Gloor P
Electroencephalogr Clin Neurophysiol Suppl. 1978(34):245-9.
A hypothesis for the mechanism of generalized spike and wave discharge in human generalized epilepsy is proposed in the light of findings obtained in feline generalized penicillin epilepsy. It is postulated that generalized bilaterally synchronous spike and wave discharge depends upon a diffuse and relatively mild state of cortical hyperexcitability which increases the responsiveness of cortical neurons. Afferent thalamo-cortical volleys normally involved in the genesis of spindles and recruiting responses are most likely to precipitate spike and wave discharges under these conditions. The spike and wave pattern probably results from the activation of a recurrent intracortical inhibitory pathway which becomes activated when cortical neurons discharge in greater number and more repetitively than is normally the case. During spike and wave discharges a large number of neurons oscillate between short periods of excitation, corresponding to the spike, and longer periods of inhibition, corresponding to the slow wave component of the spike and wave complex. This disrupts the normal transactional processes of cortical neurons which are presumably responsible for mental activity, particularly for the close integration of perception, cognition and voluntary motor responsiveness. The degree of this interference varies greatly and in mild absence seizure it is not justified to speak of "loss of consciousness". The fundamental disturbance in absence seizures brought about by the generalized cortical spike and wave discharges is therefore better regarded as a "clouding of the mind". Loss of consciousness can be said to occur only when the interference with mental activity becomes particularly intense. Loss of consciousness in absence seizures can therefore not be used as an argument in favor of primary involvement of higher brain-stem mechanisms.
根据猫的全身性青霉素癫痫实验结果，提出了一种关于人类全身性癫痫中全身性棘波和慢波放电机制的假说。假定双侧全身性同步棘波和慢波放电取决于皮质兴奋性过高的弥漫且相对较轻的状态，这种状态会增加皮质神经元的反应性。在这种情况下，通常参与纺锤波和募集反应产生的丘脑 - 皮质传入冲动最有可能引发棘波和慢波放电。棘波和慢波模式可能是由皮质内反复抑制性通路的激活所致，当皮质神经元放电数量比正常情况更多且更频繁时，该通路就会被激活。在棘波和慢波放电期间，大量神经元在短时间兴奋（对应棘波）和长时间抑制（对应棘波和慢波复合波的慢波成分）之间振荡。这扰乱了皮质神经元正常的交互过程，而这些过程大概是负责精神活动的，特别是负责感知、认知和自主运动反应的紧密整合。这种干扰程度差异很大，在轻度失神发作时，说“意识丧失”是不合理的。因此，全身性皮质棘波和慢波放电引起的失神发作的根本干扰，更好地应被视为“意识模糊”。只有当对精神活动的干扰变得特别强烈时，才可以说发生了意识丧失。因此，失神发作中的意识丧失不能作为支持高级脑干机制原发性受累的论据。
