Mathieu P A
Biomedical Engineering Institute, Université de Montréal, Canada.
Electromyogr Clin Neurophysiol. 1995 Dec;35(8):503-13.
Following a cerebro-vascular accident, motor deficits are usually associated with a selective atrophy of fast fatiguable muscle fibers. The reduction of output torque in spastic patients is considered to be caused by unfused twitches resulting from the reduction in the motor unit firing rate. To regain control of a paretic limb, these patients have to learn, through training, how to recruit an adequate number of intact motor units to generate the required functional movement. In hemiplegia, intra-subject variability makes difficult the assessment of the effects of any therapy treatments. Our objective here was thus to address the problem of the data variability and to analyze the electromyographic signal obtained from hemiplegic patients under biofeedback training. The experimental situation chosen was a very isolated but controlled motor activity (an isometric shoulder forward flexion). The results show that after training, 5 out of 11 patients could produce EMG signal from their affected deltoid whose mean value was 50% greater than before the training, while no appreciable change was observed for their unaffected deltoid. While these EMG changes on the HEMI side are correlated with greater torque output, the coefficient of correlation is slightly smaller after than before the training (r = 0.87 vs 0.89). It can be hypothesized that while the training was directed toward the deltoid, the patients in some ways developed new strategies for contracting their shoulder.
脑血管意外后，运动功能障碍通常与快速疲劳性肌纤维的选择性萎缩有关。痉挛患者输出扭矩的降低被认为是运动单位放电频率降低导致的不完全强直收缩所致。为了重新控制瘫痪肢体，这些患者必须通过训练学习如何募集足够数量的完整运动单位来产生所需的功能性运动。在偏瘫患者中，个体内部的变异性使得评估任何治疗方法的效果变得困难。因此，我们这里的目标是解决数据变异性问题，并分析偏瘫患者在生物反馈训练下获得的肌电信号。所选择的实验情况是一种非常孤立但可控的运动活动（等长肩部前屈）。结果表明，训练后，11名患者中有5名能够从患侧三角肌产生肌电信号，其平均值比训练前高出50%，而未受影响的三角肌未观察到明显变化。虽然患侧的这些肌电变化与更大的扭矩输出相关，但训练后的相关系数略小于训练前（r = 0.87对0.89）。可以推测，虽然训练针对三角肌，但患者在某些方面发展出了收缩肩部的新策略。
