Abstract
<jats:p>Focal task-specific dystonia (FTSD) is an isolated dystonia in which abnormal muscle contractions occur only during a particular motor task while most other movements remain relatively spared. In this Hypothesis article, we propose that FTSD arises within a task-specific motor synergy (TSMS) in primary motor cortex (M1), a local excitatory-inhibitory ensemble supporting a specific movement component of the affected task. We hypothesize that excitatory synapses within the affected TSMS become disproportionately strong relative to parvalbumin (PV)-centered inhibitory circuitry, creating a hyperexcitable dystonic synergy recruited when attempted task intensity exceeds the capacity of the residual functional synergy. A change in movement coordination is proposed to reduce the capacity of a previously established TSMS, producing task-specific true weakness at higher intensities. Repeated overreaching beyond this reduced capacity may then favor excitatory over inhibitory strengthening, consolidate the dystonic synergy, and generate the symptom-threshold phenomenon. A spiking neural network provides a conditional proof of concept that specified functional and E/I-imbalanced conditions can exhibit an input-dependent crossover in relative population firing. Finally, we propose below- or at-threshold retraining (BATR), in which symptom-free practice may promote inhibitory rebalancing and raise the symptom-threshold. This framework offers an experimentally testable M1-centered account of FTSD.</jats:p>