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1897年 Sherrington 的经典实验证明刺激旧小脑可抑制去大脑强直。Moruzzi 观察到施于猫的小脑皮质的高频刺激(200～300cps)抑制去大脑强直,而低频刺激(5～15cps)则使之加重。1955年 Cooke 和 Snider 证实刺激小脑可改变抽搐发作的电发现,用60V 刺激猫大脑引起的发作,可被低于7V 刺激小脑皮质而完全停止发作。1965年 Dow 等发现小脑对癫痫主要为抑制性影响。1964年 Ito 和Yoshida 证明慢性小脑皮质刺激使整个小脑皮质蒲肯野细胞传出抑制性放电。1972年Julien 证实青霉素所致癫痫灶的猫和正常猫自发的蒲肯野细胞发放率用苯妥英钠后戏剧性地增加,故得出结论药物抗癫痫作用有赖于小脑皮质,其蒲肯野细胞放电增加可能降低大脑活性,而蒲肯野细胞活动丧失则增加大脑兴奋性。基于上述认识,从1972年开始,Cooper 提
In 1897, Sherrington’s classic experiments demonstrated that stimulating the old cerebellum can inhibit brain denervation. Moruzzi observed that high-frequency stimulation (200-300 cps) applied to the cerebellum of the cat suppressed denervation of the brain and was aggravated by low-frequency stimulation (5-15 cps). Cooke and Snider (1955) confirmed that stimulating the cerebellum can alter the electrical findings of convulsions, and that the 60-V stimulation of the cat’s brain caused an episode to stop completely by stimulating the cerebellar cortex below 7V. In 1965, Dow et al found that the cerebellum had mainly suppressive effects on epilepsy. In 1964, Ito and Yoshida demonstrated that chronic cerebellar cortical stimulation induces an inhibitory discharge in the entire cerebellar Purkinje cell. In 1972 Julien confirmed penicillin-induced epileptic foci cats and normal cat spontaneous Purkinje cell distribution rate increased significantly with phenytoin sodium, it concluded that the drug antiepileptic effect depends on the cerebellar cortex, the Purkinje cell discharge increased May reduce brain activity, while Purkinje cell loss of activity increases brain excitability. Based on the above understanding, since 1972, Cooper mentioned