A Proposed Cause, Mechanism, and Rehabilitation for Focal Task-Specific Dystonia: A Theoretical-Empirical Approach

Focal task-specific dystonia (FTSD) poses a complex interplay of maladaptive neuroplasticity and motor circuit imbalance. Traditional theories often implicate subcortical nuclei but fail to explain why symptoms remain so tightly bound to a singular, highly practiced skill. Here we propose that the primary driver of FTSD is a newly formed "dystonic synergy" within the primary motor cortex (M1), in which excitatory circuit synapses are adequate relative to under-strengthened inhibitory circuit synapses, triggering involuntary contractions once the skill's intensity demands surpass the functional synergy's excitatory and inhibitory circuit capacity (synaptic strength). In short, we use an extensive single-case observation as the core empirical foundation and chronicle how a decade of stable piano performance deteriorated following a sudden technical change that forced the finger flexion motor synergy to "overreach". The patient's initial phase was dominated by "true weakness," a condition of task-specific paresis where the motor system is physically unable to generate the required excitatory inhibitory (E/I) drive to match the attempted movement speed. Over repetitive attempts to override that limitation, the excitatory circuit strengthened while the inhibitory circuit lagged, culminating in a fully formed dystonic synergy within three weeks. This maladaptive synergy then manifested in both piano playing and typing, a related digit-based skill, greatly disabling normal function in both tasks. We illustrate that once formed, the dystonic synergy remains stable but not spontaneously progressive, consistent with a saturable excitatory capacity. Moreover, a spiking neural network simulation provides proof of concept for the hypothesis and identifies the input strength threshold at which the network shifts from balanced to hyperexcitable output. Finally, we propose and describe a non-invasive motor retraining approach for reversing FTSD, "below or at-threshold retraining" (BATR), in which the inhibitory circuit of the dystonic synergy is methodically strengthened by strict practice at or below the individual symptom threshold. This motor strategy, validated in the single-case longitudinal data and in other published studies using similar methods, reveals that the dysregulated synergy can be rebalanced to restore fully normal motor function and highlights a noninvasive avenue for rehabilitation and prevention in FTSD.