Journal of Sleep Research最新文献

Lucid dreaming, defined as the experience of becoming aware of dreaming while dreaming, offers a unique window into a state of consciousness characterised by a blending of the sensory vividness of REM sleep with the self-awareness of wakefulness. While past functional imaging has shed light on the neural activity supporting lucid dreaming, the structural brain correlates of lucid dream frequency as an individual trait varying in the normal population, remain largely unexplored. Moreover, the possibility of separating ordinary dreams from lucid dreaming has been only partially explored. In this exploratory study, we employed a data-driven, multimodal neuroimaging approach known as mCCA + jICA, to identify joint and modality-specific grey matter (GM) and white matter (WM) morphometric features associated with the individual differences in lucid and non-lucid dream recall measured by a validated self-report measure. Results revealed that lucid dreaming frequency was associated with one joint GM-WM component, encompassing frontal, temporal, parietal, and cerebellar regions implicated in metacognition, imagery, and volitional control, as well as one GM-specific component involving visual and attentional areas including the cuneus. In contrast, ordinary dream recall frequency was associated exclusively with two WM-specific components, showing no overlap with those linked to lucid dreaming. These findings suggest that the tendency to experience lucid dreams is rooted in distributed, structurally covarying brain systems, distinct from those underlying general dream recall. The presence of joint components supports the view that lucid dreaming depends on the integration of cortical and subcortical systems mediating self-awareness and internal simulation.

Dual orexin receptor antagonists (DORAs) such as suvorexant are effective treatments for insomnia but are associated with rapid eye movement (REM) sleep-related adverse effects. While sleep paralysis and hypnagogic hallucinations are recognised, cataplexy is not typically reported. We describe a 39-year-old male US Navy Veteran with chronic pain, long-standing insomnia and anxiety who developed recurrent, emotionally triggered episodes of bilateral ptosis, slurred speech, unsteadiness and subjective "euphoric" sensations shortly after initiating suvorexant. Neurologic evaluation, electroencephalography, electromyography and brain imaging were unrevealing. Multiple sleep latency testing demonstrated normal mean sleep latency without sleep-onset REM periods, excluding narcolepsy. Polysomnography revealed mild obstructive sleep apnea. Symptoms diminished substantially following suvorexant discontinuation and multimodal treatment including cognitive behavioural therapy for insomnia, escitalopram and continuous positive airway pressure therapy, though mild residual symptoms persisted. This case suggests that suvorexant may provoke cataplexy-like phenomena via REM-intrusion mechanisms in susceptible individuals. Clinicians should monitor for atypical motor or speech symptoms in patients prescribed DORAs, particularly those with psychiatric comorbidity or sleep fragmentation.

We investigated whether sleep microstructures show spatial differences in young children with autism compared with typically developing peers. 32-channel electroencephalography (EEG) during natural sleep after 5-6 h of partial sleep deprivation was recorded from 53 children (26 with autism, 27 typically developing; 1.1-5.1 years). Quantified EEG features included spindle density, frequency, morphology, slow oscillations and the relative power of infraslow oscillations (0.005-0.03 Hz). Clinical associations were examined using the Autism Diagnostic Observation Schedule, the Childhood Autism Rating Scale and the Gesell Developmental Schedules. Children with autism showed greater modulation of spindle frequency by the phase of slow oscillations at a right frontal scalp electrode (F8). An infraslow peak slightly below 0.02 Hz was present in both groups. Although group differences in infraslow power did not remain significant after correction for multiple comparisons, infraslow power correlated positively with autism severity in males, over posterior and temporal regions. These findings indicate that sleep microstructures in early childhood reflect thalamocortical and cortical dysfunction with sex-specific clinical associations.

Psychotic-like experiences are subclinical psychotic symptoms that are usually accompanied by sleep problems, negative emotions, and poorer cognitive functioning. However, their night-to-day associations remain understudied in older adults. 72 participants aged 50-79 took part in a home-based sleep study. After an intelligence test, they reported their sleep quality, dream and morning emotions, psychotic-like experiences, and subjective cognitive failures for 7 days, in addition to wearing an electroencephalographic headband. Results showed that poorer subjective sleep quality was associated with higher levels of psychotic-like experiences the following day, a relationship mediated by negative morning and dream emotions. Furthermore, higher subjective cognitive failures and lower IQ were related to more psychotic-like experiences. Objective sleep parameters were not linked to next-day psychotic-like experiences. The results demonstrate that negative emotions play a mediating role between poor sleep quality and psychotic-like experiences in older adults. Additionally, improved cognitive performance, both subjective and objective, seems to protect against the occurrence of psychotic-like experiences. The study indicates that sleep, emotions, and cognitive functions are key contributors to daytime psychotic-like experiences in older adults.

Multimorbidity and cognitive decline are highly prevalent among older adults. Although sleep disturbances are known to be associated with both conditions, the underlying mechanisms connecting multimorbidity to cognitive impairment remain poorly understood. To address this gap, a multi-center, population-based cross-sectional study was conducted to investigate the potential mediating role of sleep quality in the relationship between multimorbidity and cognitive decline. From June 2023 to March 2024, a total of 3574 community-dwelling adults aged 65 years or older were recruited from eight communities in Shanghai. After excluding participants with missing data (n = 672), the final analytical sample comprised 2902 individuals. Data were analysed using R Statistical Software. Among the 2902 participants (mean age 73.8 ± 7.9 years), fully adjusted models revealed two key findings: first, a significant association was observed between multimorbidity and cognitive decline (odds ratio = 1.152 per unit increase in the Chinese Multimorbidity Weighted Index); and second, sleep quality mediated 12.1% of this relationship (p = 0.004), a result that was confirmed through bootstrap validation for robustness. In conclusion, sleep quality partially mediates the positive association between multimorbidity burden and cognitive decline, accounting for approximately one-eighth of the total effect.

The international Swiss Primary Hypersomnolence and Narcolepsy Cohort Study (iSPHYNCS) is a multicentre study aimed at identifying novel biomarkers for central disorders of hypersomnolence (CDH). We analysed questionnaires and metadata to uncover distinct clusters of participants and explore phenotypic variability within CDH. Data were collected from 227 patients with CDH and 33 healthy controls. Participants completed validated clinical questionnaires and study-specific questions addressing CDH-related symptoms such as excessive daytime sleepiness, fatigue, cataplexy, disrupted sleep, and sleep paralysis. Demographic metadata (age, gender, BMI) were included. After excluding participants with missing over 30% of data (n = 40), missing values were imputed using a multiple random forest algorithm. A robust clustering pipeline was employed: (1) random sampling of 60% of the dataset, (2) dimensionality reduction via UMAP, (3) K-means clustering, and (4) consensus clustering across 500 iterations. Post hoc analysis was performed to identify biomarkers in data not used for clustering. We identified four distinct clusters. One predominantly comprised healthy controls, while another primarily contained individuals with narcolepsy type 1 (NT1). Two clusters represented predominantly the narcolepsy borderland group (NBL), with one distinctly characterised by higher symptom severity and psychiatric comorbidities. The clustering pipeline produced reproducible results, with the NT1 and healthy control clusters serving as internal validation. The differentiation between the two NBL clusters aligns with prior studies, suggesting a possible NBL subtype marked by increased fatigue and psychiatric comorbidities. These findings emphasise the phenotypic heterogeneity of CDH and the potential for cluster-based approaches in management. Trial Registration: ClinicalTrials.gov identifier: NCT04330963.

Sleep is fundamental for infant development and health, playing a critical role in cognitive, socio-emotional, and physical growth. However, environmental factors can impact the quality and duration of sleep in infants. This review synthesises current evidence on the associations between environmental chemical exposures and infant sleep outcomes, with a focus on the first 1000 days of life. Infants may be exposed to environmental pollutants before birth, through the placenta, or after birth, via breastfeeding, diet, and external sources such as inhalation, dust contact, or hand-to-mouth exposure. Given their ongoing development, foetuses and infants are particularly vulnerable to these pollutants. This period of rapid growth and maturation represents a highly sensitive window for environmental exposures. This review covers various categories of environmental pollutants, including persistent organic pollutants (PCBs, dioxins), non-persistent pollutants (phthalates, BPA), air pollutants (particulate matter, second-hand smoke), and water contaminants (nitrates, microplastics). Environmental chemicals exposure could be assessed using parental questionnaires or biological monitoring, while sleep is evaluated using actigraphy, polysomnography, or parental reporting. Some evidence suggests that both prenatal and postnatal exposure to environmental contaminants may be associated with sleep disturbances in children, particularly in girls. Despite the numerous studies on adults and the mechanisms associated with these pollutants (neurotoxicity, endocrine disruption), which suggest an effect on sleep, there is a lack of studies in children, resulting in limited associations in the literature. Therefore, it is imperative to conduct studies on environmental pollutants present in breast milk, diet, and/or ambient air to understand their impact on infant sleep.

Sleep is increasingly understood as a socially embedded phenomenon. This study examined how structural and functional aspects of social support, as well as loneliness, relate to sleep health in a German sample of middle-aged adults (N = 5388). Drawing on the socio-ecological model of sleep health, we assessed the contributions of social support dimensions while accounting for age, sex, and socioeconomic status, as well as psychological covariates. The results of the binary logistic regression showed that functional support (ESSI), friend network size (LSNS6), and loneliness (CES-D item 14) significantly (p < 0.001) predicted sleep health (PSQI), while family network size did not. The portion of explained variance was small (4%-5%). Results remained robust after adjusting for age, sex, and socioeconomic status, but no longer when including psychological covariates (GAD-7, SWLS, CES-D), in which case only the friend network size remained significant (p = 0.019). Women were significantly more affected by poor sleep health than men, and with higher socioeconomic status, fewer people reported suffering from poor sleep (all: p < 0.001). Additional subgroup analysis revealed higher age as a risk factor for worse sleep health in women only, while the friend network was only relevant in men. Our findings highlight the importance of distinguishing between structural and functional dimensions of social support in sleep health research and interventions, and suggest a potential sex-by-age interaction. Future research should promote equity by including diverse populations and longitudinally examine how social support, especially friend networks, affects sleep across genders, ages, and contexts.

Distinguishing non-epileptic events from epileptic seizures remains a clinical challenge, particularly when occurring exclusively during sleep. Sleep-related rhythmical movement disorder (SRRMD) is a benign condition typically seen in early childhood, characterised by stereotyped, rhythmical repetitive movements involving large muscle groups, predominantly during Stage II of non-REM sleep. These movements can closely mimic features of sleep parasomnias, hypermotor seizures or psychogenic non-epileptic seizures (PNES), complicating the diagnostic approach. We present a case of an adolescent female with comorbid SRRMD and PNES and a clinical approach to distinguish between them.

Insomnia is the most prevalent sleep disorder, affecting up to one third of the adult population and is increasingly recognised as a potential contributor to cardiovascular disease (CVD), a leading cause of global morbidity and mortality. This narrative review examines the complex relationship between insomnia and CVD, integrating epidemiological, genetic and mechanistic evidence to assess whether insomnia represents a causal cardiovascular risk factor. Large prospective cohort studies and meta-analyses consistently show that insomnia symptoms and clinically diagnosed insomnia are associated with increased risks of hypertension, myocardial infarction, stroke, heart failure and cardiovascular mortality, with stronger associations observed in individuals with short sleep duration or persistent insomnia. Mendelian randomization studies involving millions of participants further support a likely causal link, suggesting that genetic liability to insomnia increases the risk of multiple cardiometabolic outcomes. Biological plausibility is supported by evidence of autonomic imbalance, hypothalamic-pituitary-adrenal axis activation, inflammation and adverse blood pressure profiles in individuals with insomnia. However, insomnia is a heterogeneous condition, frequently coexisting with other sleep disorders and influenced by psychosocial and circadian factors, which complicates causal inference. Importantly, evidence that treatment of insomnia reduces cardiovascular risk remains limited. While cognitive behavioural therapy for insomnia improves sleep outcomes and some cardiometabolic biomarkers, randomised trials have not demonstrated clear benefits on blood pressure or other cardiovascular endpoints and some pharmacological treatments may even be associated with harm. Overall, current evidence suggests that insomnia is a plausible and potentially causal risk factor for CVD, but definitive proof of reversibility through treatment is lacking. Well-powered, rigorously designed trials targeting patients with clinically defined insomnia are needed to determine whether effective insomnia treatment can meaningfully reduce cardiovascular risk and inform future prevention strategies.