Sleep Continuity Disruption Research Articles

The insensitivity of sleep to an unfamiliar sleeping environment in patients with insomnia disorder.

Sleeping in an unfamiliar environment, such as a sleep laboratory, is thought to disturb sleep in healthy individuals and could express a hyperarousal state called the first night effect. Insomnia disorder (ID) is a highly prevalent health problem characterized by increased arousal during the night and daytime. Whether or nota similar phenomenon occurs in patients with ID is unclear. This study aimed to investigate the effect of an unfamiliar environment on the sleep of patients with ID. In an unfamiliar sleep laboratory, polysomnographic recording testing was performed for two consecutive nights in patients with ID and age- and sex-matched healthy controlsubjects (HC). We collected sleep diaries and questionnaires regarding sleep, medical conditions, psychological status, and health history. Sleep continuity and architecture in both groups were compared and analyzed for two consecutive nights. Participants with ID(n = 39) and HC(n = 35) demonstrated differentially poor sleep on laboratory adaptation after exposure to the sleep laboratory. Patients with ID had longer rapid eye movement (REM) latency on the first night than on the second sleep night. HC showed increased duration and percentage of N1, decreased duration and percentage of N3, and decreased REM percentage during initial nights compared to subsequent nights. The other sleep variables showed no differences between the first and second sleep nights in patients with ID and HC. An unfamiliar sleep environment does not aggravate the disruption of sleep continuity and sleep architecture but only affects the REM latency in patients with ID compared with HC.

First-night effect in insomnia disorder: a systematic review and meta-analysis of polysomnographic findings.

Polysomnographic studies have been performed to investigate the first-night effect in insomnia disorder. However, these studies have revealed discrepant findings. This meta-analysis aimed to summarise and quantify the characteristics of the first-night effect in insomnia disorder. We performed a systematic search of the PubMed, Medline, EMBASE, Web of Science and PsycINFO databases to identify studies published through October 2019. A total of 11,862 articles were identified, and seven studies with eight independent populations were included in the meta-analysis. A total of 639 patients with insomnia disorder and 171 healthy controls underwent more than 2 consecutive nights of in-laboratory polysomnography. Pooled results demonstrated that both variables of sleep continuity and sleep architecture, other than slow-wave sleep were significantly altered in the first-night effect in insomnia disorder. Furthermore, the results indicated that patients with insomnia disorder had a disruption of sleep continuity in the first-night effect, including increased sleep onset latency and reduced total sleep time, compared to healthy controls. Overall, the findings show that patients with insomnia disorder experience the first-night effect, rather than reverse first-night effect, and the profiles of the first-night effect in patients with insomnia are different from healthy controls. These indicate that an adaptation night is necessary when sleep continuity and sleep architecture is to be studied in patients with insomnia disorder. More well-designed studies with large samples are needed to confirm the results.

P100 Different effect of sleep loss paradigms on various pain types in healthy subjects: A systematic review and meta-analysis

Abstract Introduction Sleep disturbances are comorbid with chronic pain, exacerbating pain conditions. Experimental studies have implemented different sleep loss paradigms combined with quantitative sensory testing to better understand the sleep-pain relationship. However, knowledge of which sleep loss paradigms are most detrimental regarding hyperalgesia is lacking. The current review aims to differentiate the effect of fragmented sleep from partial or total sleep deprivation and determine whether sleep-loss-related hyperalgesia is due to curtailed/deprived consolidated sleep or sleep continuity disruption. Methods We searched the databases, including EBSCO, MEDLINE, Psychological Information Database (Psych INFO), Science Direct, and Web of Science, to identify 36 experimental studies involving 928 participants. The studies implemented different sleep loss paradigms, such as total sleep deprivation, sleep restriction, and disrupted sleep continuity on heat, cold, pressure, and mechanical pain thresholds in the general population. In addition, we considered the sex-dependent effect of sleep loss on various pain types. Results Total sleep deprivation exerted the strongest (SMD = -1.721; CI95: -2.358, -1.073; P<0.001), while fragmented sleep protocols induced the least (SMD = -0.294; CI95: -0.478, -0.110; P=0.007) hyperalgesic effect. The effect of sleep loss on heat pain was greatest, whereas on pressure pain was smallest. The sleep loss-related hyperalgesia on heat and pressure pain differed between men and women, while the cold pain threshold was sex-independent. Conclusion This meta-analysis confirms that depriving sleep entirely greatly affects pain perception while disrupted sleep continuity induces a small effect and requires two consecutive nights of disruptions.

Disruption of Sleep Continuity During the Perimenopause: Associations with Female Reproductive Hormone Profiles.

Nocturnal vasomotor symptoms (nVMS), depressive symptoms (DepSx), and female reproductive hormone changes contribute to perimenopause-associated disruption in sleep continuity. Hormonal changes underlie both nVMS and DepSx. However, their association with sleep continuity parameters resulting in perimenopause-associated sleep disruption remains unclear. We aimed to determine the association between female reproductive hormones and perimenopausal sleep discontinuity independent of nVMS and DepSx. Daily sleep and VMS diaries, and weekly serum assays of female reproductive hormones were obtained for 8 consecutive weeks in 45 perimenopausal women with mild DepSx but no primary sleep disorder. Generalized estimating equations were used to examine associations of estradiol, progesterone, and follicle stimulating hormone (FSH) with mean number of nightly awakenings, wakefulness after sleep onset (WASO) and sleep-onset latency (SOL) adjusting for nVMS and DepSx. Sleep disruption was common (median 1.5 awakenings/night, WASO 24.3 and SOL 20.0 minutes). More awakenings were associated with estradiol levels in the postmenopausal range (β = 0.14; 95% CI, 0.04 to 0.24; P = 0.007), and higher FSH levels (β [1-unit increase] = 0.12; 95% CI, 0.02 to 0.22; P = 0.02), but not with progesterone (β [1-unit increase] = -0.02; 95% CI, -0.06 to 0.01; P = 0.20) in adjusted models. Female reproductive hormones were not associated with WASO or SOL. Associations of more awakenings with lower estradiol and higher FSH levels provide support for a perimenopause-associated sleep discontinuity condition that is linked with female reproductive hormone changes, independent of nVMS and DepSx.

Increased variability in total sleep time is associated with reduced psychomotor vigilance impairment following experimental sleep continuity disruption

Increased variability in total sleep time is associated with reduced psychomotor vigilance impairment following experimental sleep continuity disruption

The effect of sleep continuity disruption on multimodal emotion processing and regulation: a laboratory-based, randomised, controlled experiment in good sleepers.

Previous research shows that experimental sleep deprivation alters emotion processing, suggesting a potential mechanism linking sleep disruption to mental ill-health. Extending previous work, we experimentally disrupted sleep continuity in good sleepers and assessed next-day emotion processing and regulation using tasks with established sensitivity to depression. In a laboratory-based study, 51 good sleepers (37 female; mean [SD] age 24[3.63]years), were randomised to 1 night of uninterrupted sleep (n=24) or sleep continuity disruption (n=27). We assessed emotion perception, attention, and memory the following day. Participants also completed an emotion regulation task and measures of self-reported affect, anxiety, sleepiness, overnight declarative memory consolidation, and psychomotor vigilance. Confirming the effects of the manipulation, sleep continuity disruption led to a marked decrease in polysomnography-defined total sleep time (229.98 versus 434.57 min), increased wake-time after sleep onset (260.66 versus 23.84 min), and increased sleepiness (d=0.81). Sleep continuity disruption led to increased anxiety (d=0.68), decreased positive affect (d=-0.62), reduced overnight declarative memory consolidation (d=-1.08), and reduced psychomotor vigilance (longer reaction times [d=0.64] and more lapses [d=0.74]), relative to control. However, contrary to our hypotheses, experimental sleep disruption had no effect on perception of, or bias for, emotional facial expressions, emotional memory for words, or emotion regulation following worry induction. In conclusion, 1 night of sleep continuity disruption had no appreciable effect on objective measures of emotion processing or emotion regulation in response to worry induction, despite clear effects on memory consolidation, vigilance, and self-reported affect and anxiety.

0548 Overnight Memory Consolidation in Insomnia versus Normal and Experimentally Disrupted Sleep

Abstract Introduction Healthy sleep is assumed to play an important role in the consolidation of newly acquired memories. Evidence suggest that periods of sleep after learning facilitates memory consolidation relative to wakefulness. Insomnia is associated with cognitive impairment but few studies have assessed overnight memory consolidation. We compared overnight consolidation in people with insomnia to a group of good sleepers who were randomised to either a normal night of sleep (uninterrupted sleep, US) or one night of sleep continuity disruption via forced awakenings (FA). Methods 51 good sleepers (37 female; mean age: 24 years, SD: 3.63), randomised to either one night of US (n=24) or one night of FA (n=27), were compared to 27 participants meeting criteria for insomnia disorder (23 female; mean age: 53 years, SD: 8.34) who were assessed at baseline as part of a randomised controlled trial of digital cognitive-behavioural therapy. Overnight memory consolidation (difference in correctly recalled word pairs between evening and morning recall) was assessed using the same word-pair task and protocol in the two lab-based studies. Results Overnight memory consolidation was significantly lower in the insomnia (mean: 5.4, SD: 5.8, p=0.001) and the FA (mean: 6.7, SD: 4.1, p<0.001) group compared to the US group (mean: 11.6, SD: 5.3). However, when adjusted for age only the FA group, but not the insomnia group, showed significantly lower memory performance than the US group. Conclusion While our findings suggest that overnight memory consolidation is impaired in insomnia relative to normal sleep we cannot rule out an age-related explanation given the difference in ages between the study samples. Future work will assess whether overnight consolidation improves following cognitive behavioural therapy. Support The research was supported by the National Institute for Health Research (NIHR) Oxford Biomedical Research Centre (BRC) and the Dr Mortimer and Theresa Sackler Foundation. The views expressed are those of the authors and not necessarily those of the NHS, the NIHR or the Department of Health.

One night of sleep continuity disruption engenders impairment in overnight memory consolidation and vigilance but not emotion perception or regulation: results from a randomised, lab-based experimental study

One night of sleep continuity disruption engenders impairment in overnight memory consolidation and vigilance but not emotion perception or regulation: results from a randomised, lab-based experimental study

0119 The Effect Of Sleep Continuity Disruption On Threat-related Attentional Bias: Randomised Controlled Experiment In Good Sleepers

0119 The Effect Of Sleep Continuity Disruption On Threat-related Attentional Bias: Randomised Controlled Experiment In Good Sleepers

Partial Sleep Deprivation Attenuates the Positive Affective System: Effects Across Multiple Measurement Modalities.

Ample behavioral and neurobiological evidence links sleep and affective functioning. Recent self-report evidence suggests that the affective problems associated with sleep loss may be stronger for positive versus negative affective state and that those effects may be mediated by changes in electroencepholographically measured slow wave sleep (SWS). In the present study, we extend those preliminary findings using multiple measures of affective functioning. In a within-subject randomized crossover experiment, we tested the effects of one night of sleep continuity disruption via forced awakenings (FA) compared to one night of uninterrupted sleep (US) on three measures of positive and negative affective functioning: self-reported affective state, affective pain modulation, and affect-biased attention. The study was set in an inpatient clinical research suite. Healthy, good sleeping adults (N = 45) were included. Results indicated that a single night of sleep continuity disruption attenuated positive affective state via FA-induced reductions in SWS. Additionally, sleep continuity disruption attenuated the inhibition of pain by positive affect as well as attention bias to positive affective stimuli. Negative affective state, negative affective pain facilitation, nor negative attention bias were altered by sleep continuity disruption. The present findings, observed across multiple measures of affective function, suggest that sleep continuity disruption has a stronger influence on the positive affective system relative to the negative affective affective system.

(190) Effects of sleep continuity disruption on cold pain tolerance and accompanying pain catastrophizing in healthy, good sleepers

Chronic sleep problems, such as those associated with insomnia, have been shown to increase vulnerability for chronic pain at the population level. However, there is limited understanding of the mechanisms linking sleep and pain. Cold pain tolerance (CPT) is a predictor of clinical pain severity in chronic pain patients. Pain catastrophizing, a maladaptive cognitive coping strategy, is associated with lower pain tolerance and higher clinical pain. In the present study, we investigated the effects of sleep continuity disruption -- an experimental model of sleep deprivation with ecological validity for comorbid chronic pain and insomnia -- on CPT and accompanying catastrophizing cognitions. Healthy good sleepers underwent one night of uninterrupted sleep (US) and one night of forced awakenings (FA) in a randomized, within-person, counter-balanced design. On the day following each sleep condition, participants placed their dominant hand palm-down in a 4°C circulating water bath for a maximum of 300 seconds and were instructed to remove their hand when the pain became intolerable. CPT was measured as the time to withdrawal. Participants completed a self-report pain catastrophizing scale immediately following CPT. A total of 33 subjects provided usable data on these measures. Results indicated that CPT was significantly lower following FA compared to US (p<0.05). Pain catastrophizing was not significantly different between sleep conditions. Together these findings indicate that a single night of sleep continuity disruption is associated with a reduction in CPT that does not appear to be driven by catastrophizing. The present data suggest that the association of sleep continuity disruption and pain tolerance may be one avenue through which chronic sleep disorders, such as insomnia, increase vulnerability to chronic pain.

The Effects of Sleep Continuity Disruption on Positive Mood and Sleep Architecture in Healthy Adults.

The purpose of this study was to test an experimental model of the effects of sleep continuity disturbance on sleep architecture and positive mood in order to better understand the mechanisms linking insomnia and depression. Participants were randomized to receive 3 consecutive nights of sleep continuity disruption via forced nocturnal awakenings (FA, n = 21), or one of two control conditions: restricted sleep opportunity (RSO, n = 17) or uninterrupted sleep (US, n = 24). The study was set in an inpatient clinical research suite. Healthy, good-sleeping men and women were included. Polysomnography was used to measure sleep architecture, and mood was assessed via self-report each day. Compared to restricted sleep opportunity controls, forced awakenings subjects had significantly less slow wave sleep (P < 0.05) after the first night of sleep deprivation, and significantly lower positive mood (P < 0.05) after the second night of sleep deprivation. The differential change in slow wave sleep statistically mediated the observed group differences in positive mood (P = 0.002). To our knowledge, this is the first human experimental study to demonstrate that, despite comparable reductions in total sleep time, partial sleep loss from sleep continuity disruption is more detrimental to positive mood than partial sleep loss from delaying bedtime, even when controlling for concomitant increases in negative mood. With these findings, we provide temporal evidence in support of a putative biologic mechanism (slow wave sleep deficit) that could help explain the strong comorbidity between insomnia and depression.

Optogenetic disruption of sleep continuity impairs memory consolidation

Memory consolidation has been proposed as a function of sleep. However, sleep is a complex phenomenon characterized by several features including duration, intensity, and continuity. Sleep continuity is disrupted in different neurological and psychiatric conditions, many of which are accompanied by memory deficits. This finding has raised the question of whether the continuity of sleep is important for memory consolidation. However, current techniques used in sleep research cannot manipulate a single sleep feature while maintaining the others constant. Here, we introduce the use of optogenetics to investigate the role of sleep continuity in memory consolidation. We optogenetically targeted hypocretin/orexin neurons, which play a key role in arousal processes. We used optogenetics to activate these neurons at different intervals in behaving mice and were able to fragment sleep without affecting its overall amount or intensity. Fragmenting sleep after the learning phase of the novel object recognition (NOR) task significantly decreased the performance of mice on the subsequent day, but memory was unaffected if the average duration of sleep episodes was maintained at 62-73% of normal. These findings demonstrate the use of optogenetic activation of arousal-related nuclei as a way to systematically manipulate a specific feature of sleep. We conclude that regardless of the total amount of sleep or sleep intensity, a minimal unit of uninterrupted sleep is crucial for memory consolidation.

Sleep deprivation and pain perception

Chronically painful conditions are frequently associated with sleep disturbances, i.e. changes in sleep continuity and sleep architecture as well as increased sleepiness during daytime. A new hypothesis, which has attracted more and more attention, is that disturbances of sleep cause or modulate acute and chronic pain. Since it is well-known that pain disturbs sleep the relationship between the two has since recently been seen as reciprocal. To fathom the causal direction from sleep to pain we have reviewed experimental human and animal studies on the effects of sleep deprivation on pain processing. According to the majority of the studies, sleep deprivation produces hyperalgesic changes. Furthermore, sleep deprivation can interfere with analgesic treatments involving opioidergic and serotoninergic mechanisms of action. The still existing inconsistency of the human data and the exclusive focus on REM sleep deprivation in animals so far do not allow us to draw firm conclusions as to whether the hyperalgesic effects are due to the deprivation of specific sleep stages or whether they result from a generalized disruption of sleep continuity.

REM-Sleep in patients with dementia of Alzheimer and frontotemporal type under long term treatment with cholinesterase inhibitors

Besides cognitive impairment, patients with dementia commonly present with a sleep disturbance. The most robust polysomnographic finding in Alzheimer’s dementia (DAT) is reduction of REM-sleep. Cholinsterase inhibitors (Che-I) are able to increase REM-sleep in volunteers. The objective of this study was to evaluate the effects of Che-I on REM-sleep in DAT and frontotemporal dementia (FTD) during long-term treatment. So far, 13 patients with low to moderate dementia could be examined. 7 patients were classified as having DAT and 6 patients as having FTD. A polysomnography was performed in all patients who were free of psychotropic medication before therapy with a Che-I and after 5–10 months, while patients were on monotherapy with a Che-I. In all patients sleep continuity disruption was observed. In DAT a more accentuated REM sleep reduction in comparison to FTD was found. Treatment with Che-I did not improve sleep continuity. However, REM-sleep increased in patients with DAT, but not in patients with FTD. Furthermore, REM-latency was reduced in DAT after treatment with Che-I. The observed REM-sleep reduction in patients with DAT compared to FTD may suggest that cholinergic neurotransmission is more impaired in DAT than in FTD. However, it remains unclear whether the increase of REM-sleep after long-term treatment with Che-I in DAT may only reflect a mere pharmacological effect or whether this increase may be related to the efficacy of anti-dementia treatment

The effect of sleep deprivation on pain.

Chronic pain syndromes are associated with alterations in sleep continuity and sleep architecture. One perspective of this relationship, which has not received much attention to date, is that disturbances of sleep affect pain. To fathom this direction of cause, experimental human and animal studies on the effects of sleep deprivation on pain processing were reviewed. According to the majority of the studies, sleep deprivation produces hyperalgesic changes. Furthermore, sleep deprivation can counteract analgesic effects of pharmacological treatments involving opioidergic and serotoninergic mechanisms of action. The heterogeneity of the human data and the exclusive interest in rapid eye movement sleep deprivation in animals so far do not allow us to draw firm conclusions as to whether the hyperalgesic effects are due to the deprivation of specific sleep stages or whether they result from a generalized disruption of sleep continuity. The significance of opioidergic and serotoninergic processes as mediating mechanisms of the hyperalgesic changes produced by sleep deprivation are discussed.

Microstructure of the non-rapid eye movement sleep electroencephalogram in patients with newly diagnosed Parkinson's disease: effects of dopaminergic treatment.

We investigated non-rapid eye movement (non-REM) sleep in patients with newly diagnosed Parkinson's disease (PD) who had never previously received dopaminergic medication. There were no significant differences in the conventional sleep parameters between de novo patients with PD and a healthy control group, but the length of stage 1 sleep and the number of awakenings increased significantly upon administration of dopaminergic drugs. Analyzing the quantitative electroencephalogram (EEG), we observed a significant reduction in the low-delta frequency range and a nonsignificant increase in the sigma frequency range in de novo patients with PD. The dopaminergic medication also nonsignificantly reduced the low-delta and sigma frequencies, the latter to the level of the controls. Possible mechanisms that may account for the observed differences are discussed. It is suggested that Parkinson's disease as well as the application of dopaminergic drugs exerts a desynchronizing effect on the sleep EEG that is reflected in a disruption of sleep continuity.