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中风后患者行走时反应性平衡控制策略的机械有效性受损。

Impairments in the mechanical effectiveness of reactive balance control strategies during walking in people post-stroke.

作者信息

Liu Chang, McNitt-Gray Jill L, Finley James M

机构信息

Department of Biomedical Engineering, University of Southern California, Los Angeles, CA, United States.

Department of Biological Science, University of Southern California, Los Angeles, CA, United States.

出版信息

Front Neurol. 2022 Oct 31;13:1032417. doi: 10.3389/fneur.2022.1032417. eCollection 2022.

DOI:10.3389/fneur.2022.1032417
PMID:36388197
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9659909/
Abstract

People post-stroke have an increased risk of falls compared to neurotypical individuals, partly resulting from an inability to generate appropriate reactions to restore balance. However, few studies investigated the effect of paretic deficits on the mechanics of reactive control strategies following forward losses of balance during walking. Here, we characterized the biomechanical consequences of reactive control strategies following perturbations induced by the treadmill belt accelerations. Thirty-eight post-stroke participants and thirteen age-matched and speed-matched neurotypical participants walked on a dual-belt treadmill while receiving perturbations that induced a forward loss of balance. We computed whole-body angular momentum and angular impulse using segment kinematics and reaction forces to quantify the effect of impulse generation by both the leading and trailing limbs in response to perturbations in the sagittal plane. We found that perturbations to the paretic limb led to larger increases in forward angular momentum during the perturbation step than perturbations to the non-paretic limb or to neurotypical individuals. To recover from the forward loss of balance, neurotypical individuals coordinated reaction forces generated by both legs to decrease the forward angular impulse relative to the pre-perturbation step. They first decreased the forward pitch angular impulse during the perturbation step. Then, during the first recovery step, they increased the backward angular impulse by the leading limb and decreased the forward angular impulse by the trailing limb. In contrast to neurotypical participants, people post-stroke did not reduce the forward angular impulse generated by the stance limb during the perturbed step. They also did not increase leading limb angular impulse or decrease the forward trailing limb angular impulse using their paretic limb during the first recovery step. Lastly, post-stroke individuals who scored poorer on clinical assessments of balance and had greater motor impairment made less use of the paretic limb to reduce forward momentum. Overall, these results suggest that paretic deficits limit the ability to recover from forward loss of balance. Future perturbation-based balance training targeting reactive stepping response in stroke populations may benefit from improving the ability to modulate paretic ground reaction forces to better control whole-body dynamics.

摘要

与神经正常的个体相比,中风后人群跌倒的风险增加,部分原因是无法产生适当的反应来恢复平衡。然而,很少有研究调查偏瘫缺陷对步行过程中向前失去平衡后反应控制策略力学的影响。在此,我们描述了跑步机皮带加速引起的扰动后反应控制策略的生物力学后果。38名中风后参与者和13名年龄匹配、速度匹配的神经正常参与者在双带跑步机上行走,同时接受导致向前失去平衡的扰动。我们使用节段运动学和反作用力计算全身角动量和角冲量,以量化前后肢体在矢状面响应扰动时产生冲量的效果。我们发现,与对非偏瘫肢体或神经正常个体的扰动相比,对偏瘫肢体的扰动在扰动步骤中导致向前角动量的增加更大。为了从向前失去平衡中恢复,神经正常的个体协调双腿产生的反作用力,以相对于扰动前步骤减少向前角冲量。他们首先在扰动步骤中减少向前俯仰角冲量。然后,在第一个恢复步骤中,他们通过前导肢体增加向后角冲量,并通过后随肢体减少向前角冲量。与神经正常的参与者不同,中风后人群在扰动步骤中没有减少支撑肢体产生的向前角冲量。他们在第一个恢复步骤中也没有使用偏瘫肢体增加前导肢体角冲量或减少后随肢体向前角冲量。最后,在平衡临床评估中得分较低且运动障碍较大的中风后个体较少使用偏瘫肢体来减少向前动量。总体而言,这些结果表明偏瘫缺陷限制了从向前失去平衡中恢复的能力。未来针对中风人群反应性跨步反应的基于扰动的平衡训练可能受益于提高调节偏瘫地面反作用力以更好地控制全身动力学的能力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa0f/9659909/46a218544f3e/fneur-13-1032417-g0008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa0f/9659909/bf9797b7a7d8/fneur-13-1032417-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa0f/9659909/28bef83c9448/fneur-13-1032417-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa0f/9659909/2d918175683f/fneur-13-1032417-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa0f/9659909/cd57e7d62a0f/fneur-13-1032417-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa0f/9659909/62c9c77ef4e5/fneur-13-1032417-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa0f/9659909/e23eac8c5042/fneur-13-1032417-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa0f/9659909/088255d0bd79/fneur-13-1032417-g0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa0f/9659909/46a218544f3e/fneur-13-1032417-g0008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa0f/9659909/bf9797b7a7d8/fneur-13-1032417-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa0f/9659909/28bef83c9448/fneur-13-1032417-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa0f/9659909/2d918175683f/fneur-13-1032417-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa0f/9659909/cd57e7d62a0f/fneur-13-1032417-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa0f/9659909/62c9c77ef4e5/fneur-13-1032417-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa0f/9659909/e23eac8c5042/fneur-13-1032417-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa0f/9659909/088255d0bd79/fneur-13-1032417-g0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/aa0f/9659909/46a218544f3e/fneur-13-1032417-g0008.jpg

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