Objective
To investigate the change of motor evoked potential (MEP) in the cerebral infarction, and observe the effect of stimulation intensity and location of cerebral infarction, using rat model of cerebral ischemia induced by endothelin-1 (ET-1). Method: Middle cerebral artery (MCA) infarct, cortical infarct, and internal capsular infarct were induced in Spraugue- Dawley rats, by injecting ET-1 stereotaxically. MEP was recorded in forelimb by transcranial magnetic stimulation at 100%, 120%, and 150% of motor threshold by a small figure-8 coil. The location of cerebral infarction was confirmed histologically by 2,3,5-triphenyltetrazolium chloride (TTC) staining. Results: In MCA infarct, MEP was not recorded at all intensity. In internal capsular infarct, no MEP was recorded at 100% of motor threshold, and amplitude was decreased at 120%. In cortical infarct, MEP was not recorded at 100%, but amplitude was maintained at 120% and 150%. Latency did not change significantly at all intensity. Conclusion: Amplitude of MEP decreased after cerebral infarction, but latency did not change. Decrease in amplitude was larger with deeper location of cerebral infarction. Cerebral cortex was stimulated at 100% of motor threshold, subcortical structure was stimulated at 120%, and deeper structure was stimulated at 150%, respectively. (J Korean Acad Rehab Med 2010; 34: 381-386)

Objective
To investigate the changes of motor and soma-tosensory evoked potentials found in focal cerebral cortical ischemia induced by endothelin-1 (ET-1), one of the common models of cerebral infarct in rats. Method: A total of twenty Sprague-Dawley rats were studied. Focal cerebral cortical ischemia was induced by steterotaxic injection of ET-1 into forelimb region of cerebral cortex. Pellet retrieval test, motor evoked potential (MEP), and somatosensory evoked potential (SEP) were compared before and after cerebral ischemia. The location and extent of cerebral ischemia were confirmed histologi-cally. Results: Success rate of pellet retrieval test decreased significantly after induction of cerebral ischemia, demon-strating sensorimotor deficit in the contralateral forelimb. The latency and amplitude of MEP did not changed significantly despite weakness of forelimb. However, SEP showed reversal of the positive peaks. Conclusion: The results suggest that the changes of MEP and SEP in focal cerebral cortical ischemia are different from those in cerebral ischemia by large artery occlusion. When evaluating MEP and SEP in focal cerebral ischemia model, interpretation of evoked potentials should be cautious. (J Korean Acad Rehab Med 2009; 33: 147-153)