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与工作相关的肌肉骨骼疾病大鼠模型中的正中神经损伤

Median nerve trauma in a rat model of work-related musculoskeletal disorder.

作者信息

Clark Brian D, Barr Ann E, Safadi Fayez F, Beitman Lisa, Al-Shatti Talal, Amin Mamta, Gaughan John P, Barbe Mary F

机构信息

Department of Physical Therapy, College of Allied Health Professions, Temple University, Philadelphia, Pennsylvania 19140, USA.

出版信息

J Neurotrauma. 2003 Jul;20(7):681-95. doi: 10.1089/089771503322144590.

Abstract

Anatomical and physiological changes were evaluated in the median nerves of rats trained to perform repetitive reaching. Motor degradation was evident after 4 weeks. ED1-immunoreactive macrophages were seen in the transcarpal region of the median nerve of both forelimbs by 5-6 weeks. Fibrosis, characterized by increased immunoexpression of collagen type I by 8 weeks and connective tissue growth factor by 12 weeks, was evident. The conduction velocity (NCV) within the carpal tunnel showed a modest but significant decline after 9-12 weeks. The lowest NCV values were found in animals that refused to participate in the task for the full time available. Thus, both anatomical and physiological signs of progressive tissue damage were present in this model. These results, together with other recent findings indicate that work-related carpal tunnel syndrome develops through mechanisms that include injury, inflammation, fibrosis and subsequent nerve compression.

摘要

对训练进行重复性伸手动作的大鼠正中神经的解剖学和生理学变化进行了评估。4周后运动功能退化明显。到5 - 6周时,在前肢正中神经的腕横区域可见ED1免疫反应性巨噬细胞。纤维化在8周时表现为I型胶原蛋白免疫表达增加,在12周时表现为结缔组织生长因子增加,较为明显。9 - 12周后,腕管内的传导速度(NCV)出现适度但显著的下降。在拒绝全程参与任务的动物中发现了最低的NCV值。因此,该模型中存在进行性组织损伤的解剖学和生理学迹象。这些结果与其他近期发现表明,与工作相关的腕管综合征是通过包括损伤、炎症、纤维化和随后的神经压迫在内的机制发展而来的。

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