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脊髓损伤后恢复运动功能的组合式电-药理神经假体接口。

Combinatory electrical and pharmacological neuroprosthetic interfaces to regain motor function after spinal cord injury.

机构信息

Experimental Neurorehabilitation Laboratory, Department of Neurology, University of Zurich, CH-8006 Zurich, Switzerland.

出版信息

IEEE Trans Biomed Eng. 2009 Nov;56(11 Pt 2):2707-11. doi: 10.1109/TBME.2009.2027226. Epub 2009 Jul 24.

DOI:10.1109/TBME.2009.2027226
PMID:19635690
Abstract

Severe lesions of the rodent or human spinal cord lead to permanent paralysis of the legs. Here, we review novel evidences suggesting that interventions combining pharmacological and electrical stimulations of the spinal cord have a high potential to promote the recovery of locomotion following severe spinal cord injuries in humans. These strategies are based on the existence of webs of circuits and receptors embedded in the spinal motor infrastructure that each modulate specific aspects of locomotor movements. We show that chemical or electrical stimulations can engage specific elements of this spinal machinery, thus resulting in distinct patterns of locomotion in paralyzed spinal rats. In turn, simultaneous chemical stimulations of neural receptors and/or electrical stimulations of multiple spinal segments can synergistically facilitate locomotor movements. These preliminary results provide a strong rationale for the development of neuroprosthetic chemotrode and electrode arrays that would enable a detailed and distributed access to the different elements of the spinal motor infrastructure. Such novel biomedical technologies may offer unparalleled potential to induce multiple and flexible locomotor states in paralyzed subjects.

摘要

严重的啮齿动物或人类脊髓损伤会导致腿部永久性瘫痪。在这里,我们回顾了新的证据,表明结合脊髓的药理学和电刺激的干预措施具有很大的潜力,可以促进人类严重脊髓损伤后的运动功能恢复。这些策略基于存在于脊髓运动基础设施中的电路和受体网络,它们各自调节运动运动的特定方面。我们表明,化学或电刺激可以激活这种脊髓机制的特定元件,从而导致瘫痪的脊髓大鼠出现不同的运动模式。反过来,同时对神经受体进行化学刺激和/或对多个脊髓节段进行电刺激可以协同促进运动运动。这些初步结果为神经假体化学刺激电极和电极阵列的开发提供了强有力的依据,这些技术可以实现对脊髓运动基础设施的不同元件的详细和分布式访问。这些新的生物医学技术可能为诱导瘫痪受试者的多种灵活运动状态提供无与伦比的潜力。

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