G.P.293: Peripheral nerve conduction abnormalities in amyotrophic lateral sclerosis

Abstract

In amyotrophic lateral sclerosis (ALS), the distal latency (DL) prolongation of median nerve is usually detected by motor nerve conduction study. It depends on a reduction of the compound muscle action potential (CMAP) of median nerve in most cases. But in some cases though the reduction of CMAP is not severe, the DL is strongly prolonged. In these cases, prolonged distal latencies cannot be explained by primary axonal damages in ALS. To investigate the pathogenesis of peripheral nerve conduction abnormalities in ALS. Forty-six patients with ALS (22 men and 24 women; mean age 67.8 years; mean duration of illness 17.0 months) were studied. We analysed the values of DL, CMAP amplitude, motor conduction velocity (MCV), F-wave latency (F-lat), sensory nerve action potential (SNAP) amplitude and sensory conduction velocity (SCV). DL of median, ulnar nerve was prolonged in 28 and 12 patients, respectively. CMAP amplitude of median, ulnar nerve was reduced in 22 and 16 patients. MCV of median, ulnar nerve was slowed in 12 and 6 patients. F-lat of median, ulnar nerve was prolonged in 5 and 3 patients. SCV of median, ulnar nerve was slowed in 9 and 5 patients. Abnormalities were obviously milder in sensory nerves than in motor nerves. Only DL prolongation without CMAP reduction of median, ulnar nerve is shown in 11 and 3 patients, respectively. Significant correlations were found between DL and CMAP, CMAP and MCV, MCV and F-lat only in median nerve. The peripheral nerve conduction slowing may partly be caused by motor axonal degeneration in ALS. But nerve conduction slowing without muscle wasting is found in some early ALS patients. The underlying mechanism remains to be solved about nerve conduction abnormalities in ALS. In amyotrophic lateral sclerosis (ALS), the distal latency (DL) prolongation of median nerve is usually detected by motor nerve conduction study. It depends on a reduction of the compound muscle action potential (CMAP) of median nerve in most cases. But in some cases though the reduction of CMAP is not severe, the DL is strongly prolonged. In these cases, prolonged distal latencies cannot be explained by primary axonal damages in ALS. To investigate the pathogenesis of peripheral nerve conduction abnormalities in ALS. Forty-six patients with ALS (22 men and 24 women; mean age 67.8 years; mean duration of illness 17.0 months) were studied. We analysed the values of DL, CMAP amplitude, motor conduction velocity (MCV), F-wave latency (F-lat), sensory nerve action potential (SNAP) amplitude and sensory conduction velocity (SCV). DL of median, ulnar nerve was prolonged in 28 and 12 patients, respectively. CMAP amplitude of median, ulnar nerve was reduced in 22 and 16 patients. MCV of median, ulnar nerve was slowed in 12 and 6 patients. F-lat of median, ulnar nerve was prolonged in 5 and 3 patients. SCV of median, ulnar nerve was slowed in 9 and 5 patients. Abnormalities were obviously milder in sensory nerves than in motor nerves. Only DL prolongation without CMAP reduction of median, ulnar nerve is shown in 11 and 3 patients, respectively. Significant correlations were found between DL and CMAP, CMAP and MCV, MCV and F-lat only in median nerve. The peripheral nerve conduction slowing may partly be caused by motor axonal degeneration in ALS. But nerve conduction slowing without muscle wasting is found in some early ALS patients. The underlying mechanism remains to be solved about nerve conduction abnormalities in ALS.