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脑瘫的肌肉挛缩与被动力学

Muscle contracture and passive mechanics in cerebral palsy.

机构信息

Shirley Ryan AbilityLab, Chicago, Illinois.

Departments of Physical Medicine and Rehabilitation and Biomedical Engineering, Northwestern University , Chicago, Illinois.

出版信息

J Appl Physiol (1985). 2019 May 1;126(5):1492-1501. doi: 10.1152/japplphysiol.00278.2018. Epub 2018 Dec 20.

Abstract

Skeletal muscle contractures represent the permanent shortening of a muscle-tendon unit, resulting in loss of elasticity and, in extreme cases, joint deformation. They may result from cerebral palsy, spinal cord injury, stroke, muscular dystrophy, and other neuromuscular disorders. Contractures are the prototypic and most severe clinical presentation of increased passive mechanical muscle force in humans, often requiring surgical correction. Intraoperative experiments demonstrate that high muscle passive force is associated with sarcomeres that are abnormally stretched, although otherwise normal, with fewer sarcomeres in series. Furthermore, changes in the amount and arrangement of collagen in the extracellular matrix also increase muscle stiffness. Structural light and electron microscopy studies demonstrate that large bundles of collagen, referred to as perimysial cables, may be responsible for this increased stiffness and are regulated by interaction of a number of cell types within the extracellular matrix. Loss of muscle satellite cells may be related to changes in both sarcomeres and extracellular matrix. Future studies are required to determine the underlying mechanism for changes in muscle satellite cells and their relationship (if any) to contracture. A more complete understanding of this mechanism may lead to effective nonsurgical treatments to relieve and even prevent muscle contractures.

摘要

骨骼肌肉挛缩是肌肉-肌腱单元的永久性缩短,导致弹性丧失,在极端情况下会导致关节变形。它们可能由脑瘫、脊髓损伤、中风、肌肉营养不良和其他神经肌肉疾病引起。挛缩是人类增加被动机械肌肉力量的典型和最严重的临床表现,通常需要手术矫正。术中实验表明,高肌肉被动力与异常拉伸的肌节有关,尽管肌节通常正常,但串联的肌节较少。此外,细胞外基质中胶原蛋白的数量和排列的变化也会增加肌肉僵硬。结构光照和电子显微镜研究表明,大量胶原束,称为肌周缆,可能是导致这种僵硬增加的原因,并且受到细胞外基质中许多细胞类型相互作用的调节。肌肉卫星细胞的丧失可能与肌节和细胞外基质的变化有关。需要进一步的研究来确定肌肉卫星细胞变化的潜在机制及其与挛缩的关系(如果有的话)。对这一机制的更全面了解可能会导致有效的非手术治疗来缓解甚至预防肌肉挛缩。

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