Electrophysiological studies in carpal tunnel syndrome

The exact reason for the decrease in median nerve motor conduction velocity in the forearm segment in patients with Carpal tunnel syndrome (CTS) is not known. However, some studies support the hypothesis of blockage of large myelinated fibers in the carpal tunnel and retrograde axonal degeneration. In this study, it was aimed to determine the decrease in the median nerve motor conduction velocities of the second lumbrical and APB muscles recorded in the forearm segment in CTS patients compared to the control group, and also to compare the motor nerve conduction velocities in the forearm segment among severe CTS patients and others. Data on both hands of 51 CTS patients and 20 healthy control participants were included in the study. There was no significant difference in age and gender distribution between patients and volunteers. CTS patients were divided into 4 groups according to the severity of the involvement as minimal (group 1), mild (group 2), moderate (group 3) and severe (group 4). The median nerve motor conduction velocity in the forearm was found to be slower in CTS patients with positive motor weakness, sensory deficit, Phalen's test, and Tinel's sign compared to the patients without examination findings (p=0.006, p=0.025, p=0.019, p=0.017, respectively). In addition, in patients with motor weakness and APB muscle atrophy, the motor conduction velocity of the median nerve recorded to the second lumbrical muscle in the forearm segment was decreased (p=0.003, p=0.001, respectively). According to ROC curve analysis, sensitivities of median-ulnar motor response latency difference recorded to second lumbrical-interossei muscle, median motor distal latency in wrist recorded from APB muscle, median motor conduction velocity in carpal tunnel, first finger median-radial sensory latency difference, fourth finger median-ulnar sensory latency difference, second finger median sensory nerve peak latency measurements were 81.4%, 86.1%, 87.1%, 90.6%, 91.5%, respectively, the specificities were 90%, 90%, 92.5%, 92.5%, 100% and 90%, respectively. Similarly to the literature, the highest sensitivity was found in the fourth finger median-ulnar sensory latency difference and second finger median sensory response peak latency electrophysiological examinations. However, there was no significant difference with other findings. In CTS patients, we found that the mean value of the median nerve motor conduction velocity recorded to APB muscle in the forearm segment was 53,8 m/s (±4,2) and the mean value of the median nerve motor conduction velocity recorded to second lumbrical muscle was 54,3 m/s (±5,6). There was a significant difference when compared with the control group (p<0.001, p=0.012, respectively). The median nerve motor conduction velocity recorded to second lumbrical muscle was significantly decresed in the severe patient group (group 4) compared to the other three groups (p<0.001). The median nerve motor conduction velocity recorded to second lumbrical and APB muscles in forearm segment, no decrease was observed in the median nerve motor conduction velocities in parallel with the marked decrease in the median motor conduction velocity in the wrist canal. This makes us think that the decrease in conduction velocity in the forearm segment is primarily secondary to retrograde axonal degeneration. However, the increase in conduction velocity proportional to the increased fiber thickness in the proximal segment is known, it cannot exclude the blockage of large myelinated fibers in the wrist canal. We think that the presence of axonal degeneration is related to the severity of the disease.