Journal of Sleep Research最新文献

Sleep reactivity-an individual's susceptibility to sleep disruptions due to stress-has been linked to increased insomnia risk. Investigating how sleep reactivity moderates the 'stress → pre-sleep arousal → sleep' pathway may help mitigate sleep disturbances and enhance treatment outcomes. In the present study, full-time university students without sleep disorders completed the Ford Insomnia Response to Stress Test (FIRST), which assesses sleep reactivity. From 264 students, 30 students with the lowest and 30 with the highest FIRST scores were selected for further study. They provided daily actigraphy, Pre-sleep Arousal Scale ratings, pre-sleep heart rate (via an ŌURA ring), and perceived stress scores over 2 weeks. Multilevel moderated mediation analyses were conducted using 800 nights of data to examine within- and between-individual associations. At the within-individual level, days with higher-than-usual perceived stress were associated with reduced total sleep time and increased sleep onset latency (p's < 0.05). These effects were mediated by heightened pre-sleep cognitive arousal (p's < 0.05) but not moderated by the FIRST group. In contrast, between-individual analyses revealed a significant moderation by the FIRST group (p < 0.05). High sleep-reactive individuals reported significantly greater average levels of perceived stress and pre-sleep cognitive arousal, leading to prolonged wakefulness after sleep onset (b = 0.123, Monte Carlo confidence interval [MCCI] = 0.006-0.292), compared to low-reactive sleepers. Overall, on a day-to-day basis, both groups showed increased pre-sleep cognitive arousal and sleep disruptions in response to elevated daily stress. However, between individuals, high sleep reactivity significantly amplified the effect of pre-sleep cognitive (but not physiological) arousal, leading to more pronounced sleep disturbances compared to low-reactive sleepers.

PSG, a cornerstone diagnostic instrument in sleep medicine, is recommended for the diagnosis of numerous sleep disorders and might be used as a benchmark for evaluating therapeutical effectiveness. However, PSG has its limitations, and its usefulness in the future warrants reappraisal. First, it is a complex test that requires highly-trained personnel to correctly place the electrodes, monitor the patient, and manually analyse the data. This constitutes a significant economic burden for both society and healthcare systems. PSG also presents few technical limitations: variability of data between nights and variable reliability of scoring between readers. The results given to patients are also limited to the macrostructure of sleep, risking the loss of important information that escapes detection when relying solely on polysomnographic evaluation based on macro sleep stages. The current sleep scoring guidelines raise some doubts about their ability to capture the dynamic and complex nature of human sleep in both clinical and physiological contexts. On the other hand, advanced PSG analysis can provide key information for diagnosis particularly through the microstructural analysis of NREM oscillatory pattern, characterisation of spindles and slow waves, eye movement density, spectrum analysis with hypnodensity and sleep propensity with odd ratio products (ORP). These elements provide a better understanding of the differences between insomnia and poor sleep perception. Furthermore, these methods take into account the dynamics of sleep states, going beyond the mere distinction of sleep into macro stages, which poorly reflects the dynamic nature of sleep itself and including in the assessment of sleep function all the complex associations that sleep itself has with autonomic and cardiorespiratory variables. These insights will transform the role of technicians and clinicians in PSG analysis, with a shift towards training in digital data analysis and algorithms to better inform patients about their PSG results.

Sleep is essential for normal physiological functioning, and sleep deprivation is typically compensated by increasing subsequent sleep duration and/or intensity. However, a recent study showed that barnacle geese (Branta leucopsis) exhibit seasonal variation in sleep homeostasis, with full recovery of sleep after sleep deprivation in summer but no sleep rebound after similar deprivation in winter based on electroencephalography (EEG). This lack of sleep rebound could suggest that geese in winter do not build up sleep pressure during wakefulness or that accumulated sleep need is not reflected in EEG-based sleep measures. The current study investigated whether geese in winter accumulate sleep pressure during extended wakefulness, using behavioural activity and reactivity to stimulation as alternative indicators of sleep drive. If sleep deprivation increases sleep pressure, we expected geese to adopt more sleep postures and show elevated arousal thresholds in response to stimulation. Fifteen barnacle geese were implanted with epidural electrodes for EEG recordings and housed in a semi-natural enclosure during winter. We carefully observed and approached the geese at 10-min intervals during the night for 8-h following sunset. Although sleep was suppressed during this period, it did not lead to significant EEG changes and most of the lost sleep was not recovered. However, the behavioural observations revealed that geese exhibited increased sleep postures and diminished responsiveness to being approached. Our findings suggest that prolonged wakefulness in barnacle geese increases behavioural indicators of sleep pressure, also in winter, even though this rise in sleep drive is not clearly reflected in EEG-based sleep measures.

This overview with re-analysis of systematic reviews (SRs) aims to assess the effectiveness of orofacial myofunctional therapy (MT) for Obstructive Sleep Apnea (OSA) patients. We searched PubMed, Embase, and the Cochrane Library up to July 2024. SRs with meta-analyses on OSA in adults or children who underwent MT intervention compared to any control were included. Primary outcomes were severity of sleep apnea, oxygen saturation, sleep efficiency, and daytime sleepiness, while secondary outcomes included snoring intensity, frequency, and sleep quality. We included nine SRs, encompassing 21 unique primary studies (13 RCTs, 8 pre-post studies; n = 716 participants). The methodological quality of the SRs was generally critically low (5/9 SRs). After re-analyzing outcome data (primary studies overlap: 13.44%), MT seems to be more effective than control in reducing severity of sleep apnea (MD -9.54; CIs 95% -14.04, -5.04), daytime sleepiness (MD -3.62; CIs 95% -6.61, -0.63), sleep quality (MD -2.23; CIs 95% -2.93, -1.53), and in improving minimum oxygen saturation (MD 3.19; CIs 95% 1.47, 4.91) in adults. No differences were found in mean oxygen saturation and sleep efficiency. Meta-analyses comparing pre-MT to post-MT showed improvements post-MT. Sparse evidence was found for other outcomes and for children. MT may improve multiple clinical outcomes in OSA. Results should be interpreted cautiously, as most primary studies are at high risk of bias. More research is needed on the pediatric population.

This study aimed to assess the associations between the frequency of episodes of disorders of arousal (sleepwalking and sleep terrors) and emotional-behavioural problems in a longitudinal cohort of healthy children aged 4 and 5 years. Mother-child dyads (N = 345) were recruited during pregnancy for a longitudinal cohort study. Mothers completed validated questionnaires when children were 4 and 5 years old. Linear regressions assessed (1) the concurrent association between the frequency of disorders of arousal episodes (i.e., sleepwalking and sleep terrors) and emotional-behavioural problems in children at 4 and 5; and (2) the association between the frequency of disorders of arousal episodes at 4 and emotional-behavioural problems at 5. Models included the following covariates: child's sex, child's nighttime sleep duration, socioeconomic status and maternal depressive symptoms. More frequent episodes of disorders of arousal at age 4 were significantly associated with more concurrent internalising (B = 2.659, p = 0.001), and externalising problems (B = 2.740, p = 0.006). At age 5, the frequency of episodes was not associated with concurrent internalising and externalising problems (p > 0.05). More frequent episodes at age 4 were associated with more externalising problems at 5 (B = 2.462, p = 0.039). Although sleep terrors and sleepwalking are often benign, our results show that even in a non-clinical cohort, these sleep phenomena can be associated with emotional-behavioural problems in children as young as 4. While the mere presence of sleep terrors or sleepwalking is not alarming, screening for emotional-behavioural problems seems appropriate for children with frequent episodes.

Recent studies have shown that acoustic stimulation, a common neuromodulation technique, can enhance slow-wave activity (SWA), which is associated with immune, autonomic nervous system activity and cognitive health benefits. Despite some disagreement, many studies suggest that maximising tone-evoked SWA depends on the timing of the acoustic stimulus in relation to ongoing cortical slow oscillations. Given the close connection between the central and peripheral systems during sleep, particularly at the cortico-cardiac level, we here aimed to examine the overlooked relationship between the timing of stimulation and the dominant cortical and cardiac rhythms. We evaluated the effect of acoustic stimulation in different phases of the EEG slow oscillation (SO; ~0.8 Hz) component of SWA (0.5-4 Hz) and heart rate (HR) low-frequency (LF) (0.04-0.15 Hz) and high-frequency (HF) (0.15-0.4 Hz) oscillations on tone-evoked EEG slow activity and HR profiles. One hundred thirty-three adolescents underwent overnight polysomnography where acoustic tones (80 dB at 1000 Hz for 50 msec) were played with a random 15-30 s interstimulus interval. The analysis was limited to artefact and arousal-free episodes of NREM sleep. Playing acoustic tones in the upstate phases of EEG SOs, upstate phases of HR LF oscillations and downstate phases of HR HF oscillations induced significantly higher peak-to-peak amplitude EEG SOs (110%, 16% and 7%, respectively) (p < 0.001) and HR oscillations (16%, 56% and 25%, respectively) (p < 0.001), produced a greater number of EEG SOs (22%, 12% and 5%, respectively) and increased the SWA (3%, 14% and 3%, respectively) (p < 0.05) in contrast to playing tones in the other phase (downstate phases of EEG SOs, downstate phases of LF oscillations and upstate phases of HR HF oscillations). Our findings reveal complex interactions between the central and peripheral nervous systems in processing external stimuli, leading to significant variations in postcortical and cardiac oscillations. These results have potential implications for developing deep sleep enhancement technologies using adaptive interventions based on multidimensional oscillations.

Restless legs syndrome (RLS) is a common sensorimotor disorder, and the most common sleep-related movement disorder with a prevalence of up to 15% in the European and US population. This review addresses key aspects of RLS, focusing on novel data that have or will likely have an impact on clinical practice. These include novel insights into pathophysiology and motor activity during sleep, with a key focus on implications for RLS treatment. Along this line, we discuss the problem of augmentation before introducing new treatment paradigms and insights into new drug targets from genetics. Besides RLS, restless sleep disorder, neck myoclonus, fragmentary myoclonus, propriospinal myoclonus at the wake–sleep transition, and facio-mandibular myoclonus are discussed. This review provides an overview of the most recent insights into sleep-related movement disorders, and of how they are changing clinical practice.

Sleep deprivation (SD) causes large disturbances in mood and cognition. The molecular basis for these effects can be explored using transcriptional profiling to quantify brain gene expression. In this report, we used a meta-analysis of public transcriptional profiling data to discover SD effects on gene expression that are consistent across studies and paradigms. To conduct the meta-analysis, we used pre-specified search terms related to rodent SD paradigms to identify relevant studies within Gemma, a database containing > 19,000 re-analysed microarray and RNA-Seq datasets. Eight studies met our systematic inclusion/exclusion criteria. These studies characterised the effect of 18 SD interventions on gene expression in the mouse cerebral cortex (collective n = 293). For each gene with sufficient data (n = 16,290), we fit a random effects meta-analysis model to the SD effect sizes (log(2) fold changes). Our meta-analysis revealed 182 differentially expressed genes in response to SD (false discovery rate: FDR < 0.05), most of which (115/182) showed similar effects (FDR < 0.05) in an independent large dataset (GSE114845: n = 86 RNA-Seq samples from n = 222 mice). Gene-set enrichment analysis revealed down-regulation in pathways related to stress response (e.g., glucocorticoid receptor Nr3c1), vasculature, growth and development, and upregulation related to stress, inflammation, and neuropeptide signalling. Exploratory analyses suggested that recovery sleep (included in six contrasts: range: 1-18 h) could reverse the impact of SD on gene expression. Our meta-analysis provides a useful reference database illustrating the diverse molecular impact of SD on the rodent cerebral cortex.

Problems with initiating and maintaining sleep are among the most common health complaints, with prevalence rates exceeding 50% depending on the survey. Preventing the progression to chronic insomnia may reduce public healthcare costs and prevent secondary illnesses. This study examined the effectiveness of a novel app-based digital course using cognitive behavioural therapy for insomnia (CBT-I) in preventing the manifestation of insomnia among individuals with sub-threshold to moderate symptoms. Participants were assigned to an intervention group (N = 191, ages 20-75) or a waitlist control group (N = 72, ages 22-77) and assessed at three time points: Pre-intervention (T0), Post-intervention (T1, after 7-week course) and Follow-up (T2, 3 months after course initiation) using the Insomnia Severity Index (ISI), Sleep Hygiene Index (SHI) and sleep diary entries. Results showed a significant reduction in insomnia severity (-4.8 ± 3.7 ISI points) and improved sleep hygiene (-3.5 ± 4.5 SHI points) from T0 to T1 (d = 1.35, and d = 0.69, respectively), with stable effects maintained at the 3-month follow-up. Remission was achieved by 48% of the intervention group compared to 18% of the control group. Improvements were also observed in sleep latency, sleep efficiency and reductions in nocturnal awakenings and wake time after sleep onset (d = 0.25-0.71). Activating evening activates, napping, irregular bedtimes, uncomfortable sleep environment, perceived stress and rumination significantly reduced (d = 0.16-0.59). Notably, 68% of users reported sustained improvements in their sleep. The findings indicate that various sleep hygiene behaviours can be effectively modified through an app-based CBT-I intervention. Trial Registration: This study was pre-registered at Open Science Framework https://osf.io/yj2va.

Motor memory consolidation is a process by which newly acquired skills become stable over time in the absence of practice. Sleep facilitates consolidation, yet it remains unknown whether sleep-dependent consolidation is intact in people with Parkinson's disease. Here, we investigated whether a post-learning nap-as compared to wakefulness-improves motor memory consolidation in Parkinson. Thirty-two people with Parkinson's disease and 32 healthy older adults learnt a finger-tapping sequence task before a nap or wake intervention (pseudo-randomised assignment). Consolidation was measured as the change in performance between pre- and post-intervention and at 24-h retention. Automaticity was measured with dual-task cost, assessed at post-intervention and at post-night. Sleep architecture and electrophysiological markers of plasticity were extracted from the post-learning nap, to assess their association with performance change. The behavioural results suggest similar consolidation effects after sleep and wakefulness in both populations. Moreover, there was no effect of napping automaticity. Results also suggest positive associations between performance improvement and slow wave amplitude and slope in people with Parkinson's disease, and inconclusive associations between cross-frequency coupling and performance change in both populations. To conclude, napping did not have a beneficial effect on the consolidation of a finger-tapping task as compared to wakefulness in either people with Parkinson's disease or healthy older adults. Finally, in patients, sleep markers of plasticity were associated with performance improvements, implying that equivalent memory consolidation may be differently associated to sleep-related processes in Parkinson's and healthy ageing. Trial Registration: NCT04144283.