Kamper Derek G, Fischer Heidi C, Cruz Erik G, Rymer William Z
Sensory Motor Performance Program, Rehabilitation Institute of Chicago, Chicago, IL 606011, USA.
Arch Phys Med Rehabil. 2006 Sep;87(9):1262-9. doi: 10.1016/j.apmr.2006.05.013.
To assess the relative contributions of several neurologic and biomechanic impairment mechanisms to overall finger and hand impairment in chronic hemiparetic stroke survivors.
Repeated-measures design.
Clinical research laboratory.
Thirty stroke survivors with chronic hemiparesis. Fifteen subjects had severe hand motor impairment and 15 had moderate impairment, as measured with the Chedoke-McMaster Stroke Assessment.
Not applicable.
The biomechanic factors stiffness and resting flexion torque, together with the neurologic factors spasticity, strength, and coactivation, were quantified by using a custom hand manipulator, a dynamometer, and electromyographic recordings. Both passive and active rotations of the metacarpophalangeal joints of the fingers were examined.
Although subjects in the severely impaired group exhibited statistically greater passive stiffness and resting flexion torque than their moderately impaired counterparts (P<.05), the overall effect of these biomechanic changes appeared small in relation to the deficits attributable to neurologic changes such as spasticity and, especially, weakness. In fact, weakness in grip strength and isometric extension accounted for the greatest portion of the variance between the 2 groups (eta(2)=.40 and eta(2)=.23, respectively).
Thus, deficits in hand motor control after stroke seem to derive mainly from weakness, which may be attributable to the loss of descending corticospinal pathway activation of motoneurons.
评估几种神经和生物力学损伤机制对慢性偏瘫性卒中幸存者手指和手部整体损伤的相对影响。
重复测量设计。
临床研究实验室。
30名慢性偏瘫性卒中幸存者。根据Chedoke-McMaster卒中评估量表，15名受试者存在严重手部运动损伤，15名存在中度损伤。
不适用。
使用定制的手部操作器、测力计和肌电图记录，对生物力学因素（僵硬度和静息屈曲扭矩）以及神经因素（痉挛、力量和共同激活）进行量化。检查手指掌指关节的被动和主动旋转。
尽管严重损伤组受试者的被动僵硬度和静息屈曲扭矩在统计学上高于中度损伤组受试者（P<0.05），但与痉挛尤其是无力等神经学变化导致的功能缺陷相比，这些生物力学变化的总体影响似乎较小。事实上，握力和等长伸展力的减弱在两组之间的差异中占最大比例（分别为η² = 0.40和η² = 0.23）。
因此，卒中后手运动控制缺陷似乎主要源于无力，这可能归因于皮质脊髓束下行通路对运动神经元激活的丧失。
