version of this article.
- Issue online: 6 MAY 2014
- Version of Record online: 7 APR 2014
- Manuscript Accepted: 13 FEB 2014
- Manuscript Revised: 13 JAN 2014
- Manuscript Received: 2 OCT 2013
- motor cortex
The authors hypothesized that a deficient premotor–motor inhibitory network contributes to the unwanted involuntary movements in dystonia. The authors studied nine controls and nine patients with writer's cramp (WC). Dorsal premotor–motor cortical inhibition (dPMI) was tested by applying conditioning transcranial magnetic stimulation (TMS) to the dorsal premotor cortex and then a test pulse to the ipsilateral motor cortex at an interval of 6 ms. The authors used an H-reflex in flexor carpi radialis paired with TMS over the premotor cortex to assess for spinal cord excitability change. Finally, the authors interrupted a choice reaction time task with TMS over dorsal premotor cortex to assess performance in a nondystonic task. The results showed that WC patients exhibited dPMI at rest (88.5%, the ratio of conditioned to unconditioned test pulse), in contrast to controls, who did not show dPMI (109.6%) (P = 0.0198). This difference between patients and controls persisted during contraction (100% vs. 112%) and pen-holding (95.6% vs. 111%). The H-reflex in the arm was not modulated by the premotor cortex stimulation. The WC patients made more errors, and the error rate improved with TMS over the premotor cortex. These results suggest that abnormal premotor–motor interactions may play a role in the pathophysiology of focal dystonia. The dPMI was not modulated by task in either group, but was constantly greater in the patients. The significance of the increased inhibition is likely to be compensatory. It appears to be a robust finding and, in combination with other features, could be further explored as a biomarker. © 2014 International Parkinson and Movement Disorder Society