Corticospinal tract conduction block results in the prolongation of central motor conduction time in compressive cervical myelopathy.

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%. 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. Conclusions: Insight was provided into the mechanism of corticospinal dysfunction in compressive cervical myelopathy.