Epileptic activity was recorded electroencephalographically in at least one sibling in 22 (51.16%) of 43 patients with rolandic epilepsy and/or centrotemporal spikes. In 26 of 69 (37.68%) siblings, epileptic discharges were observed. These were recorded only in waking in 1 subject (1.5%), in waking and sleep in 13 (18.8%), and in sleep only in 12 (17.4%). The greatest number of epileptic discharges was noted in waking during hyperventilation (52.4%) and in sleep stage C (88%). Foci were recorded in only 4 (5.8%) of the 26 cases with epileptic discharges, and generalized spike-wave complexes were recorded in 22 (31.9%). In one sibling, the sharp-wave focus was located in the right centrotemporal area, in a second in the left occipital, and in a third in the left frontal region with spreading to the centrotemporal; in the fourth, two independent foci were observed in the left and right centrotemporal area. One epileptic discharge was observed every 74.9 s in waking and every 150.9 s in sleep. Epileptic activity was greatest in the group between 5 and 12 years of age (54.3%). The same activation rates were noted in siblings of patients with (47.2%) and without seizures (42.9%), and no differences were noted in siblings with (40%) or without (37.5%) seizures. Family history and sex of the siblings of patient did not play a role in the rate of activation. An autosomal dominant inheritance is assumed, but further investigations are necessary.

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Epileptic activity was recorded in the waking and sleep EEG of 62.5% of 80 siblings of 38 patients with absence seizures. Epileptic discharges were noted in waking only in 8.7%, in waking as well as sleep in 28.8%, and in sleep only in 25%. Generalized, partly irregular, and slow spike-wave complexes were found, twice with lateral emphasis. Spike-wave complexes were recorded in 72% of 50 siblings of patients with idiopathic absence and in 46.7% of 30 siblings of patients with symptomatic absence. One epileptic discharge was observed every 108.6 s on the average, without striking differences between siblings of patients with idiopathic (99.7 s) and symptomatic absence (119.3 s). Without any differences between siblings of children with idiopathic and symptomatic absence, the most epileptic discharges were activated in sleep stages C and D, followed by stages A and B. The highest activation rate was observed in the 7-14-year-old group (73.5%) and to a somewhat lesser degree in the group between 15 and 20 years of age (66.7%); fewer epileptic discharges were recorded in younger (25%) and older patients (28.6%). The higher activation rates in the male sex were significant only in siblings of patients with idiopathic absence. Although only five patients (13.2%) were photosensitive, a photosensitivity was found in 24% of siblings of children with idiopathic absence and in 20% of siblings of patients with symptomatic absence. Three siblings of patients with idiopathic absence also had absence seizures; in one of them a febrile seizure occurred at an earlier age. All of them showed generalized spike wave discharges in waking as well as sleep. Occipital theta delta activity with generalization was observed more frequently in siblings of patients with idiopathic absence (82.2%) than in those of patients with symptomatic absence (63.6%). Our waking and sleep EEG recordings prove that concerning etiology-genetic factors play a striking role in idiopathic absence, but are also of considerable significance in the symptomatic types.

The purpose of the study was to investigate whether the sleep EEG after sleep deprivation has a stronger provocative effect than the drug-induced sleep EEG. For this purpose a sleep EEG, induced by 2 mg/kg body weight of promazine hydrochloride, was recorded. On the following day a sleep EEG of the same patient was recorded after sleep deprivation of 24--26 h. If only patients whose wake EEGs were free from epileptic activity are considered, the rate of provocation was 58%. As epileptic activity could be recorded even in the sleep EEG without sleep deprivation in 45%, the advantage gained by recording a sleep EEG after sleep deprivation (52%) is only relatively small. The occurrence of epileptic activity was shown to be significantly more frequent amongst women and those who developed epilepsy at a younger age. For practical purposes it is recommended that for those patients whose wake EEGs are free from epileptic activity, a sleep EEG--possibly drug-induced--should be recorded. Only in instances where epileptic activity can not then be recorded should a wake EEG after sleep deprivation be carried out, and followed immediately, if necessary, by a sleep EEG.

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.