CAJ | 학술논문

目的　探索非完全性脊髓损伤（discomplete SCI）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35 gcf损伤组70 gcf损伤组，100 gcf损伤组），分别测定10只正常大鼠和40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。100gcf损伤组及脊髓横断组损伤水平以下MEP信号消失，而35 gcf损伤组MEP波幅降低，潜伏期延迟。70 gcf损伤组的20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晚期病人潜在的治疗方法。
목적　탐색비완전성척수손상（discomplete SCI）적직접전생리증거이급4-안기필정(4-AP)적영향。 방법　채용Allen's타격모형조성T8-T9척수불동정도손상（공백조35 gcf손상조70 gcf손상조，100 gcf손상조），분별측정10지정상대서화40지척수손상대서적경막외운동유발전위（scMEP）화세포외운동유발전위(exMEP)，병채용사판시험화Tarlov평분계통판단척수신경공능。 결과　초역치경피층자격하정상대서적운동유발전위（MEP）포괄3-4개조기부향파봉（N1, N2, N3, N4），이급후속불은정적만기성분。최대파폭적N1화N2분포재척수전속화복외측속，즉추체외계전도도경。100gcf손상조급척수횡단조손상수평이하MEP신호소실，이35 gcf손상조MEP파폭강저，잠복기연지。70 gcf손상조적20지대서중,18지안림상표준속전탄，단신경생이학검사증실기중7지대서적척수손상절단잉유전도공능，례여scMEP혹exMEP적N1화N2파잉보류。급여4-AP후，잔존적MEP파폭현저증고，분포범위확대。 결론　경피층자격유발적MEP주요경추체외계전도。MEP감측가제공일충직접검측SCI후척수운동전도속공능상태적방법，심지가발현비완전성SCI중부분잔류적운동신경섬유。이사용4-AP혹기타K+통도조체제가능시치료중、중도SCI만기병인잠재적치료방법。
Objective　To research the direct electrophysiological evidence of discomplete spinal cord injury (SCI) and the effect of 4-aminopyridine on it. Methods　Motor evoked potentials (MEPs), both spinal cord recorded MEPs (scMEPs) and extracellularly recorded MEPs (exMEPs) were recorded and characterized on a T13 epidural electrode (scMEPs) and an extracellular microelectrode (exMEPs) for 10 normal rats and 40 rats with lesions of various severity (sham, 35?g*cm force (gcf), 70?gcf, 100?gcf impact injury) at the T8-T9 cord using the Allen's drop model. The incline plane and Tarlov techniques were used to assess clinical neurological function. Results　MEPs in the normal rats were elicited by applying transcortical suprathreshold stimulation consisting of 3-4 early negative peaks (N1, N2, N3 and N4) followed by several late waves. The N1 and N2 peaks were largest in the anterior and ventrolateral funiculus, respectively, which was indicative of extrapyramidal pathways. The 100?gcf impact injuries and the cord transection abolished the MEP distal to the lesion, whereas the 35?gcf injuries resulted in a latency shift and amplitude decrement of the MEP peaks. Eighteen of the 20 rats with 70?gcf injuries showed clinical paraplegia. Among them, 7 rats had neurophysiological evidence of residual conduction pathways through the lesioned cord segment, such as the presence of N1 and N2 peaks in the scMEPs or exMEPs. After 4-aminopyridine (4-AP) administrations (1?mg/kg), the amplitude of the spared exMEP increased significantly and spread more widely. Conclusions　MEPs evoked by transcortical stimulation travel mostly in the extrapyramidal tract. MEP monitoring could provide an excellent method of detecting the functional integrity of the motor tracts after SCI, and could even detect spared motor fibers after discomplete SCI. Furthermore, the use of 4-AP or other K+ channel blocking agents may be a potential treatment for patients with chronic moderate to severe SCI.