OBJECTIVES: To study motor unit number estimation (MUNE) in acutely transected peripheral nerves, and to retest our previous observation which had revealed a discordance between the loss of compound muscle action potential (CMAP) size and decrease in MUNE during Wallerian degeneration. METHODS: In eight patients with nine transected median or ulnar nerves, a total of 18 electrophysiological studies were performed before the complete nerve degeneration ensues. CMAP recordings and incremental MUNE studies were performed by stimulation of the nerves at the wrist level and recording from the appropriate hand muscles. The same studies repeated on the contralateral side. RESULTS: Injury side to intact side ratios of the MUNEs were significantly higher than the CMAP ratios. Mean step areas in MUNE studies were found to be lower on the transected sides after 72 hours post-injury. DISCUSSION: These findings support the existence of an electrophysiologically observable asynchrony in neuromuscular synapse dysfunction during Wallerian degeneration.
OBJECTIVES: To study motor unit number estimation (MUNE) in acutely transected peripheral nerves, and to retest our previous observation which had revealed a discordance between the loss of compound muscle action potential (CMAP) size and decrease in MUNE during Wallerian degeneration. METHODS: In eight patients with nine transected median or ulnar nerves, a total of 18 electrophysiological studies were performed before the complete nerve degeneration ensues. CMAP recordings and incremental MUNE studies were performed by stimulation of the nerves at the wrist level and recording from the appropriate hand muscles. The same studies repeated on the contralateral side. RESULTS: Injury side to intact side ratios of the MUNEs were significantly higher than the CMAP ratios. Mean step areas in MUNE studies were found to be lower on the transected sides after 72 hours post-injury. DISCUSSION: These findings support the existence of an electrophysiologically observable asynchrony in neuromuscular synapse dysfunction during Wallerian degeneration.