Objective: Using a novel methodology combining neuroimaging and transcranial magnetic stimulation(TMS), we explored the difference in the interactions between the principal nodes of the fine motor control network in task-specific dystonia(TSD) patients and healthy controls.

Background: Humans have a distinguishing ability for fine motor control which is sub-served by a highly evolved corticomotoneuronal network. The acquisition of a particular motor skill involves a long series of practice movements, trial and error, adjustment and refinement. At the cortical level, this acquisition begins in the parieto-temporal sensory regions and is subsequently consolidated and stratified in the premotor-motor cortex. TSD can be viewed as a corruption or loss of motor control confined to a single motor skill.

Method: 9 patients with TSD and 13 HV underwent clinical assessment, structural and fMRI during finger tapping task. Anatomical images co-registered with the fMRI during task were used for target selection and neuro-navigation for TMS. TMS evaluation included measurement of the input-output recruitment curve (IOC), cortical silent period (CSP), and amplitude of the motor evoked potentials (MEP) conditioned by 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.

Results: 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 inhibition of dIPL node, baseline aIPL-M1 interactions became significantly inhibitory and the prior inhibitory interaction PMv-M1 trended towards facilitation, only for the TSD group.

Conclusion: 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.

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MDS Abstracts - https://www.mdsabstracts.org/abstract/interactions-within-fine-motor-control-network-in-task-specific-dystonia/