Sleep physiology in toddlers: Effects of missing a nap on subsequent night sleep

Lassonde, Jonathan M.; Rusterholz, Thomas; Kurth, Salomé; Schumacher, Allyson M.; Achermann, Peter; LeBourgeois, Monique K.

doi:10.1016/j.nbscr.2016.08.001

Cited by 21 publications

(23 citation statements)

References 50 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…SWE was obtained by cumulating mean SWA of artifact-free NREM sleep epochs in 30 min segments multiplied by the number of NREM sleep epochs in that segment [34]. The values of SWE at the end of sleep are indicators of the level of dissipated sleep pressure during the night.…”

Section: Sleep Latency and Efficiencymentioning

confidence: 99%

“…Both conditions were followed by total sleep deprivation. Several markers of sleep homeostasis were quantified, some of which were compared with predictions of the two-process model of sleep regulation [11,12,14,16,33,34]. We aimed to test whether adaptation to the imposed conditions occurred and whether this resulted in deviations from predictions based on a sleep homeostasis model.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Response to chronic sleep restriction, extension, and subsequent total sleep deprivation in humans: adaptation or preserved sleep homeostasis?

Skorucak

Arbon

Dijk

et al. 2018

Sleep

Self Cite

View full text Add to dashboard Cite

Sleep is regulated by a homeostatic process which in the two-process model of human sleep regulation is represented by electroencephalogram slow-wave activity (SWA). Many studies of acute manipulation of wake duration have confirmed the precise homeostatic regulation of SWA in rodents and humans. However, some chronic sleep restriction studies in rodents show that the sleep homeostatic response, as indexed by SWA, is absent or diminishes suggesting adaptation occurs. Here, we investigate the response to 7 days of sleep restriction (6 hr time in bed) and extension (10 hr time in bed) as well as the response to subsequent total sleep deprivation in 35 healthy participants in a cross-over design. The homeostatic response was quantified by analyzing sleep structure and SWA measures. Sleep restriction resulted primarily in a reduction of rapid eye movement (REM) sleep. SWA and accumulated SWA (slow-wave energy, SWE) were not much affected by sleep extension/restriction. The SWA responses did not diminish significantly in the course of the intervention and did not deviate significantly from the predictions of the two-process model. The response to total sleep deprivation consisted of an increase in SWA and rise rate of SWA and SWE and did not differ between the two conditions. The data show that changes in sleep duration within an ecologically relevant range have a marked effect on REM sleep and that SWA responds in accordance with predictions based on a saturating exponential increase during wake and an exponential decline in sleep of homeostatic sleep pressure during both chronic sleep restriction and extension.Key words: chronic sleep restriction; chronic sleep extension; sleep deprivation; homeostasis; allostasis; Process S; simulations; adaptation Statement of SignificanceBoth chronic short and long sleep are associated with negative health consequences. It is therefore important to understand sleep regulation during sleep restriction and extension. Sleep homeostasis refers to the sleep-wake dependent aspect of sleep regulation and slowwave sleep is often considered of particular importance. We observed that 1 week of sleep restriction primarily leads to deficits in rapid eye movement sleep while slow-wave activity is little affected throughout the week long sleep restriction and sleep extension in accordance with predictions of the two-process model. The data imply that there is no significant adaptation to insufficient or excessive sleep.

show abstract

Section: Sleep Latency and Efficiencymentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Response to chronic sleep restriction, extension, and subsequent total sleep deprivation in humans: adaptation or preserved sleep homeostasis?

Skorucak

Arbon

Dijk

et al. 2018

Sleep

Self Cite

View full text Add to dashboard Cite

show abstract

“…As first proposed by Borbély, the homeostatic process dictates that sleep propensity builds with increasing time awake and dissipates during periods of sleep [ 12 ]. Sleep electroencephalography (EEG) findings from adults and toddlers indicate reduced nocturnal nighttime sleep drive as a function of daytime napping (e.g., longer sleep onset latency, decreased slow wave activity in non-rapid eye movement sleep, 0.75–4.5 Hz) [ 13 – 15 ]. Additionally, evidence linking naps, nighttime sleep, and the homeostatic process in children is inferred from studies using parent-reports or actigraphy suggesting that preschoolers who nap longer during the day are more likely to sleep less the following night [ 1 , 16 , 17 ].…”

Section: Introductionmentioning

confidence: 99%

The Timing of the Circadian Clock and Sleep Differ between Napping and Non-Napping Toddlers

et al. 2015

Self Cite

View full text Add to dashboard Cite

The timing of the internal circadian clock shows large inter-individual variability across the lifespan. Although the sleep-wakefulness pattern of most toddlers includes an afternoon nap, the association between napping and circadian phase in early childhood remains unexplored. This study examined differences in circadian phase and sleep between napping and non-napping toddlers. Data were collected on 20 toddlers (34.2±2.0 months; 12 females; 15 nappers). Children followed their habitual napping and non-napping sleep schedules (monitored with actigraphy) for 5 days before an in-home salivary dim light melatonin onset (DLMO) assessment. On average, napping children fell asleep during their nap opportunities on 3.6±1.2 of the 5 days before the DLMO assessment. For these napping children, melatonin onset time was 38 min later (p = 0.044; d = 0.93), actigraphically-estimated bedtime was 43 min later (p = 0.014; d = 1.24), sleep onset time was 59 min later (p = 0.006; d = 1.46), and sleep onset latency was 16 min longer (p = 0.030; d = 1.03) than those not napping. Midsleep and wake time did not differ by napping status. No difference was observed in the bedtime, sleep onset, or midsleep phase relationships with DLMO; however, the wake time phase difference was 47 min smaller for napping toddlers (p = 0.029; d = 1.23). On average, nappers had 69 min shorter nighttime sleep durations (p = 0.006; d = 1.47) and spent 49 min less time in bed (p = 0.019; d = 1.16) than non-nappers. Number of days napping was correlated with melatonin onset time (r = 0.49; p = 0.014). Our findings indicate that napping influences individual variability in melatonin onset time in early childhood. The delayed bedtimes of napping toddlers likely permits light exposure later in the evening, thereby delaying the timing of the clock and sleep. Whether the early developmental trajectory of circadian phase involves an advance associated with the decline in napping is a question necessitating longitudinal data as children transition from a biphasic to monophasic sleep-wakefulness pattern.

show abstract

“…This has been shown in children with childhood epilepsy with centrotemporal spikes, ‘partial refractory’ epilepsies, idiopathic generalized epilepsies, and epileptic encephalopathies, and has been demonstrated even in a drug‐naive cohort . Additionally, children with focal lesional epilepsies may have increased SWS versus controls . Despite the heterogeneity of these data, they provide evidence first that most children with epilepsy will be relatively REM‐deprived compared to peers, and second that both epileptic activity and antiepileptic therapy likely contribute to this derangement.…”

Section: Sleep In Children With Epilepsy: Disrupted and Intact Aspectsmentioning

confidence: 99%

“…43 Additionally, children with focal lesional epilepsies may have increased SWS versus controls. 34 Despite the heterogeneity of these data, they provide evidence first that most children with epilepsy will be relatively REM-deprived compared to peers, and second that both epileptic activity and antiepileptic therapy likely contribute to this derangement. SWS, however, is likely to be found in normal or higher amounts.…”

Section: Data From Polysomnographymentioning

confidence: 99%

Sleep architecture and homeostasis in children with epilepsy: a neurodevelopmental perspective

Chan¹

2019

Develop Med Child Neuro

View full text Add to dashboard Cite

Although the influence of sleep on epilepsy has long been recognized, this relationship has yet to be fully exploited to benefit patients. The past decade has seen significant advances in understanding paediatric sleep, providing a framework by which to properly evaluate the sleep of children with epilepsy, which itself has been subject to increasing scrutiny. The role of sleep in learning and the potential for interictal discharges to disrupt sleep‐related memory consolidation provide a novel perspective for understanding the association of childhood epilepsy with a high rate of intellectual disability. In this review, I outline the evolution of sleep duration, architecture, and homeostasis across childhood, relating this to the development of cognitive functions. I describe how these may be disrupted or preserved in children with epilepsy; in particular, collating data from polysomnography. Finally, I explore how sleep may, in the future, be modulated to improve cognitive outcome in these patients. What this paper adds Children with epilepsy have less rapid eye movement sleep than controls, but this improves with seizure cessation. Deep or slow‐wave sleep is highly conserved in children with epilepsy. Sleep homeostasis may be disrupted either at a local or global level by the presence of interictal epileptiform discharges.

show abstract

Sleep physiology in toddlers: Effects of missing a nap on subsequent night sleep

Cited by 21 publications

References 50 publications

Response to chronic sleep restriction, extension, and subsequent total sleep deprivation in humans: adaptation or preserved sleep homeostasis?

Response to chronic sleep restriction, extension, and subsequent total sleep deprivation in humans: adaptation or preserved sleep homeostasis?

The Timing of the Circadian Clock and Sleep Differ between Napping and Non-Napping Toddlers

Sleep architecture and homeostasis in children with epilepsy: a neurodevelopmental perspective

Contact Info

Product

Resources

About