Center for Neuroscience and Neurological Recovery, Methodist Rehabilitation Center, Jackson, MS, USA.
Exp Brain Res. 2020 Dec;238(12):2909-2919. doi: 10.1007/s00221-020-05936-2. Epub 2020 Oct 15.
It is unclear whether muscle coactivation during gait is altered early after stroke and among which muscles. We sought to characterize muscle coactivation during gait in subacute stroke subjects without hypertonia and explore the relationship with temporospatial parameters. In 70 stroke (23 ± 12 days post-onset) and 29 age-matched healthy subjects, surface electromyography signals were used to calculate coactivation magnitude and duration between rectus femoris and medial hamstring (knee antagonistic coactivation), tibialis anterior and medial gastrocnemius (ankle antagonistic coactivation), and rectus femoris and medial gastrocnemius (extensor synergistic coactivation) during early double-support (DS1), early single-support (SS1), late single-support (SS2), late double-support (DS2), and swing (SW). Compared to both free and very-slow speeds of controls, stroke subjects had bilaterally decreased ankle coactivation magnitude in SS2 and duration in SS1 and SS2 as well as increased extensor coactivation magnitude in DS2 and SW. Both non-paretic knee and ankle coactivation magnitudes in SS2 moderately correlated with most temporospatial parameters (|r| ≥ 0.40). Antagonistic and synergistic coactivation patterns of the knee and ankle muscles during gait are altered bilaterally in subacute stroke subjects without lower limb hypertonia suggesting impairments in motor control. Greater coactivation magnitudes in the non-paretic knee and both ankles during the terminal stance (SS2) are associated with the overall worse gait performance. Unlike previously reported excessive coactivation or no change in chronic stroke, bilaterally decreased and increased coactivation patterns are present in subacute stroke. These findings warrant longitudinal studies to examine the evolution of changes in muscle coactivation from subacute to chronic stroke.
在卒中后早期,并且在哪些肌肉中,步态中的肌肉协同收缩是否改变尚不清楚。我们试图描述亚急性卒中患者中无痉挛的步态中的肌肉协同收缩,并探索其与时空参数的关系。在 70 名卒中患者(发病后 23±12 天)和 29 名年龄匹配的健康对照者中,使用表面肌电图信号来计算股直肌和内侧半腱肌(膝关节拮抗协同收缩)、胫骨前肌和内侧比目鱼肌(踝关节拮抗协同收缩)以及股直肌和内侧比目鱼肌(伸肌协同收缩)在早期双支撑(DS1)、早期单支撑(SS1)、晚期单支撑(SS2)、晚期双支撑(DS2)和摆动(SW)期间的协同收缩幅度和持续时间。与健康对照者的自由和非常慢的速度相比,卒中患者在 SS2 中双侧踝关节协同收缩幅度减小,在 SS1 和 SS2 中协同收缩持续时间缩短,在 DS2 和 SW 中伸肌协同收缩幅度增加。SS2 中非瘫痪侧膝关节和踝关节协同收缩幅度与大多数时空参数中度相关(|r|≥0.40)。亚急性卒中患者在下肢无痉挛的情况下,双侧膝关节和踝关节肌肉在步态中的协同收缩模式发生改变,提示运动控制受损。在终末站立(SS2)期间,非瘫痪侧膝关节和双侧踝关节协同收缩幅度越大,整体步态表现越差。与慢性卒中中报道的过度协同收缩或无变化不同,亚急性卒中中存在双侧协同收缩幅度减小和增加的模式。这些发现需要进行纵向研究,以检查从亚急性到慢性卒中的肌肉协同收缩变化的演变。