EPILEPSY AND SLEEP

This review discusses several aspects of epilepsy and sleep. The level of wakefulness is controlled by transmitters such as acetylcholine, n orepinephrine, serotonin, and histamine. These neurotransmitters are i nvolved in modulatory neurotransmission of the ascending brain stem sy stems, which play an important role in controlling the sleep-wake cycl e. Experimental evidence suggests that rapid eye movement sleep atonia is induced by increased endogenous acetylcholine release. Regarding s leep factors, recent data suggest that prolactin may stimulate rapid e ye movement sleep and that growth hormone-releasing factor is involved in non-rapid eye movement sleep regulation. The neuropharmacologic fe atures of several animal models of epilepsy have been investigated. Ep ileptiform discharges of genetic absence seizures in rats have been fo und to be suppressed by cholinergic drugs. The beta-carboline abecarni l has a strong antiepileptic effect on spike-wave discharges in rats t hat generate spontaneous spike-wave discharges, and it may be useful a s an antiepileptic drug. Sleep epilepsy has been studied in a model of amygdala-kindled kittens. During the postkindling development, multif ocal epilepsy with convulsions occurred that were distributed througho ut the sleep-wake cycle; this finding agrees with the clinical literat ure. A typical feature of juvenile myoclonic epilepsy is the occurrenc e of seizures in a strict relationship to the sleep-wake cycle. There is now some neurophysiologic evidence that this syndrome also causes d isturbance of sleep stability with increased arousal reactions. Noctur nal paroxysmal dystonia is not a homogeneous entity. Several clinical reports indicate that the short-lasting variant is most likely a form of frontal lobe epilepsy, but the nature of the longer-lasting variant s is still obscure.