Whether cerebrospinal fluid (CSF)-dynamics-related glymphatic alterations occur in middle-aged and older adults with chronic insomnia (CI) remains unknown. We therefore examined global and network-level blood oxygenation level-dependent (BOLD)-CSF coupling in this population and assessed the effects of low-frequency repetitive transcranial magnetic stimulation (LF-rTMS) during standardized hypnotic tapering. This two-stage study included a cross-sectional comparison and a randomized, double-blind, parallel-group, sham-controlled trial. In Stage 1, 43 CI patients and 40 matched healthy controls completed sleep assessments and resting-state functional magnetic resonance imaging to quantify global and network-level BOLD-CSF coupling. In Stage 2, 26 CI patients were randomized (1:1) to receive 4weeks of active or sham LF-rTMS during hypnotic tapering. Sleep was assessed at baseline, 2weeks, 4weeks, and 12months. Neuroimaging was acquired at baseline and 4weeks. CI patients showed significantly reduced global BOLD-CSF coupling, particularly in frontoparietal network (FPN) and default mode network (DMN). Global and FPN coupling correlated with sleep quality. In the randomized trial, LF-rTMS produced greater improvements in sleep at 4weeks than sham resulted in fewer participants resuming hypnotics at 12months. LF-rTMS increased global and DMN BOLD-CSF coupling, and these changes were associated with improvements in sleep. Middle-aged and older adults with chronic insomnia exhibit reduced global BOLD-CSF coupling, indicating alterations in CSF dynamics that may relate to glymphatic function. LF-rTMS improved insomnia symptoms and modulated this coupling, indicating therapeutic potential for chronic insomnia.Trial Registration: ChiCTR2100049455. This trial is registered with the Chinese Clinical Trial Registry (ChiCTR; ChiCTR2100049455), titled "Application of neurodegenerative techniques for insomnia and cognitive impairment in the elderly," with the registry record available at: https://www.chictr.org.cn/bin/project/edit?pid=130047. This study demonstrates that middle-aged and older adults with chronic insomnia show reduced global blood oxygenation level-dependent (gBOLD)-cerebrospinal fluid (CSF) coupling, indicating alterations in CSF-related dynamics that may reflect glymphatic-relevant processes at the cortical functional level. These alterations were most pronounced in high-order brain networks and were associated with poorer sleep quality. Low-frequency repetitive transcranial magnetic stimulation (LF-rTMS) applied to the right dorsolateral prefrontal cortex modulated gBOLD-CSF coupling and improved sleep symptoms, with benefits maintained at 12months. These findings suggest that disrupted CSF-dynamics coupling may be a functional marker associated with chronic insomnia in later adulthood and support LF-rTMS as a feasible non-pharmacological approach for long-term management, potentially enabling targeted modulation of CSF-dynamics-related processes.

Sleep loss significantly disrupts cognitive and emotional functioning, yet the neural consequences of different types of sleep deprivation remain unclear. In a within-subject resting-state fMRI study, we examined how acute total sleep deprivation (TSD) and chronic sleep restriction (CSR) alter intrinsic functional brain organization in 28 healthy adults scanned under three conditions: rested wakefulness (RW), after one night of TSD, and after five nights of CSR.To quantify network-level disruption, we applied graph-theoretical analyses, including a novel within-subject adaptation of the Hub Disruption Index and Covariate-Constrained Manifold Learning (CCML), an unsupervised embedding technique sensitive to subject-level covariates. Moreover, we assessed subjective sleep quality, sleepiness, and circadian traits. Both TSD and CSR were associated with a consistent reorganization of graph topology relative to RW. Furthermore, direct comparisons revealed that TSD and CSR affect different brain hubs. Regional changes in degree, closeness, and clustering coefficients were most prominent in subsystems of the default mode network, frontoparietal network, and cerebellum. These differences were also captured in CCML embeddings, supporting the hypothesis that acute and chronic sleep deprivation exert divergent effects on brain connectivity. Findings were robust across graph thresholds, brain atlases, and nodal metrics. Moreover, these results were further supported by subjective measures - sleepiness was associated with reduced network integration in RW, and circadian phenotype emerged as a key determinant of individual sensitivity to sleep loss. Our results show that TSD and CSR induce divergent alterations in brain functional organization, offering new insights into their neural impact.

Sleep resilience is the ability to maintain effective emotional, cognitive, and physical functioning despite disruptions to sleep/circadian rhythms. While conceptually related to sleep health, no validated measure currently exists. This cross-sectional survey study aimed to validate a novel self-report measure of sleep resilience, the Sleep Resilience Questionnaire (SRQ), and examine its associations with demographic features, sleep disturbance, and sleep-related impairment. Our convenience sample included 455 adults (Mean age=45±17) in the United States who completed a demographic survey, PROMIS Sleep Disturbance (PROMIS-SD) and Sleep-Related Impairment (PROMIS-SRI), and retrospective and prospective SRQ forms (English version 1). Exploratory and confirmatory factor analyses (EFA and CFA) evaluated the SRQ's factor structure and internal consistency, and structural equation modeling examined associations with demographics, PROMIS-SD, and PROMIS-SRI. EFA and CFA supported a highly correlated two-factor retrospective SRQ structure and a unidimensional prospective SRQ structure with excellent fit and internal consistency (CFI & TLI>.99, RMSEA<.07, ω>.92). Lower sleep resilience was associated with greater sleep-related impairment (p<0.05) but not sleep disturbance. Younger age, men, higher education, greater number of dependents, and higher income were associated with lower sleep resilience in specific retrospective or prospective domains (p<0.05). Findings suggest sleep resilience is a meaningful dimension of sleep health, associated with demographic and sleep-related impairments, and the SRQ forms appear to validly measure it. Despite limitations of the cross-sectional design, the SRQ may be useful for future research aimed at identifying potential intervention targets to improve sleep-related impairments.

Nighttime environmental noise (EN) exposure disturbs sleep and increases morbidity and mortality. Affordable and effective countermeasures are needed, but rigorous research is scarce. This study investigates the efficacy of pink noise (PN) and earplugs for mitigating the effects of intermittent EN on sleep. Twenty-five healthy adults (mean ± SD age 28.5 ± 5.9years, seven male) participated in a seven-night polysomnographic laboratory study with different noise conditions including exposure to EN (93 events; maximum sound pressure level 45 to 65dBA), PN (40 or 50dBA), earplugs, and their combination. In the morning, participants completed cognitive tests, cardiovascular measurements, hearing tests, and surveys. Compared to a noise-free control night, EN reduced N3 deep sleep (p < .0001) while PN reduced REM sleep (p < .001). Adding PN to EN worsened sleep structure, despite minor dose-dependent improvements of EN-induced sleep fragmentation and N3 sleep increases. Earplugs mitigated nearly all EN effects on sleep but started failing at the highest EN level (65 dBA). Morning cognition, cardiovascular measures, and hearing were not affected by nighttime noise, but subjective assessments of sleep, alertness and mood were significantly worse after EN and PN exposure. In contrast to PN, earplugs proved efficacious in mitigating the effects of EN on sleep. Considering the importance of REM sleep for memory, emotion regulation, and neurodevelopment, the negative effects of PN on REM sleep caution against the widespread and indiscriminate use of broadband noise (BN). Additional research on optimal BN color/level and long-term use is needed, especially in vulnerable populations. Registered at clinicaltrials.gov under "Broadband Sound and Sleep"; https://clinicaltrials.gov/study/NCT05774977; registration # NCT05774977.

Idiopathic hypersomnia (IH) is a rare chronic neurological condition that may be characterized by excessive daytime sleepiness (EDS), and/or prolonged nocturnal sleep, and also sleep inertia, yet its underlying mechanisms and diagnostic boundaries remain poorly defined. A key challenge is distinguishing excessive sleep duration from EDS, as patients may present one or both features, and similar symptoms can arise from diverse medical, psychiatric, and sleep disorders. Current diagnostic criteria rely heavily on the multiple sleep latency test, which frequently underestimates hypersomnia in patients with long sleep need, demonstrates poor test-retest reliability, and separates IH from narcolepsy type 2 based on an unstable count of sleep-onset REM periods. Accurate measurement of long sleep is an unmet need. Actigraphy and sleep diaries frequently misestimate true sleep duration, while extended polysomnography, the gold standard, is rarely feasible outside research. Defining abnormal sleep quantity remains difficult given individual variability and the heterogeneity of IH phenotype. The pathophysiology of IH remains largely speculative. No definitive biomarker has been identified, and proposed mechanisms, including genetic susceptibility, circadian alterations, abnormal slow-wave dynamics, and neurobiology disturbances lack consistent validation. Clinical overlap between IH and hypersomnolence associated with depression suggests potential shared disruptions in arousal and circadian-homeostatic systems, though their neurobiological bases remain unclear. Therapeutic approaches are still limited. Low-sodium oxybate offers symptomatic improvement, and orexin receptor agonists represent an encouraging emerging class. Advancing the field will require better phenotyping, standardized sleep extension methods, and biomarkers to define IH as a distinct multidimensional disorder rather than a diagnosis of exclusion.