A multifactorial conceptual model of peripheral neuromusculoskeletal predisposing factors in task-specific focal hand dystonia in musicians: etiologic and therapeutic implications

Abstract

A model is presented showing how peripheral factors may cause a process of movement adaptation that leads to task-specific focal hand dystonia in musicians (FHDM). To acquire a playing technique, the hand must find effective and physiologically sustainable movements within a complex set of functional demands and anatomic, ergonomic, and physiological constraints. In doing so, individually discriminating constraints may become effective, such as limited anatomic independence of finger muscles/tendons, limited joint ranges of motion, or (subclinical) neuromusculoskeletal defects. These factors may, depending on the instrument-specific playing requirements, compromise or exclude functional playing movements. The controller (i.e., the brain) then needs to develop alternative motions to execute the task, which is called compensation. We hypothesize that, if this compensation process does not converge to physiologically sustainable muscle activation patterns that satisfy all constraints, compensation could increase indefinitely under the pressure of practice. Dystonic symptoms would become manifest when overcompensation occurs, resulting in motor patterns that fail in proper task execution. The model presented in this paper only concerns the compensatory processes preceding such overcompensations and does not aim to explain the nature of the dystonic motions themselves. While the model considers normal learning processes in the development of compensations, neurological predispositions could facilitate developing overcompensations or further abnormal motor programs. The model predicts that if peripheral factors are involved, FHDM symptoms would be preceded by long-term gradual changes in playing movements, which could be validated by prospective studies. Furthermore, the model implies that treatment success might be enhanced by addressing the conflict between peripheral factors and playing tasks before decompensating/retraining the affected movements.

Fig. 1

Multifactorial model of peripheral factors in focal hand dystonia in musicians. For explanation, see text. RoM (block 1): range of motion

Fig. 2

Playing technique changes with practice over time–hypothesis. (1) Unconstrained hand: playing movements become practice-invariant. (2) Constrained hand with effective and physiologically feasible compensated movements: longer learning process, but playing movements also become practice-invariant. (3–5) Hands at FHDM risk. (3) Playing technique does not become practice-invariant, but exposure (amount of practice) remains too small for FHDM development. (4) Greater practice intensity leads to FHDM, with resulting run-away changes in movements.(5) Trigger event provoking FHDM development. (6) Physiological muscle capacities may increase/decrease over time, increasing or reducing the critical physiological load for FHDM development

Fig. 3

Schematized are the control and overarching feedback loops that determine the development of a playing technique. Musculoskeletal hand factors or defects, musculoskeletal mechanics, and instrument manipulation requirements are beyond voluntary control (dashed boxes). The limit of control is muscle activation. The brain’s sole means of solving conflicts between factors in the dashed box is the production of motor patterns leading to effective movements. Depending on the factors, effective and physiologically feasible motor patterns to solve the instrument-technical playing problems may or may not exist. Damage to peripheral nerves (compressions) may diminish the responsiveness of muscles to fine control and thus make the hand more vulnerable to developing inadequate motor patterns. Voluntary components in developing playing motions relate to auditory (task achievement) and visual (playing posture) feedback