The Diagnostic Value of the Sleep EEG With and Without Sleep Deprivation in Patients With Atypical Absences

Hitherto it has not been known whether or not the sleep EEG after sleep deprivation is more effective than the simple or drug-induced sleep EEG. To investigate this, we recorded for 32 patients both sleep EEGs without sleep deprivation and, on the following day, sleep EEGs after 24 h of sleep deprivation. All the patients had atypical absences which were almost exclusively combined with generalized seizures or some other seizure types. All patients were receiving antiepileptic therapy. Sleep without sleep deprivation was induced by oral administration of 2 mg/kg body weight Protactyl (promazine hydrochloride). In patients showing no epileptic activity in the routine EEG, epileptic discharges could be provoked in 78% without sleep deprivation and in 72% after sleep deprivation. Epileptic activity was already seen in 28.1% of the cases in the awake EEG without sleep deprivation, recorded immediately before the sleep EEG, and in 50% of the cases in the awake EEG after sleep deprivation. It is unlikely that promazine hydrochloride in the dose used here has an additional inherent provocative effect. Generalized spike-and-wave complexes or sharp slow wave complexes which were combined twice with foci and runs of rapid spikes were recorded. In the sleep EEG without sleep deprivation, epileptic discharges were seen in the somewhat shallower stages (C leads to A leads to B leads to D) and, in the sleep EEG after sleep deprivation, in the somewhat deeper stages (D leads to C leads to B leads to A). Fewer epileptic discharges were elicited in patients who were older at the time of their first seizure. The illness was mild in patients whose sleep EEGs showed no epileptic activity. It is concluded that, as a rule, it is not necessary to record an EEG after sleep deprivation in patients with atypical absences whose routine EEGs show no epileptic activity; the drug-induced sleep EEG shows the same provocative effect.