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慢性迷走神经刺激会增加丘脑皮质体感诱发电位的潜伏期。

Chronic vagus nerve stimulation increases the latency of the thalamocortical somatosensory evoked potential.

作者信息

Naritoku D K, Morales A, Pencek T L, Winkler D

机构信息

Division of Neurology, Southern Illinois University School of Medicine, Springfield 62794-9230.

出版信息

Pacing Clin Electrophysiol. 1992 Oct;15(10 Pt 2):1572-8. doi: 10.1111/j.1540-8159.1992.tb02935.x.

Abstract

The Neurocybernetic Prosthesis (NCP) is a pacemaker-like device that has been designed to provide chronic intermittent vagus nerve stimulation. It is currently under study for the treatment of refractory partial onset epilepsy, and preliminary studies have indicated that partial onset seizures are improved by this therapy. The mechanisms by which it exerts its antiepileptic effect are not well understood. Although there are extensive pathways to the forebrain from the nuclei of the vagus nerve, the evidence that the NCP alters neural transmission outside the vagal system is limited. We prospectively examined somatosensory and brain stem auditory evoked potentials (BAEPs) in three patients receiving NCP implantation to determine if changes in these studies occur as a result of chronic vagus nerve stimulation. The results demonstrate a significant prolongation of the cervicomedullary to thalamocortical potential (N13-N20) interval on somatosensory evoked potential (SSEP) studies following activation of the device. No other significant changes were seen on SSEP or BAEP in the NCP implanted patients or normal controls. The findings suggest that chronic vagus nerve stimulation does alter neuronal networks outside of the brain stem vagus system, and may potentially provide a means to clinically monitor and titrate this therapy.

摘要

神经控制假体(NCP)是一种类似起搏器的装置,其设计目的是提供慢性间歇性迷走神经刺激。目前正在研究其用于治疗难治性部分性发作癫痫,初步研究表明这种疗法可改善部分性发作。其发挥抗癫痫作用的机制尚不清楚。尽管从迷走神经核到前脑有广泛的通路,但NCP改变迷走神经系统外神经传递的证据有限。我们前瞻性地检查了3例接受NCP植入患者的体感诱发电位和脑干听觉诱发电位(BAEP),以确定这些检查中的变化是否由慢性迷走神经刺激引起。结果显示,在激活该装置后,体感诱发电位(SSEP)研究中颈髓至丘脑皮质电位(N13-N20)间期显著延长。在植入NCP的患者或正常对照的SSEP或BAEP中未观察到其他显著变化。这些发现表明,慢性迷走神经刺激确实会改变脑干迷走神经系统外的神经元网络,并可能为临床监测和调整这种疗法提供一种方法。

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