Chang Ming Hong, Wei Shiew Jue, Chen Lee Wei
Section of Neurology, Taichung Veterans General Hospital, No. 160, Chung Kang Road, Section 3, 40705, Taichung, Taiwan, ROC.
Clin Neurophysiol. 2003 Jun;114(6):1091-5. doi: 10.1016/s1388-2457(03)00057-9.
The exact cause of decreased forearm median motor conduction velocity (FMMCV) in carpal tunnel syndrome (CTS) is still a subject of controversy. A conduction block or an axonal loss in the large myelinating fibers upon wrist compression, or retrograde axonal atrophy, is suspected.
In order to attempt a determination of the cause, 10 patients with clinical symptoms and signs of CTS, confirmed using standard electrodiagnosis and with a slowed FMMCV <50m/s, were included in this study. Serial standard median motor conduction studies were performed at baseline, 1 week, 2 weeks, 4 weeks, 8 weeks, and 12 weeks after endoscopic ligament release. Serial median motor distal latencies (MMDL), compound muscle action potential (CMAP) amplitudes, and FMMCV, were determined and compared.
Significant improvement in MMDL had occurred at the 1-week follow-up examination; however, no such improvement in FMMCV was observed. Furthermore, a significant increase in CMAP amplitude was evidenced beginning 4 weeks after surgery. The results revealed an improvement in median motor conduction, across the wrist segment, that did not parallel the increase in FMMCV, suggesting that a conduction block or axonal loss at wrist compression was not the likely cause of the decreased FMMCV.
Retrograde axonal atrophy, not selective damage to the large myelinating fibers at the wrist, is the direct cause of decreased FMMCV in CTS.
