Walker Department of Mechanical Engineering, The University of Texas at Austin, Austin, TX, USA.
Ralph H Johnson VA Medical Center, Charleston, SC, USA.
J Neuroeng Rehabil. 2022 Jun 3;19(1):55. doi: 10.1186/s12984-022-01029-z.
Successful walking requires the execution of the pre-swing biomechanical tasks of body propulsion and leg swing initiation, which are often impaired post-stroke. While excess rectus femoris activity during swing is often associated with low knee flexion, previous work has suggested that deficits in propulsion and leg swing initiation may also contribute. The purpose of this study was to determine underlying causes of propulsion, leg swing initiation and knee flexion deficits in pre-swing and their link to stiff knee gait in individuals post-stroke.
Musculoskeletal models and forward dynamic simulations were developed for individuals post-stroke (n = 15) and healthy participants (n = 5). Linear regressions were used to evaluate the relationships between peak knee flexion, braking and propulsion symmetry, and individual muscle contributions to braking, propulsion, knee flexion in pre-swing, and leg swing initiation.
Four out of fifteen of individuals post-stroke had higher plantarflexor contributions to propulsion and seven out of fifteen had higher vasti contributions to braking on their paretic leg relative to their nonparetic leg. Higher gastrocnemius contributions to propulsion predicted paretic propulsion symmetry (p = 0.005) while soleus contributions did not. Higher vasti contributions to braking in pre-swing predicted lower knee flexion (p = 0.022). The rectus femoris had minimal contributions to lower knee flexion acceleration in pre-swing compared to contributions from the vasti. However, for some individuals with low knee flexion, during pre-swing the rectus femoris absorbed more power and the iliopsoas contributed less power to the paretic leg. Total musculotendon work done on the paretic leg in pre-swing did not predict knee flexion during swing.
These results emphasize the multiple causes of propulsion asymmetry in individuals post-stroke, including low plantarflexor contributions to propulsion, increased vasti contributions to braking and reliance on compensatory mechanisms. The results also show that the rectus femoris is not a major contributor to knee flexion in pre-swing, but absorbs more power from the paretic leg in pre-swing in some individuals with stiff knee gait. These results highlight the need to identify individual causes of propulsion and knee flexion deficits to design more effective rehabilitation strategies.
成功行走需要执行身体推进和腿摆动启动的摆动前生物力学任务，这些任务在中风后通常会受到损害。虽然摆动时股直肌过度活跃通常与膝关节屈曲度低有关，但之前的研究表明，推进和腿摆动启动的缺陷也可能导致这种情况。本研究旨在确定摆动前推进、腿摆动启动和膝关节屈曲度缺陷的根本原因，并探讨其与中风后个体僵硬膝关节步态的关系。
为中风后个体（n=15）和健康参与者（n=5）建立了肌肉骨骼模型和正向动力学模拟。使用线性回归评估了峰值膝关节屈曲度、制动和推进对称性以及个体肌肉对制动、推进、摆动前膝关节屈曲度和腿摆动启动的贡献之间的关系。
在 15 名中风后个体中，有 4 名个体的患侧推进时的比目鱼肌贡献更高，有 7 名个体的患侧制动时的股四头肌贡献更高。推进时的比目鱼肌贡献越高，预示着患侧推进对称性越好（p=0.005），而腓肠肌的贡献则没有。摆动前的股四头肌贡献越高，预示着膝关节屈曲度越低（p=0.022）。与股四头肌相比，股直肌在摆动前对膝关节下膝加速度的贡献较小。然而，对于一些膝关节屈曲度较低的个体，在摆动前，股直肌吸收了更多的力量，而髂腰肌对患侧的贡献较少。摆动前患侧的总肌肉肌腱做功并不能预测摆动时的膝关节屈曲度。
这些结果强调了中风后个体推进不对称的多种原因，包括推进时比目鱼肌贡献不足、制动时股四头肌贡献增加以及依赖代偿机制。结果还表明，股直肌在摆动前不是膝关节屈曲的主要贡献者，但在一些僵硬膝关节步态的个体中，在摆动前会从患侧吸收更多的力量。这些结果突出了识别推进和膝关节屈曲缺陷的个体原因以设计更有效的康复策略的必要性。
