摘要
To determine whether the pathological changes caused by injury to the spinal cord can be correlated with values obtained by the Magnetic Motor Evoked Potential (MEPs) technique, we studied spinal cords from 41 adult cats who were divided into 4 groups. The groups ranged from normal cats whose spinal cords were not compressed, to slightly, moderately and severely injured. MEPs were recorded before compression and in 30 minutes, 6 hours, 1 week, 2 week and 4 week after the compression unit was installed. Pathological changes with increased pressure were seen in blood vessels, nerve cells and fibers, Nissl substance and the central canal. A reversal of pathological changes was observed in slight or moderate injury during the 4 weeks of the experiment. Extensive injury, however, caused irreversible changes in the nerve cells with loss of motor function. The latency of MEPs at 30 minutes and 6 hours in the slightly injured group was 037 and 038 times greater than the baseline and returned to normal levels in 4 weeks. In the moderately injured group, the latency was increased 077 and 081 times and in the severely injured 132 and 136 times over the baseline. Recovery in the second group was partial and not at all in the severely injured. Thus, there appears to be good correlation between observed pathological changes, motor functions and MEPs.
To determine whether the pathological changes caused by injury to the spinal cord can be correlated with values obtained by the Magnetic Motor Evoked Potential (MEPs) technique, we studied spinal cords from 41 adult cats who were divided into 4 groups. The groups ranged from normal cats whose spinal cords were not compressed, to slightly, moderately and severely injured. MEPs were recorded before compression and in 30 minutes, 6 hours, 1 week, 2 week and 4 week after the compression unit was installed. Pathological changes with increased pressure were seen in blood vessels, nerve cells and fibers, Nissl substance and the central canal. A reversal of pathological changes was observed in slight or moderate injury during the 4 weeks of the experiment. Extensive injury, however, caused irreversible changes in the nerve cells with loss of motor function. The latency of MEPs at 30 minutes and 6 hours in the slightly injured group was 037 and 038 times greater than the baseline and returned to normal levels in 4 weeks. In the moderately injured group, the latency was increased 077 and 081 times and in the severely injured 132 and 136 times over the baseline. Recovery in the second group was partial and not at all in the severely injured. Thus, there appears to be good correlation between observed pathological changes, motor functions and MEPs.
