Journal of Sleep Research最新文献

Treating obstructive sleep apnea (OSA) has been shown to improve concomitant insomnia symptoms, but whether treating OSA translates into reducing sedative medication use is unknown. We evaluated the association between initiating incident positive airway pressure (PAP) therapy and continued benzodiazepine drug receipt among chronic benzodiazepine users. This was a retrospective, population-based cohort study, analysing Ontario health administrative data from January 1, 2012-March 31, 2020. Persons aged 18 years and older, who were chronic benzodiazepine users, were included. The association of new PAP receipt on benzodiazepine drug discontinuation was evaluated at 3-9 months. Propensity score matching was used to account for potential differences in 40 relevant covariates between new and non-PAP users to minimise bias. We identified 249,516 chronic benzodiazepine users, of whom 10,688 (4.3%) newly received PAP. In the matched cohort, there was no significant difference in benzodiazepine discontinuation between new PAP and non-PAP users at 3-9 months follow-up (8.2% vs. 8.3%, relative risk [RR] 0.98, 95% confidence interval [CI] 0.90-1.07). New PAP receipt was not observed to influence stopping benzodiazepines at 3-9 months after PAP initiation. Therefore, our findings raise some uncertainty about the potential effectiveness of administering PAP therapy to improve concomitant insomnia.

The chronotype (CT) refers to an individual's diurnal preference towards morningness (M) or eveningness (E). The aim of this study was to determine the influence of chronotype on 20-km cycling performance throughout the day. Seventy-six competitive male cyclists and triathletes completed the Morningness-Eveningness Questionnaire to determine chronotype. Only participants categorised as 'definite' M- (n = 10) and E-types (n = 7) were included in the study. In a randomised order and separated by 2-7 days, participants performed four self-paced 20-km cycling time trials at four different times of the day (06:00 h, 12:00 h, 18:00 h, 22:00 h). Mental readiness was assessed before each trial. Performance across all participants was significantly better in the evening compared to the morning (change: 2.1% ± 3.8%; p = 0.008). Related to individual's mean performance E-types performed significantly better in the evening compared to the morning (p = 0.02). Specifically, athletes were 40 s faster at 18:00 h compared to 06:00 h. Mental readiness in E-type athletes was significantly lower at 06:00 h compared to all other times (p < 0.04). The present study indicates that E-type athletes perform better later in the day. This might be important for the scheduling of training times and the preparation for competition, especially in the morning.

This prospective observational study reports on the feasibility and adequacy of Level 2 polysomnography involving children with autism spectrum disorder during an interventional-randomised controlled trial. Multiple level 2 polysomnographic studies were performed using Nox-A1 devices worn between October 2023 and September 2024. Study feasibility was determined by the child's compliance and primary caregiver report, while signal quality (key channels present for at least 90% of sleep time) was used to define study adequacy. A cost analysis was also conducted. Twenty children (6-12 years, 9.1 + 1.55 years; 16 males) with autism spectrum disorder (level 2) and reported sleep difficulties participated in the study. Eighty (89%) of 90 polysomnographic studies were feasible. All infeasible studies, except one, were unrelated to the study. Seventy-four (93%) of the eighty studies resulted in adequate study quality. Most (n = 6, 7%) inadequate studies were due to electroencephalogram signal artefact/absence. The participants did not have a sleep disorder requiring medical attention. The cost of a study was estimated at $AUD 258. The study indicates the feasibility, adequacy, and cost-effectiveness of level 2 polysomnography in evaluating sleep outcomes in children with autism spectrum disorder during an interventional randomised controlled trial. This preliminary study provides valuable insights into the field of paediatric sleep medicine. Repeat studies of this method using diverse and larger sample sizes are warranted.

Despite the high prevalence of insomnia, the availability of cognitive behavioural therapy for insomnia (CBT-I) in Italy remains limited. This study aimed to verify the effectiveness and feasibility of CBT-I in a real-world outpatient sample of the Santagostino Psiche in the Santagostino clinical centre. The baseline psychometric assessment was conducted using the Insomnia Severity Index (ISI), the Dysfunctional Beliefs and Attitudes about Sleep questionnaire (DBAS-30), and the Morningness-Eveningness Questionnaire (MEQ). Sociodemographic and clinical characteristics were also collected during the clinical interview and analysed. Results showed a significant reduction in insomnia severity and dysfunctional beliefs and attitudes about sleep in all the patients, except for the causal attributions of insomnia subscale. No differences in CBT-I effectiveness were found between in-person and online treatments. Psychiatric comorbidities (mainly anxiety and mood disorders) reduced the amount of improvement in insomnia symptoms, although they remained clinically relevant. Reductions in dysfunctional beliefs and attitudes about sleep were greater with higher baseline concerns about the consequences of insomnia, perceived control over sleep, and false beliefs about sleep and sleep hygiene practices. Overall, the results confirmed the effectiveness of CBT-I within the Santagostino clinical context and suggest the possible impact of psychiatric comorbidities and cognitive concern in modulating the symptomatic progress in a real-world treatment.

As sleep restriction has negative effects on performance, ensuring sufficient sleep for shift workers is essential. Quick returns (< 11 h off between shifts) shorten sleep and are associated with increased fatigue and risk of accidents, but there is limited research on other aspects of cognitive performance and work performance. The aim of the present quasi-experimental field study was to investigate the effects of quick returns on objective and subjective measures of sleep, fatigue and cognitive performance. In total 36 newly graduated nurses were followed during two pre-scheduled work periods, with and without a quick return (evening-day-day vs. day-day-day). They kept diaries of sleep and work, wore actigraphy wristbands to record sleep and performed 3 × 3 min smartphone-based cognitive tests (simple reaction time, episodic memory and Stroop) several times daily. Quick returns were found to shorten sleep by 46 min on average, and participants felt less rested in the morning and sleepier throughout the day. Sleep fragmentation and sleep efficiency did not differ between conditions but participants reported poorer sleep quality. Although the nurses reported cognitive impairments after a quick return, the estimated effects on simple attention, episodic memory and Stroop were small and overlapped zero. There were also indications of lingering fatigue on the second day shift after a quick return, but estimates are uncertain. In sum, quick returns shorten sleep and decrease subjective alertness, which could contribute to increased fatigue-related risk at work, but people seem able to mobilise necessary resources to maintain performance on short cognitive tasks.

The mouse sleep is mostly recorded with only epidural electrodes and divided simply into NREM and REM stages. With the help of distributed intracerebral triplet electrodes, we searched for possible new electrophysiological signatures to characterise more specific sleep substages within the timeframe of seconds to tens of minutes. We implanted 17 C57BL/6J male mice with double or triple wire electrodes into the hippocampus, somatosensory cortex and olfactory bulb, conventional skull screw electrodes and neck EMG electrodes. Sessions with at least 1 h of sleep of the 3-h total recording time were included in the analysis. We could identify N1, N2 and N3 stages in the mouse NREM. N2 could be further divided into N2s with spindles and N2n without spindles. Furthermore, N3 following N2n vs. N2s showed different features and were therefore coined N3s and N3n, respectively. The REM could be divided into asynchronous (aREM), synchronous (sREM) and phasic (pREM) substages. The EEG power between 5 and 30 Hz showed quasi-periodic fluctuation at an infra-slow range (0.005-0.02 Hz). The sequence of sleep stages followed reliably this fluctuation, so that the onset of N2n co-occurred with a low power, N2s halfway on the rise, aREM or N3s near the peak and sREM on the descending phase. The infra-slow fluctuation was temporarily abolished by damaging the locus coeruleus noradrenergic axons with the selective neurotoxin DSP-4 or by administration of the alpha-2 adrenergic agonist medetomidine. As a result, the brain got locked in a continuous N3-like state and no REM was present.

Automatic sleep stage classification is essential for enabling non-invasive, at-home monitoring. However, current methods often rely on electroencephalogram (EEG) signals and ad-hoc development approaches that limit reproducibility. We present a reproducible engineering framework for a deep learning model based on the U-Net architecture that classifies sleep into five stages (Wake, N1, N2, N3 and REM) or four (Wake, Light Sleep, Deep Sleep and REM) using only three easily acquired physiological signals: oxygen saturation (SpO), heart rate (HR) and abdominal respiratory effort (AbdRes). In contrast to most previous studies, our model provides sleep stage predictions on a per-second basis, thus overcoming the limitations associated with fixed 30-s epochs. The model was trained on the Sleep Heart Health Study-Visit 2 (SHHS2) dataset and externally validated on the Multi-Ethnic Study of Atherosclerosis (MESA). Optimisation of the model was achieved via Keras Tuner with the Hyperband algorithm. The study achieved weighted F1-scores of 68% (five-stage) and 71% (four-stage) with Cohen's Kappa of 0.61 and 0.67 on SHHS2, with consistent performance on MESA. These results demonstrate strong generalisation and suggest that this lightweight, EEG-free approach offers a practical path towards scalable, clinically relevant sleep monitoring.

While previous research has identified emotional dysregulation and repetitive thinking as contributors to insomnia, the interplay between these factors remains unclear. Building upon data previously collected in our laboratory, this exploratory study extends prior findings by examining the mediating role of rumination, worry and rapid eye movement (REM) sleep instability in the relationship between emotional dysregulation and the functional impact of insomnia and depressive symptoms, aiming to generate hypotheses about the psychological and neurophysiological mechanisms linking these constructs. Using the same cohort of 23 patients with insomnia disorder and 23 matched healthy sleepers, participants underwent overnight polysomnography and completed validated questionnaires assessing emotional dysregulation, worry, rumination and the functional impact of insomnia. Novel mediation models were used to examine whether worry, rumination and REM sleep instability mediated the link between emotional dysregulation and daytime consequences of insomnia. Compared to controls, individuals with insomnia showed significantly greater emotional dysregulation, rumination and worry. Mediation analysis indicated that rumination, but not worry, significantly mediated the relationship between emotional dysregulation and daytime consequences of insomnia. Furthermore, higher scores on the dimension 'difficulties in distracting with emotions' were associated with increased REM sleep instability, which also mediated the effect of emotional dysregulation on daytime consequences of insomnia. These findings highlight the crucial role of rumination in sustaining the functional impact of insomnia and suggest that interventions targeting repetitive negative thinking and emotional regulation may improve sleep outcomes.

Sleep dysfunction can impair cognition and may play a causal role in the development of hallucinations. Deficits in cognitive control have been implicated in cognitive models of hallucinations. To better understand the underpinning role of cognition in the relationship between sleep and hallucinations, the current study aimed to investigate the impact of sleep deprivation on cognitive control mechanisms such as intentional inhibition and working memory, as well as auditory signal detection. Forty-five participants were allocated to either a sleep-deprivation condition (N = 15) or a rested control group condition (N = 30). Cognitive control assessments were applied at three timepoints for each condition: baseline (T1), post-sleep deprivation/post-habitual sleep (T2), and post-recovery sleep/post-habitual daily activity (T3). Results showed significant effects of sleep deprivation on intentional inhibition and working memory, but not auditory signal detection. Findings support current neurocognitive theories and suggest that sleep deprivation may lead to hallucinations through effects on intrusive thoughts and memories. Future research should continue to explore the potential mechanistic pathway between cognitive control and sleep, to inform future intervention work. The study pre-registration, open materials, data, and code are available on the Open Science Framework (doi.org/10.17605/OSF.IO/28SRW).

Central hypersomnia disorder (CHD) may result in a higher risk of injury/accident. The present study aims to investigate the real-world risk by tracing patients in a clinical cohort for 4 years. We tracked the injury/accident risk of CHD clinical cohort patients from Taiwan's National Health Insurance Research Database (NHIRD) and compared it with controls. Data were collected based on the International Classification of Diseases, Tenth Revision. Patients were categorised by diagnosis, gender and age, with each subgroup compared to age- and gender-matched controls. Group differences were analysed using the Chi-square test and t-test. Bonferroni correction was used for post hoc analysis. A total of 386 CHD clinical cohort patients were included. Narcolepsy type 1 patients had the highest subjective and objective symptom severity (p < 0.001). Compared to controls, CHD patients had a significantly higher risk of injury and accident of up to 61.92% and 7.51% during the 4-year follow-up, necessitating clinical visits. Narcolepsy type 2 patients have the highest risk of injury (p = 0.005). Age/gender differences were found. Males had a higher specific-site injury risk (p = 0.045) than females, while females had a higher transportation accident risk than controls (p = 0.048). Children/adolescents had a higher risk in total injury and multiple-site injury than controls (p = 0.024, p = 0.014), and adults had a higher risk in specific-site injury and transportation accident (p = 0.020, p = 0.004). In conclusion, CHD patients had a higher risk of injury/accident, even among those with milder symptoms. Gender and age differences in these risks were observed. Our findings highlight the importance of hypersomnia treatment and individualised considerations in clinical practice.