Functional MRI reveals increased connectivity in the somato-cognitive action network, suggesting a shared pathology across dystonia types.
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.
No takes yet. Share an insight, caveat, or question.
Wang et al. (2025) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: