Leijnse J N A L, Hallett M, Sonneveld G J
Department of Bio-, Electro- and Mechanical Systems (BEAMS), Faculty of Applied Sciences, Université Libre de Bruxelles, Av. Fr. Roosevelt 50, 1050, Brussels, Belgium,
Biol Cybern. 2015 Feb;109(1):109-23. doi: 10.1007/s00422-014-0631-5. Epub 2014 Oct 17.
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.
本文提出了一个模型,展示了外周因素如何引发运动适应过程,进而导致音乐家出现特定任务性局灶性手部肌张力障碍(FHDM)。为了习得一种演奏技巧,手部必须在一系列复杂的功能需求以及解剖学、人体工程学和生理学限制条件下,找到有效且生理上可持续的运动方式。在此过程中,个体差异导致的限制因素可能会发挥作用,比如手指肌肉/肌腱的解剖学独立性有限、关节活动范围受限,或者(亚临床)神经肌肉骨骼缺陷。根据乐器特定的演奏要求,这些因素可能会损害或排除功能性演奏动作。此时,控制器(即大脑)需要开发替代动作来执行任务,这一过程称为补偿。我们假设,如果这种补偿过程无法收敛到满足所有限制条件的生理上可持续的肌肉激活模式,那么在练习压力下,补偿可能会无限增加。当出现过度补偿时,肌张力障碍症状就会显现,导致运动模式无法正确执行任务。本文提出的模型仅涉及此类过度补偿之前的补偿过程,并非旨在解释肌张力障碍动作本身的性质。虽然该模型考虑了补偿发展过程中的正常学习过程,但神经学易感性可能会促使过度补偿或进一步发展出异常运动程序。该模型预测,如果涉及外周因素,FHDM症状之前演奏动作会有长期的逐渐变化,这一点可通过前瞻性研究得到验证。此外,该模型还意味着,在对受影响的动作进行失代偿/再训练之前,通过解决外周因素与演奏任务之间的冲突,可能会提高治疗成功率。