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Obstructive sleep apnea represents a common disorder with potentially high morbidity and mortality. Its clinical significance and treatment options have not been fully defined. Excessive daytime sleepiness and the cardiovascular complications of obstructive sleep apnea constitute a significant public health problem. Clinical features and treatment are discussed.
Obstructive sleep apnea syndrome (OSAS) is the most common organic disorder of excessive daytime somnolence. In cross-sectional studies the minimum prevalence of OSAS among adult men is about one per cent. Prevalence is highest among men aged 40-65 years. The highest figures for this age group indicate that their prevalence of clinically significant OSAS may be 8.5% or higher. Habitual snoring is the most common symptom of OSAS (70-95%). The most significant risk factor for OSAS is obesity, especially upper body obesity. Other risk factors for snoring, and for OSAS, are male gender, age between 40 and 65 years, cigarette smoking, use of alcohol, and poor physical fitness. Upper airway obstruction with snoring or sleep apnea are commonly seen in children of all ages. Snoring is very common among infants and children with Pierre Robin syndrome and among infants with nasal obstruction. Snoring and obstructive sleep apnea are also very common in men with acromegaly. Many other syndromes or diseases exist in which the upper airway is narrowed. Prevalence of snoring and sleep apnea is increased in all such situations. It has been suggested that sleep apnea may be one mechanism contributing to sleep-related mortality. The prevalence of every night snoring seems to decrease after the age of 65. However, more than 25% of persons over 65 have more than five apneas per hour of sleep. It remains to be seen whether this finding has clinical significance. Partial upper airway obstruction, even without apneas, may influence pulmonary arterial pressure and may cause daytime sleepiness and some health consequences.(ABSTRACT TRUNCATED AT 250 WORDS)
BACKGROUND: Obstructive Sleep Apnea (OSA) is a common chronic disease that affects more than 20% of the adult population. One of the most frequent and characteristic symptoms of OSA is excessive daytime sleepiness (EDS). This symptom is typically treated in patients with OSA with the application of continuous positive airway pressure (CPAP), the gold-standard treatment for this disease. In some patients who are adequately treated with CPAP, residual excessive daytime sleepiness (REDS) persists. The prevalence, associations, and outcomes associated with REDS remain poorly understood. METHODS: Multicenter, prospective, observational cohort study including 1000 patients. Participants will undergo a sleep study for the diagnosis of obstructive sleep apnea (OSA), 24-h ambulatory blood pressure monitoring, clinical assessment, quality-of-life questionnaires, Epworth Sleepiness Scale, and collection of biochemical variables and biological samples. Patients with OSA will receive standard care, and those prescribed continuous positive airway pressure (CPAP) will be monitored for treatment adherence. OSA patients will be assessed at baseline and at 6, 12, and 24 months. DISSCUSION: We aim to establish a prospective observational cohort of patients with obstructive sleep apnea (OSA) treated with CPAP, with and without REDS. The HYPNOSA project will create the largest available registry of patients with OSA and REDS using real-world data, providing accurate prevalence estimates and long-term outcomes. Biological samples will be analyzed to assess the role of specific biomarkers. TRIAL REGISTRATION: Registered at ClinicalTrials.gov. Identifer: NCT06514482.
Obstructive sleep apnea, a sleep disorder, is becoming more prevalent and requires prompt and effective treatment by the dental and medical specialties. Conservative treatment modalities (ie, intraoral devices that prevent or minimize airway obstruction by the tongue) are recommended for treating mild to moderate forms of OSA. This article describes a simplified technique for fabricating an intraoral OSA prosthesis.
Obstructive sleep apnea may contribute to the development of pulmonary hypertension and RVF primarily through pulmonary vasoconstriction secondary to hypoxia. Several recent studies indicate, however, that intermittent apnea-related hypoxia is not sufficient to cause sustained pulmonary hypertension. These studies have been consistent in showing that pulmonary hypertension and RVF are almost invariably seen in the presence of diurnal hypoxia. Sustained pulmonary hypertension, therefore, appears to be associated with sustained hypoxia as is the case in COPD. Patients with OSA who have hypoxia while awake are, as a rule, obese and have mild-to-moderate diffuse obstructive airways disease. Thus, most cases of pulmonary hypertension in association with OSA result from a combination of OSA, obesity, and diffuse obstructive airways disease, a so-called overlap syndrome. However, from the therapeutic viewpoint, it is apparent that treatment of OSA by NCPAP or tracheostomy, in such cases, is usually sufficient to reverse pulmonary hypertension and RVF. More recent work has provided strong evidence that OSA can play a role in the pathogenesis of LV heart failure in patients with CHF of otherwise unknown etiology. It is likely that this occurs through a combination of increased LV afterload related to exaggerated negative Pit swings during obstructive apneas, to intermittent hypoxia, and to chronically elevated sympathoadrenal activity. Reversal of OSA by NCPAP in these patients may relieve LV heart failure. These findings add a new dimension to our understanding of the pathophysiologic effects of OSA on the cardiovascular system by demonstrating that the LV is a structure that may suffer functional impairment secondary to the stresses imposed by OSA. Finally, it has now become apparent that CSR in patients with CHF can cause symptoms of a sleep apnea syndrome when associated with intermittent hypoxia and arousals from sleep. Reversal of CSR during sleep by NCPAP can lead to alleviation of these symptoms and possibly to reduced cardiac dyspnea and LV systolic function as well. Taken together, this suggests that much more extensive use of polysomnography may be warranted in the investigation of cardiovascular disease. The reasons are compelling: sleep apnea disorders are common and eminently treatable conditions whose reversal can result in improved right and left heart function and symptomatic improvement in patients with impaired myocardial function.
Obstructive sleep apnea syndrome (OSAS) and heavy snoring during sleep, without sleep apnea, has been well described in children and adults. We report a case series of 25 full-term infants, prospectively obtained from a database of nearly 700 "apparent life-threatening event" (ALTE) cases, who presented between 3 weeks and 4 1/2 months of age an ALTE and who progressively developed more florid symptomatology and polygraphic findings. All of them were classified as OSAS patients by five years of age. These index cases are compared with two other ALTE infant groups followed in parallel during the first year of life but whose symptoms were short-lived. The index cases presented more frequently a positive family history of OSAS and an early report of snoring or noisy breathing during sleep. Usage of an esophageal balloon to monitor esophageal pressure (Pes) and usage of nasal continuous positive airway pressure (CPAP) as a test may help in the early recognition of these infants, who appear to make more effort to breathe during sleep, based on the indirect evidence of Pes measurements. It is suggested that anatomic features, including a small posterior airway space leading to an abnormal degree of upper airway resistance, may be the cause of the symptoms presented by these infants. Considering the parental anxiety generated by persistence of symptoms after the first year of life in ALTE infants, recognition of this subgroup is important.
Sleep obstructive apnea syndrome (SOAS) is a common condition with a strong male predominance. Its incidence is more than 1 percent in the population as a whole. It exists in snorers. Both snoring and SOAS are linked to the presence of abnormalities (congenital or acquired) of the upper respiratory tract. The nocturnal cardiovascular consequences of SOAS are directly linked to apnea. Bradycardia occurs during apnea and tachycardia when ventilation restarts. Paroxysmal nocturnal hypertension is a constant feature. Even in individuals who are normotensive during the day, each restarting of ventilation is accompanied by peaking of blood pressure. The pulmonary artery pressure curve follows that of systemic blood pressure. Complications begin when SOAS has been present for several years: 1) Chronic: permanent systemic hypertension is common (56 percent of SOAS). It is often refractory to antihypertensive treatment. 2) Acute: the onset of myocardial infarction and of cerebrovascular accidents explains the heavy mortality of SOAS (37 percent at 8 years in untreated individuals with a number of episodes of apnea exceeding 20 per hour of sleep). Other acute complications are less common: acute pulmonary edema, nocturnal sudden death. These events may be prevented by treatment suppressing apnea: actuarial survival curves are then superimposable upon those of the population as a whole. Thus SOAS is a cardiovascular risk factor which is remarkably reversible by specific treatment, though which most often passes unrecognized.
BACKGROUND: Obstructive sleep apnea (OSA) is highly prevalent but remains substantially underdiagnosed. Polysomnography (PSG) is the reference standard, but its cost and limited availability constrain large-scale case identification. AI-based screening tools may support risk stratification and referral prioritization, but their diagnostic accuracy across apnea-hypopnea index (AHI) thresholds remains uncertain. OBJECTIVE: This review aimed to systematically evaluate the diagnostic accuracy of AI-based OSA screening tools at AHI thresholds of ≥5, ≥15, and ≥30 events/hour, with emphasis on models using non-PSG-derived inputs. METHODS: PubMed, Embase, Scopus, and Web of Science were searched for studies published from January 1, 2016, to May 3, 2026. Eligible studies included adults evaluated for suspected OSA or recruited from population-based cohorts, assessed AI-based models intended or interpretable for OSA screening, risk prediction, or screening-oriented severity classification, used PSG as the reference standard, and reported sufficient data to construct or reconstruct 2×2 contingency tables. Diagnostic accuracy was synthesized separately by AHI threshold and input source using bivariate random-effects models, with 95% CIs and prediction intervals (PIs). Risk of bias and certainty of evidence were assessed using QUADAS-2 (Quality Assessment of Diagnostic Accuracy Studies 2) and GRADE (Grading of Recommendations Assessment, Development, and Evaluation), respectively. RESULTS: A total of 60 studies were included, of which 47 contributed data to the meta-analysis. At AHI thresholds of ≥5, ≥15, and ≥30 events/hour, pooled sensitivities were 0.94 (95% CI 0.92-0.96; 95% PI 0.71-0.99), 0.87 (95% CI 0.84-0.89; 95% PI 0.66-0.96), and 0.83 (95% CI 0.79-0.87; 95% PI 0.61-0.94), respectively; the corresponding specificities were 0.77 (95% CI 0.69-0.84; 95% PI 0.30-0.96), 0.81 (95% CI 0.75-0.85; 95% PI 0.39-0.96), and 0.91 (95% CI 0.87-0.94; 95% PI 0.55-0.99), respectively. The corresponding areas under the summary receiver operating characteristic curves were 0.943, 0.907, and 0.920. For non-PSG-derived tools, sensitivities were 0.92, 0.85, and 0.81, and specificities were 0.70, 0.74, and 0.85 at the 3 thresholds, respectively. For PSG-derived models, sensitivities were 0.96, 0.90, and 0.85, and specificities were 0.82, 0.88, and 0.96, respectively. Exploratory subgroup analyses suggested performance variation across selected study and model characteristics, including region, algorithmic framework, data source, and validation method. CONCLUSIONS: AI-based tools showed generally favorable screening performance for OSA across clinically relevant AHI thresholds, although wide PIs suggest variable performance across future comparable populations and settings. By synthesizing diagnostic accuracy across 3 AHI thresholds and distinguishing non-PSG-derived from PSG-derived models, this review extends previous broad or modality-specific reviews and offers a clinically interpretable, pathway-specific basis for linking model performance to intended use. The findings may clarify potential roles for non-PSG-derived tools in front-end screening and referral prioritization and for PSG-derived models in reduced-channel assessment and sleep-laboratory workflow support. Given substantial heterogeneity, limited external validation, and low or very low certainty of evidence, prospective validation is needed before routine implementation.
BACKGROUND: The verification of the results of weight loss as a therapy in the obstructive apnea sleep syndrome (OSAS) is reported given the scarcity of bibliography concerning the same, despite most patients being obese. METHODS: One hundred thirty-five patients fulfilling the polysomnographic requisites of OSAS and who had lost more that 50% of their excess weight limit with a diet of 1,000 kcal/day as their only therapy were studied. Two groups of patients were established; the first being made up of 89 obese patients (excess weight greater than 15%) and the second 46 non obese patients. Polysomnography was performed prior to and following the diet and the apnea hypopnea index (AHI) were compared with the diminution being related to the loss of weight. RESULTS: The 89 obese patients had a mean excess of weight of 35% (+/- 20) and an AHI of 64 (+/- 24). Following the loss of weight the same were 11% (+/- 14) and 34 (+/- 28) respectively (p less than 0.001). The 46 non obese patients had an initial medium excess of weight of 9% (+/- 6) and an AHI of 45 (+/- 21) with the same being 1% (+/- 2) and 28 (+/- 26) (p less than 0.001) following the diet. A cure was achieved (AHI less than 10) in 29 cases (33%) in the obese group and in 19 (41%) in the non obese group. CONCLUSIONS: The efficacy of weight loss in the treatment of patients with OSAS is confirmed. Although the percentages of cure may seem low the innocuousness of this therapeutic method is recommended as an initial measure prior to the decision of surgery.
STUDY OBJECTIVES: To evaluate the effect of daridorexant on nighttime respiratory function and sleep in adults with severe obstructive sleep apnea (OSA) without insomnia. MATERIALS AND METHODS: This randomized, double-blind, placebo-controlled, two-period, crossover trial was conducted at a single sleep center in 16 adults (≥18 years) with severe OSA without insomnia. In each period, daridorexant 50 mg or placebo was administered every evening for 5 days. Primary and secondary endpoints were the treatment differences (daridorexant-placebo) for apnea/hypopnea index (AHI) and oxygen saturation (SpO2) during total sleep time (TST), respectively, after last dosing. A mean increase in AHI ≥10 events/h and mean decrease in nocturnal SpO2 ≤-2% were the minimum changes considered to be clinically meaningful negative effects. Other endpoints included TST, latency to persistent sleep (LPS), and wake after sleep onset (WASO). RESULTS: Mean baseline AHI was 51.2 events/h (range 30.8, 82.2) and mean SpO2 during TST was 92.1% (range 88.5, 94.3). No clinically meaningful effect of daridorexant on AHI or SpO2 during TST was detected. Treatment differences were -3.7 events/h (one-sided 95% CI ≤ +4.2) and - 0.12 % (one-sided 95% CI ≥ -0.6), respectively. Compared with placebo, daridorexant increased TST by 32.5 min (90% CI: 6.9, 58.2), associated with shorter LPS (-10.3 min [90% CI: -20.6, -0.02]) and a trend towards reduced WASO (-15.2 min [-31.2, 0.9]). Four adverse events were reported (daridorexant n = 3; placebo n = 1), all of mild intensity and none related to respiratory function. CONCLUSION: Short-term treatment with daridorexant does not impair sleep-disordered breathing and may improve sleep in patients with severe OSA. CLINICAL TRIAL: ClinicalTrials.gov, https://clinicaltrials.gov/study/NCT05458193, NCT05458193. Statement of Significance Obstructive sleep apnea (OSA) is highly prevalent and associated, in 30%-50% of cases, with insomnia-related symptoms, yet the safety of insomnia medications in OSA remains unclear. Daridorexant, a dual orexin receptor antagonist for the treatment of adults with insomnia disorder, previously showed no negative effect on sleep-disordered breathing in participants with mild/moderate OSA. This randomized, double-blind, placebo-controlled, crossover trial evaluates daridorexant 50 mg (maximum therapeutic dose) in participants with severe OSA without insomnia. Repeated dosing (5 nights) did not impair nighttime respiratory function, as assessed by apnea/hypopnea index and nocturnal oxygen saturation. Moreover, improvements in sleep characteristics were observed with daridorexant, extending evidence that daridorexant 50 mg is safe and well-tolerated and may improve sleep in adults with severe OSA.
Patients with obstructive sleep apnea (OSA) syndrome are known to exhibit nocturnal natriuresis/diuresis. We studied plasma and urinary levels of atrial natriuretic peptide (ANP), a potent natriuretic hormone released from the heart, and plasma antidiuretic hormone (ADH) levels in patients with OSA during awake and sleeping periods, to compare with those of normal subjects. Seven patients with OSA and 6 normal subjects were studied. Arterial blood samples were drawn during the awake and the sleeping period, while in patients with OSA, blood samples were obtained during the apneic period. Urine samples were collected over two 12-hour periods (9 a.m.-9 p.m. and 9 p.m.-9 a.m.) In patients with OSA, plasma ANP as well as urinary ANP excretion increased during the apneic period compared with the awake period. There was a significant negative correlation between plasma levels of ANP and ADH in patients with OSA. On the other hand, normal subjects had no apparent differences in plasma and urinary ANP levels between the two periods. It is suggested that nocturnal increase in ANP and decrease in ADH are responsible for the nocturnal diuresis and natriuresis associated with OSA.
Obstructive sleep apnea syndrome (OSAS) is associated with severe cardiac arrhythmias and conduction abnormalities. Cor pulmonale and right-sided heart failure may ensue. Uvulopalatopharyngoplasty (UPPP) is one of several treatment modalities suggested for OSAS. Tracheotomy and CPAP treatment in adult OSAS patients and adenotonsillectomy in children with OSAS were shown to lead to improvement in some cardiac parameters. Cardiac function was prospectively evaluated in 19 OSAS patients before and after UPPP. No significant changes after surgery were noted on electrocardiographic studies. Improvement in global and regional function of both ventricles was seen in 91% of the patients. A trend toward significant elevation in left ventricular ejection fraction and a statistically significant increase in right ventricular ejection fraction were observed (45% +/- 9% to 50% +/- 7% [p = 0.007]). Our results support performance of UPPP in selected OSAS patients for relief of potentially life-threatening cardiac pathologies.
Although obstructive sleep apnea (OSA) occurs in the pediatric population, diagnostic criteria have not been established. Since criteria for adult OSA are well established, we asked whether commonly used adult criteria, such as the apnea index (based on the number of obstructive apnea [OA] events per hour), would identify children with serious sleep-related upper airway obstruction. Polysomnographic data were analyzed from 20 children (ages 8 months to 16 yr) with clinical evidence of upper airway obstruction during sleep (loud snoring and labored breathing) and who had cyclic oscillations of oxyhemoglobin saturation (SaO2) during sleep. The overnight studies included sleep state (EEG, EOG, and EMG), SaO2, ECG, nasal (end-tidal CO2) and oral (thermistor) airflow, chest and abdominal movement (inductance plethysmography), and video camera and behavioral observations. Measurements included the number of obstructive events > or = 10 s, the number of desaturations (> or = 5% decrease lasting > or = 5 s), the number of desaturation episodes to < 90%, < 85%, and < 80% lasting > 5 s, and the percentage of sleep time with SaO2 values < 90%. Gas exchange was impaired as evidenced by cyclic decreases in SaO2 and elevated PETCO2 values (maximum value 58 +/- 6 mm Hg). The children experienced 175 +/- 168 (range 6 to 609) episodes of decreased SaO2 > 5%, with an average minimum SaO2 of 66 +/- 13% (range 30 to 85%). The average number of apnea events was only 1.9 +/- 3.2 events/h (range 0 to 10.4).(ABSTRACT TRUNCATED AT 250 WORDS)
Healthcare contributes significantly to global greenhouse gas (GHG) emissions, yet the environmental impact of sleep medicine, particularly the diagnosis and therapy of obstructive sleep apnea (OSA), remains poorly characterized. We systematically searched PubMed, Scopus, and Embase (2015-2025) for studies on OSA care reporting environmental metrics (carbon footprint, energy use, resource consumption) or healthcare resource utilization. Supplementary searches identified additional non-peer-reviewed sustainability-focused studies that have been presented at conferences. Of 19 primary peer-reviewed studies on OSA care and utilization, only one reported environmental metrics (telemedicine CO2 savings related to reduction in travel-related emissions). Supplementary sources revealed that OSA care has a measurable carbon footprint driven by disposable equipment, device electricity, and travel and that OSA diagnostics create significant solid waste with opportunities for waste reduction through the use of reusable equipment. This review shows that while the environmental impact of sleep medicine has been rarely studied to this date, available evidence suggests significant opportunities for sustainability through virtual care, home testing, and equipment optimization. Future research should incorporate environmental impact into the assessment of clinical pathways.
A retrospective study of pediatric patients with obstructive sleep apnea who underwent adenotonsillectomy between 1987 and 1990 was undertaken to determine the frequency of postoperative respiratory compromise and to determine if risk factors for its development could be identified. Sixty-nine patients less than 18 years old had polysomnographically documented obstructive sleep apnea and were observed postoperatively in the pediatric intensive care unit. Of these, 16 (23%) had severe respiratory compromise, defined as intermittent or continuous oxygen saturation of 70% or less, and/or hypercapnia, requiring intervention. Compared with patients without respiratory compromise, these patients were younger (3.4 +/- 4 vs 6.1 +/- 4 years) and had more obstructive events per hour of sleep on the polysomnogram (49 +/- 41 vs 19 +/- 30). They were more likely to weight less than the fifth percentile for age (odds ratio [OR], 5.1; 95% confidence interval [CI], 1.4 to 18.7), to have an abnormal electrocardiogram and/or echocardiogram (OR, 4.5; 95% CI, 1.3 to 15.1), and to have a craniofacial abnormality (OR, 6.2; 95% CI, 1.5 to 26). Multiple logistic regression analysis revealed the most significant risk factors were age below 3 years and an obstructive event index greater than 10. Children with obstructive sleep apnea are at risk for respiratory compromise following adenotonsillectomy; young age and severe sleep-related upper airway obstruction significantly increase this risk. We recommend in-hospital postoperative monitoring for children undergoing adenotonsillectomy for obstructive sleep apnea.
BACKGROUND: Obstructive sleep apnea (OSA) promotes endothelial activation and a prothrombotic milieu through intermittent hypoxia, oxidative stress, and systemic inflammation, mechanisms closely linked to atherosclerosis progression. The vascular effects of continuous positive airway pressure (CPAP) therapy in patients with established coronary artery disease (CAD) remain incompletely understood. OBJECTIVE: To evaluate the longitudinal effects of CPAP treatment on endothelial adhesion molecules and fibrinolytic balance in patients with CAD and OSA. METHODS: In this randomized controlled analysis from the RICCADSA trial, 210 revascularized CAD patients with moderate-to-severe OSA were assigned to CPAP (n = 104) or no-CPAP (n = 106) and had available biomarker measurements at baseline and 12 months. Circulating intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and plasminogen activator inhibitor-1 (PAI-1) were assessed. Linear mixed-effects models were used to examine longitudinal changes and time-by-treatment interactions adjusted for cardiometabolic covariates. RESULTS: For ICAM-1, no significant time-by-treatment interaction was observed. For PAI-1, a borderline time-by-treatment interaction suggested a numerically smaller increase in the CPAP group compared with no-CPAP (p = 0.09). CPAP treatment was associated with a significantly greater reduction in VCAM-1 over time compared with no-CPAP (time-by-treatment interaction p = 0.045 in adjusted models). CONCLUSIONS: CPAP treatment was associated with selective modulation of vascular biomarkers in patients with CAD and OSA, characterized by attenuation of endothelial activation reflected by reduced VCAM-1 levels, while fibrinolytic imbalance appeared largely resistant to intervention. These findings support pathway-specific vascular responses to CPAP and provide mechanistic insight into residual atherosclerotic risk in this high-risk population.
Two sons and their father had severe hypersomnolence and obstructive sleep apnea. A third son, although asymptomatic, was shown to have upper-airway obstruction during sleep. Electromyographic recordings of genioglossus activity in the two symptomatic sons revealed loss of tonic activity in early stages of sleep at times when sleep apnea occurred. The asymptomatic son showed loss of tonic activity during rapid-eye-movement sleep, the sleep period when upper-airway obstruction occurred. Two sudden deaths occurred in this family. A 30-year-old brother died at home while asleep, and a child of the asymptomatic brother died at the age of four months from presumed sudden-infant-death syndrome. Obstructive sleep apnea may have a familial basis; the tongue may be involved in the genesis of upper-airway obstruction during sleep.
BACKGROUND: Obstructive sleep apnea is common, but its long-term association with site-specific cancers remains unclear. In this study, we examined 15-year risks of site-specific cancers in people with obstructive sleep apnea compared with the general population and to people with overweight or obesity. METHODS: We conducted a nationwide population-based cohort study using Danish registries, 1995-2021. People diagnosed with obstructive sleep apnea were compared with the general population and to people with overweight or obesity. Adjusted (weighted) 15-year risks, risk differences, and risk ratios (RRs) were estimated using the Aalen-Johansen estimator. Confounding was addressed using standardized morbidity ratio weighting. RESULTS: The study included 114,264 people with obstructive sleep apnea, 115,497 members of the general population, and 113,034 with overweight or obesity. After weighting, the distributions of sex (74% male), age (median 53 years), and comorbidities were comparable across the three cohorts. Obstructive sleep apnea was associated with an increased risk of cancers of the brain (adjusted 15-year risk: 5.78 vs. 3.61 per 1,000 persons; aRR 1.60 [95% CI 1.43-1.78]) and spinal cord (1.65 vs. 1.17 per 1,000 persons; aRR 1.41 [95% CI 1.16-1.72]) compared with the general population. Associations persisted when the obstructive sleep apnea cohort was compared with those with overweight or obesity. No associations were observed for other site-specific cancers. CONCLUSION: Obstructive sleep apnea was associated with an increased risk of brain and spinal cord cancers. These findings highlight the importance of effective prevention of obstructive sleep apnea and the need for further research on treatment.