2026-03-08T18:25:51Z https://hiroshima.repo.nii.ac.jp/oai

oai:hiroshima.repo.nii.ac.jp:02006667 2025-02-21T08:07:26Z 1730444907710

Corticospinal tract conduction block results in the prolongation of central motor conduction time in compressive cervical myelopathy Nakanishi, Kazuyoshi Nakanishi Kazuyoshi Tanaka, Nobuhiro Tanaka Nobuhiro Fujiwara, Yasushi Fujiwara Yasushi Kamei, Naosuke Kamei Naosuke Ochi, Mitsuo Ochi Mitsuo open access Copyright (c) 2006 Elsevier Ltd. motor evoked potentials central motor conduction time spinal cord evoked potentials cervical myelopathy transcranial magnetic stimulation 490 Objective: The objective of this study was to analyze corticospinal function in patients with compressive cervical myelopathy and to elucidate the mechanism underlying its prolonged central motor conduction time (CMCT). Methods: Motor evoked potentials following transcranial magnetic stimulation (TMS) and peripheral conduction time in the ulnar and tibial nerves following electrical stimulation were measured from the abductor digiti minimi (ADM) and abductor hallucis (AH) muscles in 24 patients with compressive cervical myelopathy and used to calculate CMCT. Spinal cord evoked potentials (SCEPs) following transcranial electric stimulation were recorded intraoperatively from the C2-3 to C6-7 intervertebral levels. Correlations between prolonged CMCT and SCEP values were then estimated. Results: The shorter/longer CMCT between the patients' right and left ADM and AH were 8.5 ± 2.9/11.5 ± 3.3 and 16.2 ± 3.1/18.4 ± 3.3 ms, respectively (mean ± SD). The SCEPs amplitude at C6-7, compared to C2-3, was 25.7 ± 21.0 %.0 The attenuation of SCEP amplitude, but not latency, at C6-7 correlated significantly with CMCT prolongation. Conclusions: Our data support the view that CMCT prolongation is primarily due to corticospinal conduction block, rather than conduction delay. Significance: Insight was provided into the mechanism of corticospinal dysfunction in compressive cervical myelopathy. Elsevier 2006-03 eng journal article AO https://hiroshima.repo.nii.ac.jp/records/2006667 10.1016/j.clinph.2005.11.010 16442342 http://dx.doi.org/10.1016/j.clinph.2005.11.010 1388-2457 AA11309888 Clinical Neurophysiology Clinical Neurophysiology 117 3 623 623 627 https://hiroshima.repo.nii.ac.jp/record/2006667/files/ClinNeur_117_623.pdf 361.4 KB