scholarly journals Effects of sleep restriction on the sleep electroencephalogram of adolescents

SLEEP ◽  
2021 ◽  
Author(s):  
Ian G Campbell ◽  
Alejandro Cruz-Basilio ◽  
Nato Darchia ◽  
Zoey Y Zhang ◽  
Irwin Feinberg

Abstract Study Objectives This report describes findings from an ongoing longitudinal study of the effects of varied sleep durations on wake and sleep electroencephalogram (EEG) and daytime function in adolescents. Here, we focus on the effects of age and time in bed (TIB) on total sleep time (TST) and nonrapid eye movement (NREM) and rapid eye movement (REM) EEG. Methods We studied 77 participants (41 male) ranging in age from 9.9 to 16.2 years over the 3 years of this study. Each year, participants adhered to each of three different sleep schedules: four consecutive nights of 7, 8.5, or 10 h TIB. Results Altering TIB successfully modified TST, which averaged 406, 472 and 530 min on the fourth night of 7, 8.5, and 10 h TIB, respectively. As predicted by homeostatic models, shorter sleep durations produced higher delta power in both NREM and REM although these effects were small. Restricted sleep more substantially reduced alpha power in both NREM and REM sleep. In NREM but not REM sleep, sleep restriction strongly reduced both the all-night accumulation of sigma EEG activity (11–15 Hz energy) and the rate of sigma production (11–15 Hz power). Conclusions The EEG changes in response to TIB reduction are evidence of insufficient sleep recovery. The decrease in sigma activity presumably reflects depressed sleep spindle activity and suggests a manner by which sleep restriction reduces waking cognitive function in adolescents. Our results thus far demonstrate that relatively modest TIB manipulations provide a useful tool for investigating adolescent sleep biology.

2012 ◽  
Vol 302 (5) ◽  
pp. R533-R540 ◽  
Author(s):  
Irwin Feinberg ◽  
Nicole M. Davis ◽  
Evan de Bie ◽  
Kevin J. Grimm ◽  
Ian G. Campbell

We recorded sleep electroencephalogram longitudinally across ages 9–18 yr in subjects sleeping at home. Recordings were made twice yearly on 4 consecutive nights: 2 nights with the subjects maintaining their ongoing school-night schedules, and 2 nights with time in bed extended to 12 h. As expected, school-night total sleep time declined with age. This decline was entirely produced by decreasing non-rapid eye movement (NREM) sleep. Rapid eye movement (REM) sleep durations increased slightly but significantly. NREM and REM sleep durations also exhibited different age trajectories when sleep was extended. Both durations exceeded those on school-night schedules. However, the elevated NREM duration did not change with age, whereas REM durations increased significantly. We interpret the adolescent decline in school-night NREM duration in relation to our hypothesis that NREM sleep reverses changes produced in plastic brain systems during waking. The “substrate” produced during waking declines across adolescence, because synaptic elimination decreases the intensity (metabolic rate) of waking brain activity. Declining substrate reduces both NREM intensity (i.e., delta power) and NREM duration. The absence of a decline in REM sleep duration on school-night sleep and its age-dependent increase in extended sleep pose new challenges to understanding its physiological role. Whatever their ultimate explanation, these robust findings demonstrate that the two physiological states of human sleep respond differently to the maturational brain changes of adolescence. Understanding these differences should shed new light on both brain development and the functions of sleep.


SLEEP ◽  
2021 ◽  
Vol 44 (Supplement_2) ◽  
pp. A87-A87
Author(s):  
Mohammad Sibai ◽  
Timothy Roehrs ◽  
Gail Koshor ◽  
Jelena Verkler ◽  
Leslie Lundahl

Abstract Introduction Sleep disturbances are commonly reported by chronic marijuana (MJ) users and often identified as reasons for MJ relapse and/or other drug use. In the current study we compared the sleep architecture of 12 heavy MJ users to 11 normal controls. Methods Participants in the marijuana group met DSM-V criteria for cannabis use disorder but were otherwise healthy individuals. On the first study day, individuals smoked (1330-1400 hr) 11 puffs from a cannabis cigarette (7% THC). During the next four days, under varying experimental contingencies participants smoked an average of 4.58 (±3.48) day 1, 4.92 (±3.62) day 2, 4.75 (±3.52) day 3, and 4.17 (±3.56) day 4 puffs from cannabis cigarettes (7% THC). Their sleep was recorded the first four study nights using standard polysomnography procedures at Henry Ford Sleep and Research Center Hospital, under an 8-hr fixed time in bed (2300-0700 hr). Controls (n=11) had no history of illicit drug use or medical illness and were not shift workers. Neither group reported a history of sleep-related disorders. PSG recordings were scored using Rechtschaffen and Kales standard criteria. Sleep measures included sleep efficiency (total sleep time/time in bed * 100), latency to persistent sleep, and percent of time spent in Stage 1, 2, 3/4, and rapid eye movement (REM). Results PSGs taken across all four nights of inpatient stay showed that MJ users spent significantly more time in REM sleep compared to controls (means 24.91, 24.64, 24.42, 24.13 vs 18.81, p<.001) and less time in stage 3/4 sleep (means 4.33, 4.79, 4.53, 6.91 vs 15.68, p<.001). MJ users showed reduced sleep efficiency compared to controls on night 4 (means 82.03 vs 90.32, p=0.039), and increased latency to persistent sleep on night 1 (means 6.04 vs 17.77, p=0.026). Conclusion These data show reduced sleep efficiency, lightened sleep (reduced stage 3/4), as well as an increased duration during REM sleep in heavy MJ users during decreased use, findings that are predictive of relapse in other drug abuse populations. Support (if any) NIH/NIDA R21 DA040770 (LHL)


Circulation ◽  
2020 ◽  
Vol 141 (Suppl_1) ◽  
Author(s):  
Xiaoyue Liu ◽  
Jeongok G Logan ◽  
Younghoon Kwon ◽  
Jennifer Lobo ◽  
Hyojung Kang ◽  
...  

Introduction: Blood pressure (BP) variability (BPV) is a novel marker for cardiovascular disease (CVD) independent of high BP. Sleep architecture represents the structured pattern of sleep stages consisting of rapid eye movement (REM) and non-rapid eye movement (NREM), and it is an important element in the homeostatic regulation of sleep. Currently, little is known regarding whether BPV is linked to sleep stages. Our study aimed to examine the relationship between sleep architecture and BPV. Methods: We analyzed in-lab polysomnographic studies collected from individuals who underwent diagnostic sleep studies at a university hospital from 2010 to 2017. BP measures obtained during one year prior to the sleep studies were included. BPV was computed using the coefficient of variation for all individuals who had three or more systolic and diastolic BP data. We conducted linear regression analysis to assess the relationship of systolic BPV (SBPV) and diastolic BPV (DBPV) with the sleep stage distribution (REM and NREM sleep time), respectively. Covariates that can potentially confound the relationships were adjusted in the models, including age, sex, race/ethnicity, body mass index, total sleep time, apnea-hypopnea index, mean BP, and history of medication use (antipsychotics, antidepressants, and antihypertensives) during the past two years before the sleep studies. Results: Our sample (N=3,565; male = 1,353) was racially and ethnically diverse, with a mean age 54 ± 15 years and a mean BP of 131/76 ± 13.9/8.4 mmHg. Among the sleep architecture measures examined, SBPV showed an inverse relationship with REM sleep time after controlling for all covariates ( p = .033). We subsequently categorized SBPV into four quartiles and found that the 3 rd quartile (mean SBP SD = 14.9 ± 2.1 mmHg) had 3.3 fewer minutes in REM sleep compared to the 1 st quartile ( p = .02). However, we did not observe any relationship between DBPV and sleep architecture. Conclusion: Greater SBPV was associated with lower REM sleep time. This finding suggests a possible interplay between BPV and sleep architecture. Future investigation is warranted to clarify the directionality, mechanism, and therapeutic implications.


SLEEP ◽  
2020 ◽  
Vol 43 (Supplement_1) ◽  
pp. A115-A115
Author(s):  
O R Larson ◽  
C W Jones ◽  
M Basner ◽  
D F Dinges

Abstract Introduction Mood progressively deteriorates over consecutive days of sleep restriction. The neurobiological processes active during sleep that influence the risk of mood disturbance are unknown. This study investigated the relationships between physiological sleep parameters (i.e., slow-wave activity (SWA), slow-wave energy (SWE), rapid eye-movement (REM) sleep duration and latency), and self-reported measures of mood across sleep restriction. Methods N=181 healthy participants (48.1% female; 30±6.8 yrs) had valid polysomnography (PSG) and mood data. The study design included two baseline nights (8h time in bed [TIB]) followed by five nights of 4h TIB. PSG (EEG derivations C3-A2, Fz-A1, O2-A1) was collected on the second baseline night (B2), first night of 4h TIB (SR1), and the fifth night of 4h TIB (SR5). The Profile of Mood States was assayed on days following PSG. Power spectral analysis for SWE and SWA was conducted (delta power; band: 0.5-4.5 Hz). General linear regression models were used to independently assess the slope of SWE, SWA, percent REM of total sleep time (TST), and REM latency on mood disturbance across sleep restriction. Results At baseline, higher SWE (unadjusted; r=0.21; P=0.004) and SWA (unadjusted; r=0.19; P=0.007) were associated with greater mood disturbance; these relations were attenuated when adjusted for age and sex. No relation was found between mood and REM latency or REM percent of TST. The slope of mood disturbance from B2 to SR5 was associated with greater percentage increases in C3 SWA on SR5 relative to B2 (β=0.039; P=0.008); this association was not observed for SWE (β=-0.016; P=0.48). The slope of REM latency and REM percent of TST were not associated with the slope of mood disturbance. Conclusion Our results indicate that greater SWA due to sleep restriction was associated with greater mood disturbance, suggesting that less SWA may confer resilience to mood disturbances resulting from sleep restriction. Support This work was supported by National Institute of Health NIH R01NR004281 and National Space and Biomedical Research Institute NSRBI NCC 5-98.


SLEEP ◽  
2019 ◽  
Vol 43 (6) ◽  
Author(s):  
Sjoerd J van Hasselt ◽  
Maria Rusche ◽  
Alexei L Vyssotski ◽  
Simon Verhulst ◽  
Niels C Rattenborg ◽  
...  

Abstract Most of our knowledge about the regulation and function of sleep is based on studies in a restricted number of mammalian species, particularly nocturnal rodents. Hence, there is still much to learn from comparative studies in other species. Birds are interesting because they appear to share key aspects of sleep with mammals, including the presence of two different forms of sleep, i.e. non-rapid eye movement (NREM) and rapid eye movement (REM) sleep. We examined sleep architecture and sleep homeostasis in the European starling, using miniature dataloggers for electroencephalogram (EEG) recordings. Under controlled laboratory conditions with a 12:12 h light–dark cycle, the birds displayed a pronounced daily rhythm in sleep and wakefulness with most sleep occurring during the dark phase. Sleep mainly consisted of NREM sleep. In fact, the amount of REM sleep added up to only 1~2% of total sleep time. Animals were subjected to 4 or 8 h sleep deprivation to assess sleep homeostatic responses. Sleep deprivation induced changes in subsequent NREM sleep EEG spectral qualities for several hours, with increased spectral power from 1.17 Hz up to at least 25 Hz. In contrast, power below 1.17 Hz was decreased after sleep deprivation. Sleep deprivation also resulted in a small compensatory increase in NREM sleep time the next day. Changes in EEG spectral power and sleep time were largely similar after 4 and 8 h sleep deprivation. REM sleep was not noticeably compensated after sleep deprivation. In conclusion, starlings display signs of NREM sleep homeostasis but the results do not support the notion of important REM sleep functions.


1994 ◽  
Vol 77 (4) ◽  
pp. 1811-1818 ◽  
Author(s):  
C. P. O'Donnell ◽  
E. D. King ◽  
A. R. Schwartz ◽  
P. L. Smith ◽  
J. L. Robotham

The effect of sleep deprivation on sleep architecture and respiratory responses to repetitive airway obstruction during sleep was investigated in four chronically instrumented tracheostomized dogs during 12-h nocturnal experiments. A 24-h period of prior sleep deprivation increased (P < 0.05) the rate at which airway obstruction could be induced from 20 +/- 3 (SE) to 37 +/- 10 times/h compared with non-sleep-deprived dogs. During non-rapid-eye-movement sleep the duration of obstruction, minimum arterial hemoglobin saturation, and peak negative inspiratory effort at arousal were 20.5 +/- 1.0 s, 91.7 +/- 0.5%, and 28.4 +/- 1.8 mmHg, respectively, in non-sleep-deprived dogs. Sleep deprivation increased (P < 0.01) the duration of obstruction to 28.0 +/- 0.9 s, worsened (P < 0.05) the minimal arterial hemoglobin desaturation to 85.4 + 3.1%, and increased (P < 0.025) the peak negative inspiratory effort at arousal to 36.1 +/- 1.6 mmHg. Sleep deprivation also caused increases (P < 0.025) in total sleep time, rapid-eye-movement (REM) sleep time, and percentage of time in REM sleep in a 2-h recovery period without airway obstruction at the end of the study. We conclude that airway obstruction in the sleeping dog can reproduce the disturbances in sleep architecture and respiration that occur in obstructive sleep apnea and that prior sleep deprivation will increase apnea severity, degree of somnolence, and REM sleep rebound independent of change in upper airway collapsibility.


1977 ◽  
Vol 233 (5) ◽  
pp. R213-R221 ◽  
Author(s):  
J. M. Walker ◽  
S. F. Glotzbach ◽  
R. J. Berger ◽  
H. C. Heller

Electroencephalogram (EEG), electrooculogram, electromyogram, and electrocardiogram were recorded from ground squirrels (Citellus beldingi and C. lateralis) during the summer and also during the hibernation season. Summer recordings revealed that the animals spent an average of 66% of the 24-h period asleep (49% of the 12-h light period and 84% of the 12-h dark period); 19% of the total sleep time (TST) consisted of rapid-eye-movement (REM) sleep, and 81% of TST consisted of slow-wave sleep (SWS). Recordings obtained during the hibernation season showed that hibernation was entered through sleep, but the distribution of sleep states was different than in euthermic sleep. During the early entrance when brain temperature (Tbr) was between 35 and 25 degrees C, the animals were asleep 88% of the time, but only 10% of the TST was spent in REM sleep. The EEG amplitude declined with decreased Tbr so that classical sleep stages could not be identified below a Tbr of 25 degrees C. The frequency of the EEG increased as Tbr decreased; but activity in the 0–4 cycles/s band occupied the majority of the record even at a Tbr of 10 degrees C. Below a Tbr of 10 degrees C the EEG was isoelectric except for intermittent bursts of spindles. It was concluded from these and other results that the entrance into hibernation represents an extension of the thermoregulatory adjustments that occur during SWS.


2010 ◽  
pp. 821-829 ◽  
Author(s):  
H Wu ◽  
WS Stone ◽  
X Hsi ◽  
J Zhuang ◽  
L Huang ◽  
...  

Sleep is regulated by complex biological systems and environmental influences, neither of which is fully clarified. This study demonstrates differential effects of partial sleep deprivation (SD) on sleep architecture and psychomotor vigilance task (PVT) performance using two different protocols (sequentially) that each restricted daily sleep to 3 hours in healthy adult men. The protocols differed only in the period of sleep restriction; in one, sleep was restricted to a 3-hour block from 12:00 AM to 3:00 AM, and in the other, sleep was restricted to a block from 3:00 AM to 6:00 AM. Subjects in the earlier sleep restriction period showed a significantly lower percentage of rapid-eye-movement (REM) sleep after 4 days (17.0 vs. 25.7 %) and a longer latency to the onset of REM sleep (L-REM) after 1 day (78.8 vs. 45.5 min) than they did in the later sleep restriction period. Reaction times on PVT performance were also better (i.e. shorter) in the earlier SR period on day 4 (249.8 vs. 272 ms). These data support the view that earlier-night sleep may be more beneficial for daytime vigilance than later-night sleep. The study also showed that cumulative declines in daytime vigilance resulted from loss of total sleep time, rather than from specific stages, and underscored the reversibility of SR effects with greater amounts of sleep.


Author(s):  
Sophie West

Typically, disorders of sleep cause disturbance either to the sufferer or to their bed partner. If total sleep time is reduced, this may lead to problems with excessive daytime sleepiness, which can affect work, driving, concentration, and relationships. ‘Sleepiness’ implies an intrusive desire to fall asleep, caused by some form of sleep deprivation or sedative drugs; this is different from ‘tiredness’, which implies general fatigue, lethargy, and exhaustion and is caused by a range of conditions, including depression, chronic disease, or a busy lifestyle. Adults sleep on average for 8 hours a night. Normal sleep consists of periods of deep or slow-wave sleep, interspersed with shorter periods of dreaming or rapid-eye-movement (REM) sleep. Periods of REM sleep lengthen towards the morning and hence some people remember their dreams on waking. Different disorders of sleep can affect any of these sleep stages.


SLEEP ◽  
2020 ◽  
Vol 43 (Supplement_1) ◽  
pp. A123-A123
Author(s):  
I G Campbell ◽  
A Cruz Basilio ◽  
Z Y Zhang ◽  
N Darchia ◽  
I Feinberg

Abstract Introduction Over the past 18 years, our laboratory has been carrying out longitudinal studies of sleep and sleep need across adolescence. Our current study uses a dose-response design to examine daytime performance and sleep EEG after varied sleep durations. Here we present results for 1-30 Hz EEG power in NREM and REM sleep. Methods Home EEG recording in children 10-16 years old (N=77, mean age = 13.2). Adhering to their habitual rise time participants kept an assigned TIB schedule of 7, 8.5, or 10 hours for four consecutive nights. Participants completed all three conditions each year of the 3 year study. EEG recordings from the fourth night of each condition were scored and analyzed with FFT. Results Reducing TIB from 10 to 7 hours effectively decreased total sleep time (TST) from an average of 531 min to an average of 407 min. Decreasing TIB (from 10 to 7 h) produced a small increase (4.6%, p=0.0004) in delta (1-4 Hz) power and a larger decrease (9.0%, p=0.0032) in alpha (8-11 Hz) power in the first 5 h of NREM sleep. In REM periods 2 and 3, the same TIB reduction also increased (12.1%, p&lt;0.0001) delta power and decreased (14.2%, p&lt;0.0001) alpha power. Decreasing TIB reduced (11%, p&lt;0.0001) sigma (11-15 Hz) power in the first 5h of NREM sleep and reduced (28%, p&lt;0.0001) all night NREM sigma energy. Conclusion Reducing TST changes EEG power in several frequency bands. The increase in NREM delta power, expected from homeostatic models, may be too small to be biologically significant. The larger loss of sigma power may be of greater consequence. Sigma frequency activity is an indicator of sleep spindles which have been affected in aging, learning, memory and psychopathology. The sigma response to sleep restriction could be used to study these relations. Support PHS grant R01 HL116490 supported this work.


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