Motor cortex rTMS restores defective intracortical inhibition in chronic neuropathic pain
Motor cortex rTMS restores defective intracortical inhibition in chronic neuropathic pain
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DOI：
10.1212/01.wnl.0000242731.10074.3c
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发表时间：
2006-11-14
期刊：
影响因子：
9.9
通讯作者：
Nguyen, J. P.
中科院分区：
文献类型：
--
作者：
Lefaucheur, J. P.;Drouot, X.;Nguyen, J. P.
目的：评估慢性神经性疼痛患者在基线和运动皮层重复经颅磁刺激（rTMS）后的皮层兴奋性变化。研究方法：在22例单侧手部疼痛的各种神经起源和22个年龄匹配的健康对照组，我们研究了以下参数的皮质兴奋性：运动阈值在休息，运动诱发电位振幅比在两个强度，皮质沉默期（CSP），和皮质内抑制（ICI）和皮质内促进。我们比较了健康受试者和基线患者的这些参数。我们还研究了兴奋性的变化，对应于疼痛的手的患者后，积极或假rTMS的皮质区域在1或10 Hz的运动皮层。结果如下：在基线时，与健康受试者相比，患者的两个半球的CSP缩短，与疼痛评分相关，而ICI仅在与疼痛的手相对应的运动皮层减少。关于rTMS的影响，单一的显着变化是ICI增加对应于疼痛的手，积极的10 Hz rTMS后，与疼痛缓解相关的运动皮层。结论：慢性神经性疼痛与运动皮层去抑制相关，表明GABA能神经传递受损与疼痛的某些方面或潜在的感觉或运动障碍有关。运动皮层刺激产生的镇痛作用可能至少部分是由于皮质内抑制过程的恢复。
Objective: To assess cortical excitability changes in patients with chronic neuropathic pain at baseline and after repetitive transcranial magnetic stimulation (rTMS) of the motor cortex. Methods: In 22 patients with unilateral hand pain of various neurologic origins and 22 age-matched healthy controls, we studied the following parameters of cortical excitability: motor threshold at rest, motor evoked potential amplitude ratio at two intensities, cortical silent period (CSP), and intracortical inhibition (ICI) and intracortical facilitation. We compared these parameters between healthy subjects and patients at baseline. We also studied excitability changes in the motor cortex corresponding to the painful hand of patients after active or sham rTMS of this cortical region at 1 or 10 Hz. Results: At baseline, CSP was shortened for the both hemispheres of patients vs healthy subjects, in correlation with pain score, while ICI was reduced only for the motor cortex corresponding to the painful hand. Regarding rTMS effects, the single significant change was ICI increase in the motor cortex corresponding to the painful hand, after active 10-Hz rTMS, in correlation with pain relief. Conclusion: Chronic neuropathic pain was associated with motor cortex disinhibition, suggesting impaired GABAergic neurotransmission related to some aspects of pain or to underlying sensory or motor disturbances. The analgesic effects produced by motor cortex stimulation could result, at least partly, from the restoration of defective intracortical inhibitory processes.