全身性癫痫伴尖波发作是一种促进睡眠功能的癫痫性疾病。

P Halász
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摘要

本文结合相关文献和个人调查,对全身性癫痫伴尖峰波发作的发病机制提出了新的假说。第一部分是对社会经济学理论发展的批判性概述。本文概述了中心化理论,关于皮层下与皮层起源的争论,Gloor的“皮质网状”假说,以及Niedermeyer的“畸形”概念。在下一节中,我们会发现在睡眠和清醒之间,在快速眼动睡眠和慢波睡眠之间存在一个特别的最佳区域,这个区域非常有利于尖波发作的发生。根据我们对这个临界区域内动态的调查,尖波发作总是伴随着意识水平的特征波动而出现,在这种波动中,向觉醒的变化总是伴随着向睡眠的反弹。因此,这个不稳定边界区的动力学性质在尖波发作的发生中变得特别有趣。研究表明,即使没有癫痫,在睡眠深度的微振荡中也可以观察到一种动态,这种动态可以根据相互诱导调节模型来解释。在我们的概念中,入睡的过程是从睡眠促进系统的反弹中产生的,这是对来自外部环境的感官输入的响应。根据这个模型,唤醒对睡眠的影响具有促进睡眠的作用。我们这样解释所有由感觉刺激引起的同步脑电图反应,我们认为k -复合体型同步反应是入睡过程的“基石”,它包含了整个过程的浓缩形式。证明了k -配合物与尖波模式之间的多种相似性。在此基础上,尖波发作可以被看作是反映在k复合体现象中的睡眠诱导动量的癫痫“漫画”。因此,GESw是睡眠促进功能的癫痫性障碍。这一假设解决并解释了我们对这一机制的认识中许多相互矛盾的特征,并为进一步的研究提供了一个新的生物学导向的框架。根据这一假说,人们试图解释GESw的一些特征:基因决定、年龄依赖性、与睡眠-觉醒周期的联系以及功能解剖特征和癫痫发作的症状。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Generalized epilepsy with spike-wave paroxysms as an epileptic disorder of the function of sleep promotion.

A new hypothesis is offered regarding the pathomechanism of generalized epilepsy with spike-wave paroxysms (GESw) based on the pertaining literature and personal investigations. The first section is devoted to a critical overview of the development of theories regarding GESw. The centrencephalic theory, the debate on subcortical versus cortical origin, the "corticoreticular" hypothesis of Gloor and, finally, the "dyshormic" concept of Niedermeyer are outlined. In the next section it is shown that there is a particular optimum zone between sleep and wakefulness and between REM and slow wave sleep which highly favours the occurrence of spike-wave paroxysms. According to our investigations into the dynamics within this critical zone, the spike-wave paroxysms always appear with characteristic fluctuations of the level of consciousness where the changes towards awakening are always followed by rebounds towards sleep. Hence, the dynamic properties of this unstable border zone become especially interesting in the genesis of spike-wave paroxysms. It has been shown that even without epilepsy, a dynamics can be observed in the micro-oscillations in the depth of sleep which could be interpreted according to the reciprocal induction regulation model. In our concept the process of falling asleep emerges from rebounds of the sleep promoting system in response to sensory inputs streaming in from the external environment. According to this model, arousal influences in sleep have a sleep promoting effect. We interpret in this way all synchronized EEG reactions elicited by sensory stimuli and we consider K-complex type synchronization reactions as a "building stone" of the process of falling asleep which contains the whole process in concentrated form. The manifold similarities between the K-complex and the spike-wave pattern are demonstrated. On this basis spike-wave paroxysms can be regarded as an epileptic "caricature" of the sleep induction momentum reflected in the K-complex phenomenon. Hence, the GESw is the epileptic disorder of the sleep promotion function. This hypothesis resolves and explains many contradictory features of our knowledge about this mechanism and gives a new biologically oriented framework for further research. In the light of the hypothesis it has been attempted to interpret some of the characteristic features of the GESw: the genetic determination, the age dependency, the link with the sleep-waking cycle as well as the functional-anatomical characteristics and the symptoms of the seizures.

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