Search Results (156)

Background: Sleep-disordered breathing (SDB) is frequently accompanied by autonomic nervous system (ANS) dysfunction, which is closely associated with an increased incidence of cardiovascular diseases and elevated mortality risk. Heart rate variability (HRV) serves as a classic metric for evaluating sympathovagal balance; however, the specific impacts of four distinct types of respiratory events—obstructive apnea (OA), central apnea (CA), mixed apnea (MA), and hypopnea (HYP)—on HRV remain underinvestigated. Utilizing ultra-short-term HRV analysis, this study aimed to evaluate the immediate effects of different respiratory events on ANS function, while further exploring the modulatory roles of arousal, Apnea–Hypopnea Index (AHI) severity and sleep stages (non-rapid eye movement [NREM] vs. rapid eye movement [REM]). Methods: A total of 108 patients with SDB undergoing overnight polysomnography (PSG) were included. A total of 19,862 respiratory events, including obstructive apnea (OA), central apnea (CA), mixed apnea (MA), and hypopnea (HYP), were analyzed using 15 s ECG segments. Linear mixed-effects models (LMMs) and estimated marginal means (EMMs) with Sidak-adjusted pairwise comparisons were constructed to evaluate differences in ECG-derived features and to analyze differences between event types. Results: Central apnea (CA) was associated with significantly reduced HRV and heart rate indices, including Standard Deviation of Successive Differences (SDSD), Root Mean Square of the Successive (RMSSD), Standard Deviation 1 (SD1), and heart rate (HR), compared with other respiratory event types (all p < 0.05). Across all event types, HRV metrics exhibited consistent dynamic changes before, during, and after respiratory events (all p < 0.001), characterized by a decrease during the event followed by post-event recovery. In the interaction effect of sleep stage, SDSD was significantly lower in CA compared with both OA (estimate = −11.67, 95% CI −18.78 to −4.59, p < 0.001) and HYP (estimate = −11.38, 95% CI −18.55 to −4.20, p < 0.001) during NREM sleep. No significant differences in HRV parameters, heart rate, or QRS duration were observed between OA and HYP (all p > 0.05). Conclusions: This study is the first to elucidate the differential impacts of four distinct types of sleep respiratory events on ultra-short-term HRV, confirming that CA events exert the most profound effects on autonomic function. These findings suggest that the proportion of CA occurrences could serve as a more precise biomarker for identifying individuals at high risk for cardiovascular diseases within the SDB population. Full article

Current diagnostic methods for OSA and CSA are costly, unreliable, and the therapeutic options are limited, with varying efficacy across patients. As the prevalence of sleep apnea and cardiovascular disease continue to rise, identifying innovative therapies through advances in biomedicine and personalized medicine has become increasingly critical. This review discusses the mechanistic links between sleep apnea and subsequent cardiovascular outcomes from a technical perspective, focusing on innovations currently applied to the diagnosis and treatment of sleep apnea, and opportunities for further advancement in the field. Full article

Background: Frequent nocturnal arousals are a core feature of comorbid insomnia and obstructive sleep apnea (COMISA), yet the underlying central mechanisms remain unclear. Identifying brain functional correlates of nocturnal awakenings may help clarify arousal-related mechanisms and inform potential interventional targets. Methods: A total of 99 participants (COMISA, insomnia alone, OSA alone, and healthy controls) underwent clinical assessments, polysomnography, and brain magnetic resonance imaging (MRI). MRI metrics were compared across groups, followed by correlation and regression analyses with the arousal index, adjusting for respiratory events and insomnia-related factors. Results: Patients with COMISA exhibited more severe insomnia symptoms, greater daytime dysfunction, and more frequent nocturnal awakenings than those with insomnia alone, although their arousal index did not differ from that of the OSA group. Patients with COMISA exhibited altered activity in the right cerebellar lobule VIII (Cerebelum_8_R), left middle temporal gyrus, and right inferior frontal gyrus, opercular part. Lower fractional amplitude of low-frequency fluctuations (fALFF) in the Cerebelum_8_R was associated with a higher arousal index. This association remained significant after controlling for insomnia severity and sleep efficiency but was attenuated after adjustment for AHI. Conclusions: Reduced functional activity in the Cerebelum_8_R was independently associated with sleep fragmentation in COMISA, independent of insomnia severity but potentially mediated by respiratory events. These findings suggest this region may be involved in arousal-related neural regulation and could represent a therapeutic target for the complex symptoms of COMISA. Trial Registration: Chinese Clinical Trial Registry, ChiCTR2500095809. Full article

Glucagon-like peptide-1 receptor agonists (GLP-1RAs) have transformed the management of type 2 diabetes and obesity, yet their actions extend beyond glycemic control and weight loss. This narrative review synthesizes current preclinical and clinical evidence examining the bidirectional relationship between glucagon-like peptide-1 (GLP-1) receptor agonists and circadian biology. A structured literature search was conducted in PubMed using combinations of the terms ‘GLP-1,’ ‘circadian,’ ‘chronobiology,’ ‘sleep,’ ‘obesity,’ and ‘type 2 diabetes’ through January 2026. Accumulating evidence indicates that GLP-1 physiology is closely coupled to circadian timing systems and sleep–wake regulation. In this narrative review, we synthesize emerging data that reframe GLP-1RAs as chronometabolic modulators, acting at the intersection of metabolism, circadian biology, and sleep. We review circadian control of GLP-1 secretion by intestinal L-cells, emphasizing the role of core clock genes and the vulnerability of incretin rhythms to circadian misalignment from shift work, nocturnal light exposure, and sleep loss. We then examine GLP-1 receptor signaling within central and peripheral clock networks, including feedback effects on hypothalamic and hepatic circadian regulation. Emerging data suggest that GLP-1 signaling is under circadian regulation and may, in turn, influence central and peripheral clock systems. Comparative discussion of semaglutide, liraglutide, and tirzepatide highlights agent-specific pharmacokinetics and emerging clinical data linking GLP-1RA therapy to sleep outcomes, particularly obstructive sleep apnea. Finally, we outline translational opportunities for chronotherapy and precision medicine, positioning GLP-1RAs as integrative tools for metabolic and sleep-related disease rather than purely weight-centric therapies. We propose that GLP-1 receptor agonists may function as chronometabolic modulators, with potential implications for personalized chronopharmacological strategies in metabolic disease. Full article

Background/Objectives: Primary aldosteronism (PA), the leading cause of secondary hypertension, results from autonomous aldosterone hypersecretion. It is characterized by increased extracellular volume, elevated cardiac output, and greater arterial stiffness compared with essential hypertension, reflecting aldosterone-mediated hemodynamic dysregulation. The prevalence and morbidity of PA are increasingly acknowledged; however, PA continues to be underdiagnosed because of limited screening and diagnostic complexity. Methods: A narrative review was conducted using PubMed (2015–2025), with terms targeting PA epidemiology, excluding treatment-focused studies. From 971 articles, 133 relevant studies (original research studies, reviews, meta-analyses) were included, addressing prevalence, risk factors, comorbidities, genetics, and diagnostic issues. Results: PA prevalence in hypertensive populations is 5–10%, rising to 17.8% in young-onset and 20–30% in resistant hypertension. Screening indications include resistant/severe hypertension, hypokalemia, adrenal incidentaloma, young-onset disease, obstructive sleep apnea (59.8% comorbidity in hypertensive PA), and familial history, while a link may exist with papillary thyroid cancer. The aldosterone–renin ratio (ARR) is the primary screening tool, limited by assay variability and confounders (e.g., sodium intake). Confirmatory testing (such as with the saline infusion test) is often challenging to perform in routine practice. Adrenal venous sampling (AVS) is useful for subtyping unilateral (aldosterone-producing adenoma; APA; ~35–50%) vs. bilateral (idiopathic hyperaldosteronism; IHA) disease, despite technical challenges. Somatic mutations (e.g., KCNJ5, more frequent in Asians) and rare familial forms drive PA. Complications include cardiovascular events (Major Adverse Cardiovascular Events; MACE: 13.6% at 5.8 years), stroke, renal impairment (decreased eGFR, proteinuria), metabolic disorders (diabetes, obesity), and novel associations (vertebral fractures, renal stones, normal-tension glaucoma). Psychiatric comorbidities (depression/anxiety in 30–70% of patients) have been associated with central mineralocorticoid receptor effects, with sleep disturbances being prominent in females. Subclinical PA predicts hypertension and arterial stiffness. Conclusion: Improved screening protocols, standardized ARR cutoffs, and advanced imaging and genetic analyses are needed to enhance PA detection. Future research should validate cost-effective screening and clarify psychiatric-metabolic links for optimized management. Full article

Background: Obstructive sleep apnea (OSA) is a major modifiable risk factor for atrial fibrillation (AF), promoting arrhythmogenesis through intermittent hypoxia, autonomic activation, and atrial remodeling. Although continuous positive airway pressure (CPAP) effectively treats OSA, real-world evidence linking objectively measured CPAP exposure to clinically relevant AF recurrence remains limited. Aims: We aimed to evaluate the association between CPAP adherence and risk of recurrent paroxysmal AF, and to compare time to first recurrence between patients with mean nightly CPAP use ≥4 h/night versus <4 h/night. Materials and Methods: In this prospective observational cohort (2017–2024), consecutive hospitalized and outpatient adults with severe obstructive sleep apnea (OSA; apnea–hypopnea index > 30 events/h) and documented paroxysmal atrial fibrillation (AF) were enrolled. Persistent and long-standing persistent AF were excluded to ensure a homogeneous population with respect to atrial substrate. OSA was assessed using home sleep apnea testing (ResMed ApneaLink), and all patients initiated continuous positive airway pressure (CPAP) therapy (ResMed AirSense 10). Objective adherence data were obtained via the ResMed AirView telemonitoring platform. Exclusion criteria included permanent AF, prior pulmonary vein isolation, central sleep apnea, left ventricular ejection fraction < 50%, end-stage chronic kidney disease (eGFR < 15 mL/min/1.73 m² or dialysis), or inability to initiate or maintain CPAP therapy. Patients were followed for 12 months. The primary endpoint was time to first documented recurrence of paroxysmal AF (≥30 s on 12-lead electrocardiography or 24-h Holter monitoring). Progression to permanent AF, defined after unsuccessful rhythm control attempts and subsequent transition to a rate control strategy, was assessed as a secondary endpoint. Time-to-event analyses used Kaplan–Meier estimates with log-rank testing, and Cox proportional hazards regression adjusted for age, body mass index, apnea–hypopnea index, heart failure, left atrial volume index, and antiarrhythmic drug therapy. Results: The final analysis included 91 patients (mean age 62.15 ± 8.29 years; 68.13% men). Mean nightly CPAP use was ≥4 h/night in 49 patients and <4 h/night in 42 patients. During follow-up, paroxysmal AF recurrence occurred in 12/49 (24.5%) patients in the ≥4 h/night group and 16/42 (38.1%) in the <4 h/night group. Mean arrhythmia-free survival at 12 months was numerically higher in the ≥4 h/night group (11.25 vs. 10.51 months), without a statistically significant difference in Kaplan–Meier curves (log-rank p = 0.11). In multivariable Cox regression, binary adherence (≥4 h/night) was not independently associated with recurrence (HR 0.52, p = 0.13), whereas mean nightly CPAP use analyzed as a continuous variable remained independently associated with delayed recurrence (per 1-h increase: HR 0.66, 95% CI 0.48–0.91, p = 0.01). Progression to permanent AF occurred in 4/49 (10.0%) versus 9/42 (17.6%) patients, respectively (p = 0.29). Conclusions: In this real-world cohort of patients with severe OSA and paroxysmal AF, higher objectively measured CPAP exposure was independently associated with delayed AF recurrence when analyzed as a continuous variable, suggesting a graded association between objectively measured CPAP exposure and AF recurrence. Larger studies with extended follow-up and continuous rhythm monitoring are warranted to confirm long-term rhythm benefits and effects on AF progression. Full article

Sleep disorders and primary headache syndromes frequently coexist, and accumulating evidence suggests that this relationship is bidirectional and biologically mediated rather than coincidental. Patients with migraine, tension-type headache, and cluster headache commonly report poor sleep quality, insomnia symptoms, and irregular sleep patterns, while individuals with sleep disorders such as insomnia, obstructive sleep apnea, restless legs syndrome, and narcolepsy experience a higher prevalence, severity, and chronification of headache disorders. This narrative review synthesizes current clinical, epidemiologic, and translational evidence supporting shared neurobiological mechanisms linking sleep and headache disorders. We focus on five major overlapping pathways: dopaminergic dysfunction, iron deficiency, hypothalamic and circadian dysregulation, central sensitization, and neuroinflammation. Evidence from population-based studies, clinical cohorts, neuroimaging, genetic research, and experimental models demonstrates that these mechanisms converge within hypothalamic, brainstem, and trigeminovascular circuits that regulate arousal, pain processing, and homeostasis. Conditions such as insomnia, obstructive sleep apnea, restless legs syndrome, and circadian disruption not only exacerbate headache burden but may act as modifiable risk factors that promote headache onset and progression. Recognizing sleep disorders as integral components of headache pathophysiology has important clinical implications, emphasizing the need for systematic sleep assessment and targeted sleep interventions as part of comprehensive headache management strategies. Full article

Pulmonary hypertension (PH) is a progressive disorder characterized by elevated pulmonary arterial pressure and the extensive remodeling of pulmonary vasculature. Chronic intermittent hypoxia (CIH), a hallmark of obstructive sleep apnea (OSA), is a well-established contributor to the pathogenesis of PH. OSA is defined by repetitive episodes of upper airway obstruction during sleep, leading to cycles of hypoxia and reoxygenation that trigger a cascade of deleterious events including oxidative stress, inflammation, endothelial dysfunction, and vascular remodeling. Growing evidence underscores the critical role of transient receptor potential canonical (TRPC) channels in mediating hypoxia-induced vascular alterations that contribute to the development of PH. TRPC channels are non-selective cation channels that regulate calcium influx in response to mechanical stimuli, pro-inflammatory cytokines, oxidative stress, and hypoxia. These channels are expressed in both pulmonary arterial smooth muscle cells (PASMCs) and pulmonary artery endothelial cells (PAECs), where they modulate key processes such as proliferation, migration, apoptosis, endothelial permeability, and vasoconstriction. Under hypoxic conditions, the upregulation of TRPC1, TRPC3, TRPC4, and TRPC6 has been implicated in dysregulation of calcium homeostasis and activation of pathological signaling pathways that contribute to increased pulmonary arterial pressure. In this review, we propose that upregulation and functional modulation of TRPC channels under CIH represents a central pathogenic mechanism linking OSA to PH. We hypothesize that TRPC1, TRPC3, TRPC4, and TRPC6 act as critical molecular effectors mediating hypoxia-driven calcium influx and downstream signaling pathways that lead to pulmonary vascular remodeling, endothelial dysfunction, and increased pulmonary arterial pressure. This framework allows us to integrate mechanistic insights from molecular, cellular, and translational studies, and to evaluate the therapeutic potential of targeting TRPC channels in OSA-associated PH. Full article

We report a thirty-six-year-old woman with intellectual disability who was referred for evaluation of suspected obstructive sleep apnea. The initial clinical impression suggested a syndromic case, so comprehensive genetic testing was undertaken. Overnight polysomnography revealed a severe rapid eye movement–predominant obstructive sleep apnea syndrome with an apnea–hypopnea index of 31.9 events per hour, rapid eye movement apnea–hypopnea index of 113.8 events per hour, and lowest oxygen saturation of 66%. Treatment with continuous positive airway pressure improved respiratory and sleep quality indices and was well tolerated. Whole-exome sequencing identified a de novo splice site variant in the pleckstrin homology domain interacting protein gene (c.41-1G > A), confirming a molecular diagnosis of Chung–Jansen Syndrome. Chung–Jansen syndrome is a rare neurodevelopmental disorder caused by heterozygous pathogenic variants in the pleckstrin homology domain interacting protein gene, marked by developmental delay, intellectual disability, behavioral abnormalities, dysmorphism, and progressive obesity. PHIP influences central and peripheral pathways controlling satiety, pancreatic function, and body weight. Despite frequent reports of sleep problems, systematic evaluation of sleep-disordered breathing has been limited. This adult case provides the first polysomnographic confirmation in the syndrome, supporting proactive screening for obstructive sleep apnea—especially in those with obesity. Integrating genetic assessment into sleep care can reduce diagnostic delays and better guide therapy and prognosis. Full article

Objectives: Unexplained syncope (US) persists despite extensive diagnostic evaluations, with autonomic dysfunction as a central mechanism. Sleep apnea (SA) may contribute through intermittent hypoxemia and autonomic imbalance. We evaluated the impact of SA treatment on syncope recurrence, nocturnal heart rate variability (HRV), and quality of life in patients with US. Methods: We conducted a prospective multicentre study in three hospitals in Galicia (Spain), including adults with US who underwent home respiratory polygraphy. SA was diagnosed according to guideline criteria, and treatment was prescribed when indicated (positive airway pressure therapy, positional therapy, and/or weight management). Symptoms, syncope burden, nocturnal heart rate variability derived from the ECG signal, and quality of life (SF-36 and a 0–100 visual analogue scale) were assessed at baseline and after 12 months. Results: Of 141 patients, 99 met treatment criteria, and 67 completed the 12-month follow-up. Mean age was 64.5 years; 59.6% were men; mean AHI was 25.9/h. After therapy, daytime sleepiness (Epworth score decreased from 8 to 5; p = 0.001), fatigue, nocturnal awakenings, and syncopal episodes decreased from 62.6% to 16.2%, 56.6% to 16.2%, and 3 to 0, respectively (all p < 0.001). HRV showed increased RR interval (p < 0.001) and RMSSD (p = 0.04). Quality of life improved in vitality (SF-36 vitality domain increased from 44 to 50; p = 0.02) and on the visual analogue scale (0–100: 50 to 70; p = 0.002). Conclusions: In this prospective cohort of patients with US and SA, therapy for SA was associated with fewer syncope recurrences, improvements in nocturnal respiratory indices, and selected heart rate variability measures, and better self-reported fatigue and vitality. Given the single-arm design and potential adherence and selection biases, these findings should be interpreted with caution and warrant confirmation in controlled studies. Full article

The interpretation and diagnosis of central sleep apnea in pediatrics by nocturnal polysomnography is challenging due to its technical complexity, which involves the simultaneous recording of multiple physiological parameters related to sleep and wakefulness. Furthermore, the unfamiliar environment of a sleep laboratory can hinder sleep evaluation, and diagnostic backlogs are common due to restricted capacity at specialist tertiary centers. The ability to undertake home sleep studies in a familiar environment using simple, robust, and low-cost technology is attractive. The potential to repurpose the PneumoWave biosensor, a UKCA Class 1 device, registered as an accelerometer-based monitoring device that is intended to capture and store chest motion data continuously over a period of time for retrospective analysis, was explored in an in vitro model of central sleep apnea. The PneumoWave system contains a biosensor (PW010), which was able to record simulated apnea episodes of 5 to 20 s across physiologically relevant pediatric breathing rates using an in vitro manikin model and manual annotation. The findings confirm that the PneumoWave biosensor could be a useful technology to support home sleep apnea testing and warrant further exploration. Full article

Background/Objectives: Obstructive sleep apnea (OSA) is often accompanied by metabolic syndrome (MetS), forming a high-risk phenotype with elevated cardiometabolic burden. The contribution of lifestyle behaviors—particularly eating mechanics and psychological eating cues—to disease severity remains unclear. This study examined independent associations of dietary behaviors and physical activity (PA) with OSA severity, sleep quality, and metabolic health. Methods: Forty-four OSA patients (mean age 38.3 ± 9.1 years; 89% male) underwent attended polysomnography, dual-energy X-ray absorptiometry, and metabolic profiling. Validated questionnaires assessed dietary behaviors, PA, and sleep quality. Hierarchical logistic regression identified predictors of MetS, severe OSA, and poor sleep quality. Results: The prevalence of MetS was 45%. Compared with those with OSA alone, participants with MetS demonstrated significantly greater central adiposity and more severe nocturnal hypoxemia, despite similar apnea–hypopnea indexes. In multivariable models, MetS was independently associated with higher body mass index (adjusted odds ratio [aOR] = 1.64; p = 0.008) and reward eating (aOR = 3.34; p = 0.041), whereas higher total PA was associated with reduced odds (aOR = 0.96; p = 0.026). Poor subjective sleep quality was significantly associated with younger age (aOR = 0.91; p = 0.037). For severe OSA, slow chewing was associated with significantly reduced odds (aOR = 0.24; p = 0.038), while emotional eating was associated with increased odds (aOR = 2.40; p = 0.048). Conclusions: This hypothesis-generating study identifies a high-risk OSA phenotype marked by metabolic dysfunction and hypoxemia. Eating speed (a proxy for mindful eating), emotional and reward-driven eating, and PA independently shape metabolic and respiratory outcomes. These findings support incorporating behavioral nutrition into multidisciplinary OSA management. Full article

Background: Sleep-disordered breathing (SDB) and intracerebral hemorrhage (ICH) share a bidirectional relationship: SDB may increase ICH risk, while ICH can induce or exacerbate SDB. However, the prevalence and characteristics of post-ICH SDB remain poorly defined. Objective: To estimate the prevalence of SDB among ICH survivors and examine associated clinical factors, including the relative burden of obstructive (OSA) versus central sleep apnea (CSA). Methods: A systematic review and meta-analysis were performed across PubMed, Scopus, CINAHL, and ClinicalTrials.gov. Studies assessing SDB in adults with ICH using American Academy of Sleep Medicine (AASM) category 1–4 diagnostic devices were included. Random-effects models estimated pooled prevalence at varying apnea–hypopnea index (AHI) thresholds, with subgroup analyses by setting, timing, geography, and diagnostic factors. Results: Seventeen studies met inclusion criteria. Pooled SDB prevalence was 85% (95% CI: 80–91%) at AHI > 5, with 49% (95% CI: 42–57%) experiencing moderate SDB (AHI > 15), and 21% (95% CI: 15–27%) experiencing severe SDB (AHI > 30). The prevalence of OSA predominated 73% (95% CI: 64% to 82%),while CSA occurred in 5% (95% CI: 2–9%), corresponding to a pooled RR of 7.44 and OR of 53.08 for OSA versus CSA. Conclusions: SDB—primarily OSA—is highly prevalent following ICH, underscoring the need for early, routine screening and intervention to improve neurological and cardiovascular outcomes. Full article

Sleep disordered breathing can cause serious health issues, yet current diagnostic methods are cumbersome and prone to error. Thoracic electrical bio-impedance (BioZ) is a promising alternative, but it remains unclear whether the measured BioZ variations reflect lung volume changes. We leverage linear reductions in lung volume during central sleep apnea (CSA) events to assess whether BioZ measurements capture changes in lungs. BioZ signals from 92 sleep studies were analyzed using linear regression to quantify their slope and linearity ($R^2$). Group differences were assessed, and a linear mixed-effects model was used to evaluate the impact of the body mass index (BMI), gender, and sleeping position. Welch’s ANOVA showed significant differences between CSA and breathing segments. A chi-squared analysis showed that CSA events were more likely to exhibit negative slopes. The mixed-effects model found no BMI or gender effects, but the supine posture was significantly associated with more negative linear trends. These findings indicate that BioZ captures lung volume changes and that the sleeping position significantly modulates how clearly these changes appear in the signal. Full article

Background and Objective: Lennox–Gastaut syndrome (LGS) is a severe developmental and epileptic encephalopathy characterized by multiple seizure types, distinctive electroencephalography (EEG) abnormalities, and cognitive impairment. Sleep disturbances are highly prevalent in LGS and contribute substantially to reduced quality of life. However, no comprehensive analysis has yet been conducted to systematically examine key aspects of sleep—including architecture, microstructure, sleep-disordered breathing, and circadian regulation—leaving critical knowledge gaps. To address this, we conducted a scoping review to map the current evidence on sleep abnormalities in LGS and to identify priorities for future research. Method: A scoping review was conducted following PRISMA-ScR guidelines. PubMed, Embase, Ovid, and ClinicalTrials.gov from inception to October 2025 for studies evaluating sleep parameters in individuals with LGS or mixed epilepsy cohorts with ≥50% LGS cases. Eligible designs included observational and interventional studies using polysomnography, video-EEG, actigraphy, or sleep questionnaires. Data were synthesized narratively due to heterogeneity, and methodological quality was assessed using relevant Joanna Briggs Institute (JBI) checklists. Results: After screening 1242 articles, eleven studies met inclusion criteria, spanning 1986–2025 and conducted across four continents. Most were small single-center observational studies (5–16 LGS participants) using polysomnography as the primary assessment, with others employing wearable monitoring, surface and intracranial EEG, or circadian biomarker analyses. Across studies, individuals with LGS demonstrated markedly disrupted sleep architecture—notably reduced or absent rapid eye movement (REM) sleep, fragmented non-rapid eye movement (NREM) sleep, and attenuated spindles. Microstructural analysis showed elevated cyclic alternating pattern (CAP) rates, with epileptiform discharges clustering in CAP phase A. Sleep-disordered breathing (SDB) was common, particularly in adults, and associated with tonic seizures and central apneas. Circadian rhythm dysregulation, including altered melatonin and cortisol profiles, was also reported. A feasibility study demonstrated that home-based wearable devices and sleep apnea monitors were both acceptable and practical for use in children with LGS. No interventional studies have evaluated whether addressing sleep abnormalities modifies seizure or cognitive outcomes. Interpretation: Sleep in LGS is profoundly disrupted at both macrostructural and microstructural levels. These abnormalities may exacerbate seizure burden, cognitive impairment, and SUDEP risk, representing a potentially modifiable contributor to disease severity. Larger, prospective studies integrating polysomnography, wearable monitoring, and interventional approaches are needed to clarify causal mechanisms and therapeutic potential. Full article