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站立平衡的联合平移和旋转扰动揭示了脑瘫儿童平衡障碍中交互抑制减少的贡献。

Combined translational and rotational perturbations of standing balance reveal contributions of reduced reciprocal inhibition to balance impairments in children with cerebral palsy.

机构信息

Department of Movement Sciences, KU Leuven, Leuven, Belgium.

Department of Rehabilitation Sciences, KU Leuven-UZ Leuven, Leuven, Belgium.

出版信息

PLoS Comput Biol. 2024 Jun 13;20(6):e1012209. doi: 10.1371/journal.pcbi.1012209. eCollection 2024 Jun.

DOI:10.1371/journal.pcbi.1012209
PMID:38870205
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11206838/
Abstract

Balance impairments are common in cerebral palsy. When balance is perturbed by backward support surface translations, children with cerebral palsy have increased co-activation of the plantar flexors and tibialis anterior muscle as compared to typically developing children. However, it is unclear whether increased muscle co-activation is a compensation strategy to improve balance control or is a consequence of reduced reciprocal inhibition. During translational perturbations, increased joint stiffness due to co-activation might aid balance control by resisting movement of the body with respect to the feet. In contrast, during rotational perturbations, increased joint stiffness will hinder balance control as it couples body to platform rotation. Therefore, we expect increased muscle co-activation in response to rotational perturbations if co-activation is caused by reduced reciprocal inhibition but not if it is merely a compensation strategy. We perturbed standing balance by combined backward translational and toe-up rotational perturbations in 20 children with cerebral palsy and 20 typically developing children. Perturbations induced forward followed by backward movement of the center of mass. We evaluated reactive muscle activity and the relation between center of mass movement and reactive muscle activity using a linear feedback model based on center of mass kinematics. In typically developing children, perturbations induced plantar flexor balance correcting muscle activity followed by tibialis anterior balance correcting muscle activity, which was driven by center of mass movement. In children with cerebral palsy, the switch from plantar flexor to tibialis anterior activity was less pronounced than in typically developing children due to increased muscle co-activation of the plantar flexors and tibialis anterior throughout the response. Our results thus suggest that a reduction in reciprocal inhibition causes muscle co-activation in reactive standing balance in children with cerebral palsy.

摘要

平衡障碍在脑瘫中很常见。当平衡受到向后的支撑面平移的干扰时,与正常发育的儿童相比,脑瘫儿童的足底屈肌和胫骨前肌的协同激活增加。然而,增加的肌肉协同激活是改善平衡控制的补偿策略,还是由于抑制减少的结果尚不清楚。在平移干扰期间,由于协同激活导致的关节刚度增加可能有助于通过抵抗身体相对于脚的运动来辅助平衡控制。相比之下,在旋转干扰期间,由于增加的关节刚度会使身体与平台旋转耦合,因此会阻碍平衡控制。因此,如果协同激活是由于抑制减少引起的,而不是仅仅是补偿策略,我们预计会对旋转干扰产生增加的肌肉协同激活。我们通过向后平移和脚趾向上旋转的组合来干扰站立平衡在 20 名脑瘫儿童和 20 名正常发育的儿童中。扰动会引起质心的向前和向后运动。我们使用基于质心运动学的线性反馈模型来评估反应性肌肉活动以及质心运动与反应性肌肉活动之间的关系。在正常发育的儿童中,扰动会引起足底屈肌平衡校正肌肉活动,随后是胫骨前肌平衡校正肌肉活动,这是由质心运动驱动的。在脑瘫儿童中,由于整个反应过程中足底屈肌和胫骨前肌的协同激活增加,从足底屈肌到胫骨前肌的活动转换不如正常发育的儿童明显。因此,我们的结果表明,抑制减少会导致脑瘫儿童在反应性站立平衡中产生肌肉协同激活。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0813/11206838/05501c46813a/pcbi.1012209.g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0813/11206838/9a108e6707f0/pcbi.1012209.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0813/11206838/aea6b5461f97/pcbi.1012209.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0813/11206838/2b64db6141fc/pcbi.1012209.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0813/11206838/645c6e2d465f/pcbi.1012209.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0813/11206838/6226bb6eea9d/pcbi.1012209.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0813/11206838/c059d892160f/pcbi.1012209.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0813/11206838/18d3c5b46248/pcbi.1012209.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0813/11206838/85bf42f39188/pcbi.1012209.g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0813/11206838/05501c46813a/pcbi.1012209.g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0813/11206838/9a108e6707f0/pcbi.1012209.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0813/11206838/aea6b5461f97/pcbi.1012209.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0813/11206838/2b64db6141fc/pcbi.1012209.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0813/11206838/645c6e2d465f/pcbi.1012209.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0813/11206838/6226bb6eea9d/pcbi.1012209.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0813/11206838/c059d892160f/pcbi.1012209.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0813/11206838/18d3c5b46248/pcbi.1012209.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0813/11206838/85bf42f39188/pcbi.1012209.g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0813/11206838/05501c46813a/pcbi.1012209.g009.jpg

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