Understanding Motor Impairment in the Paretic Lower Limb After a Stroke: A Review of the Literature
Understanding Motor Impairment in the Paretic Lower Limb After a Stroke: A Review of the Literature
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DOI：
10.1310/tsr1605-346
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发表时间：
2009-09-01
影响因子：
2.2
通讯作者：
Hidler, J.
中科院分区：
文献类型：
--
作者：
Arene, N.;Hidler, J.
除了脊髓上中枢损伤导致的肌肉无力之外，多种机制可能会导致中风后瘫痪下肢的运动障碍。中风后，偏瘫肌肉及其运动单位的生理变化、激动剂激活的被动或主动抑制以及异常的肌肉激活模式都会发生，并减少肌肉力量的产生。其他因素（例如被动张力增加）可能会阻碍主动肌和拮抗肌扭矩的产生，而异常的运动激活和肌肉运动控制的改变可能会产生异常的步态模式。相对的下肢肌肉的共同激活有助于关节僵硬和姿势稳定性；瘫痪下肢的异常共激活可能导致姿势稳定性缺陷。肌肉激活时间异常也会导致肌肉工作输出减少，进而导致肢体功能下降。当感觉缺陷伴随肌肉无力时，传入信号处理受损可能会导致异常肌肉激活、异常步态模式以及对步态和站立期间扰动的异常反应。本文回顾了这些不同因素单独和组合对中风后瘫痪下肢运动功能受损的影响。
In addition to muscle weakness caused by injury to supraspinal centers, several mechanisms may contribute to motor impairment in the paretic lower limb following a stroke. Physiological changes in the paretic muscles and their motor units, passive or active restraint of agonist activation, and abnormal muscle activation patterns have been shown to occur after a stroke and to reduce muscle force generation. Other factors such as increased passive tone may impede agonist and antagonist muscle torque generation, while abnormal motor activation and altered motor control of muscles can produce abnormal gait patterns. Co-activation of opposing lower limb muscles contributes to joint stiffness and postural stability; abnormal co-activation in paretic lower limbs can lead to deficits in postural stabilization. Abnormal timing of muscle activation can also yield reduced muscle work output and, in turn, reduced limb function. When sensory deficits accompany muscle weakness, impaired processing of afferent signals may contribute to abnormal muscle activation, abnormal gait patterns, and abnormal responses to perturbation during gait and stance. This article reviews the impact of these various factors, individually and in combination, on impaired motor function in the paretic lower limb after a stroke.