Nakanishi Kazuyoshi, Tanaka Nobuhiro, Kamei Naosuke, Hamasaki Takahiko, Nishida Koji, Touten Yoriko, Ochi Mitsuo
Department of Orthopaedic Surgery, Programs for Applied Biomedicine, Division of Clinical Medical Science, Graduate School of Biomedical Sciences, Hiroshima University, Kasumi 1-2-3, Hiroshima, Japan.
J Neurol Sci. 2007 May 15;256(1-2):71-4. doi: 10.1016/j.jns.2007.02.009. Epub 2007 Mar 26.
We examined the relationship between the CMCT and features of spinal cord evoked potentials (SCEPs) among 25 patients with compressive cervical myelopathy to elucidate the mechanism underlying the prolonged central motor conduction time (CMCT) in patients with compressive cervical myelopathy. CMCT values were calculated by measuring motor evoked potentials from the abductor digiti minimi muscles (ADMs) and abductor hallucis muscles (AHs) following transcranial magnetic stimulation and peripheral conduction times determined in the ulnar and tibial nerves. SCEPs following transcranial electrical stimulation were recorded intraoperatively from C2-3, C6-7 and T11-12. The shorter/longer CMCTs between the patients' right and left ADMs and AHs were 9.5+/-3.2/11.5+/-3.8 and 16.2+/-2.8/18.8+/-3.3 ms, respectively (mean+/-SD). The percentage ratio of the amplitude of the D-wave at C6-7 or T11-12 to that at C2-3 was 19.4+/-14.2 or 3.2+/-3.1%, respectively. The CMCT value was significantly correlated with the attenuation of SCEP amplitude, but not with SCEP latency both at C6-7 and T11-12, suggesting that CMCT prolongation is primarily due to corticospinal conduction block rather than conduction delay. Spinal motor neurons might need more time to fire in patients with compressive cervical myelopathy when corticospinal potentials, but not conduction, are attenuated, thereby resulting in prolonged CMCT.
我们研究了25例压迫性颈椎病患者的中枢运动传导时间（CMCT）与脊髓诱发电位（SCEPs）特征之间的关系，以阐明压迫性颈椎病患者CMCT延长的潜在机制。CMCT值通过在经颅磁刺激后测量小指展肌（ADMs）和拇短展肌（AHs）的运动诱发电位以及在尺神经和胫神经中测定的周围传导时间来计算。术中记录经颅电刺激后的SCEPs，记录部位为C2-3、C6-7和T11-12。患者左右ADMs和AHs之间较短/较长的CMCT分别为9.5±3.2/11.5±3.8和16.2±2.8/18.8±3.3毫秒（平均值±标准差）。C6-7或T11-12处D波振幅与C2-3处D波振幅的百分比分别为19.4±14.2或3.2±3.1%。CMCT值与C6-7和T11-12处SCEP振幅的衰减显著相关，但与SCEP潜伏期无关，这表明CMCT延长主要是由于皮质脊髓传导阻滞而非传导延迟。当皮质脊髓电位而非传导减弱时，压迫性颈椎病患者的脊髓运动神经元可能需要更多时间来放电，从而导致CMCT延长。
