"Tapping" into neural inhibition in focal hand dystonia: an evaluation of a finger-tapping task using TMS and fMRI.

BACKGROUND

Focal hand dystonia (FHD) is a task-specific movement disorder characterized by involuntary muscle contractions during skilled hand use. Impaired intracortical inhibition is a core feature of FHD, yet its relationship to functional brain activity during motor tasks remains poorly understood. This study combined transcranial magnetic stimulation (TMS) and functional MRI (fMRI) to investigate the relationship between intracortical inhibition, as measured by the cortical silent period (cSP), and task-based brain activation in individuals with FHD.

METHODS

Sixteen individuals with FHD and 18 age-matched healthy controls completed cSP assessments and fMRI. Participants performed self-paced finger tapping with each hand separately. For FHD participants with left-hand symptoms (n = 4), left-right labels were flipped during analysis so that right-hand data represented the symptomatic hand and left-hand data represented the non-symptomatic hand across all participants. We analyzed activation in sensorimotor regions and tested voxel-wise correlations between cSP duration and BOLD responses.

RESULTS

FHD participants demonstrated greater activation in the inferior parietal lobule (IPL) within the posterior parietal cortex (PPC) during both right- and left-hand finger tapping. Notably, during left-finger tapping (non-symptomatic hand), cSP duration positively correlated with cerebellar activation, suggesting altered integration of inhibitory circuits during motor execution. No such correlations were found during right-finger tapping (symptomatic hand) or for control participants.

CONCLUSION

These findings suggest that individuals with FHD may selectively recruit cerebellar sensorimotor circuits to modulate inhibition during movement of the non-symptomatic hand, though this pattern was not observed during movement of the symptomatic hand. The cerebellum may play a central role in adaptive motor control in FHD. Future work should leverage symptom-inducing tasks and alternative inhibitory markers to further clarify these mechanisms.