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

Abstract

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.

Increasing the Yield of EEG

“…There is an activating effect from SD on IEDs aside from the sampling effect or the activating effects of sleep. IEDs may occur with greater frequency during wakefulness after SD in the interval before sleep than in wakefulness without SD (Degen and Degen, 1981;Degen and Degen, 1983;Degen and Degen, 1991;Degen et al, 1987). However, the activating effect of SD was greatest during sleep in most but not all studies (Mendez and Radtke, 2001).…”

What is the role for EEG after sleep deprivation in the diagnosis of epilepsy? Issues, controversies, and future directions

“…Many studies suggest a specific activating effect of SD per se, pointing out that EEG activation is already present during the waking phases of the EEG recorded after SD (Degen, 1980;Degen and Degen, 1983;Degen et al, 1987;DeRoos et al, 2009;Mattson et al, 1965;Pratt et al, 1968;Schwarz and Zangemeister, 1978;So et al, 1994;Tartara et al, 1980). Fountain et al (1998) specifically addressed this aspect and showed significant IED incidence both during wakefulness and sleep SD EEG epochs, inferring that the EEG activation was exclusively due to SD, rather than to the occurrence of sleep.…”

“…Recent seizures occurrence Degen (1980), Degen and Degen (1983), Gandelman-Marton and Theitler (2011), Pratt et al (1968) Earlier or recent seizure onset Degen (1980), Degen andDegen (1991, 1983), Degen et al (1987) Previous history of repeated seizures DeRoos et al (2009), Gandelman-Marton and Theitler (2011) Higher seizure frequency Degen and Degen (1983) Delayed psychomotor development Degen (1980), Degen and Degen (1983), Degen et al (1987) Coexistent neuropathological conditions Degen (1980), Degen and Degen (1983), Degen et al (1987) Personality changes Degen and Degen (1983) Family history of epilepsy Degen et al (1987) Female gender Degen andDegen (1991, 1981), Degen et al (1987) Children and young patients Degen (1980), Degen and Degen (1991), Degen et al (1987), Roth et al (1986), DeRoos et al (2009 in the 1960s performed an additional basal EEG in those patients in whom SD EEG had shown IEDs. The proportion of SD-positive patients showing IEDs in a second basal EEG ranged from 18.8% (Mattson et al, 1965) to 12.8% (Pratt et al, 1968) and to a striking 0% in Geller et al (1969).…”

Sleep and Epilepsy: What We Know, Don’t Know, and Need to Know

“…Several studies have suggested that TSD can be useful in activating IEDs in wakefulness, especially in patients with IGE (Degen et al, 1980;Degen et al, 1981;Degen et al, 1983;Degen et al, 1987;El-Ad et al, 1994;Fountain et al, 1998;Geller et al, 1969;Klinger et al, 1991;Pratt et al, 1968;Ropakiotis et al, 2000;Roth et al, 1986;Scollo Lavizzari et al, 1977;Tartura et al, 1980;Veldhuizen et al, 1983). Fountain et al (1998) found that 7% of subjects had IEDs during wakefulness only after TSD.…”

“…In a series of studies in the 1980s, Degen and colleagues compared the effects of TSD on EEGs of subjects with different seizure types and epilepsy syndromes (Degen et al, 1981;Degen et al, 1983;Degen et al, 1987). For most seizure types, they found that spontaneous sleep and sleepdeprived recordings produced similar activation rates (awakening grand mal, 77% versus 71%; atypical absence, 78% versus 72%; absence epilepsy, 69% versus 71%; CPS, 49% versus 51%).…”