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维拉帕米对多发性硬化症患者中枢传导的影响。

Verapamil-induced changes in central conduction in patients with multiple sclerosis.

作者信息

Gilmore R L, Kasarskis E J, McAllister R G

出版信息

J Neurol Neurosurg Psychiatry. 1985 Nov;48(11):1140-6. doi: 10.1136/jnnp.48.11.1140.

Abstract

The electrophysiological characteristics of demyelinated axons are sensitive to changes in plasma calcium concentration. This study investigated the effect of verapamil, a calcium antagonist drug, on brainstem auditory, visual, and somatosensory evoked potentials in multiple sclerosis patients. Eight clinically stable patients with abnormal visual and/or brainstem auditory evoked potentials and four normal volunteers were studied. During intravenous infusions of verapamil (mean plasma concentration = 130.0 +/- 56.4 ng/ml), the latencies of peaks III and V were shortened (p less than 0.05) in multiple sclerosis patients with abnormally prolonged BAEPs. The I-III (delta = 0.08 ms), III-V (delta = 0.46 ms), and I-V (delta = 0.53 ms) interpeak intervals, and the P100 latency (delta = 10.15 ms) of the visual evoked potential were similarly affected in these patients. In contrast, normal evoked potentials of both multiple sclerosis patients and control subjects were not altered compared to baseline recordings obtained 24 hours earlier. Intravenous verapamil, therefore, alters the BAEPs and VEPs of some multiple sclerosis patients with demyelinated auditory and visual pathways by shortening pathologically prolonged latencies toward normal. The present study suggests pharmacological manipulation of calcium-dependent processes, possibly at the level of the demyelinated axon, can acutely facilitate central conduction of electrical impulses in some patients with clinically stable multiple sclerosis.

摘要

脱髓鞘轴突的电生理特性对血浆钙浓度的变化敏感。本研究调查了钙拮抗剂药物维拉帕米对多发性硬化症患者脑干听觉、视觉和体感诱发电位的影响。研究了8名视觉和/或脑干听觉诱发电位异常的临床稳定患者以及4名正常志愿者。在静脉输注维拉帕米期间(平均血浆浓度 = 130.0 +/- 56.4 ng/ml),脑干听觉诱发电位异常延长的多发性硬化症患者中,峰III和峰V的潜伏期缩短(p < 0.05)。这些患者的I-III(δ = 0.08 ms)、III-V(δ = 0.46 ms)和I-V(δ = 0.53 ms)峰间间期以及视觉诱发电位的P100潜伏期(δ = 10.15 ms)也受到类似影响。相比之下,与24小时前获得的基线记录相比,多发性硬化症患者和对照受试者的正常诱发电位没有改变。因此,静脉注射维拉帕米通过将病理延长的潜伏期缩短至正常,改变了一些听觉和视觉通路脱髓鞘的多发性硬化症患者的脑干听觉诱发电位和视觉诱发电位。本研究表明,对钙依赖性过程进行药理操作,可能在脱髓鞘轴突水平,可在一些临床稳定的多发性硬化症患者中急性促进电冲动的中枢传导。

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