Daytime Sleepiness In Obstructive Sleep Apnea Research Articles

Influence of social jetlag on daytime sleepiness in obstructive sleep apnea.

Social jetlag is the discrepancy between socially determined sleep timing on workdays and biologically determined sleep timing on days free of social obligation. Poor circadian timing of sleep may worsen sleep quality and increase daytime sleepiness in obstructive sleep apnea (OSA). We analysed de-identified data from 2,061 participants (75.2% male, mean [SD] age 48.6[13.4]years) who completed Sleep Apnea Global Interdisciplinary Consortium (SAGIC) research questionnaires and underwent polysomnography at 11 international sleep clinic sites. Social jetlag was calculated as the absolute difference in the midpoints of sleep between weekdays and weekends. Daytime sleepiness was assessed using the Epworth Sleepiness Scale (ESS). Linear regression analyses were performed to estimate the association between social jetlag and daytime sleepiness, with consideration of age, sex, body mass index, ethnicity, insomnia, alcohol consumption, and habitual sleep duration as confounders. Of the participants, 61.5% had <1 h of social jetlag, 27.5% had 1 to <2 h, and 11.1% had ≥2 h. Compared to those with <1 h of social jetlag, those with ≥2 h of social jetlag had 2.07 points higher ESS (95% confidence interval [CI] 0.77-3.38, p=0.002), and those with 1 to <2 h of social jetlag had 0.80 points higher ESS (95% CI 0.04-1.55, p=0.04) after adjustment for potential confounding. Interaction with OSA severity was observed; social jetlag appeared to have the greatest effect on daytime sleepiness in mild OSA. As social jetlag exacerbates daytime sleepiness in OSA, improving sleep timing may be a simple but novel therapeutic target for reducing the impact of OSA.

Reduced Cross-Frequency Coupling and Daytime Sleepiness in Obstructive Sleep Apnea Patients.

Simple SummaryObstructive sleep apnea (OSA) is one of the most common breathing-related sleep disorders. The processes that take place in specific areas of the brain during distinct sleep stages and specific respiratory events are suspected to be impaired in OSA patients. These brain processes may be described in complex (mathematical) terms. Using one of these descriptions (phase–amplitude cross-frequency coupling), we demonstrated in electroencephalographic (EEG) recordings of OSA patients that the process sequences in certain areas of the brain are altered in distinct sleep stages of OSA patients compared to patients who do not suffer from clinically relevant OSA. In addition, we were able to find a physiological marker that assesses the severity of daytime sleepiness, one of the main symptoms of OSA. This study supports the hypothesis that OSA is a neuronal/neuromuscular disorder. Thus, it contributes to a better understanding of the so-far-unexplained cause for the development of OSA and opens new possibilities for the exploration of alternative therapeutic approaches.Obstructive sleep apnea (OSA) is associated with sleep-stage- and respiratory-event-specific sensorimotor cortico-muscular disconnection. The modulation of phase–amplitude cross-frequency coupling (PACFC) may influence information processing throughout the brain. We investigated whether sleep-stage-specific PACFC is impaired at the sensorimotor areas in OSA patients. C3 and C4 electrode EEG polysomnography recordings of 170 participants were evaluated. Different frequency band combinations were used to compute CFC modulation index (MI) to assess if MI differs between OSA and non-significant OSA patients in distinct sleep stages. We tested if the CFC-MI could predict daytime sleepiness in OSA. Theta–gamma CFC-MI at cortical sensorimotor areas was significantly reduced during all sleep stages; the delta–alpha CFC-MI was significantly reduced during REM and N1 while increasing during N2 in patients with respiratory disturbance index (RDI) > 15/h compared to those with RDI ≤ 15/h. A sleep stage classification using MI values was achieved in both patient groups. Theta–gamma MI during N2 and N3 could predict RDI and Epworth Sleepiness Scale, while delta–alpha MI during REM predicted RDI. This increase in disconnection at the cortical sensorimotor areas with increasing respiratory distress during sleep supports a cortical motor dysfunction in OSA patients. The MI provides an objective marker to quantify subjective sleepiness and respiratory distress in OSA.

The association between beta-blocker therapy and daytime sleepiness in obstructive sleep apnoea

Daytime sleepiness is a cardinal symptom of obstructive sleep apnoea (OSA) and a well-recognised side effect of beta-blockers, therefore patients with OSA under this treatment may have worse sleepiness. However, the interaction between daytime sleepiness and beta-blockers use has not been thoroughly investigated in patients with OSA before. We analysed the data of 2183 individuals (1852 patients with OSA and 331 snorer controls) from 3 countries (Greece, Hungary and Moldova). Medical history, including medication usage and the Epworth Sleepiness Scale (ESS) were recorded. Patients and controls were divided into somnolent (ESS ≥ 11) and non-somnolent (ESS < 11) groups, and the association between-blocker use with the somnolent group was investigated with multivariate logistic regression analysis adjusted for confounders. Sensitivity analyses were performed in each cohort, in the severity subgroups, in patients who did not take statins and in those who had polysomnography as a diagnostic test. There was no relationship between beta-blocker usage and the somnolent OSA (p = 0.24) or control (p = 0.64) groups. These results were similar in sensitivity analyses (all p > 0.05). ESS was related to BMI (ρ = 0.25), total sleep time (ρ = 0.07), AHI (ρ = 0.32), oxygen desaturation index (ρ = 0.33) and minimum oxygen saturation (ρ = – 0.32, all p < 0.05) in OSA, and was higher in patients with hypertension, diabetes and cerebro/cardiovascular disease and those who took statins (all p < 0.05). In general, beta-blockers are not associated with increased daytime sleepiness in OSA. Thus, the diagnosis of OSA should not discourage initiation of beta-blocker treatment, if it is clinically indicated.

Inspiratory Muscle Training in the Severity of Obstructive Sleep Apnea, Sleep Quality and Excessive Daytime Sleepiness: A Placebo-Controlled, Randomized Trial.

PurposeExercise programs have been considered as an adjuvant treatment in obstructive sleep apnea (OSA). However, few studies have focused on the effects of the inspiratory muscle training (IMT) in reducing the severity and the symptoms of OSA.Patients and MethodsA randomized controlled trial was conducted and approved by the local Ethics Committee. All subjects signed the informed consent form and were randomized into 2 groups: a) IMT group (n = 8), 8 weeks of IMT with 75% of maximal inspiratory pressure (MIP) and b) placebo group (n = 8): subjects performed IMT without load.ResultsIMT group showed reduction in the apnea–hypopnea index (AHI) (p = 0.01), in the Berlin questionnaire score (p = 0.001) and an increase in inspiratory muscle strength (p = 0.018). IMT group demonstrated a reduction in the AHI (31.7 ± 15.9 events/h vs 29.9 ± 15.8 events/h; p <0.001), in the Berlin questionnaire scores (2.6 ± 0.5 vs 1.2 ± 0.5; p = 0.016), Pittsburgh Sleep Quality Index (PSQI) score (7.2 ± 3.6 vs 3.7 ± 1.3; p = 0.008), in the Epworth Sleepiness Scale (ESS) (12.5 ± 4.0 vs 7.7 ± 3.0; p = 0.008) and increase in MIP (83.6 ± 26.5 cmH2O and 127.9 ± 32.5 cmH2O; p = 0.010).ConclusionThe IMT promotes discrete changes in the AHI and improves sleep quality and excessive daytime sleepiness in OSA. Moreover, IMT is a cheap, useful and simple home-based training program and can be considered as an adjunct therapy for OSA patients.

Metabolic syndrome, insulin resistance and sleepiness in real-life obstructive sleep apnoea

The metabolic syndrome shows a variable prevalence in obstructive sleep apnoea (OSA), and its association with insulin resistance or excessive daytime sleepiness in OSA is unclear. This study assessed the following in consecutive patients with newly diagnosed OSA: 1) the prevalence of metabolic syndrome; and 2) its association with insulin resistance and daytime sleepiness. Metabolic syndrome (National Cholesterol Education Program Adult Treatment Panel (NCEP-ATP) III criteria), insulin resistance (Homeostatic Model Assessment (HOMA) index, n = 288) and daytime sleepiness (Epworth Sleepiness Scale) were assessed in 529 OSA patients. The prevalence of metabolic syndrome was 51.2%, which increased with OSA severity. Each metabolic syndrome component correlated with apnoea/hypopnoea index, but only blood pressure retained significance after correction for confounders. Both obesity and OSA contributed to metabolic abnormalities, with different sex-related patterns, since diagnosis of metabolic syndrome was significantly associated with neck circumference, age, body mass index and lowest arterial oxygen saturation in males, and with age and arousal index in females. The number of metabolic syndrome components increased with HOMA index (p<0.001). Prevalence of sleepiness was the same in patients with and without metabolic syndrome. The metabolic syndrome occurs in about half of "real-life" OSA patients, irrespective of daytime sleepiness, and is a reliable marker of insulin resistance.

Obstructive sleep apnoea, insulin resistance and sleepiness

Our understanding of obstructive sleep apnoea (OSA) has advanced much beyond that of the condition being a noisy breathing abnormality during sleep which classically presents with daytime sleepiness, to a...

Use of the Epworth Sleepiness Scale to demonstrate response to treatment with nasal continuous positive airways pressure in patients with obstructive sleep apnoea

The Epworth Sleepiness Scale (ESS) was used to measure the degree of daytime sleepiness in two groups of patients with obstructive sleep apnoea (OSA), before and after treatment with nasal continuous positive airways pressure (CPAP). One group (50 patients) were assessed after 2 months CPAP treatment after which the mean ESS fell from 16·4 [standard error of mean ( sem) 0·52] to 7·0 ( sem 0·56). A second group (25 patients) were assessed after 1 yr of treatment: a similar fall in mean ESS was seen from 15·2 ( sem 1·13) before treatment to 6·0 ( sem 0·72). These results imply that the ESS can be used clinically to demonstrate the response of daytime sleepiness in OSA to treatment with CPAP, and that the fall in ESS seen after 2 months is sustained after 1 yr of treatment. It is also possible that this approach could be used to monitor the progress of treatment with CPAP.