We hypothesize that a deficient premotor-motor inhibitory network contributes to the unwanted involuntary movements in dystonia.

We 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 6ms. We used an H-reflex in flexor carpi radialis paired with TMS over the premotor cortex to assess for spinal cord excitability change. Finally, we interrupted a choice reaction time task with TMS over dorsal premotor cortex to assess performance in a non-dystonic task.

Our results showed that WC patients exhibited dPMI at rest (88.5%, the ratio of conditioned to unconditioned test pulse) in contrast to our 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. 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. 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.