Introduction

Epilepsy is a chronic condition characterized by recurring seizures. In most epileptic syndromes spontaneous seizures are random, i.e they occur independently from the patient's state of arousal. However, the role of the sleep state, and particularly different stages of sleep, in facilitating ictal or interictal discharges, has been the object of several studies and recent reviews (Shouse et al., 1997a, b).

The synchronized EEG activity and preserved muscular tone characterizing the early stage of sleep facilitate the propagation of interictal discharges and seizure onset, whereas inhibited muscular tone and desynchronized EEG activity prevent seizure onset during Rem sleep. Moreover, thalamocortical drive evoking physiological sleep transients (K-complexes and spindles activity) and burst-pause firing in cortical neurons during NRem sleep may facilitate the spread of bisynchronous discharges in generalized epilepsies.

The most common epileptic situations related to sleep include some forms of idiopathic generalized epilepsies such as epilepsy with grand mal (GTC) on awakening and juvenile myoclonic epilepsy (JME) in which myoclonic jerks or generalized convulsion appear typically after awakening and are provoked by sleep deprivation. Sleep is a strong seizure trigger in benign epilepsy of childhood with centrotemporal spikes (BECT) a form of idiopathic (with age-related onset) localization-related epilepsies, in which partial motor seizures occur in sleep in 70–80% of cases and interictal spikes appear only during sleep in about 30% of patients.

Other very rare conditions in which sleep plays a fundamental role in the pathogenetic epileptic process are the Landau–Kleffer syndrome (LKS) and the situation named continuous spikes and waves during sleep (CSWS).