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Contribution of thixotropy, spasticity, and contracture to ankle stiffness after stroke

机译:触变性,痉挛和挛缩对踝关节的贡献 中风后的僵硬

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摘要

OBJECTIVES—Increasedresistance to stretch of muscles after stroke may be the result ofcentrally mediated neural factors such as spasticity or local,peripheral factors such as muscle contracture or thixotropy. The aimwas to investigate evidence for an abnormal thixotropic response andcompare this with two other factors—contracture and spasticity—whichcould potentially contribute to muscle stiffness after stroke.
METHODS—Thirtypatients with stroke whose calf muscles were assessed clinically asstiff and 10 neurologically normal subjects were recruited. To measurethixotropy, their calf muscles were stretched through two cycles aftertwo prestretch conditions: one in which the muscles were maintained ina shortened position and one in which they were maintained in alengthened position. Spasticity was defined as the presence of tonicstretch reflexes in relaxed muscles. Contracture was defined as beingpresent when maximum passive ankle dorsiflexion fell at least 2 SDbelow the mean value of the control subjects.
RESULTS—Both controlsand patients with stroke exhibited a thixotropic response but this wasno greater in the patients than the controls. About one third of thepatients displayed muscle contracture and most exhibited spasticity.Contracture made a significant contribution (p=0.006) to the clinical measure of calfmuscle stiffness while spasticity made a significant contribution(p=0.004) to the laboratory measure of calfmuscle stiffness.
CONCLUSIONS—Measuringthixotropy at the level of joint movement was sufficiently sensitive todetermine the thixotropic response in both neurologically normalsubjects and patients impaired after stroke. The thixotropic responsewas not higher than normal after stroke, suggesting that whereasthixotropy may produce enough immediate resistance to impede movementin those who are very weak, it is not a substantial contributor to longterm muscle stiffness. Contracture did significantly contribute tomuscle stiffness, supporting the importance of prevention ofcontracture after stroke. Spasticity contributed to muscle stiffnessonly when the limb was moved quickly.


机译:目的—中风后增加的对肌肉拉伸的抵抗力可能是中央介导的神经因素(如痉挛)或局部,周围因素(如肌肉挛缩或触变性)的结果。目的是调查触变反应异常的证据,并将其与其他两个因素(收缩和痉挛)进行比较,这可能会导致中风后肌肉僵硬。方法— 30例中风患者的小腿肌肉经临床评估为僵硬,并招募了10名神经系统正常的受试者。为了测量触变性,在两种预拉伸条件后,将它们的小腿肌肉拉伸两个周期:其中一个将肌肉保持在缩短的位置,另一个将它们保持在伸长的位置。痉挛被定义为在松弛的肌肉中出现强直反射。当最大被动踝背屈比对照受试者的平均值下降至少2 SD时,出现挛缩。结果:对照组和中风患者均表现出触变性,但在患者中并不比对照组大。约三分之一的患者表现出肌肉挛缩,大多数表现出痉挛性。收缩对小腿僵硬的临床测量有显着贡献(p = 0.006),而痉挛对小腿僵硬的实验室测量有显着贡献(p = 0.004)。结论:在关节运动水平上测量触变性足以确定神经系统正常受试者和中风后受损患者的触变性反应。中风后触变性反应不高于正常水平,这表明尽管触变性可能在非常虚弱的人中产生足够的直接阻力来阻止运动,但对长期的肌肉僵硬并不是实质性贡献。挛缩确实显着促进了肌肉僵硬,支持了预防中风后挛缩的重要性。痉挛仅在快速移动肢体时才导致肌肉僵硬。

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