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

被引:18
作者
Leijnse, J. N. A. L. [1 ,2 ]
Hallett, M. [3 ]
Sonneveld, G. J. [4 ]
机构
[1] Univ Libre Bruxelles, Fac Sci Appl, Dept Bio Electro & Mech Syst BEAMS, Av Fr Roosevelt 50, B-1050 Brussels, Belgium
[2] Univ Libre Bruxelles, Erasme Univ Hosp, Dept Orthoped & Traumatol, B-1050 Brussels, Belgium
[3] NINDS, Human Motor Control Sect, Med Neurol Branch, NIH, Bethesda, MD 20892 USA
[4] Bethesda Hosp, Hoogeveen, Netherlands
关键词
Hand; Biomechanics; Control; Focal dystonia; Overuse; Musicians; FLEXOR DIGITORUM PROFUNDUS; MEASURING FORCE TRANSFERS; MULTI-FINGER TASKS; OVERUSE SYNDROME; MOTOR CORTEX; DEEP FLEXORS; BRAIN; PLASTICITY; PATHOPHYSIOLOGY; BLEPHAROSPASM;
D O I
10.1007/s00422-014-0631-5
中图分类号
TP3 [计算技术、计算机技术];
学科分类号
0812 ;
摘要
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.
引用
收藏
页码:109 / 123
页数:15
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