뇌경색 흰쥐에서 뇌병변 위치와 자극강도에 따른 운동유발전위의 변화
Effect of Stimulation Intensity and Location of Cerebral Infarction on Motor Evoked Potentials in the Rat
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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)
Abstract
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)
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