Neurogenic motor evoked potential changes after acute experimental spinal cord i njury

OBJECTIVE: To better understand the characte ristics of the neurogenic motor evoked potential (NMEP) before and after acute s pinal cord injury. METHODS: We recorded and characterized the spinal cord NMEP fro m 48 normal rats and from 38 rats with spinal cord hemisection lesion. Spinal co rd NMEPs were elicited by applying a range of current intensities with bipolar m icroelectrode stimuli to the C4 cord segment and recording the responses from sc iatic nerves with bipolar microelectrodes placed in the neurilemma. RESULTS: The evoked potentials consisted of three stable and re producible negative and three positive peaks. The meanplus minusSD latencies of N1 were 2.89plus minus0.22 ms on the right side and 2.89plus minus0.24 ms on th e left side. The mean conduction velocity was 47.9 m/s. The meanplus minusSD am plitudes of N1 were 3.61plus minus2.10 muV on the right side and 3.83plus minus2.3 2 muV on the left side. The amplitudes of N1 were signific antly different among the eight stimulus intensity groups (right side: F=2.22, df=7201, P=0.03; left side: F=2.11, df=7206, P=0.04). The amplitude was largest when the stimulus intensity was 1.1-2.5 mA. The latencies of N1 were not si gnificantly different among the eight stimulus intensity groups (right side: F=0.40, df=7201, P=0.9; left side: F=1.20, df=7206, P=0.3. The amplitudes and latencies of N2, N3 were not significantly different among the eight stimulus intensity groups. There were no significant changes in latency and amplitude between the left and the right side nerve responses. Thirty-eight rats underwent T9 cord right side hemisection. Among them, 20 (53%), 30 (79%), and 32 (84%) rats could not be reco rded in corresponding to N1, N2, and N3, respectively, in the right-side sciati c nerves; and 13 (79%), 18 (47%), and 21 (55%), in corresponding to N1, N2, and N3 in the left-side sciatic nerves. The latency was significantly delayed on th e both right and left sides. The amplitude N1 was significantly depressed on the both sides, with N3 significantly depressed on the right side and N2 not signif icantly depressed. CONCLUSIONS: The amplitude of N is significantly different amon g the eight stimulus intensity groups. The amplitude is largest when the stimulu s intensity is 1.1-2.5 mA. The light injury results in a significant la tency delay in N1, N2, and N3 waves and a significant amplitude attenuation in N1. The N1 amplitude is sensitive to the degree of the lesion and conducts bilate rally. N2 and N3 conduct mainly along the ipsilateral posterolaterial tracts in the rats.