Department of Physical Therapy, University of Toronto, Toronto, Ontario, Canada.
J Appl Physiol (1985). 2010 Nov;109(5):1337-46. doi: 10.1152/japplphysiol.00804.2009. Epub 2010 Aug 19.
The contributions of nervous system muscle activation and muscle atrophy to poststroke weakness have not been evaluated together in the same subject. Maximal voluntary contraction (MVC) torque, voluntary activation (twitch interpolation), and electromyographic (EMG) amplitude were determined bilaterally in the plantar flexors of seven chronic stroke survivors (40-63 yr, 24-51 mo poststroke). Volumes of the plantar flexor muscles were determined bilaterally with magnetic resonance imaging (MRI). The mean (±SD) contralesional (paretic) MVC torque was less than one-half of the ipsilesional leg: 56.7 ± 57.4 vs. 147 ± 35.7 Nm (P = 0.006). Contralesional voluntary activation was only 48 ± 36.9%, but was near complete in the ipsilesional leg, 97 ± 1.9% (P = 0.01). The contralesional MVC EMG amplitude (normalized to the maximum M-wave peak-to-peak amplitude) of the gastrocnemii and soleus were 36.0 ± 28.5 and 36.0 ± 31.0% of the ipsilesional leg. Tibialis anterior (TA) EMG coactivation was not different between the contralesional (23.2 ± 24.0% of TA MVC EMG) and ipsilesional side (12.3 ± 5.7%) (P = 0.24). However, TA EMG coactivation was excessive (71%) in one subject and accounted for ~8% of her weakness based on the estimated antagonist torque. Relative (%ipsilesional leg) plantar flexor and gastrocnemii volumes were 88 ± 6% (P = 0.004) and 76 ± 15% (P = 0.01), respectively. Interlimb volume differences of the soleus, deep plantar flexors, and peronei were not significant. Preferred walking speed (0.83 ± 0.33 m/s) was related to the contralesional MVC torque (r(2) = 0.57, P = 0.05, N = 7), but the two subjects with the greatest weakness walked faster than three others. Our findings suggest that plantar flexor weakness in mobile chronic stroke survivors reflects mostly voluntary activation failure, with smaller contributions from antagonist activity and atrophy.
神经系统肌肉活动和肌肉萎缩对卒中后无力的影响尚未在同一受试者中同时进行评估。在 7 名慢性卒中幸存者（40-63 岁，卒中后 24-51 个月）的足底屈肌双侧分别测定最大自主收缩（MVC）扭矩、自愿激活（抽搐插值）和肌电图（EMG）幅度。使用磁共振成像（MRI）双侧确定足底屈肌的体积。患侧（瘫痪侧）的平均（±SD）MVC 扭矩小于健侧的一半：56.7 ± 57.4 与 147 ± 35.7 Nm（P = 0.006）。患侧的自愿激活仅为 48 ± 36.9%，但在健侧几乎完全为 97 ± 1.9%（P = 0.01）。患侧 MVC EMG 幅度（相对于最大 M 波峰峰值幅度归一化）的比目鱼肌和腓肠肌为健侧的 36.0 ± 28.5 和 36.0 ± 31.0%。胫骨前肌（TA）EMG 共激活在患侧（TA MVC EMG 的 23.2 ± 24.0%）和健侧之间无差异（12.3 ± 5.7%）（P = 0.24）。然而，一名受试者的 TA EMG 共激活过度（71%），根据估计的拮抗肌扭矩，这占她无力的~8%。足底屈肌和比目鱼肌的相对（健侧腿）体积分别为 88 ± 6%（P = 0.004）和 76 ± 15%（P = 0.01）。腓肠肌、深部足底屈肌和腓骨肌的肢体间体积差异无显著性。首选步行速度（0.83 ± 0.33 m/s）与患侧 MVC 扭矩相关（r(2) = 0.57，P = 0.05，N = 7），但两名无力最大的受试者的步行速度快于其他三人。我们的研究结果表明，移动性慢性卒中幸存者的足底屈肌无力主要反映自愿激活失败，而拮抗剂活性和萎缩的贡献较小。
