Somato‐Cognitive Action Network in Focal Dystonia
Name
Movement Disorders - 2025 - Wang - Somato‐Cognitive Action Network in Focal Dystonia.pdf
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2.79 MB
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Author(s)
Wang, Yuchao
Huynh, Baothy
Ren, Jianxun
Chen, Mo
Zhang, Wei
Hu, Dan
Li, Shasha
Liu, Hesheng
Kimberley, Teresa J.
Date Issued
August 28, 2025
Journal
Movement Disorders
Publisher
Wiley
Citation
Wang, Y., Huynh, B., Ren, J., Chen, M., Zhang, W., Hu, D., Li, S., Liu, H. and Kimberley, T.J. (2025), Somato-Cognitive Action Network in Focal Dystonia. Mov Disord.
Version
Final published version
Abstract
Background
The central pathology causing idiopathic focal dystonia remains unclear. The recently identified somato-cognitive action network (SCAN) has been implicated.
Objective
We tested whether the effector-agnostic SCAN may constitute a central pathology shared across dystonia subtypes, whereas the effector-specific regions in the primary sensorimotor cortex may show distinct functional changes specific to the dystonic body part.
Methods
We collected functional magnetic resonance imaging (MRI) from patients with focal dystonia (laryngeal dystonia [LD], N = 24; focal hand dystonia [FHD], N = 18) and healthy control participants (N = 21). Regions of interest were selected a priori within the basal ganglia-thalamo-cortical and cerebello-thalamo-cortical sensorimotor pathways. We investigated dystonia-dependent resting-state connectivity changes: between SCAN and related cortical regions, between cortical and noncortical regions, and among noncortical regions. Cortical network boundaries were individualized based on resting-state data. Separately, individualized hand and mouth/larynx regions were also generated from task-based MRI (finger-tapping and phonation, respectively) for comparison.
Results
Both focal dystonia subtypes showed significant functional changes (P = 0.048 for LD, P = 0.017 for FHD) compared to controls, driven by SCAN's higher functional connectivity to task-based mouth/larynx region and concomitantly lower connectivity to the cingulo-opercular network. No significant subcortical or cerebellar changes were observed when LD and FHD were modeled as independent groups. However, exploratory analysis combining LD and FHD suggested a dystonia-dependent asynchronization between SCAN and sensorimotor cerebellum (P = 0.010) that may indicate a pathological rather than compensatory process.
Conclusions
We demonstrate that SCAN is uniquely associated with focal dystonia dysfunction beyond the dystonic effector regions, offering insights into pathophysiology and treatments. © 2025 The Author(s). Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society.
MIT Department
Massachusetts Institute of Technology. Department of Brain and Cognitive Sciences
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DOI of Published Version
https://doi.org/10.1002/mds.70021
