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Introduction Insomnia is a prevalent yet under-characterized disorder, particularly regarding the heterogeneity of patients and their associated responses to different treatment modalities. This often leads to suboptimal management. There is a need to consider personalized approaches tailored to the characteristics of insomnia phenotypes with regard to objective evidence of shortened sleep duration (< 6 h). This study will examine whether there is a differential treatment response to cognitive behavioral therapy for insomnia (CBT-I) versus pharmacotherapy (lemborexant) as a function of insomnia phenotypes (i.e., ± 6 h of sleep). Methods This study is a three-arm pragmatic randomized clinical trial, which will enroll 90 adults with chronic insomnia disorder and anxiety/depressive symptoms. Eligible participants will be randomized to one of three conditions (1:1:1) involving CBT-I, lemborexant (Dual Orexin Receptor Antagonist) or placebo medication. Treatment outcomes will be assessed at post-treatment and 6-month follow-up. Insomnia symptom severity as measured by the Insomnia Severity Index will serve as the primary outcome for treatment comparisons. Secondary outcomes will include daily sleep/wake variables derived from the Consensus Sleep Diary, subjective measures of fatigue, mood, mental well-being, functional impairments, and sleep-related beliefs and attitudes. In addition, changes in cognitive performance will be examined as an exploratory outcome. Sleep reactivity and arousal level will be evaluated as potential mediators of treatment-related changes in CBT-I and pharmacotherapy. Discussion This study will contribute to the development of personalized medicine for managing different insomnia phenotypes and will have implication for knowledge mobilization of sleep research. Trial registration ClinicalTrials.gov. Identifier: NCT06779149. Registered on 12 January 2025.

Purpose The purpose of this study was to investigate apnea–hypopnea index (AHI) across two polysomnographies (PSGs) to examine AHI variability and impact on clinical diagnosis. Materials and methods Two-night PSGs of 193 sleep clinic patients were reviewed, and the AHI variability was analyzed. Anonymized records from five patients with significant night-to-night AHI variability were used in this study: the two-night PSGs from two patients were represented as four individual PSGs; the two-night PSG for two others were represented as being obtained from two different sleep clinics; the last patient’s PSG was shown as a two-night study. Twenty-two sleep experts attending the Associated Professional Sleep Societies meeting were recruited to make diagnoses based on the PSGs. They were told that the PSGs were from seven patients: four with single-night PSG; two with two PSGs, each one from a different clinic; and one patient with a two-night PSG. Results Twenty-one percent of the 193 sleep clinic patients had a nightly PSG AHI variability of greater than 5. Forty-eight percent of all patients had a significantly higher AHI on the first night, and 41% had a significantly higher AHI on the second night. Using an AHI > 15 diagnostic criteria, sleep apnea would have been undetected in 20% ( n  = 39) of patients due to low AHI on one night. Furthermore, 13% of all patients had a more severe sleep apnea classification based on the second night of PSG. For the seven cases, 27–36% of sleep experts failed to identify sleep apnea especially when presented with the PSG containing the lower AHI. Incidences of missed sleep apnea diagnoses were reduced to 15–18% when information from two PSGs was presented to the sleep experts. Conclusions Utilizing a large patient population, this study supports the significant night-to-night variability in PSG respiratory variables. Identification of sleep apnea in some patients is reduced when sleep experts are provided with only one PSG recording. The clinical implication is that about 13% of sleep clinic patients might benefit from a second night of PSG.

Abstract Study Objective: To compare cognitive behavioral therapy for insomnia (CBT-I) + antidepressant medication (AD) against treatments that target solely depression or solely insomnia. Design: A blinded, randomized split-plot experimental study. Setting: Two urban academic clinical centers. Participants: 107 participants (68% female, mean age 42 ± 11) with major depressive disorder and insomnia. Interventions: Randomization was to one of three groups: antidepressant (AD; escitalopram) + CBT-I (4 sessions), CBT-I + placebo pill, or AD + 4-session sleep hygiene control (SH). Measurements and Results: Subjective sleep was assessed via 2 weeks of daily sleep diaries (use of medication was covaried in all analyses); although there were no statistically significant group differences detected, all groups improved from baseline to posttreatment on subjective sleep efficiency (SE) and total wake time (TWT) and the effect sizes were large. Objective sleep was assessed via overnight polysomnographic monitoring at baseline and posttreatment; analyses revealed both CBT groups improved on TWT (p = .03), but the AD + SH group worsened. There was no statistically significant effect for PSG SE (p = .07). There was a between groups medium effect observed for the AD + SH and CBT + placebo group differences on diary TWT and both PSG variables. All groups improved significantly from baseline to posttreatment on the Hamilton Rating Scale for Depression (HAMD-17); the groups did not differ. Conclusions: Although all groups self-reported sleeping better after treatment, only the CBT-I groups improved on objective sleep, and AD + SH’s sleep worsened. This suggests that we should be treating sleep in those with depression with an effective insomnia treatment and relying on self-report obscures sleep worsening effects. All groups improved on depression, even a group with absolutely no depression-focused treatment component (CBT-I + placebo). The depression effect in CBT-I only group has been reported in other studies, suggesting that we should further investigate the antidepressant properties of CBT-I.

Visible light is the principal stimulus for resetting the mammalian central circadian pacemaker. Circadian phase resetting is most sensitive to short-wavelength (blue) visible light. We examined the effects of removing short-wavelengths <500 nm from polychromatic white light using optical filters on circadian phase resetting in rats. Under high irradiance conditions, both long- (7 hours) and short- (1 hour) duration short-wavelength filtered (<500 nm) light exposure attenuated phase-delay shifts in locomotor activity rhythms by (~40-50%) as compared to unfiltered light exposure. However, there was no attenuation in phase resetting under low irradiance conditions. Additionally, the reduction in phase-delay shifts corresponded to regionally specific attenuation in molecular markers of pacemaker activation in response to light exposure, including c-FOS, Per1 and Per2. These results demonstrate that removing short-wavelengths from polychromatic white light can attenuate circadian phase resetting in an irradiance dependent manner. These results have important implications for designing and optimizing lighting interventions to enhance circadian adaptation.

Abstract Study Objectives To assess the efficacy and safety of FT218, a novel once-nightly formulation of sodium oxybate (ON-SXB), in patients with narcolepsy in the phase 3 REST-ON trial. Methods Narcolepsy patients aged ≥16 years were randomized 1:1 to uptitration of ON-SXB (4.5, 6, 7.5, and 9 g) or placebo. Three coprimary endpoints were change from baseline in mean sleep latency on the Maintenance of Wakefulness Test, Clinical Global Impression-Improvement rating, and weekly cataplexy attacks at 9, 7.5, and 6 g. Secondary endpoints included change from baseline on the Epworth Sleepiness Scale. Safety included adverse drug reactions and clinical laboratory assessments. Results In total, 222 patients were randomized; 212 received ≥1 dose of ON-SXB (n = 107) or placebo (n = 105). For the three coprimary endpoints and Epworth Sleepiness Scale, all three doses of ON-SXB demonstrated clinically meaningful, statistically significant improvement versus placebo (all p < 0.001). For ON-SXB 9 g versus placebo, increase in mean sleep latency was 10.8 versus 4.7 min (Least squares mean difference, LSMD [95% CI], 6.13 [3.52 to 8.75]), 72.0% versus 31.6% were rated much/very much improved on Clinical Global Impression-Improvement (OR [95% CI], 5.56 [2.76 to 11.23]), change in mean weekly number of cataplexy attacks was –11.5 versus –4.9 (LSMD [95% CI], –6.65 [–9.32 to –3.98]), and change in Epworth Sleepiness Scale was –6.5 and –2.7 (LSMD [95% CI], –6.52 [–5.47 to –2.26]). Common adverse reactions included nausea, vomiting, headache, dizziness, and enuresis. Conclusions ON-SXB significantly improved narcolepsy symptoms; its safety profile was consistent with SXB. ON-SXB conferred efficacy with a clearly beneficial single nighttime dose. Clinical Trial Registration ClinicalTrials.gov: NCT02720744, https://clinicaltrials.gov/ct2/show/NCT02720744.

Background Continuous positive airway pressure (CPAP) is an effective treatment for obstructive sleep apnea syndrome (OSAS). Consistent adherence to CPAP improves the patient’s longevity and quality of life as well as public safety. However, nonadherence is a significant contributor to the growing burden of untreated OSAS, and is associated with negative consequences for the patient, public safety, and the healthcare system. Objective The use of CPAP is a classic example of an effective treatment for which adherence is extremely variable. This paper examines a multiplicity of factors that influence CPAP adherence. Factors These factors are traditionally thought of in terms of patient and equipment variables, but in addition physician, family, healthcare facility, and governmental issues all contribute to CPAP adherence. Discussion These factors are reviewed and pragmatic recommendations are made for improving clinical practice.

Numerous studies have been conducted in the past few decades on obstructive sleep apnea (OSA) as an independent risk factor for the development and progression of cardiac arrhythmia. Treatment with continuous positive airway pressure (CPAP) therapy lowers blood pressure, improves ejection fraction in patients with heart failure, and decreases the need of revascularization procedures in patients with coronary artery disease. However, there has been little published discussion regarding the effect of CPAP treatment on cardiac arrhythmia in patients with OSA. We aimed to summarize scientific evidence regarding the utility of CPAP treatment in managing the recurrence and severity of different types of cardiac arrhythmia. We retrieved articles published in English before December 2016, through database search of PubMed, CENTRAL, and Embase. All peer-reviewed experimental, comparative, and other observational studies focused on adults were considered eligible. Several studies documented positive changes in arrhythmia frequency and severity with CPAP application, irrespective of type of arrhythmia, study methodology, or setting. However, the available evidence on the impact of CPAP treatment on the frequency and severity of cardiac arrhythmia is limited by heterogeneity of data. The duration of CPAP application, compliance with treatment, and baseline severity of OSA and cardiac pathology are important confounding factors that influence the effect of CPAP treatment. We emphasize the need for agreement on a core set of relevant predictors of the magnitude of the effect. Future research should carefully address these factors and their influence on the potential therapeutic ability of CPAP treatment to improve cardiac outcomes and reduce the risks of adverse cardiac and noncardiac effects associated with untreated OSA.

PurposeObstructive sleep apnea (OSA) has been recognized as an independent risk factor for the development and progression of atrial fibrillation (AF). We aimed to investigate the changes in heart rate and atrial and ventricular ectopy after continuous positive airway pressure (CPAP) treatment in patients with OSA and AF.MethodsConsecutive patients with AF underwent ambulatory sleep monitoring, and OSA was defined as an Apnea-Hypopnea-Index (AHI) ≥ 5/h. Treated patients completed in-laboratory CPAP titration study. A 24-h ECG Holter was performed at baseline and at 3 and 6 months after CPAP treatment.ResultsOne hundred patients (70% males) with AF were included in the final analysis. OSA was diagnosed in 85% of patients. There were no significant changes in mean 24-h heart rate in patients with paroxysmal or permanent AF at 3 and 6 months of treatment compared to baseline. In patients with paroxysmal AF (n = 29), atrial and ventricular ectopy counts/24 h significantly decreased at 3 months compared to baseline (median (IQR) 351 (2049) to 57 (182), P = 0.002; 68 (105) to 16 (133), P = 0.01 respectively). At 6 months follow-up, the atrial ectopy count/24 h significantly decreased in patients with paroxysmal AF compared to baseline (median (IQR) 351 (2049) to 31 (113), P = 0.016, n = 14). In patients with permanent AF (n = 15), there was a significant reduction in ventricular ectopy count/24 h at 3 months compared to baseline (median (IQR) 100 (1116) to 33 (418), P = 0.02).ConclusionsThere is a significant decrease in atrial and ventricular ectopy count/24 h in patients with AF and OSA at 3 and 6 months of CPAP treatment compared to baseline.

The purpose of this review is to provide an update of the research regarding the etiology, diagnosis and management of psychogenic non-epileptic seizures (PNES). A literature search using Pubmed, Ovid MEDLINE and EMBASE database was performed from 2000 up to August 2017. We have evaluated the different factors leading to PNES as well as the diagnostic approach and management of this disorder which continue to be very difficult. The coexistence of epilepsy and PNES poses special challenges and requires the coordinated efforts of the family physicians, psychiatrists, psychologists and neurologists. Although this condition has an overall poor prognosis, a multidisciplinary approach in the diagnosis and management of this disorder would likely improve the outcomes. We have proposed a diagnostic and treatment algorithm for PNES and suggested a national registry of patients suffering from this condition. The registry would contain data regarding treatment and outcomes to aid in the understanding of this entity. Vue d’ensemble des crises psychogènes non-épileptiques: étiologie, diagnostic et prise en charge. L’objectif de cet article est de présenter une mise à jour des activités de recherche qui concernent l’étiologie, le diagnostic et la prise en charge des crises psychogènes non-épileptiques (CPNE). Pour ce faire, nous avons mené de 2000 à août 2017 une recherche bibliographique au moyen des bases de données suivantes : PubMed, Ovid MEDLINE et Embase. Nous avons procédé à l’évaluation des divers facteurs causant les CPNE, des approches diagnostiques et de la prise en charge de ce trouble, laquelle continue à être très difficile. La coexistence de l’épilepsie et des CPNE présente aussi des défis particuliers et exige des efforts coordonnés de la part des médecins de famille, des psychiatres, des psychologues et des neurologues traitants. Bien que les pronostics au sujet de cette condition soient généralement réservés, une approche multidisciplinaire dans l’établissement d’un diagnostic et la prise en charge des CPNE contribueraient probablement à améliorer l’évolution de l’état de santé des patients. À cet égard, nous avons proposé, en plus d’un registre national des patients atteints de ce trouble, un algorithme de diagnostic et de traitement pour les CPNE. À noter que ce registre contiendrait des données portant sur les modalités de traitement et leur résultat afin de favoriser la compréhension du cadre clinique des CPNE.