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在双侧跖屈肌无力的个体中,将运输代谢成本降至最低可预测在一系列踝足矫形器刚度下步态力学的变化。

Minimization of metabolic cost of transport predicts changes in gait mechanics over a range of ankle-foot orthosis stiffnesses in individuals with bilateral plantar flexor weakness.

作者信息

Kiss Bernadett, Waterval Niels F J, van der Krogt Marjolein M, Brehm Merel A, Geijtenbeek Thomas, Harlaar Jaap, Seth Ajay

机构信息

Department of Biomechanical Engineering, Delft University of Technology, Delft, Netherlands.

Amsterdam UMC Location University of Amsterdam, Rehabilitation Medicine, Amsterdam, Netherlands.

出版信息

Front Bioeng Biotechnol. 2024 May 23;12:1369507. doi: 10.3389/fbioe.2024.1369507. eCollection 2024.

DOI:10.3389/fbioe.2024.1369507
PMID:38846804
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11153850/
Abstract

Neuromuscular disorders often lead to ankle plantar flexor muscle weakness, which impairs ankle push-off power and forward propulsion during gait. To improve walking speed and reduce metabolic cost of transport (mCoT), patients with plantar flexor weakness are provided dorsal-leaf spring ankle-foot orthoses (AFOs). It is widely believed that mCoT during gait depends on the AFO stiffness and an optimal AFO stiffness that minimizes mCoT exists. The biomechanics behind why and how an optimal stiffness exists and benefits individuals with plantar flexor weakness are not well understood. We hypothesized that the AFO would reduce the required support moment and, hence, metabolic cost contributions of the ankle plantar flexor and knee extensor muscles during stance, and reduce hip flexor metabolic cost to initiate swing. To test these hypotheses, we generated neuromusculoskeletal simulations to represent gait of an individual with bilateral plantar flexor weakness wearing an AFO with varying stiffness. Predictions were based on the objective of minimizing mCoT, loading rates at impact and head accelerations at each stiffness level, and the motor patterns were determined via dynamic optimization. The predictive gait simulation results were compared to experimental data from subjects with bilateral plantar flexor weakness walking with varying AFO stiffness. Our simulations demonstrated that reductions in mCoT with increasing stiffness were attributed to reductions in quadriceps metabolic cost during midstance. Increases in mCoT above optimum stiffness were attributed to the increasing metabolic cost of both hip flexor and hamstrings muscles. The insights gained from our predictive gait simulations could inform clinicians on the prescription of personalized AFOs. With further model individualization, simulations based on mCoT minimization may sufficiently predict adaptations to an AFO in individuals with plantar flexor weakness.

摘要

神经肌肉疾病常常导致踝关节跖屈肌肌无力,这会损害步态中踝关节蹬离力量和向前推进力。为了提高步行速度并降低运输代谢成本(mCoT),为患有跖屈肌无力的患者提供了背叶弹簧式踝足矫形器(AFO)。人们普遍认为,步态期间的mCoT取决于AFO的刚度,并且存在使mCoT最小化的最佳AFO刚度。然而,关于为何存在最佳刚度以及它如何使跖屈肌无力个体受益背后的生物力学原理,目前尚未得到充分理解。我们假设AFO会减少所需的支撑力矩,从而减少站立期踝关节跖屈肌和膝关节伸肌的代谢成本贡献,并降低启动摆动期时髋屈肌的代谢成本。为了验证这些假设,我们生成了神经肌肉骨骼模拟模型,以代表一名双侧跖屈肌无力患者穿着不同刚度AFO时的步态。预测基于使mCoT最小化的目标、每个刚度水平下着地时的加载速率和头部加速度,并且通过动态优化确定运动模式。将预测的步态模拟结果与双侧跖屈肌无力患者在不同AFO刚度下行走的实验数据进行比较。我们的模拟结果表明,随着刚度增加mCoT的降低归因于支撑中期股四头肌代谢成本的降低。mCoT超过最佳刚度后的增加归因于髋屈肌和腘绳肌代谢成本的增加。我们从预测性步态模拟中获得的见解可以为临床医生开具个性化AFO提供参考。随着模型进一步个体化,基于mCoT最小化的模拟可能足以预测跖屈肌无力个体对AFO的适应性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d23c/11153850/3609db5216ea/fbioe-12-1369507-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d23c/11153850/237febeb8aa5/fbioe-12-1369507-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d23c/11153850/159b4753ab0a/fbioe-12-1369507-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d23c/11153850/9a6fa7e034c3/fbioe-12-1369507-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d23c/11153850/3a780dd5a0a6/fbioe-12-1369507-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d23c/11153850/da570ad70f2a/fbioe-12-1369507-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d23c/11153850/3609db5216ea/fbioe-12-1369507-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d23c/11153850/237febeb8aa5/fbioe-12-1369507-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d23c/11153850/159b4753ab0a/fbioe-12-1369507-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d23c/11153850/9a6fa7e034c3/fbioe-12-1369507-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d23c/11153850/3a780dd5a0a6/fbioe-12-1369507-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d23c/11153850/da570ad70f2a/fbioe-12-1369507-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d23c/11153850/3609db5216ea/fbioe-12-1369507-g006.jpg

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