GENERALIZED EPILEPSY WITH SPIKE-WAVE PAROXYSMS AS AN EPILEPTIC DISORDER OF THE FUNCTION OF SLEEP PROMOTION

Abstract

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 1st section is devoted to a critical overview of the development of theories regarding GESw. The centrencephalic theory, the debate on subcortical vs. cortical origin, the corticoreticular hypothesis of Gloor and the dyshormic concept of Niedermeyer are outlined. The 2nd section discusses the particular optimum zone between sleep and wakefulness and between REM [rapid eye movement] and slow wave sleep which highly favors the occurrence of spike-wave paroxysms. According to investigations into the dynamics within this critical zone, spike-wave paroxysms always appear with characteristic fluctuations of the consciousness level where changes towards awakening are always followed by rebounds towards sleep. The dynamic properties of this unstable border zone become especially interesting in the genesis of spike-wave paroxysms. Even without epilepsy, changes occur in the micro-oscillations in the depth of sleep, which could be interpreted according to the reciprocal induction regulation model. 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. All synchronized EEG reactions elicited by sensory stimuli were interpreted in this way and K-complex type synchronization reactions are considered 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. The GESw is the epileptic disorder of the sleep promotion function. This hypothesis resolves and explains many contradictory features of knowledge about this mechanism and gives a new biologically oriented framework for further research. In the light of the hypothesis it was attempted to interpret some of the characteristic features of the GEWs: genetic determination, age dependency, the link with sleep-waking cycle and functional-anatomical characteristics and the symptoms of the seizures.