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目的 探索非完全性脊髓损伤 (discompleteSCI)的直接电生理证据以及 4 氨基吡啶 (4 AP)的影响。方法 采用Allen’s打击模型造成T8-T9脊髓不同程度损伤 (空白组 35gcf损伤组 70gcf损伤组 ,10 0gcf损伤组 ) ,分别测定 10只正常大鼠和 4 0只脊髓损伤大鼠的硬膜外运动诱发电位 (scMEP)和细胞外运动诱发电位 (exMEP) ,并采用斜板试验和Tarlov评分系统判断脊髓神经功能。结果 超阈值经皮层刺激下正常大鼠的运动诱发电位 (MEP)包括 3- 4个早期负向波峰 (N1,N2 ,N3,N4 ) ,以及后续不稳定的晚期成分。最大波幅的N1和N2 分布在脊髓前束和腹外侧束 ,即锥体外系传导途径。 10 0gcf损伤组及脊髓横断组损伤水平以下MEP信号消失 ,而 35gcf损伤组MEP波幅降低 ,潜伏期延迟。 70gcf损伤组的 2 0只大鼠中 ,18只按临床标准属全瘫 ,但神经生理学检查证实其中 7只大鼠的脊髓损伤节段仍有传导功能 ,例如scMEP或exMEP的N1和N2 波仍保留。给予 4 AP后 ,残存的MEP波幅显著增高 ,分布范围扩大。结论 经皮层刺激诱发的MEP主要经锥体外系传导。MEP监测可提供一种直接检测SCI后脊髓运动传导束功能状态的方法 ,甚至可发现非完全性SCI中部分残留的运动神经纤维。而使用 4 AP或其他K+通道阻滞剂可能是治疗中、重度SCI晚期病人潜在?
Objective To explore the direct electrophysiological evidence of incompletecomplete SCI and the effect of 4-aminopyridine (4 AP). Methods Toxicities of T8-T9 spinal cord were induced by Allen’s attack model (70gcf injury group and 100gcf injury group in 35gcf injury group, blank group), and 10 normal rats and 40 spinal cord injured rats were respectively induced by epidural exercise (ScMEP) and extracellular motor evoked potentials (exMEP). The spinal nerve function was evaluated by using the ramp-plate test and the Tarlov scoring system. Results Ultrathreshold normal motor evoked potentials (MEPs) in the cortical region of the normal rats included 3-4 early negative peaks (N1, N2, N3, N4) and subsequent unstable components. The maximum amplitude of N1 and N2 distribution in the anterior spinal cord and ventral lateral bundle, the extrapyramidal pathway. The MEP signal disappeared in the group of 100gcf injury and spinal cord transection, while the amplitude of MEP in 35gcf injury group was decreased and latency was delayed. Of the 20 rats in the 70 gcf-injured group, 18 were paralyzed according to clinical criteria, but neurophysiological examination confirmed that seven of the rats still had conduction function in the spinal cord injury segment, such as N1 and N2 waves of scMEP or exMEP Keep. After given 4 AP, the residual MEP amplitude increased significantly, the distribution of the scope of expansion. Conclusion MEP induced by cortical stimulation is mainly transmitted through the extrapyramidal system. MEP monitoring provides a direct method of detecting the functional status of spinal motor conduction bundles after SCI, and may even find some residual motor nerve fibers in incomplete SCI. The use of 4 AP or other K + channel blockers may be in the treatment of moderate and severe SCI patients with potential late?