Sensory Motor Performance Program, Rehabilitation Institute of Chicago, Chicago, IL 60611, USA.
J Neurophysiol. 2011 Oct;106(4):1644-51. doi: 10.1152/jn.00936.2010. Epub 2011 Jul 13.
The objective of this study was to explore motor impairment of the thumb following stroke. More specifically, we quantitatively examined kinetic deficits of the thumb. We anticipated that force deficits would be nonuniformly distributed across the kinetic workspace, due in part to varying levels of difficulty in altering the motor activation pattern to meet the task. Eighteen stroke survivors with chronic hemiparesis participated in the trials, along with nine age-matched controls. Of the stroke-survivor group, nine subjects had moderate hand impairment, and the other nine subjects had severe hand impairment. Subjects were instructed to generate maximal isometric thumb-tip force, as measured with a load cell, in each of six orthogonal directions with respect to the thumb tip. Activity of three representative thumb muscles was monitored through intramuscular and surface electrodes. Univariate split-plot analysis of variance revealed that clinical impairment level had a significant effect on measured force (P < 0.001), with the severely impaired group producing only 13% of the control forces, and the moderately impaired group generating 32% of control forces, on average. Weakness in the moderately impaired group exhibited a dependence on force direction (P = 0.015), with the least-relative weakness in the medial direction. Electromyographic recordings revealed that stroke survivors exhibited limited modulation of thumb-muscle activity with intended force direction. The difference in activation presented by the control group for a given muscle was equal to 40% of its full activation range across force directions, whereas this difference was only 26% for the moderately impaired group and 15% for the severely impaired group. This diminished ability to modify voluntary activation patterns, which we observed previously in index-finger muscles as well, appears to be a primary factor in hand impairment following stroke.
本研究旨在探讨脑卒中后手拇指运动障碍。更具体地说，我们定量检查了拇指的运动缺陷。我们预计，由于改变运动激活模式以适应任务的难度不同，力缺陷将不均匀地分布在运动学工作空间中。18 名患有慢性偏瘫的脑卒中幸存者和 9 名年龄匹配的对照组参加了试验。在脑卒中幸存者组中，9 名受试者手部中度受损，另 9 名受试者手部严重受损。要求受试者在拇指尖端的六个正交方向上用测力传感器产生最大等长拇指尖端力。通过肌内和表面电极监测三个代表性拇指肌肉的活动。单变量分块方差分析显示，临床损伤程度对测量力有显著影响（P < 0.001），严重损伤组产生的力仅为对照组的 13%，中度损伤组平均产生对照组的 32%。中度损伤组的肌力减弱与力方向有关（P = 0.015），在中间方向上的相对减弱最小。肌电图记录显示，脑卒中幸存者表现出拇指肌肉活动随预期力方向的调节有限。对照组在给定肌肉上的激活差异等于其在各力方向上的全激活范围的 40%，而中度损伤组的差异仅为 26%，严重损伤组的差异仅为 15%。这种减弱的修改自愿激活模式的能力，我们之前在食指肌肉中也观察到，似乎是脑卒中后手功能障碍的一个主要因素。
