• Kazuyoshi Nakanishi, Nobuhiro Tanaka, Naosuke Kamei, Takahiko Hamasaki, Koji Nishida, Yoriko Touten, and Mitsuo Ochi.
• 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. kazn@hiroshima-u.ac.jp
• J. Neurol. Sci. 2007 May 15;256(1-2):71-4.

AbstractWe 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.

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