Leijnse Joris N A L, Hallett Mark
Department of Mechanical Engineering, Speed School for Engineering & Price Institute for Surgical Research, University of Louisville, Kentucky 40292, USA.
Mov Disord. 2007 Sep 15;22(12):1803-8. doi: 10.1002/mds.21636.
A case study is presented in which a focal hand dystonia seems to have developed in the right hand of a classical guitarist as a result of a neuromuscular peripheral defect caused by trauma. The trauma was a near total perforation of the first web space by a splinter. Healing was uneventful without apparent functional complications. Two years later the patient noticed difficulties in extending the index in playing, for which he received various unsuccessful treatments during seven years. However, we found more severe dystonic symptoms (cocontractions) in the thumb than in the index during playing, which correlated with an undiagnosed insufficiency in the flexor pollicis brevis (FPB). This defect allowed proposing a biomechanical analysis of compensations for diminished thumb control in playing, which would explain the dysfunction in the index in playing as overcompensation for the thumb problem. If this analysis is correct, the etiology of the case can be traced back to underlying multiarticular control problems in the thumb caused by an insufficient FPB. This defect was considered irrepairable. It was concluded that even with knowledge of the underlying cause, a potentially successful treatment of the dystonia might not exist in this case. The case would demonstrate that task-specific hand dystonias can arise as overcompensations for (peripheral) neuro-musculoskeletal defects. The case is illustrated by videos of playing and functional thumb tests.
本文介绍了一个病例研究，一名古典吉他手右手因创伤导致神经肌肉外周缺陷，似乎患上了局灶性手部肌张力障碍。创伤是一根木刺几乎完全穿透了第一掌骨间隙。伤口愈合顺利，没有明显的功能并发症。两年后，患者在演奏时发现食指伸展困难，在七年中他接受了各种治疗但均未成功。然而，我们发现患者在演奏时拇指的肌张力障碍症状（共同收缩）比食指更严重，这与未被诊断出的拇短屈肌（FPB）功能不全有关。这一缺陷使得我们能够对演奏中拇指控制能力下降的代偿进行生物力学分析，这可以解释演奏时食指功能障碍是对拇指问题的过度代偿。如果这一分析正确，该病例的病因可追溯到由FPB不足引起的拇指潜在多关节控制问题。这种缺陷被认为无法修复。得出的结论是，即使知道潜在病因，在这种情况下可能也不存在对肌张力障碍的潜在成功治疗方法。该病例将证明特定任务的手部肌张力障碍可能是对（外周）神经肌肉骨骼缺陷的过度代偿。文中通过演奏视频和拇指功能测试对该病例进行了说明。
