Impaired crossed facilitation of the corticospinal pathway after cervical spinal cord injury

Impaired crossed facilitation of the corticospinal pathway after cervical spinal cord injury
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DOI:
10.1152/jn.00850.2011
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发表时间:
2012-05-01
影响因子:
2.5
通讯作者:
Perez, Monica A.
Perez, Monica A.
中科院分区:
医学3区
文献类型:
--
作者:
Bunday, Karen L.;Perez, Monica A.

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邦迪吉隆坡,佩雷斯马萨诸塞州。颈脊髓损伤后皮质脊髓通路的交叉促进受损。 J Neurophysiol 107: 2901-2911, 2012。首次发表于 2012 年 2 月 22 日; doi:10.1152/jn.00850.2011.-在未受伤的人类中,众所周知,身体一侧肌肉的自愿收缩可以促进对侧皮质脊髓通路的传播。这种交叉促进效应可能有利于肢体间协调和运动表现。慢性脊髓损伤(SCI)后皮质脊髓功能的这方面是否得以保留尚不清楚。在这里,我们使用经颅磁刺激,在慢性颈椎 SCI (C-5-C-8) 患者中显示,在对侧远端或近端手臂肌肉的随意收缩水平增加期间,静息内在手部肌肉中的运动诱发电位 (MEP) 的大小保持不变。相比之下,健康对照受试者在执行相同的运动任务时,静息手部肌肉的 MEP 大小有所增加。慢性颈椎 SCI 后自愿肌电图的强度与 MEP 大小呈负相关,而在健康对照受试者中呈正相关。为了研究 MEP 交叉促进的机制,我们通过测试 F 波和颈髓 MEP (CMEP) 来检查短间隔皮质内抑制 (SICI)、半球间抑制 (IHI) 和运动神经元行为。颈椎 SCI 后,在强烈的自主收缩期间,SICI 没有变化,与休息时相比,健康对照受试者的 SICI 有所下降。颈椎 SCI 后,F 波幅度、持续时间以及 CMEP 大小保持不变,但与休息时相比,健康对照组受试者有所增加。此外,在强烈的随意收缩期间,颈椎 SCI 中的 IHI 与休息时相比没有变化。我们的结果表明,GABA 能皮质内回路、运动皮质之间的半球间谷氨酸能投射以及食指运动神经元的兴奋性是 SCI 后观察到的缺乏交叉皮质脊髓易化的潜在神经机制,至少部分是这样的。我们的数据表明脊髓运动神经元是慢性颈椎 SCI 后调节皮质脊髓传递的关键部位。
Bunday KL, Perez MA. Impaired crossed facilitation of the corticospinal pathway after cervical spinal cord injury. J Neurophysiol 107: 2901-2911, 2012. First published February 22, 2012; doi:10.1152/jn.00850.2011.-In uninjured humans, it is well established that voluntary contraction of muscles on one side of the body can facilitate transmission in the contralateral corticospinal pathway. This crossed facilitatory effect may favor interlimb coordination and motor performance. Whether this aspect of corticospinal function is preserved after chronic spinal cord injury (SCI) is unknown. Here, using transcranial magnetic stimulation, we show in patients with chronic cervical SCI (C-5-C-8) that the size of motor evoked potentials (MEPs) in a resting intrinsic hand muscle remained unchanged during increasing levels of voluntary contraction with a contralateral distal or proximal arm muscle. In contrast, MEP size in a resting hand muscle was increased during the same motor tasks in healthy control subjects. The magnitude of voluntary electromyography was negatively correlated with MEP size after chronic cervical SCI and positively correlated in healthy control subjects. To examine the mechanisms contributing to MEP crossed facilitation we examined short-interval intracortical inhibition (SICI), interhemispheric inhibition (IHI), and motoneuronal behavior by testing F waves and cervicomedullary MEPs (CMEPs). During strong voluntary contractions SICI was unchanged after cervical SCI and decreased in healthy control subjects compared with rest. F-wave amplitude and persistence and CMEP size remained unchanged after cervical SCI and increased in healthy control subjects compared with rest. In addition, during strong voluntary contractions IHI was unchanged in cervical SCI compared with rest. Our results indicate that GABAergic intracortical circuits, interhemispheric glutamatergic projections between motor cortices, and excitability of index finger motoneurons are neural mechanisms underlying, at least in part, the lack of crossed corticospinal facilitation observed after SCI. Our data point to the spinal motoneurons as a critical site for modulating corticospinal transmission after chronic cervical SCI.