A model of human sleep homeostasis based on EEG slow-wave activity: Quantitative comparison of data and simulations

Achermann, Peter; Dijk, Derk‐Jan; Brunner, Daniel P.; Borbély, Alexander A.

doi:10.1016/0361-9230(93)90016-5

Cited by 405 publications

(304 citation statements)

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“…According to contemporary models of sleep-wake cycle regulation, the interaction of homeostatic and circadian processes regulates the sleep-wake cycle (Achermann et al, 1993;Borbély and Achermann, 2000;Broughton, 1998;Daan et al, 1984). The homeostatic process represents the accumulation of sleep pressure with increasing time awake and its dissipation during a sleep episode.…”

Section: Introductionmentioning

confidence: 99%

“…The interaction between the homeostatic and the circadian processes underlies these differences. Hence, elevated homeostatic sleep pressure induced by sleep deprivation accounts for a higher amount of SWS in daytime recovery sleep compared to night time sleep (Achermann et al, 1993). Despite the deprivation of sleep, daytime recovery sleep is more fragmented and shorter than night time sleep because it is initiated at a point in the circadian rhythm when the biological clock is providing an increasing wake signal (Dijk and Czeisler, 1994).…”

Section: Introductionmentioning

confidence: 99%

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Effects of Caffeine are more Marked on Daytime Recovery Sleep than on Nocturnal Sleep

Carrier

Fernandez‐Bolaños

Robillard

et al. 2006

Neuropsychopharmacol

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Caffeine is often used to counteract sleepiness generated by sleep deprivation, jet lag, and shift-work, and is consumed at different times of day. Caffeine also has effects on sleep. However, little is known about the interaction between sleep deprivation, circadian timing, and caffeine consumption on sleep. In this study, we compared the effects of caffeine on nocturnal sleep initiated at habitual circadian time and on daytime recovery sleep. Thirty-four moderate caffeine consumers participated in both caffeine (200 mg) and placebo (lactose) conditions in a double-blind crossover design. Seventeen subjects followed their habitual sleep-wake cycle and slept in the laboratory during the night (Night), while 17 subjects were sleep deprived for one night and recovery sleep started in the morning (DayRec). All subjects received a capsule of 100 mg of caffeine (or placebo) 3 h before bedtime, and the remaining dose 1 h before bedtime. Compared to placebo, caffeine lengthened sleep latency, increased stage 1, and reduced stage 2 and slow-wave sleep (SWS) in both groups. However, caffeine reduced sleep efficiency more strongly in the DayRec group, and decreased sleep duration and REM sleep only in that group. The stronger effects of caffeine on daytime recovery sleep compared to nocturnal sleep are probably the consequence of the combined influence of increasing circadian wake propensity drive and the dissipation of homeostatic sleep pressure. We propose that the reduction of SWS by caffeine during daytime sleep increases the impact of the circadian wake signal on sleep. These results have implications for individuals using caffeine during night time. Neuropsychopharmacology (2007) 32, 964-972.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Effects of Caffeine are more Marked on Daytime Recovery Sleep than on Nocturnal Sleep

Carrier

Fernandez‐Bolaños

Robillard

et al. 2006

Neuropsychopharmacol

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“…The timing of sleep and wakefulness and the structure of sleep are regulated by the interaction of a homeostatic, sleep-wake-dependent process S and the circadian pacemaker located in the hypothalamus et al 1981;Daan et al 1984;Dijk et al 1987;Achermann et al 1993). Recent studies have indicated that an EEG correlate of sleep propensity can also be measured during wakefulness.…”

Section: A Novel Approach To Investigate the Relationship Between Depmentioning

confidence: 99%

“…Different theories have been proposed to account for the antidepressant effects of sleep manipulations. They include prolonged major suppression of REM sleep (Vogel 1975;Vogel et al 1990), elevation of sleep propensity (Borbély and Wirz-Justice 1982), and reduction of non-REM sleep intensity (Beersma and Van den Hoofdakker 1992).The timing of sleep and wakefulness and the structure of sleep are regulated by the interaction of a homeostatic, sleep-wake-dependent process S and the circadian pacemaker located in the hypothalamus et al 1981;Daan et al 1984;Dijk et al 1987;Achermann et al 1993). Recent studies have indicated that an EEG correlate of sleep propensity can also be measured during wakefulness.…”

mentioning

confidence: 99%

“…process S) accumulates during wakefulness and dissipates during sleep. The time course of this process has been estimated from low-frequency activity (power below ‫ف‬ 8 Hz) in central electroencephalogram (EEG) recordings during sleep (Borbély et al 1981;Daan et al 1984;Dijk et al 1987;Achermann et al 1993). Recent studies have indicated that an EEG correlate of sleep propensity can also be measured during wakefulness.…”

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confidence: 99%

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Different Effects of Phenelzine Treatment on EEG Topography in Waking and Sleep in Depressed Patients

Landolt

Gillin

2002

Neuropsychopharmacology

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A novel approach to investigate the relationship between depression and changes in sleep-wake regulatory mechanisms used the monoamine oxidase inhibitor (MAOI) phenelzine that is known to suppress rapid-eye-movement (REM) sleep. Sleep architecture and EEG topography during wakefulness and sleep were studied in eight depressed patients before and after five weeks of treatment with phenelzine (30-90 mg/day), which induced a significant alleviation of depressive symptoms. Theta power (4.75-7.5 Hz) during a 5-min wake EEG prior to sleep increased two-fold during administration of phenelzine. REM sleep was almost completely eliminated. This latter effect was compensated by increased duration of stage 2, whereas total sleep time was not shortened. In non-REM sleep (stages 2, 3, and 4), treatment slightly reduced EEG power between 2. Hz band increased. Activity in the delta band Mood and the regulation of sleep are closely related. This notion is supported by the presence of frequent sleep abnormalities in depressed patients, which may affect both rapid-eye-movement (REM) sleep and nonrapid-eye-movement (non-REM) sleep (Benca et al. 1992). A tight association between sleep and mood is further suggested by the beneficial action of total and partial sleep deprivation, as well as phase advance therapies of sleep in many patients with depression (Gillin and Borbély 1985; Wirz-Justice and Van den Hoofdakker 1999). Different theories have been proposed to account for the antidepressant effects of sleep manipulations. They include prolonged major suppression of REM sleep (Vogel 1975;Vogel et al. 1990), elevation of sleep propensity (Borbély and Wirz-Justice 1982), and reduction of non-REM sleep intensity (Beersma and Van den Hoofdakker 1992).The timing of sleep and wakefulness and the structure of sleep are regulated by the interaction of a homeostatic, sleep-wake-dependent process S and the circadian pacemaker located in the hypothalamus et al. 1981;Daan et al. 1984;Dijk et al. 1987;Achermann et al. 1993). Recent studies have indicated that an EEG correlate of sleep propensity can also be measured during wakefulness. Power in the theta band ( ‫ف‬ 5-8 Hz) of the wake EEG increases during sleep deprivation (Cajochen et al. 1995;Aeschbach et al. 1997;Finelli et al. 2000). The time constant of this increase is similar to that obtained for the wake-dependent rise of delta power as measured in non-REM sleep. Furthermore, topographical analyses of the EEG during prolonged wakefulness have shown that the increase of theta activity in waking and delta activity ( ‫ف‬ 1-4 Hz) in non-REM sleep are largest in frontal EEG derivations and positively correlated (Werth et al. 1998;Cajochen et al. 1999aCajochen et al. , 1999bFinelli et al. 2000). These findings suggest that sleep regulation may exhibit local features. In other words, frontal parts of the cortex may be particularly susceptible to sleep loss and reflect the homeostatic process of sleep regulation more sensitively than other cortical regions. The monoamine oxidase inhibitor...

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Sleep and Sleep Electroencephalogram in Depressed Patients Treated With Phenelzine

Landolt¹,

Raimo²,

Schnierow³

et al. 2001

Arch Gen Psychiatry

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A model of human sleep homeostasis based on EEG slow-wave activity: Quantitative comparison of data and simulations

Cited by 405 publications

References 45 publications

Effects of Caffeine are more Marked on Daytime Recovery Sleep than on Nocturnal Sleep

Effects of Caffeine are more Marked on Daytime Recovery Sleep than on Nocturnal Sleep

Different Effects of Phenelzine Treatment on EEG Topography in Waking and Sleep in Depressed Patients

Sleep and Sleep Electroencephalogram in Depressed Patients Treated With Phenelzine

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