Wolf P, Röder-Wanner U U, Brede M
Epilepsia. 1984 Aug;25(4):467-75. doi: 10.1111/j.1528-1157.1984.tb03445.x.
Sleep is a modulator of seizure activity, and many antiepileptic drugs are modulators of sleep. Can influences on sleep organization be involved in antiepileptic drug action, and can these partly account for differences in drug response of various epileptic syndromes? Much more exact data must be collected before these questions can be adequately discussed. The polygraphic sleep of 40 unmedicated epileptic patients was recorded and compared with polygraphy after adjustment to therapeutic steady states of phenobarbital (PB) and phenytoin (DPH) (as sequential sole agents in a crossover design with random sequence). With PB, patients fell asleep more rapidly and had fewer movements, movement arousals, and arousal awakenings, all of which could be beneficial, especially for patients with generalized epilepsy. Light sleep was increased, and REM sleep decreased. The usual sleep pattern was altered, with maximal deep sleep early and maximal REM sleep late in the night. PB seemed to have maximal effect in the first REM cycle. With DPH, sleep onset also came sooner, but light sleep was decreased and deep sleep increased, with no alteration of REM sleep. In contrast to PB, the changes in sleep organization were toward leveling the distribution of deep NREM sleep. The maximal alterations were observed in the third REM cycle. With both drugs, there were some differences in the response of generalized as opposed to focal epilepsies, and of awakening as opposed to sleep epilepsies. Thus, the early REM cycles seemed to be more modifiable by drugs in patients with generalized or awakening epilepsies than in patients with focal or sleep epilepsies.(ABSTRACT TRUNCATED AT 250 WORDS)