The Change Of The Trigeminal Somatosensory Evoked Potential On Cerebral Ischemia-reperfusion Rat

ObjectiverTo investigate the change of the trigeminal somatosensory evoked potential(TSEP) on cerebral ischemia-reperfusion rats. Methods:60 mature Wistar rats were selectedj ignoring its sex, with weight 260~280g. The animal model of focal cerebral ischemia-reperfusion was established by occluding middle cerebral artery with suture; TSEPs were recorded on the contralateral epidural surface and the deficiency of nerve function assessed, before ischemia, at ischemia 30mm, 90min, 120min, at reperfusion 30min, 60min. 90min, 120min;then2ratswere randomly selected from every period of ischemia and reperfusion for makingpathologic specimen to determine reliability of the animal model. Results:Apparent and stabile TSEPs were recorded from 52 of 60 rats. The basic waveformof TSEP consisted of 2 negative direction wave(N1, N2)and 1 positive direction wave(P), viz N1-P-N2 type. The amplitude of N1-P for normal rat was 5.37± 0.85@v, the latency of N1 6.57±0.26ms, the latency of P 8.08±0.74ms. Thedeficiency of nerve function gave priory to low or middle grade, majority showedapparent symptom at ischemia 60min, symptom aggravated at ischemia-reperfusion30min among half upwards rats, then restored different degree. There wassignificant difference in the latencies between every ischemia-reperfusion group and normal control group, between every ischemic group and normal control group,P 5MX05; there was no significant difference between different ischemic groups, butthere was a tendency of prolongation in the latencies with propagation of ischemic period. There was no significant difference in the latencies between every ischemia-reperfusion group and every ischemic group, between different ischemia-reperfusion groups; but there was a tendency of restoration in the latencies with prolongation of ischemia-reperfusion period. There was significant difference in the amplitudes between every ischemia-reperfusion group and normal control group, between every ischemic group and normal control group, P < 0.05; there was no significant difference between different ischemic groups, but there, was a tendency of decrement in the amplitudes with prolongation of ischemic period. There was significant difference;the in amplitudes between 30min ischemia-reperfusion group and every ischemic group, P < 0.05; there was no significant difference between other ischemia -reperfusion group and every ischemic group. There was no significant difference between every is,cherniarreperfusion group, but there was a tendency of restoration in the amplitudes with prolongation of ischemia-reperfusion period. After ischemia-reperfusion, neurons in the focus showed apparent edema, acidophilic, changenucleus, and cytoplasm was deep stained; infarct appeared in focal area. There was no significant change in ischemia-reperfusion 120min. Conclusion: The method of TSEP - detection by electric stimulation was convenient, reliable, duplication better. The latency of N1 P and the amplitude of N1-P were sensitive to ischemia; TSEP could promptly accurately reflect the state of nerve function; TSEP could regard as standard toreflecting cerebral blood fluid; TSEP could regard as objective standard to evaluating if nerve function restored.