scholarly journals Couple Relationships Are Associated With Increased REM Sleep—A Proof-of-Concept Analysis of a Large Dataset Using Ambulatory Polysomnography

2021 ◽  
Vol 12 ◽  
Author(s):  
Henning Johannes Drews ◽  
Annika Drews

Background/Objectives: Rapid Eye Movement (REM) sleep is associated with memory consolidation and several health effects including stress response, mental health, and longevity. Recently, it has been shown that regularly co-sleeping couples have increased and stabilized REM sleep when co-sleeping as compared to sleeping individually. However, it remained unclear whether this is due to a specific effect of altering the usual sleeping environment by partner deprivation or due to a generalizable REM-sleep promoting effect of couple relationships. The present study aims to clarify this ambiguity.Methods: Married or never married individuals were taken from the Sleep Heart Health Study (n = 5,804) and matched regarding sociodemographic and health parameters. Matching was done using propensity score matching (1:1, nearest neighbor) and resulted in two groups of n = 69 each (married vs. never married). After confirmation of successful matching, samples were compared regarding REM sleep and other polysomnographic parameters (paired Students t-tests or Wilcoxon signed-rank tests).Results: Married individuals showed significantly higher levels of total and relative REM sleep as compared to never married individuals (all p's ≤ 0.003). Neither other sleep stages nor REM-sleep fragmentation differed between groups (all p's ≥ 0.29). Results regarding number of sleep cycles were ambiguous.Conclusion: This is the first between-subjects study to show that couple relationships are associated with increased REM sleep. This finding represents a necessary (but not sufficient) condition for the previously hypothesized self-enhancing feedback loop of REM sleep and sociality as well as for REM-sleep promotion as a mechanism through which couple relationships prevent mental illness.

2001 ◽  
Vol 281 (3) ◽  
pp. R846-R854 ◽  
Author(s):  
Peter Meerlo ◽  
Amy Easton ◽  
Bernard M. Bergmann ◽  
Fred W. Turek

Sleep is generally considered to be a recovery from prior wakefulness. The architecture of sleep not only depends on the duration of wakefulness but also on its quality in terms of specific experiences. In the present experiment, we studied the effects of restraint stress on sleep architecture and sleep electroencephalography (EEG) in different strains of mice (C57BL/6J and BALB/cJ). One objective was to determine if the rapid eye movement (REM) sleep-promoting effects of restraint stress previously reported for rats would also occur in mice. In addition, we examined whether the effects of restraint stress on sleep are different from effects of social defeat stress, which was found to have a non-REM (NREM) sleep-promoting effect. We further measured corticosterone and prolactin levels as possible mediators of restraint stress-induced changes in sleep. Adult male C57BL/6J and BALB/cJ mice were subjected to 1 h of restraint stress in the middle of the light phase. To control for possible effects of sleep loss per se, the animals were also kept awake for 1 h by gentle handling. Restraint stress resulted in a mild increase in NREM sleep compared with baseline, but, overall, this effect was not significantly different from sleep deprivation by gentle handling. In contrast, restraint stress caused a significant increase in REM sleep compared with handling in the C57BL/6J mice but not in BALB/cJ mice. Corticosterone levels were significantly and similarly elevated after restraint in both strains, but prolactin was increased only in the C57BL/6J mice. In conclusion, this study shows that the restraint stress-induced increase in REM sleep in mice is strongly strain dependent. The concomitant increases in prolactin and REM sleep in the C57BL/6J mice, but not in BALB/cJ mice, suggest prolactin may be involved in the mechanism underlying restraint stress-induced REM sleep. Furthermore, this study confirms that different stressors differentially affect NREM and REM sleep. Whereas restraint stress promotes REM sleep in C57BL/6J mice, we previously found that in the same strain, social defeat stress promotes NREM sleep. As such, studying the consequences of specific stressful stimuli may be an important tool to unravel both the mechanism and function of different sleep stages.


2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. 35-36
Author(s):  
Kening Jiang ◽  
Adam Spira ◽  
Kelsie Full ◽  
Emmanuel Garcia ◽  
Frank Lin ◽  
...  

Abstract Speech-in-noise performance involves central auditory and cortical processing and is fundamental to communication. We investigated cross-temporal associations of habitual sleep duration and stages (1996-1998) with speech-in-noise performance (2016-2017) in a subset of the Atherosclerosis Risk in Communities Study participated in the Sleep Heart Health Study(N=755, 61±5 years, 53% female). Speech-in-noise performance was measured by Quick Speech-in-Noise Test; range:0-30; lower scores=worse performance. Time spent in each stage (stage 1;2;3/4;rapid eye movement (REM)) was measured by polysomnography. Habitual sleep duration was calculated by self-reported duration on weekdays and weekends. In models adjusting for demographic and disease covariates, every 10-minute increase in REM sleep was associated with better speech-in-noise performance (0.10 points,95% CI:0.00,0.21); every 1-hour increase in habitual sleep duration was associated with worse speech-in-noise performance (-1.28 points,95% CI:-2.49,-0.08) among participants sleep >8 hours. Long sleep duration might be a risk marker of speech-in-noise performance, but REM sleep might be a protective factor.


SLEEP ◽  
2020 ◽  
Vol 43 (Supplement_1) ◽  
pp. A20-A20
Author(s):  
D R Mazzotti ◽  
M Younes

Abstract Introduction The odds ratio product (ORP) is a new highly-validated electroencephalogram biomarker of sleep depth. ORP has been validated as such by several studies investigating the effect of sleep disorders, responses to sleep deprivation and traffic noise. ORP during REM sleep varies considerably among individuals. Whether ORP reflects sleep depth also in REM sleep is unknown. We hypothesized that subjects with high REM ORP are more prone to REM sleep fragmentation. Methods Using data from the baseline (SHHS1; N=5,537) and follow-up (SHHS2; N=2,595) visits of the Sleep Heart Health Study, we calculated and summarized ORP in 30-second intervals corresponding to manually scored sleep stage epochs. We developed a heuristic to identify REM periods, defined as sequences of REM sleep epochs separated by no more than 10 minutes of other sleep stages or wake epochs. Using general linear models adjusted by age, sex, body mass index, race and ethnicity, we evaluated the relationship between REM ORP and total REM duration, number of awakening episodes per REM period and arousal index during REM sleep. Results Higher REM ORP was correlated with shorter total REM duration (ρ SHHS1=-0.12; p &lt 0.001, ρ SHHS2=-0.07; p &lt 0.001), more awakening episodes (ρ SHHS1=0.26; p<0.001, ρ SHHS2=0.30; p &lt 0.001) and higher arousal index (ρ SHHS1=0.18; p &lt 0.001, ρ SHHS2=0.16; p &lt < 0.001) during identified REM periods. In adjusted analyses, one-unit increase in REM ORP was associated, on average, with a 7 minute decrease in total REM duration (β=-7.10; p &lt 0.001), 1 more awakening episode per REM period (β=1.29; p &lt 0.001) and an increase of 6 arousals/hour (β=6.16; p &lt 0.001) during REM sleep periods. Conclusion We found that higher REM ORP was associated with shorter REM periods, higher proportion of awake during REM periods and higher REM arousal index. Although small, these differences suggest that ORP is consistent with the concept of sleep depth also during REM sleep. Support None


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.


Author(s):  
T. Tanaka ◽  
H. Lange ◽  
R. Naquet

SUMMARY:A longitudinal study of the effects of sleep on amygdaloid kindling showed that kindling disrupted normal sleep patterns by reducing REM sleep and increasing awake time. Few interictal spike discharges were observed during the awake stage, while a marked increase in discharge was observed during the light and deep sleep stages. No discharges were observed during REM sleep. During the immediate post-stimulation period the nonstimulated amygdala showed a much higher rate of spike discharge. On the other hand, there was an increase in spike discharge in the stimulated amygdala during natural sleep without preceding amygdaloid stimulation. Amygdaloid stimulation at the generalized seizure threshold during each sleep stage resulted in a generalized convulsion.The influence of subcortical electrical stimulation on kindled amygdaloid convulsions was investigated in a second experiment. Stimulation of the centre median and the caudate nucleus was without effect on kindled convulsions, while stimulation of the mesencephalic reticular formation at high frequency (300 Hz) reduced the latency of onset of kindled generalized convulsions. Stimulation of the nucleus ventralis lateralis of the thalamus at low frequency (10 Hz) prolonged the convulsion latency, and at high current levels blocked the induced convulsion. Stimulation in the central gray matter at low frequency (10 Hz) also blocked kindled amygdaloid convulsions.


SLEEP ◽  
2020 ◽  
Vol 43 (Supplement_1) ◽  
pp. A430-A430
Author(s):  
G S Griesbach ◽  
S E Robinson ◽  
S Howell

Abstract Introduction Traumatic Brain Injury (TBI) is frequently associated with problems with sleep and diurnal somnolence. After determining if subjective somnolence was associated with sleep disturbances, we investigated if alterations in sleep architecture were associated with cognitive, social and emotional health in a sex dependent manner. For patients receiving positive airway pressure (PAP) treatment, we determined if lack of compliance contributed to cognitive and quality of life issues. Methods Adult TBI subjects (n=57) were assessed via overnight polysomnography. Mean age was 41 years and mean TBI chronicity was 2.5 years. Overall level of disability was determined by the Mayo Portland Inventory II. Sleep measures included slow wave sleep (SWS), REM latency, percent time in all sleep stages, apnea/hypopnea index, wake after sleep onset (WASO), and arousal index. Outcome measures were the California Verbal Learning Test (CVLT), Montreal Cognitive Assessment (MoCA), Trails A and B, Beck Depression Inventory, and Neuro-QoL. Results No sex effects for reporting somnolence were found. Besides being associated with increased subjective anxiety and stigma, somnolence was associated with increased arousals, decreases in SWS and higher incidence of REM AHI. WASO and number of arousals had a negative impact on the amount of SWS and sleep efficiency. Men spent significantly more time in REM sleep, which was correlated with higher scores on the MoCA and CVLT. Women showed more disability. Longer latencies to SWS were associated with increased CVLT performance. AHI was associated with increases in emotional/behavioral dyscontrol, fatigue and self-reported sleep disturbance. All effects were statistically significant. Conclusion Female TBI patients show significant impairments in REM sleep, which may impact learning and memory. Sleep disturbances were associated with poorer cognitive performance and may ultimately affect outcome, as indicated by lower scores on quality of life measures. Support Centre for Neuro Skills


SLEEP ◽  
2019 ◽  
Vol 42 (9) ◽  
Author(s):  
Nicola Hanley ◽  
Jerome Paulissen ◽  
Brian J Eastwood ◽  
Gary Gilmour ◽  
Sally Loomis ◽  
...  

Abstract Increasing vigilance without incurring the negative consequences of extended wakefulness such as daytime sleepiness and cognitive impairment is a major challenge in treating many sleep disorders. The present work compares two closely related mGluR2/3 antagonists LY3020371 and LY341495 with two well-known wake-promoting compounds caffeine and d-amphetamine. Sleep homeostasis properties were explored in male Wistar rats by manipulating levels of wakefulness via (1) physiological sleep restriction (SR), (2) pharmacological action, or (3) a combination of these. A two-phase nonlinear mixed-effects model combining a quadratic and exponential function at an empirically estimated join point allowed the quantification of wake-promoting properties and any subsequent sleep rebound. A simple response latency task (SRLT) following SR assessed functional capacity of sleep-restricted animals treated with our test compounds. Caffeine and d-amphetamine increased wakefulness with a subsequent full recovery of non-rapid eye movement (NREM) and rapid eye movement (REM) sleep and were unable to fully reverse SR-induced impairments in SRLT. In contrast, LY3020371 increased wakefulness with no subsequent elevation of NREM sleep, delta power, delta energy, or sleep bout length and count, yet REM sleep recovered above baseline levels. Prior sleep pressure obtained using an SR protocol had no impact on the wake-promoting effect of LY3020371 and NREM sleep rebound remained blocked. Furthermore, LY341495 increased functional capacity across SRLT measures following SR. These results establish the critical role of glutamate in sleep homeostasis and support the existence of independent mechanisms for NREM and REM sleep homeostasis.


SLEEP ◽  
2020 ◽  
Vol 43 (Supplement_1) ◽  
pp. A456-A457 ◽  
Author(s):  
L Menghini ◽  
V Alschuler ◽  
S Claudatos ◽  
A Goldstone ◽  
F Baker ◽  
...  

Abstract Introduction Commercial wearable devices have shown the capability of collecting and processing multisensor information (motion, cardiac activity), claiming to be able to measure sleep-wake patterns and differentiate sleep stages. While using these devices, users should be aware of their accuracy, sources of measurement error and contextual factors that may affect their performance. Here, we evaluated the agreement between Fitbit Charge 2™ and PSG in adults, considering effects of two different sleep classification methods and pre-sleep alcohol consumption. Methods Laboratory-based synchronized recordings of device and PSG data were obtained from 14 healthy adults (42.6±9.7y; 6 women), who slept between one and three nights in the lab, for a total of 27 nights of data. On 10 of these nights, participants consumed alcohol (up to 4 standard drinks) in the 2 hours before bedtime. Device performance relative to PSG was evaluated using epoch-by-epoch and Bland-Altman analyses, with device data obtained from a data-management platform, Fitabase, via two methods one that accounts for short wakes (SW, awakenings that last less than 180s) and one that does not (not-SW). Results SW and not-SW methods were similar in scoring (96.76% agreement across epochs), although the SW method had better accuracy for differentiating “light”, “deep”, and REM sleep; but produced more false positives in wake detection. The device (SW-method) classified epochs of wake, “light” (N1+N2), “deep” (N3) and REM sleep with 56%, 77%, 46%, and 62% sensitivity, respectively. Bland-Altman analysis showed that the device significantly underestimated “light” (~19min) and “deep” (~26min) sleep. Alcohol consumption enhanced PSG-device discrepancies, in particular for REM sleep (p=0.01). Conclusion Our results indicate promising accuracy in sleep-wake and sleep stage identification for this device, particularly when accounting for short wakes, as compared to PSG. Alcohol consumption, as well as other potential confounders that could affect measurement accuracy should be further investigated. Support This study was supported by the National Institute on Alcohol Abuse and Alcoholism (NIAAA) grant R21-AA024841 (IMC and MdZ). The content is solely the responsibility of the authors and does not necessarily represent the official views the National Institutes of Health.


Author(s):  
DK Jain ◽  
M Ng

Background: Seizures are rare in REM sleep. To our knowledge, the effects of different sleep stages in anti-NMDA encephalitis have not been studied. Methods: Case report. Results: 32 year-old healthy female presented with acute fluctuating level of consciousness with episodic impulsivity, disorientation, and emotional outbursts following 3 days of headache. Her temperature was 37.8°C and she was started on ceftriaxone, vancomycin, and acyclovir. CSF only showed a total nuclear cell count of 182 and pleocytosis. MRI revealed increased T2 hyperintense right lateral temporal and parietal cortical thickening. EEG revealed right frontotemporal seizures with left sided rhythmic jerking, and an extreme delta brush pattern. Interestingly, seizures and extreme delta brush disappeared in REM sleep. After HSV PCR was negative, she was immunosuppressed with corticosteroids, IVIG, rituximab, and cyclophosphamide, given the extreme delta brush pattern. Repeat CSF analysis eventually yielded highly positive anti-NMDA antibodies. Ten weeks later, she became seizure free. Conclusions: For the first time, we report REM sleep in a case of anti-NMDA encephalitis during which there was absence of extreme delta brush and ictal EEG patterns. This observation may provide insight into the ongoing debate over whether extreme delta brush is an ictal EEG pattern.


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