Memory consolidation refers to how newly encoded memories are strengthened and retained over time, and ample evidence indicates that sleep supports this process for both procedural and declarative memories. Although sleep spindles during non-rapid eye movement (NREM) sleep have been associated with consolidation, it remains unclear whether all spindle types contribute equally. Spindles vary in frequency and topography, slow spindles (≤ 12.5 Hz) predominating frontally, fast spindles (> 12.5 Hz) parietally and recent work suggests that procedural memory consolidation relates to the temporal organization of spindles in 'trains' (events occurring < 6 s apart). We investigated whether a similar mechanism operates for declarative memory during daytime naps. Participants (Nap, N = 23; No-Nap, N = 15) completed an object-location task involving 36 item-location associations, tested immediately after learning and again following a 90-min nap opportunity or an equivalent wake period. The Nap group exhibited significantly better delayed memory, measured by combined recall-associative recognition scores and a greater proportion of nappers maintained or improved performance. Within the Nap group, memory was positively associated with local spindle density at frontal and parietal sites and with the proportion of slow frontal spindles clustered in trains during NREM2. Contrary to our expectations, however, these associations did not reach significance under two-tailed testing, possibly reflecting the limited sample size and thus lack of statistical power for an experimental design based on naps. Together, our results demonstrate a robust behavioural benefit of daytime naps for declarative memory retention and, more tentatively, point to slow frontal spindle activity as a candidate correlate for future work.

Parkinson's disease (PD) is a progressive neurodegenerative disorder caused by the loss of dopaminergic neurons in the substantia nigra pars compacta. In addition to motor symptoms, excessive daytime sleepiness (EDS) occurs frequently in patients with PD and severely impairs their quality of life. Current pharmacotherapies for EDS in PD are often associated with adverse effects. However, clinical studies have yielded inconsistent results, underscoring the need for safer, more effective treatment strategies. Histamine plays a pivotal role in maintaining wakefulness in the brain and is primarily inactivated by histamine N-methyltransferase (HNMT), the major enzyme responsible for histamine clearance in the central nervous system. We previously demonstrated that pharmacological inhibition of HNMT markedly elevates brain histamine levels and potently promotes wakefulness in mouse models of narcolepsy and idiopathic hypersomnia, suggesting that targeting HNMT may also be beneficial for treating hypersomnia in PD. Here, we investigated whether pharmacological inhibition of HNMT ameliorates hypersomnia in a 6-hydroxydopamine-induced mouse model of PD. We first confirmed dopaminergic neuronal loss and hypersomnia during the active phase in a mouse model of PD. Pharmacological inhibition of HNMT with metoprine robustly increased wakefulness, markedly reduced NREM and REM sleep, and prolonged sleep latency. Metoprine also reduced sleep-wake bout fragmentation, indicating the sustained consolidation of wakefulness. In direct comparison, metoprine produced stronger and more sustained wake-promoting effects than other wake-promoting agents. These findings indicate that HNMT inhibition represents a promising and mechanistically distinct therapeutic approach for EDS in PD.

Optimizing sleep health in healthcare professionals is a challenge, as misalignment between endogenous circadian rhythms and exogenous work schedules undermines recovery, well-being, and performance. This study evaluated a tailored recovery intervention based on cognitive-behavioural approaches for insomnia designed to support recovery to rotating night shifts. In a randomized controlled trial (REST), 72 emergency healthcare professionals were randomized to intervention or control. The intervention combined personalized sleep-wake feedback with stress management techniques. Sleep-wake rhythms were monitored via actigraphy for 3 weeks before and 1 week after the intervention. Outcomes included objective sleep duration, self-reported sleepiness, insomnia severity, and subjective sleep quality, measured using the Epworth Sleepiness Scale, Insomnia Severity Index, and Leeds Sleep Evaluation Questionnaire. Fifty-nine participants (28 intervention, 31 control) were included in the primary analyses. Even on free nights, average nocturnal sleep duration was 6 h and 21 min, below recommended levels for adults. Compared with controls, intervention participants increased nocturnal time in bed by 37 min, 95% CI [13, 62], p = 0.003, and total sleep time by 23 min, 95% CI [4, 42], p = 0.019. Perceived sleep quality also improved for the intervention group t(55) = -7.91, p < 0.001, d = 2.06, 95% CI [1.42, 2.70], and insomnia symptoms decreased (β = -2.23, 95% CI [-4.26, -0.21], p = 0.031). These findings suggest that structured occupational recovery programs can enhance sleep health and facilitate recovery across rotating night work schedules. Integrating such interventions into training may reduce burnout, improve safety, and support workforce sustainability.

Sleep disturbances are common in patients with prolonged disorders of consciousness (pDoC) and are closely correlated with clinical outcomes. With an increasing number of pDoC patients undergoing surgery under general anaesthesia (GA), this study characterized sleep patterns in pDoC patients and evaluated the effects of GA on consciousness and nocturnal sleep. We prospectively enrolled 30 pDoC patients (14 in vegetative state [VS] and 16 in minimally conscious state [MCS]) undergoing spinal cord stimulation and 12 healthy controls. Among pDoC patients, 19 (10 VS, 9 MCS) with complete pre- and postoperative PSG data were analysed for GA effects. Controls underwent one overnight polysomnography (PSG); pDoC patients underwent pre- and postoperative PSG. Consciousness was assessed with Coma Recovery Scale-Revised (CRS-R) before and after surgery. Compared with controls, pDoC patients presented significantly impaired sleep structure, including reduced total sleep time (TST), decreased NREM Stage 2 sleep, diminished slow-wave sleep (SWS), reduced rapid eye movement (REM) sleep duration and percentage relative to TST (all p < 0.05). No significant short-term changes in CRS-R scores were observed following GA. Although GA significantly prolonged TST (p = 0.039), with numerical increases in absolute NREM and SWS durations, no statistically significant changes were observed in sleep stage percentages relative to TST (all p > 0.05). Subgroup analysis showed no significant within-group changes in sleep stage percentages in either the VS or MCS group. These findings suggest that GA increases TST without statistically significant changes in sleep structure in pDoC patients.

Recurrent cycles of weekday short sleep and weekend sleep extension have been shown to result in more prominent neurobehavioural impairments during subsequent weeks of sleep restriction in adolescents and young adults. Whether the same would be observed in school-aged children is unclear. In this micro-longitudinal observational cohort study, 79 children (6-12 years old, 34 males) were tracked for 16 days at home. Sleep was measured using actigraphy. Neurobehavioural functions-processing speed, working memory, vigilance, subjective sleepiness and affect-were assessed daily through a smartphone application. Forty participants had a daily average time-in-bed of less than 9 h on weekdays but at least 9 h on weekends (short sleep group), while 39 participants had at least 9 h on both weekdays and weekends (well-rested group). There were no significant group × day interactions for any neurobehavioural measure (p > 0.61), but the short sleep group reported overall higher levels of subjective sleepiness (mean Karolinska Sleepiness Scale score [SE]: 4.51 [0.21] vs. 3.77 [0.21], p = 0.01) and lower positive affect (score on the 10-item Positive and Negative Affect Schedule for Children: 12.84 [0.64] vs. 15.15 [0.65], p = 0.01) than the well-rested group. Within the short sleep group, none of the neurobehavioural measures showed observable weekday-weekend differences or compounding impairments during the second cycle of weekday short sleep. Unlike in adolescents and young adults, recurrent cycles of short sleep on weekdays and sleep extension on weekends may not be associated with compounding neurobehavioural impairments in school-aged children.

The relationship between linear growth and obstructive sleep-disordered breathing (SDB) has not been extensively studied. Hypoxic burden (HB) is a new metric that may better capture end-organ damage in paediatric SDB compared to the traditional apnea-hypopnea index (AHI). This observational cross-sectional study examined the association between HB and linear growth in nonobese children aged 3-9 years with SDB. HB was assessed as the area under the peripheral oxygen desaturation curve, alongside standard polysomnography indices. A cohort of 164 children without comorbidities except for asthma was evaluated for suspected SDB, with demographic and anthropometric data collected. The mean ± standard deviation height z score was -0.05 ± 1.09, and the median [25th; 75th percentile] HB was 1.4 [0.4; 3.5] %min/h. Forty children (24%) had an obstructive AHI greater than 5/h. HB and frequent snoring (≥ 3 nights/week) were significantly and negatively associated with height z score (standardized β = -0.21, p = 0.036 and -0.37, p = 0.043, respectively), whereas AHI did not predict linear growth outcomes. In multivariate analyses, HB remained independently associated with lower height z score and accounted for 7.5% of its variance, compared with 12.7% for ethnicity and 6.4% for body mass index z score. The oxygen desaturation index was also a significant predictor, but it explained less variance in height z score than HB. These findings suggest that intermittent hypoxia may contribute to impaired linear growth in children with SDB, although its contribution is modest and other determinants of growth remain important.

Hypopnea-predominant OSA (HypoOSA) represents a distinct phenotype compared to apnea-predominant OSA. Nevertheless, hypopnea has been defined using varying criteria, leading to differences in the estimation of AHI. This study investigated the endotypic traits of HypoOSA, as defined by ≥ 4% desaturation (4% OD) and ≥ 3% desaturation or arousal (3% ODA) criteria for hypopnea and how AHI and endotypic traits differ by criteria. We prospectively enrolled 765 adult patients with moderate-to-severe OSA from a single sleep centre. Endotypic traits were obtained from in-laboratory polysomnographic studies. Respiratory events were scored twice using 3% ODA and 4% OD criteria. Endotypic traits characterizing HypoOSA, defined as AHI comprising < 50% apneas, were identified and compared to apnea-predominant OSA. Within-subject differences in endotypic traits between the hypopnea criteria were analysed. We observed that 4% OD and 3% ODA identified 40.3% and 57.0% patients as HypoOSA, respectively. Compared to apnea-predominant OSA, HypoOSA was characterized by a lower arousal threshold, higher compensation and less collapsible upper airway, regardless of hypopnea criteria used. Compared with the 4% OD criterion, the 3% ODA criterion for hypopnea increased AHI by 33%, whereas the proportion of time with SpO2 < 90% and endotypic traits showed less variation. Patients with low consistency in AHI estimates between the two criteria showed lower AHI and favourable upper airway pathology compared to the high consistency group. In conclusion, HypoOSA is characterized by lower arousal threshold and favourable upper airway patency. Different hypopnea criteria resulted in variation in AHI, particularly among patients with lower AHI, whereas hypoxic burden and endotypic traits remained relatively stable.

Sleep talking (ST) is a parasomnia characterized by the utterance of unaware linguistic activations during sleep. Electrophysiological evidence is scarce, and it remains unclear whether local electroencephalographic (EEG) alterations characterize the sleep of STs outside of parasomnia episodes. Findings from NREM parasomnias suggest that local slow-wave activity (SWA) abnormalities may characterize a full night's sleep beyond behavioural manifestations. Accordingly, this study investigates SWA topography and the spatial distribution of the single SWA bins across sleep stages in a group of 12 young STs compared to 10 healthy controls (HCs) matched for sex and age, who underwent overnight laboratory polysomnographic recordings. The relationship between SWA pattern and parasomnia frequency was explored, and the overnight decline in SWA was examined to assess the potential impact of homeostatic processes. Our findings point to a peculiar SWA pattern characterized by a substantially stable central increase across sleep stages and a frontopolar decrease primarily in N2 sleep, suggesting a local and frequency-specific (≥ 1 Hz) SWA regulation in STs that may interact with homeostatic processes. These results provide new insights into the sleep electrophysiology of STs and shed light on trait-like regional alterations in SWA that may facilitate parasomnia events. Our findings align with the concept of local sleep, which posits that distinct cortical regions may simultaneously exhibit diverse functional states. In this view, different parasomnias may be characterized by specific SWA topographical patterns reflecting the peculiar behaviours enacted during sleep.

Sleep disruption is a common hallmark of posttraumatic stress disorder (PTSD), causing significant distress and often persisting after remission of other symptoms. Autonomic dysregulation is commonly comorbid and has been implicated in the underlying pathophysiology of both wake- and sleep-related symptoms following trauma. However, existing self-report tools for nightmares and trauma-related sleep disruption place relatively little emphasis on autonomic symptoms such as palpitations and sweating, limiting our ability to gauge these features quantitatively, assess their impact on sleep, and track their response to treatment. Here, we describe the initial validation of a novel exploratory 11-item self-report measure, the Seattle Trauma and Autonomic Related Sleep Symptoms (STARSS) Scale, developed to assess trauma-related sleep disruption including nightmares and autonomic hyperarousal symptoms. Psychometric validation of the STARSS was assessed in a sample of 830 healthcare workers and first responders working during the COVID-19 pandemic. The full scale (STARSS-11) positively correlated with self-report measures of symptom domains often associated with nightmares and commonly elevated following trauma exposure including PTSD (PCL-5; r = 0.76), anxiety (GAD7; r = 0.65), depression (PHQ9; r = 0.63), and insomnia (ISI; r = 0.56), and displayed strong internal consistency (α = 0.89; ω = 0.93). The STARSS-11 is well-fit by a 4-factor model: hyperarousal upon waking, trauma dream intensity, and self- and partner-reported excessive physical activity during sleep. An item-reduced STARSS-9 with 3 factors is also described. These outcomes suggest STARSS is a promising tool for the assessment of sleep disturbance related to trauma and dysautonomia in research settings.

Cerebral small vessel disease (CSVD), a disorder that affects the cerebral microvasculature, is commonly associated with aging and may contribute to dementia and stroke. Increasing evidence suggests a link between CSVD and sleep disturbances, but the association remains poorly understood. This study, part of the population-based Hamburg City Health Study, integrated portable sleep diagnostics (WatchPAT-200) with brain imaging techniques sensitive to subtle microstructural (peak-width of skeletonized mean diffusivity (PSMD)) and cortical alterations. Linear and logistic regression models were performed, accounting for demographic, sleep-related covariates, and vascular risk factors, to elucidate the importance of sleep and the maintenance of cerebral vascular health in aging. In 154 participants (63.26 ± 8.19 years, 41.56% women), sleep compositions characterised by a higher proportion of light sleep relative to deep sleep were associated with higher log-transformed PSMD and lower cortical thickness. However, REM sleep relative to non-REM sleep was not associated with log-transformed PSMD or cortical thickness, and no associations were observed between sleep-stage compositions and log-transformed white matter hyperintensity (WMH) load or log-transformed perivascular space (PVS) volume. Additionally, longer TST was associated with relevant sleep apnea. High-resolution neuroimaging, combined with home sleep monitoring, suggests an association between sleep disturbances and greater CSVD-related changes in aging. PSMD serves as a sensitive biomarker for early microstructural changes before visible damage occurs, thus supporting early detection to preserve cerebrovascular health. Given our cross-sectional study design, the exact causality requires future longitudinal studies.

Idiopathic/isolated REM sleep behaviour disorder (iRBD) is widely recognized as a key prodromal condition associated with a high risk of progression to α-synucleinopathies. Despite this, disclosure of risk related to such early signs of neurodegeneration remains controversial in clinical practice. This scoping review aims to systematically analyse literature regarding the risk disclosure, focusing on attitudes and preferences of patients as well as healthcare professionals, communication strategies used, emotional and behavioural processes that emerge pre, during and post disclosure in different settings. Results found in 8 articles show that few studies have focused specifically on risk disclosure to individuals with iRBD and that, despite its recognized importance, it has not been consistently integrated into routine clinical practice. For healthcare professionals, the main obstacles include uncertainty in formulating individualized prognoses, ethical challenges linked to the principle of beneficence and concerns about the possible emotional impact of disclosure. From the patients' viewpoint, there is a clear need for comprehensive and robust information about their condition, even though obtaining accurate and trustworthy sources can be difficult. Risk disclosure is considered essential by both patients and professionals, but a systematic step-by-step approach has yet to be implemented for people with iRBD on progression to neurodegenerative diseases.

Obstructive sleep apnoea (OSA) is common, but current diagnostic pathways rely on single-night assessment and the apnoea-hypopnoea index. Both are limited for assessment of variability and linking only weakly to symptoms, comorbidity and treatment response. The current protocol addresses this gap by aiming to validate a diagnostic pathway integrating a digital platform, mobile application, multiple-night sleep testing, semiautomated analysis and a novel sleep health questionnaire, labelled as 'Sleep Revolution'. Study objectives are to compare staff time required for diagnosis between standard care and Sleep Revolution pathway, and to examine associations between multi-night sleep metrics and Positive Airway Pressure (PAP) treatment outcomes, diagnostic concordance, PAP prescription, patient satisfaction, adherence and feasibility. This multicentre, two-arm cross-over study is conducted at 23 sleep centres in Europe within the European Sleep Apnoea Database (ESADA) network. Adults referred for suspected OSA complete both standard care and the Sleep Revolution pathway in randomised order. Standard care includes single-night polygraphy or polysomnography according to local routines. The Sleep Revolution pathway comprises three nights of self-applied polysomnography (NOX-SAS), digital symptom assessment (mobile app) and the Withings ScanWatch (physical activity, physiological signals). Diagnosis and treatment decisions are based solely on the first pathway. Outcomes include staff time (primary), technical performance, diagnostic yield, patient-reported measures, PAP adherence and symptom change. The sample size is calculated as 1000 randomised participants. Ethical approval is obtained at all participating centres. The trial is registered with ISRCTN (ISRCTN17539031). Data acquisition is performed between Q1 2024 and Q2 2025; data cleaning and analyses are ongoing.

Despite sleep's multidimensional nature, previous research has focused on correlates of individual sleep dimensions. This study aimed to characterise young children's nighttime sleep profiles based on duration, timing, latency and quality, and to examine potential correlates. Parents of 320 children aged 1-5 years across Canada completed an online questionnaire on children's nighttime sleep (duration, timing, latency, quality) and potential correlates, including child demographics and behaviours, parental demographics, bedtime routine frequency, parent-child sleep interaction (preschoolers aged 3-5 years only), parental stress and sleep environment. Latent profile analysis classified sleep profiles using age-adjusted sleep dimensions. T-tests and logistic regressions were performed, weighted for classification probabilities. For results, two profiles emerged: Sleepy Koalas (59%) and Restless Racoons (41%), with the Restless Racoons having significantly shorter sleep duration, later sleep patterns, longer sleep onset latency and poorer sleep quality compared to the Sleepy Koalas. Children from households with income above $100,000 were twice as likely to belong to the Sleepy Koalas group (OR = 2.05, 95% CI: 1.26, 3.35), compared to those from lower-income households. In preschoolers, when parent-child sleep interactions were added to the model, each one-unit increase in problematic interactions was associated with 21% lower likelihood of Sleepy Koalas membership (OR = 0.79, 95% CI: 0.72, 0.86), with differences across the interquartile range corresponding to up to a 95% reduction in odds. In conclusion, there may be sleep health disparities in young children across household income groups. Fostering high-quality parent-child sleep interactions may be important for promoting healthier sleep profiles in preschoolers.