Background Prespecified outcomes form the foundation of clinical trial validity. Despite federal registration requirements under the FDAAA Final Rule, discrepancies between registered and published outcomes remain common across medical fields. The extent of outcome modifications in interventional sleep disorder trials has not been systematically examined using registry version histories. Methods We conducted a cross-sectional registry-publication comparison of 54 interventional sleep disorder trials registered on ClinicalTrials.gov between January 2017 and December 2024. Using the platform's “History of Changes” tool, we compared earliest and most recent registry versions to identify outcome modifications. Changes were classified as high, moderate, or low impact. Corresponding publications were reviewed to assess disclosure. Predictors of modification were evaluated using Firth penalized logistic regression. Results Substantive outcome modifications were present in 94.4% of trials, with a median of five modifications per trial. High-impact modifications affecting primary outcomes occurred in 48.1% of trials. Changes most frequently involved clarification or increased specification (61.1%), outcome additions (57.4%), and removals (40.7%). The majority of modifications occurred after primary completion (60.8%) or publication (37.3%). Disclosure was rare: 3.9% of trials acknowledged modifications in the registry and 5.9% in the corresponding publication. Industry funding was associated with lower odds of high-impact modification (OR 0.2, 95% CI 0.0-0.7; p = 0.01) Conclusions Outcome modifications are nearly universal in sleep disorder trials and are rarely disclosed. Strengthening preregistration practices, editorial oversight, and registry transparency may improve the reliability of the sleep medicine evidence base.
Objectives Motor vehicle accident (MVA) risk is greater in patients with obstructive sleep apnea (OSA), yet the functional domains most closely linked to driving-related impairment remain incompletely understood. This exploratory pilot study aimed to perform an integrated assessment of driving performance, eye movements, vigilance, and cognitive function in OSA and to examine their relationships with disease severity and treatment response. Methods Adult drivers with suspected OSA underwent assessment using a driving simulator, Psychomotor Vigilance Test (PVT), eye-tracking, and the Cambridge Neuropsychological Test Automated Battery (CANTAB). Participants with moderate-to-severe OSA (apnea–hypopnea index ≥20) who initiated continuous positive airway pressure (CPAP) therapy underwent re-evaluation after 6–12 months. Results At baseline, single-task reaction time in the driving simulator was positively correlated with apnea severity. In contrast, response accuracy under multitask plus steering conditions was associated with nocturnal hypoxemia (T90), suggesting differential contributions of apnea frequency and oxygen desaturation to driving performance. Eye-tracking parameters, including saccade amplitude and fixation duration, were significantly correlated with both driving performance and spatial working memory error scores. Following CPAP therapy, simple reaction times improved in both the driving simulator and PVT, whereas changes in multitasking performance and CANTAB measures were not statistically significant. Conclusions Basic psychomotor speed was associated with OSA severity and improved following CPAP therapy, suggesting within-subject improvement of vigilance-dependent processes. In contrast, integrated oculomotor and executive function measures were more closely linked to complex driving performance, indicating that multidomain assessment may better characterize driving-related impairment in OSA. These findings provide preliminary evidence to guide future hypothesis-driven studies.
Sexual dysfunction (SD) is common in patients with obstructive sleep apnoea (OSA). Although continuous positive airway pressure (CPAP) therapy improves SD, it does not consistently modify testosterone or estradiol levels, suggesting involvement of other hormonal pathways. We analysed sex hormone levels in 70 patients with OSA before and after two weeks of CPAP withdrawal. No statistically significant treatment effects were observed for testosterone, androstenedione, gestagens, dehydroepiandrosterone sulfate, luteinizing hormone or follicle-stimulating hormone, whereas dehydroepiandrosterone (DHEA) increased after CPAP withdrawal. As DHEA secretion is adrenocorticotropic hormone-responsive, this increase may point to stress-related mechanisms, rather than direct sex steroid-mediated pathways, as potential contributors to OSA-related SD.
Introduction Sleep-disordered breathing (SDB) is frequently observed in patients with pulmonary hypertension (PH) and may contribute to disease progression through recurrent nocturnal hypoxemia. However, data comparing SDB characteristics between Group 1 pulmonary arterial hypertension (PAH) and Group 4 chronic thromboembolic pulmonary hypertension (CTEPH) remain limited. Methods This cross-sectional study included 51 patients with stable precapillary PH (24 Group 1 PAH and 27 Group 4 CTEPH). Demographic characteristics, clinical findings, laboratory parameters, polysomnographic data, and right heart catheterization measurements were evaluated. All patients underwent overnight polysomnography. Statistical analyses were performed using SPSS version 25.0. Results The mean age of the study population was 55 years, and 66.7% were female. Obstructive sleep apnea syndrome (OSAS) was identified in 88.2% of patients. Nocturnal desaturation was observed in 60% of the cohort. The mean oxygen desaturation index (ODI) was 22.45 ± 20.24 events/hour among patients with OSAS and 2.82 ± 2.59 events/hour among those without OSAS. Severe OSAS was present in 55.6% of OSAS patients. Group 4 patients demonstrated significantly higher total apnea-hypopnea index (AHI) values than Group 1 patients (29.16 ± 24.37 vs. 17.65 ± 14.87 events/hour, p = 0.045). No significant differences were observed in most hemodynamic parameters according to OSAS status. Conclusions Sleep-disordered breathing is highly prevalent in patients with precapillary pulmonary hypertension. OSAS and nocturnal hypoxemia were common findings, particularly among Group 4 patients. Routine polysomnographic evaluation may facilitate early identification and appropriate management of sleep-disordered breathing in this population
Background Narcolepsy is a chronic disorder of central hypersomnia that is frequently under-recognized. Diagnostic delay, comorbid sleep-disordered breathing (SDB), and psychiatric comorbidities are well described internationally but remain poorly characterized in Saudi Arabia. Methods We retrospectively reviewed all consecutive adult patients diagnosed with narcolepsy at the sleep disorders center of King Fahad Medical City (KFMC), a tertiary referral hospital in Riyadh, between January 2015 and April 2026. Diagnosis followed the third edition of the International Classification of Sleep Disorders (ICSD-3). Patients were classified as narcolepsy type 1 (NT1) when cataplexy was present and as narcolepsy type 2 (NT2) when MSLT criteria were met without cataplexy. Sleep breathing disorders and psychiatric conditions were assessed in all patients. Diagnostic delay was defined as the interval between patient-reported symptom onset and the year of formal diagnosis. Predictors of any sleep-disordered breathing (any-SDB: apnea–hypopnea index ≥ 5/h or REM-related OSA) and of diagnostic delay were examined with multivariable logistic and linear regression; the linear regression for diagnostic delay was performed on the natural-logarithm-transformed delay (log[delay + 1]) to satisfy the normality assumption. Cerebrospinal fluid hypocretin testing was not performed. Results A total of 113 patients were analyzed (65 NT1 [57.5 %] and 48 NT2 [42.5 %]; 39 women [34.5 %]; median age 27 years [IQR 20–34]). Median body mass index (BMI) was 29.0 kg/m2 (IQR 24.9–34.0). Median diagnostic delay was 5 years (IQR 2–10; range 0–28) and increased with age (Kruskal–Wallis H = 10.7, p = 0.030; Pearson r with age = 0.43, p < 0.001). Any-SDB was present in 52/113 (46.0 %); REM-related OSA in 46/110 (40.7 %). After adjustment for narcolepsy type, BMI, and Epworth Sleepiness Scale (ESS), female sex was independently less at risk for any-SDB (adjusted odds ratio [aOR] 0.34, 95 % CI 0.13–0.88, p = 0.026) and older age conferred increased risk (aOR 1.06 per year, 95 % CI 1.01–1.11, p = 0.023). In the multivariable linear model for log-transformed diagnostic delay (adjusted R2 = 0.119), age was the only independent predictor (β = +0.020 per year on the log scale, equivalent to a 2.0 % increase in delay per year of age; 95 % CI +0.002 to +0.038, p = 0.032). ESS independently predicted dichotomized delayed diagnosis (≥ 5 years) (aOR 1.15 per ESS point, 95 % CI 1.03–1.29, p = 0.013). Cataplexy was, by definition, present in all NT1 patients (100%) and inabsent of all NT2 patients. Sleep paralysis (61.5 % vs 33.3 %, p = 0.003) and hypnagogic/hypnopompic hallucinations (50.8 % vs 16.7 %, p < 0.001) were significantly more common in NT1. Modafinil was the dominant wake-promoting agent (88.5 %); antidepressant prescribing was concentrated in NT1 (any-antidepressant 73.8 % vs 22.9 %, p < 0.001). Major depressive disorder (16.8 %) and generalized anxiety disorder (9.7 %) showed no subtype difference. Conclusions In this Saudi tertiary-center cohort, narcolepsy was associated with a substantial diagnostic delay that increased with age at presentation, and with a high prevalence of comorbid sleep-disordered breathing, in which female sex and younger age were independent predictors of lower risk for SDB. The dataset supports stronger advocacy for early MSLT testing in adult patients with chronic excessive daytime sleepiness, and for systematic screening of psychiatric comorbidity at narcolepsy diagnosis.
