Using a novel methodology combining neuroimaging and trans cranial magnetic stimulation(TMS), we explored the differences in interactions between the principal nodes of the fine motor control network and cortical excitability in TSD patients and healthy matched controls. Furthermore, we evaluated the influence of inducing an long-term depression-like (LTD-like) plastic change in the parietal multimodal sensory association region on these interactions.

Humans have a distinguishing ability for fine motor control which is sub-served by a highly evolved cortico-moto-neuronal network.  Task-specific dystonia (TSD) can be viewed as a corruption or loss of motor control confined to a single motor skill.

9 patients with TSD and 12 age and sex-matched healthy volunteers (HV) underwent clinical assessment, high resolution structural MRI for tractography, and functional MRI (fMRI) during finger tapping task. TMS evaluation included measurement of the IOC, CSP, and cortico-cortical interactions between premotor ventral (PMv)-M1, anterior inferior parietal lobe (aIPL)-M1 and dorsal inferior parietal lobe (dIPL)-M1 at baseline and repeat assessment after inhibitory continuous theta-burst stimulation (cTBS) block applied to the dIPL node using a randomized sham-controlled design.

Baseline dIPL-M1 and aIPL-M1 cortico-cortical interactions were facilitatory and inhibitory, respectively, in HV, whereas the interactions were noted to be converse and significantly different in TSD. Baseline PMv-M1 interactions were inhibitory and similar between the groups. Differences were also noted in the resting state functional connectivity between dIPL and PMv nodes with no differences noted in the structural connectivity. CSP was significantly prolonged in TSD cohort. After making a LTD-like plastic change to dIPL node, baseline aIPL-M1 interactions became significantly inhibitory and the prior inhibitory PMv-M1 interaction trended towards facilitation, only for the TSD group.

TSD should be considered as a separate nosologic entity with the likely pathophysiologic mechanism being corruption of the parieto-premotor control of a highly-refined motor skill.