Gloor P, Pellegrini A, Kostopoulos G K
Electroencephalogr Clin Neurophysiol. 1979 Mar;46(3):274-89. doi: 10.1016/0013-4694(79)90202-5.
Previous studies had suggested that the epileptic bursts of feline generalized penicillin epilepsy represent the response of hyperexcitable cortex to thalamocortical volleys normally evoking spindles. If this were the case, it should be possible to convert the epileptic bursts of generalized penicillin epilepsy into spindles by decreasing the excitability of cortical neurons. In cats exhibiting the EEG signs of feline generalized penicillin epilepsy cortical excitability was decreased by hypoxia, by the topical application to the cortex of KCl (inducing spreading depression), barbiturates, GABA, AMP or noradrenaline. During generalized penicillin epilepsy, hypoxia and KCl-induced spreading depression abolished epileptic bursts which were replaced by spindles. When spindles and epileptic complexes occurring in the same animal were compared, a direct correlation between the frequencies of these two rhythms could be demonstrated, that of the epileptic complexes being about half that of the spindle waves. These observations support the hypothesis that the epileptic bursts of feline generalized penicillin epilepsy are induced by thalamocortical volleys normally involved in spindle genesis. Topical cortical applications of barbiturates, GABA, AMP and noradrenaline reduced or inverted the negative spikes of the spike and wave complexes, while augmenting the negative slow waves, or revealing them clearly in instances in which they had been poorly developed. This effect is interpreted as being due to a selective inactivation of the superficial cortical layers. That topical cortical application of barbiturates, GABA, AMP and noradrenaline was capable of transforming into typical spike and wave complex epileptic bursts, which had not previously conformed to this pattern, indicates that the intracortical electrophysiological events of typical and atypical epileptic bursts in feline generalized penicillin epilepsy are fundamentally the same and reflect an alternation between excitatory and inhibitory sequences.
先前的研究表明，猫全身性青霉素癫痫的癫痫发作代表了过度兴奋的皮层对通常引发纺锤波的丘脑皮质冲动的反应。如果是这样的话，应该可以通过降低皮层神经元的兴奋性，将全身性青霉素癫痫的癫痫发作转化为纺锤波。在表现出猫全身性青霉素癫痫脑电图特征的猫中，通过缺氧、向皮层局部应用氯化钾（诱发扩散性抑制）、巴比妥类药物、γ-氨基丁酸（GABA）、腺苷一磷酸（AMP）或去甲肾上腺素来降低皮层兴奋性。在全身性青霉素癫痫发作期间，缺氧和氯化钾诱发的扩散性抑制消除了癫痫发作，取而代之的是纺锤波。当比较同一动物中出现的纺锤波和癫痫复合波时，可以证明这两种节律的频率之间存在直接相关性，癫痫复合波的频率约为纺锤波频率的一半。这些观察结果支持了这样一种假说，即猫全身性青霉素癫痫的癫痫发作是由通常参与纺锤波产生的丘脑皮质冲动诱发的。向皮层局部应用巴比妥类药物、GABA、AMP和去甲肾上腺素可减少或反转棘波和慢波复合波的负向尖峰，同时增强负向慢波，或者在负向慢波发育不良的情况下使其清晰显现。这种效应被解释为由于皮层浅层的选择性失活。向皮层局部应用巴比妥类药物、GABA、AMP和去甲肾上腺素能够将以前不符合典型棘波和慢波复合波模式的癫痫发作转化为典型模式，这表明猫全身性青霉素癫痫中典型和非典型癫痫发作的皮层内电生理事件在根本上是相同的，反映了兴奋和抑制序列之间的交替。
