Distinguishing active from passive components of ankle plantar flexor stiffness in stroke, spinal cord injury and multiple sclerosis

Distinguishing active from passive components of ankle plantar flexor stiffness in stroke, spinal cord injury and multiple sclerosis
复制标题

DOI:
10.1016/j.clinph.2010.02.167
复制
发表时间:
2010-11-01
影响因子:
4.7
通讯作者:
Nielsen, Jens B.
Nielsen, Jens B.
中科院分区:
医学3区
文献类型:
--
作者:
Lorentzen, Jakob;Grey, Michael J.;Nielsen, Jens B.

文献摘要

被引文献

相似文献

目的:痉挛是中枢运动通路损害的常见表现。对于正确的抗痉挛治疗,区分被动和主动对增加肌肉僵硬的作用是必不可少的。在这里,我们结合生物力学和电生理评估来区分31名健康受试者、10名中风患者、30名多发性硬化症受试者和16名脊髓损伤受试者主动反射机制和被动肌肉特性对踝关节僵硬的贡献。方法:采用计算机控制的机器人装置,以不同的速度(8-200°/S;幅度6度)对踝足底屈肌进行拉伸。用比目鱼肌肌电测定反射阈值。将扭矩和肌电数据归一化为最大扭矩和超大刺激胫神经诱发的肌电。被动阻力(对拉伸的扭矩反应)被证实是被动僵硬的一个很好的代表,当胫神经在缺血时传递被阻断时也是在较高的速度。结果:神经科受试者的被动扭矩有大于健康受试者的趋势,但除中风组外,无统计学意义(p<0.05)。在将最大刺激诱发扭矩归一化后,被确认为痉挛的神经科参与者的被动扭矩显著大于非痉挛参与者(p<0.01)。在健康受试者和神经科受试者之间,反射阈值没有显著差异。所有神经病组的反射诱发扭矩和肌电均显著大于健康组(p<0.001)。23名有足底屈肌高张的参与者(Ashworth评分=1)显示正常的反射扭矩,但没有正常化。在正常化的情况下,只有11名参与者是这样的。结论:本研究证实痉挛的临床诊断包括主动和被动肌肉特性的改变,基于常规临床检查很难区分两者。意义:数据提示,在开始抗痉挛治疗之前,应考虑比常规临床检查更有效地区分主动和被动肌肉僵硬贡献的评估技术。(C)2010年国际临床神经生理学联合会。爱思唯尔爱尔兰有限公司出版。版权所有。
Objective: Spasticity is a common manifestation of lesion of central motor pathways. It is essential for correct anti-spastic treatment that passive and active contributions to increased muscle stiffness are distinguished. Here, we combined biomechanical and electrophysiological evaluation to distinguish the contribution of active reflex mechanisms from passive muscle properties to ankle joint stiffness in 31 healthy, 10 stroke, 30 multiple sclerosis and 16 spinal cord injured participants. The results were compared to routine clinical evaluation of spasticity.Methods: A computer-controlled robotic device applied stretches to the ankle plantar flexor muscles at different velocities (8-200 deg/s; amplitude 6 degrees). The reflex threshold was determined by soleus EMG. Torque and EMG data were normalized to the maximal torque and EMG evoked by supramaximal stimulation of the tibial nerve. Passive resistance (the torque response to stretches) was confirmed to be a good representation of the passive stiffness also at higher velocities when transmission in the tibial nerve was blocked by ischemia.Results: Passive torque tended to be larger in the neurological than in the healthy participants, but it did not reach statistical significance, except in the stroke group (p < 0.05). Following normalization to the maximal stimulus-evoked torque, the passive torque was found to be significantly larger in neurological participants identified with spasticity than in non-spastic participants (p < 0.01). There was no significant difference in the reflex threshold between the healthy and the neurological participants. The reflex evoked torque and EMG were significantly larger in all neurological groups than in the healthy group (p < 0.001). Twenty three participants with evidence of hypertonia in the plantar flexors (Ashworth score >= 1) showed normal reflex torque without normalization. With normalization this was only the case in 11 participants. Increased reflex mediated stiffness was detected in only 64% participants during clinical examination.Conclusion: The findings confirm that the clinical diagnosis of spasticity includes changes in both active and passive muscle properties and the two can hardly be distinguished based on routine clinical examination.Significance: The data suggest that evaluation techniques which are more efficient in distinguishing active and passive contributions to muscle stiffness than routine clinical examination should be considered before anti-spastic treatment is initiated. (C) 2010 International Federation of Clinical Neurophysiology. Published by Elsevier Ireland Ltd. All rights reserved.