Physiology of sleep and wakefulness as it relates to the physiology of epilepsy.

Abstract

This paper reviews the present knowledge about the cellular origins of vigilance states (wakefulness and slow-wave sleep) from the perspective of their involvement in the triggering of epileptic seizures. The data stem from intracellular recordings (most of them dual impalements of pairs of neurons and glia), extracellular ionic concentrations (mainly K and Ca ) and simultaneous intracortical field potentials from the cortex of cats. These data were corroborated with recordings from naturally sleeping animals and humans. It is shown that sleep is dominated by a cortically generated slow (<1 Hz) oscillation resulting from the complex interplay within networks of neurons and glia, which are modulated by the more diffuse action of extracellular currents of ions. Wakefulness is produced through the activation of brainstem and basal forebrain structures, which disrupt sleep oscillations and elicit a global change of the extraneuronal milieu, with profound modifications of glial and cerebral blood flow parameters. Paroxysmal events arising during quiet sleep evolve within the cortex from normal slow sleep oscillations. The synchronization of large cortical and eventually subcortical territories relies on the propagation of increased currents of K through the glial syncytium, which compensate for the reduced synaptic efficacy due to the depletion of extracellular Ca.