Objective: To assess the changes of somatosensory evoked potentials (SEPs) during spinal cord ischemia and reperfusion injury and the value of SEP monitoring in evaluating neurological functions in this setting.
Methods: Spinal cord ischemia-reperfusion injury was induced in 28 rabbits by clamping the infrarenal aorta for 45 min, and the SEPs were monitored before and at 5, 10, and 15 min after ischemia, and at 15, 30, and 60 min and 2, 24 and 48 h after reperfusion. The neurological function score (NFS) of the rabbits was evaluated at 6, 12, 24 and 48 h after reperfusion, and the pathological changes of the spinal cord were observed 48 h after reperfusion.
Results: SEPs P1-wave latency significantly increased 5 min after ischemia (P<0.01) and the wave amplitude decreased 8 min after ischemia (P<0.01). SEPs disappeared 10 min after ischemia and recovered 15 min after reperfusion, but the P1-wave latency still remained longer and P1-wave amplitude lower than the measurements before ischemia (P<0.01). P1-wave amplitude became normal 15 min after the reperfusion (P>0.05), and the P1-wave latency gradually recovered 30 min after reperfusion, but still significantly longer than the preischemic value (P<0.01). P1-wave amplitude decreased again at 24 and 48 h after reperfusion (P<0.01). The NFS gradually increased at 24 and 48 h after the reperfusion (P<0.01). The changes in P1-wave amplitude at 24 and 48 h after reperfusion showed an obvious correlation to NFS (r=-0.881 and -0.925, respectively, P<0.01). Hemorrhage, swelling, and degeneration and neutrophil infiltration occurred in the spinal cord tissue 48 h after the reperfusion.
Conclusion: The changes of SEP P1-wave amplitude can better reflect the spinal cord function than the wave latency during spinal cord ischemia-reperfusion injury, and SEP monitoring provides reliable evidence for prognostic evaluation of the neurological function.