Sleep and intra-ictal epileptic electroencephalographic activities

From this review it appears that the slow wave sleep (SWS) increases the mean density of electroencephalographic paroxysmal activities (PA) whatever the epileptic syndrome. This pattern is not marked according to a bell curve among the epileptic population: about half the patients exhibit few or no PA during SWS, 20% show an increase during waking and another 20% during SWS. Begnin epilepsy with centro-temporal spikes is associated with an important sleep PA increase. In partial epilepsy, stage 3 and 4 sleep should increase the PA transmission. In children, a large increase in PA during SWS defines the continuous spike-wave during sleep syndrome, which is also observed in the syndrome of acquired aphasia with epilepsy of Landau-Kleffner; both conditions raise the issue of the neuropsychological consequences of the sleep PA. The sleep effect on the various epileptic models is analysed, showing a mean increase in PA during SWS and during transition between sleep and waking. This evidence is in agreement with the fact that during light sleep thalamocortical loops are functioning with an oscillatory pattern which facilitates PA expression. More hypothetic is the effect of sleep on the discharge rate of epileptic focus and on the cortical diffusion of the epileptic discharges. Gaba certainly participates in the thalamic influence, but its role on PA by the cortical and brain stem inhibition is speculative. Noradrenaline and acetylcholine, implicated in waking, reduce PA activity. Interindividual variations suggest that each epileptic has his own pathological neuronal organisation in which cortex and thalamocortical connexions are variously sensitive to the neurotransmitters implicated in sleep and waking.