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背景:迷走神经刺激术是一种治疗难治性癫痫的神经生理学疗法,通过刺激颈部迷走神经干可达到控制癫痫发作的目的。目的:观察间断性左侧迷走神经刺激术对致痫动物痫性发作的影响,为躯体内脏信息相互作用提供理论根据。设计:观察性实验。单位:首都医科大学神经生物学系。材料:实验于2000-03/2002-09在首都医科大学神经生物学系电生理学实验室完成。实验选用健康成年SD大鼠34只,体质量220～250g;健康成年家兔8只,体质量2.2～2.5kg。方法:①10只大鼠经肌肉注射150～160万单位青霉素致痫,通过观察迷走神经刺激术前后大鼠大脑皮质电图、行为学的变化,研究迷走神经刺激术对致痫大鼠癫痫活动的影响。②另外8只大鼠向海马内注入青霉素0.24～0.48mg致痫,观察迷走神经刺激术对致痫大鼠痫性大脑皮质电图的影响。③16只大鼠皮下注射海人藻酸致痫。经迷走神经刺激术观察致痫大鼠海马神经元放电活动、大脑皮质电图及行为学变化。④8只家兔用微量注射器向皮层滴注士的宁致痫,观察迷走神经刺激术对急性皮层损伤致痫家兔的大脑皮质电图的影响。主要观察指标:①迷走神经刺激术对青霉素致痫大鼠痫性发作的影响。②迷走神经刺激术对海人藻酸致痫的大鼠痫性发作的影响。③迷走神经刺激对士的宁致痫家兔痫性大脑皮质电图的影响。结果:34只大鼠,8只家兔均进入结果分析。迷走神经刺激可以阻抑各组致痫动物的痫性发作,痫性皮质电图、海马神经元电活动及行为学表现均呈现显著的变化,总有效率达50%以上。如在癫痫发作前先行迷走神经刺激,有效率可达80%以上。肌肉注射青霉素致痫组,行为学及大脑皮质电图明显改善分别为40%和50%。海马内注射青霉素致痫组,50%的大鼠大脑皮质电图明显改善。迷走神经刺激对海人藻酸致痫大鼠的痫性发作的有效控制率为80%。家兔大脑皮质局部滴注士的宁组,经迷走神经刺激,50%的大脑皮质电图的痫性波得到控制。结论:迷走神经刺激可有效地阻抑致痫动物的痫性发作,脑的皮质、海马神经元参与了迷走神经刺激的抗痫作用。内脏传入信息可能通过在脑的皮质、海马部位的整合作用达到有效地阻抑躯体痫性活动。
Background: Vagus nerve stimulation is a neurophysiological therapy for refractory epilepsy, which can be used to control seizures by stimulating cervical vagus nerve trunk. OBJECTIVE: To observe the effect of intermittent left vagus nerve stimulation on epileptic seizures in epileptic animals and provide theoretical basis for the interaction of somatic and visceral information. Design: Observational experiments. Unit: Department of Neurobiology, Capital Medical University. Materials: The experiment was performed at the electrophysiology laboratory of Department of Neurobiology, Capital Medical University from March 2000 to September 2002. 34 healthy adult Sprague-Dawley rats were selected and their body weight was 220 ~ 250g. Eight healthy adult rabbits with body weight of 2.2 ~ 2.5kg were selected. Methods: ①10 rats were intramuscularly injected with 1.5-1.6 million penicillin-induced epilepsy. By observing the changes of cerebral cortex electrocardiogram and behavior before and after vagus nerve stimulation in rats, the effects of vagus nerve stimulation on epileptic activity in epileptic rats . ② The other 8 rats were injected with penicillin 0.24 ~ 0.48mg into the hippocampus to induce epilepsy. The effect of vagus nerve stimulation on the epileptic cerebral cortex electrocephalus was observed. ③16 rats were injected subcutaneously with kainic acid induced epilepsy. Vagus nerve stimulation was used to observe the discharge activity of hippocampal neurons in epileptic rats and the changes of cerebral cortex and behavior. ④ 8 rabbits with microinjector to cortices Ning Ning induced epilepsy, vagus nerve stimulation to observe the impact of acute cortical injury caused by epilepsy rabbit cerebral cortex electrocardiogram. MAIN OUTCOME MEASURES: ① The effect of vagus nerve stimulation on epileptic seizures induced by penicillin in rats. ② vagus nerve stimulation of kainic acid-induced epileptic seizures in rats. Effect of vagus nerve stimulation on seizure electrocorticogram in seizures induced by strychnine in rabbits. Results: 34 rats and 8 rabbits all entered the result analysis. Vagal stimulation can inhibit epileptic seizures in each group of epileptic seizures, epileptic cortex electrophorogram, hippocampal neuronal electrical activity and behavioral performance showed significant changes, the total effective rate of 50%. As in the first vagus nerve stimulation before seizure, the effective rate of up to 80%. Intramuscular injection of penicillin epileptic group, behavioral and cerebral cortex electrogram significantly improved 40% and 50%. Hippocampal injection of penicillin-epileptic group, 50% of the rat cerebral cortex significantly improved. Vagus nerve stimulation on kainic acid-induced seizures in rats seizures effective control rate of 80%. Local cerebral cortex instillation of strychnine group, vagus nerve stimulation, 50% of the cerebral cortex epileptic wave control. Conclusion: Vagus nerve stimulation can effectively suppress epileptic seizures in epileptic animals. Cerebral cortex and hippocampal neurons are involved in the anti-epileptic effect of vagus nerve stimulation. Visceral afferent information may effectively suppress somatic seizure activity through the integration of brain cortex and hippocampus.