The cause of slowed forearm median conduction velocity in carpal tunnel syndrome

Objectives: Attempting to answer a debate concerning the etiopathogenesis of the decreased forearm median motor conduction velocity (FMMCV), we tried to use proximal stimulation at the wrist, elbow, mid-arm and axillary regions to determine segmental median motor conduction velocity (MMCV). We also correlated the FMMCV with median motor distal latency (MMDL) and compound muscle action potential (CMAP) amplitudes of the abductor pollicis brevis (APB) muscle in order to assess whether the conduction block of large myelinating fibers or retrograde axonal atrophy was the major cause of the decreased FMMCV. Background: The cause of the decreased FMMCV resulting from either the conduction block of the large myelinating fibers at the wrist or distal compression with retrograde axonal atrophy remains an unresolved issue at the moment. Animal models have supported the hypothesis that the retrograde axonal atrophy might also occur in humans. Other authors believe the standard FMMCV is calculated by subtracting the distal latency which may not represent an exact assessment of FMMCV but rather the velocity of small fibers that persist through the carpal tunnel. Subjects and methods: Patients with the clinical symptoms and signs of carpal tunnel syndrome (CTS) confirmed using standard electrodiagnosis were included. The patients were arbitrarily divided into two groups based on the FMMCV, one with reduced FMMCV (n = 20, FMMCV < 50 m/s) and the other with normal FMMCV (n = 35, FMMCV greater than or equal to 50 m/s). Age-matched volunteers served as controls. We explored motor conduction proximally at wrist, elbow, mid-arm and axillary stimulation, and recorded at the APE muscles. Based on the latency differences, we calculated the FMMCV, distal arm MMCV (DAMMCV) and proximal arm MMCV (PAMMCV), and compared the conduction velocity (CV) differences of DAMMCV-FMMCV, PAMMCV-FMMCV and PAMMCV-DAMMCV in the two patient groups and the control. Furthermore, we correlated FMMCV with MMDL and CMAP amplitudes of APE muscle because MMDL and CMAP amplitudes might reflect the integrity of the large myelinating fibers. Results: CMAP amplitudes of APE muscle at wrist stimulation and MMDL were not correlated with FMMCV in either of the two patient groups; however, the CMAP amplitude was markedly decreased and MMDL was significantly prolonged when compared with normal controls. The significant increase of CV gradient of DAMMCV-FMMCV and PAMMCV-FMMCV without an equal increase of CV gradient of PAMMCV-DAMMCV only occurred in the reduced FMMCV patient group, suggesting that the conduction block is not the primary cause. The CV gradient of DAMMCV-FMMCV and PAMMCV-DAMMCV did not show any significant difference between patients with the normal FMMCV and the control group. Conclusion: The retrograde axonal atrophy, not selective damage of the large fibers at the wrist, was the diner cause of the decreased FMMCV. (C) 2000 Elsevier Science Ireland Ltd. All rights reserved.