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利用电肌肉刺激增强主动肌-拮抗肌肌神经接口的电生理性能。

Using Electrical Muscle Stimulation to Enhance Electrophysiological Performance of Agonist-Antagonist Myoneural Interface.

作者信息

Huang Jianping, Wang Ping, Wang Wei, Wei Jingjing, Yang Lin, Liu Zhiyuan, Li Guanglin

机构信息

Shenzhen Institute of Advanced Technology of the Chinese Academy of Sciences, Shenzhen 518055, China.

CAS Key Laboratory of Human-Machine Intelligence-Synergy Systems, Shenzhen Institute of Advanced Technology, Chinese Academy of Sciences (CAS), Shenzhen 518055, China.

出版信息

Bioengineering (Basel). 2024 Sep 10;11(9):904. doi: 10.3390/bioengineering11090904.

DOI:10.3390/bioengineering11090904
PMID:39329646
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11444137/
Abstract

The agonist-antagonist myoneural interface (AMI), a surgical method to reinnervate physiologically-relevant proprioceptive feedback for control of limb prostheses, has demonstrated the ability to provide natural afferent sensations for limb amputees when actuating their prostheses. Following AMI surgery, one potential challenge is atrophy of the disused muscles, which would weaken the reinnervation efficacy of AMI. It is well known that electrical muscle stimulus (EMS) can reduce muscle atrophy. In this study, we conducted an animal investigation to explore whether the EMS can significantly improve the electrophysiological performance of AMI. AMI surgery was performed in 14 rats, in which the distal tendons of bilateral solei donors were connected and positioned on the surface of the left biceps femoris. Subsequently, the left tibial nerve and the common peroneus nerve were sutured onto the ends of the connected donor solei. Two stimulation electrodes were affixed onto the ends of the donor solei for EMS delivery. The AMI rats were randomly divided into two groups. One group received the EMS treatment (designated as EMS_on) regularly for eight weeks and another received no EMS (designated as EMS_off). Two physiological parameters, nerve conduction velocity (NCV) and motor unit number, were derived from the electrically evoked compound action potential (CAP) signals to assess the electrophysiological performance of AMI. Our experimental results demonstrated that the reinnervated muscles of the EMS_on group generated higher CAP signals in comparison to the EMS_off group. Both NCV and motor unit number were significantly elevated in the EMS_on group. Moreover, the EMS_on group displayed statistically higher CAP signals on the indirectly activated proprioceptive afferents than the EMS_off group. These findings suggested that EMS treatment would be promising in enhancing the electrophysiological performance and facilitating the reinnervation process of AMI.

摘要

激动剂 - 拮抗剂肌神经接口(AMI)是一种为控制肢体假肢重新建立生理相关本体感觉反馈的外科手术方法,已证明在驱动假肢时能够为肢体截肢者提供自然的传入感觉。AMI手术后,一个潜在的挑战是废用肌肉的萎缩,这会削弱AMI的再支配效果。众所周知,电肌肉刺激(EMS)可以减少肌肉萎缩。在本研究中,我们进行了一项动物研究,以探讨EMS是否能显著改善AMI的电生理性能。对14只大鼠进行了AMI手术,将双侧比目鱼肌供体的远端肌腱连接并置于左侧股二头肌表面。随后,将左侧胫神经和腓总神经缝合到连接的供体比目鱼肌的末端。将两个刺激电极固定在供体比目鱼肌的末端以进行EMS传递。将接受AMI手术的大鼠随机分为两组。一组接受为期八周的定期EMS治疗(称为EMS_on),另一组不接受EMS治疗(称为EMS_off)。从电诱发复合动作电位(CAP)信号中得出两个生理参数,即神经传导速度(NCV)和运动单位数量,以评估AMI的电生理性能。我们的实验结果表明,与EMS_off组相比,EMS_on组的再支配肌肉产生了更高的CAP信号。EMS_on组的NCV和运动单位数量均显著升高。此外,EMS_on组在间接激活的本体感觉传入神经上显示出统计学上高于EMS_off组的CAP信号。这些发现表明,EMS治疗在增强电生理性能和促进AMI的再支配过程方面具有前景。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/475b/11444137/02bbe8d42684/bioengineering-11-00904-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/475b/11444137/bd9b2d52fb1b/bioengineering-11-00904-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/475b/11444137/63760f03cc7c/bioengineering-11-00904-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/475b/11444137/93737c1695b0/bioengineering-11-00904-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/475b/11444137/19584a542177/bioengineering-11-00904-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/475b/11444137/02bbe8d42684/bioengineering-11-00904-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/475b/11444137/bd9b2d52fb1b/bioengineering-11-00904-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/475b/11444137/63760f03cc7c/bioengineering-11-00904-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/475b/11444137/93737c1695b0/bioengineering-11-00904-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/475b/11444137/19584a542177/bioengineering-11-00904-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/475b/11444137/02bbe8d42684/bioengineering-11-00904-g005.jpg

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本文引用的文献

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Sci Rep. 2024 Jun 12;14(1):13456. doi: 10.1038/s41598-024-63134-4.
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Nerve function restoration following targeted muscle reinnervation after varying delayed periods.不同延迟期后靶向肌肉再支配后的神经功能恢复。
Neural Regen Res. 2023 Dec;18(12):2762-2766. doi: 10.4103/1673-5374.373659.
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Autonomic modulation by low-intensity focused ultrasound stimulation of the vagus nerve.
低强度聚焦超声刺激迷走神经的自主调节。
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The Agonist-antagonist Myoneural Interface.激动剂-拮抗剂肌神经接口
Tech Orthop. 2021 Dec;36(4):337-344. doi: 10.1097/bto.0000000000000552.
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Sensory feedback for limb prostheses in amputees.截肢者的肢体假肢的感觉反馈。
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