Elsevier

Epilepsy Research

Volume 51, Issues 1–2, September 2002, Pages 123-132
Epilepsy Research

Effect of sleep deprivation on spike-wave discharges in idiopathic generalised epilepsy: a 4×24 h continuous long term EEG monitoring study

https://doi.org/10.1016/S0920-1211(02)00123-7Get rights and content

Abstract

The aim of the study was to investigate the effect of sleep and sleep deprivation on spike-wave discharges (SWD) in an idiopathic generalised epileptic patient population by continuous long term cassette EEG monitoring for 4×24 h. In ten patients with idiopathic generalised epilepsy, showing SWD during awake state and in sleep as well, EEG and sleep polygraphy was recorded for 4×24 h. Sleep was deprived during the second 24 h. Awake state, NREM1, NREM2, NREM3+4 and REM sleep duration and number of SWD episodes were evaluated in 4 min intervals by visual scoring. For analysing the effect of ‘day’ and ‘night’, ‘vigilance’ and ‘sleep deprivation’ (SD) on the density variables multi-way ANOVAs were carried out in different designs. SWD densities for different vigilance states were not significantly different during ‘day’ and ‘night’ in 24 h without SD or rebound after SD. Sleep had an activating effect SWD densities being the highest during NREM1 and NREM2. There was an increase of SWD densities in all vigilance states after SD, but SWD densities remained the highest in NREM1 andNREM2. Our results support the view that sleep dependent rather than sleep independent mechanisms cause activation of SWD after SD in generalised epilepsy. We assume that fine graded vigilance fluctuations, that are more frequent after SD, have an essential role in SWD activation in superficial sleep or even in wakefulness.

Introduction

Many studies report an increased epileptiform discharge (ED) activity following sleep deprivation (SD) (Arne-Bes et al., 1982, Degen, 1980, Degen and Degen, 1983, Degen and Degen, 1984, Drinkenburg et al., 1995, Fountain et al., 1998, Klingler et al., 1984, Logothetis et al., 1986, Marinig et al., 2000, Mattson et al., 1965, Pratt et al., 1968, Rowan et al., 1982, Scollo-Lavizzari et al., 1975, Veldhuizen et al., 1983).

It is well known that sleep itself activates EDs in partial as well as in generalised epilepsies (Autret et al., 1982, Drinkenburg et al., 1991, Gigli and Valente, 2000, Halász, 1981, Halász, 1984, Janz, 1969, Niedermeyer, 1972, Passouant, 1975). There is no general agreement whether the provocative effect of SD is caused merely by inducing sleep or SD has an independent genuine activating effect (Scollo-Lavizzari et al., 1977, Veldhuizen et al., 1983). The conclusion is based generally on retrospective studies taking records before and after SD in different time periods, in mixed epileptic population, or no ED activity under baseline conditions (Degen, 1980, Degen and Degen, 1983, Degen et al., 1987, Mattson et al., 1965, Rowan et al., 1982). Further shortcomings are that EEG recordings were short following SD (Degen and Degen, 1983, Degen et al., 1987, Logothetis et al., 1986, Scollo-Lavizzari et al., 1975, Scollo-Lavizzari et al., 1977) no control group was used and there were no records during SD. In several studies absolute numbers were used, regardless the duration of the vigilance level period where they appeared. The effect of different vigilance states with and without SD is compared only in a few studies (Fountain et al., 1998, Klingler et al., 1984, Marinig et al., 2000) and according to our knowledge, there are no published reports about the whole sleep–wake cycle, furthermore degree of activation was never measured in all vigilance levels.

Idiopathic generalised epilepsy (IGE) is underrepresented in the published studies, in spite of the well demonstrated dependence of this kind of epilepsy on vigilance (Coenen et al., 1991, Drinkenburg et al., 1991, Halász, 1984, Passouant et al., 1963, Shouse, 1987, Shouse, 1988, Snead, 1995). Here we report a prospective study of an IGE group of patients. Continuous EEG monitoring and sleep polygraphy was performed for 4×24:24 h before, 2×24 h after, and 24 h during SD.

The aim of the study was to collect more appropriate data about the nature of SWD activation through SD and the proportion of this activation with the different sleep states.

Section snippets

Study design

Ten patients with IGE, showing SWD both in spontaneous awake and sleep EEG, were selected for this study. Advantages and risks for participation were explained and informed consent was taken. Patients were admitted to the ward 1-day prior to the study, and were settled in a separate room in order to ensure undisturbed conditions and adaptation. Sleep was not recorded in the first adaptational night. EEG and sleep polygraphy was recorded for four consecutive 24 h with cassette EEG (Brain

Distribution of vigilance states during 8×12 h periods of registration

Distribution of vigilance states in the 8×12 h periods of registration (Fig. 2) showed that SD was almost complete during D2 and N2. In D1 10%, in D4 6% and in D2 no sleep was present. D3 contained rebound sleep after 24 h SD. The distribution of the five vigilance states (wakefulness, NREM1, NREM2, NREM3+4, REM) showed no significant differences among the N1, N3, and N4 nights (P>0.1 for all five ANOVA comparisons).

The ‘day’ or ‘night’ influence on SWD densities without sleep deprivation

Before studying the influence of different vigilance states and SD it was

The effect of sleep and sleep deprivation on SWD in IGE

Our study design allowed to compare SWD density in wakefulness and in different sleep stages during and after sleep deprivation in the same patients. Even with this design we had certain limitations when we tried to analyse the effect of different vigilance levels on SWD, since not all 12 h periods, contained satisfactory balance of sleep or awake states to compare them.

Our results confirm that idiopathic generalised epilepsy is a sleep, and sleep deprivation sensitive type of epilepsy. In

Acknowledgements

This study was supported the 18 Postdoctoral Ph.D. Fellowship Program (J. Filakovszky) of Semmelweis Medical University, Ministry of Culture and Education, Hungary, and Research Fund Grant of Semmelweis University TB-12/00.

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