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急性间歇性低氧暴露增强不完全性脊髓损伤患者的躯体运动功能。

Exposure to acute intermittent hypoxia augments somatic motor function in humans with incomplete spinal cord injury.

机构信息

Emory University, School of Medicine, Department of Rehabilitation Medicine, Atlanta, GA 30322, USA.

出版信息

Neurorehabil Neural Repair. 2012 Feb;26(2):163-72. doi: 10.1177/1545968311412055. Epub 2011 Aug 5.

DOI:10.1177/1545968311412055
PMID:21821826
Abstract

BACKGROUND

Neural plasticity may contribute to motor recovery following spinal cord injury (SCI). In rat models of SCI with respiratory impairment, acute intermittent hypoxia (AIH) strengthens synaptic inputs to phrenic motor neurons, thereby improving respiratory function by a mechanism known as respiratory long-term facilitation. Similar intermittent hypoxia-induced facilitation may be feasible in somatic motor pathways in humans.

OBJECTIVE

Using a randomized crossover design, the authors tested the hypothesis that AIH increases ankle strength in people with incomplete SCI.

METHODS

Ankle strength was measured in 13 individuals with chronic, incomplete SCI before and after AIH. Voluntary ankle strength was estimated using changes in maximum isometric ankle plantar flexion torque generation and plantar flexor electromyogram activity following 15 low oxygen exposures (Fio(2) = 0.09, 1-minute intervals). Results were compared with trials where subjects received sham exposure to room air.

RESULTS

AIH increased plantar flexion torque by 82 ± 33% (P < .003) immediately following AIH and was sustained above baseline for more than 90 minutes (P < .007). Increased ankle plantar flexor electromyogram activity (P = .01) correlated with increased torque (r(2) = .5; P < .001). No differences in plantar flexion strength or electromyogram activity were observed in sham experiments.

CONCLUSIONS

AIH elicits sustained increases in volitional somatic motor output in persons with chronic SCI. Thus, AIH has promise as a therapeutic tool to induce plasticity and enhance motor function in SCI patients.

摘要

背景

神经可塑性可能有助于脊髓损伤(SCI)后的运动功能恢复。在伴有呼吸功能障碍的 SCI 大鼠模型中,急性间歇性低氧(AIH)增强膈神经运动神经元的突触传入,从而通过呼吸长期易化的机制改善呼吸功能。在人类躯体运动通路中,可能也存在类似的间歇性低氧诱导的易化作用。

目的

作者采用随机交叉设计,检验 AIH 可增强不完全性 SCI 患者踝部力量的假说。

方法

13 例慢性不完全性 SCI 患者参与本研究,在接受 AIH 前后,采用 15 次低氧暴露(Fio₂=0.09,1 分钟间隔)来测量踝部力量。通过最大等长踝跖屈力矩产生和腓肠肌肌电图活动的变化来估计自愿踝部力量。将结果与接受模拟空气暴露的试验进行比较。

结果

AIH 可使踝跖屈力矩即刻增加 82±33%(P<0.003),并持续超过 90 分钟(P<0.007)。增加的踝部跖屈肌肌电图活动(P=0.01)与增加的力矩相关(r²=0.5;P<0.001)。在模拟实验中,未观察到踝部跖屈力量或肌电图活动的差异。

结论

AIH 可引发慢性 SCI 患者的随意躯体运动输出持续增加。因此,AIH 有望成为一种治疗工具,通过诱导可塑性来增强 SCI 患者的运动功能。

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