We characterized the passive mechanical properties of the affected and contralateral musculotendon units in 9 chronic stroke survivors as well as in 6 neurologically-intact controls. Using a position-controlled motor, we precisely indented the distal tendon of the biceps brachii to a 20 mm depth from skin, recording both its sagittal motion using ultrasound movies and the compression force at the tip of the indenter. Length changes of 8 equally-spaced features along the aponeurosis axis were quantified using a pixel-tracking protocol. We report that, on the aggregate and with respect to contralateral and control, respectively, the affected side initiates feature motion at a shorter indentation distance by 61% and 50%, travels further by 15% and 9%, at a lower rate of 28% and 15%, and is stiffer by 40% and 57%. In an extended analysis including the spatial location of the 8 designated features, we report that in contrast to the contralateral and control muscles, the affected musculotendon unit does not strain measurably within the imaging window. These results confirm that chronic stroke-induced spasticity changes musculotendon unit passive mechanics, causing it to not strain under stretch. The mechanisms responsible for altered passive mechanics may lie within extracellular matrix fibrosis.

中文翻译：

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慢性半球卒中幸存者体内被动肌肉力学的体内研究。

我们在9个慢性卒中幸存者以及6个神经完整的对照中表征了受影响和对侧的musendotendon单位的被动机械性能。使用位置控制马达，我们精确地将肱二头肌的远端肌腱切入距皮肤20毫米的深度，并使用超声波电影记录其矢状运动和压头尖端的压缩力。使用像素跟踪协议量化沿腱膜轴的8个等距特征的长度变化。我们报告说，总体而言，对侧和控制方面，患侧分别以较短的压痕距离（61％和50％）启动特征运动，进一步以15％和9％的速度行进，以28的较低速度行进％和15％，刚度提高40％和57％。在包括8个指定特征的空间位置的扩展分析中，我们报告说，与对侧和对照肌肉相反，受影响的肌腱末端单元在成像窗口内未可测量地拉紧。这些结果证实，慢性中风引起的痉挛改变了肌腱单元的被动力学，从而使其在拉伸下不会紧张。负责改变被动力学的机制可能在于细胞外基质纤维化。