Our results support the use of the odds ratio product (ORP) as a continuous measure of sleep depth.

Pharyngeal dilator muscles are important in the pathophysiology of obstructive sleep apnoea syndrome (OSA). We have previously shown that during wakefulness, the activity of both the genioglossus (GGEMG) and tensor palatini (TPEMG) is greater in patients with OSA compared with controls. Further, EMG activity decreases at sleep onset, and the decrement is greater in apnoea patients than in healthy controls. In addition, it is known that the prevalence of OSA is greater in middle-aged compared with younger men. Thus, we had two goals in this study. First we compared upper airway muscle activity between young and middle-aged healthy men compared with men with OSA. We also explored the mechanisms responsible for the decrement in muscle activity at sleep onset in these groups. We investigated muscle activity, ventilation (V e ), and upper airway resistance (UAR) during wakefulness and sleep onset (transition from α to θ EEG activity) in all three groups. Measurements were obtained during basal breathing (BB) and nasal continuous positive airway pressure (CPAP) was applied to reduce negative pressure-mediated muscle activation). We found that during wakefulness there was a gradation of GGEMG and UAR (younger < older < OSA) and that muscle activity was reduced by the application of nasal CPAP (to a greater degree in the OSA patients). Although CPAP eliminated differences in UAR during wakefulness and sleep, GGEMG remained greater in the OSA patients. During sleep onset, a greater initial fall in GGEMG was seen in the OSA patients followed by subsequent muscle recruitment in the third to fifth breaths following the α to θ transition. On the CPAP night,V e and GGEMG still fell further in the OSA patients compared with control subjects. CPAP prevented the rise in UAR at sleep onset along with the associated recruitment in GGEMG. Differences in TPEMG among the groups were not significant. These data suggest that the middle-aged men had upper airway function midway between that of young normal men and the abnormal airway of those with OSA. Furthermore it suggests that the initial sleep onset reduction in upper airway muscle activity is due to loss of a 'wakefulness' stimulus, rather than to loss of responsiveness to negative pressure, and that this wakefulness stimulus may be greater in the OSA patient than in healthy controls.

Study Objectives: To determine the reasons for inter-scorer variability in sleep staging of polysomnograms (PSGs). Methods: Fifty-six PSGs were scored (5-stage sleep scoring) by 2 experienced technologists, (first manual, M1). Months later, the technologists edited their own scoring (second manual, M2) based upon feedback from the investigators that highlighted differences between their scoring. The PSGs were then scored with an automatic system (Auto) and the technologists edited them, epoch-by-epoch (Edited-Auto). This resulted in 6 different manual scores for each PSG. Epochs were classified as scorer errors (one M1 score differed from the other 5 scores), scorer bias (all 3 scores of each technologist were similar, but differed from the other technologist) and equivocal (sleep scoring was inconsistent within and between technologists). Results: Percent agreement after M1 was 78.9% ± 9.0% and was unchanged after M2 (78.1% ± 9.7%) despite numerous edits (≈40/PSG) by the scorers. Agreement in Edited-Auto was higher (86.5% ± 6.4%, p < 1E−9). Scorer errors (< 2% of epochs) and scorer bias (3.5% ± 2.3% of epochs) together accounted for < 20% of M1 disagreements. A large number of epochs (92 ± 44/PSG) with scoring agreement in M1 were subsequently changed in M2 and/or EditedAuto. Equivocal epochs, which showed scoring inconsistency, accounted for 28% ± 12% of all epochs, and up to 76% of all epochs in individual patients. Disagreements were largely between awake/NREM, N1/N2, and N2/N3 sleep. Conclusion: Inter-scorer variability is largely due to epochs that are difficult to classify. Availability of digitally identified events (e.g., spindles) or calculated variables (e.g., depth of sleep, delta wave duration) during scoring may greatly reduce scoring variability.

The severity of nocturnal hypoxemia influences the magnitude of renal, but not the systemic, RAS activation independently of obesity in patients with OSA.

Background: It has been estimated that the prevalence of Alzheimer disease (AD) and related de-

No abstract

OSA and OHS are highly prevalent in obese patients with chronic awake hypoxemia, and OSA frequently coexists with COPD. Evaluation of chronic, awake hypoxemia solely based on arterial blood gas measurements and pulmonary function testing is not sufficient to identify OSA and OHS. Further diagnostic sleep testing should be performed to identify those who could benefit from alternative therapies and to avoid potential harm from treatment with supplemental oxygen alone.

RationaleHemorheological alterations are reported in obstructive sleep apnea (OSA) and reversed with continuous positive airway pressure (CPAP), observations potentially explained by intermittent hypoxia (IH)-induced oxidative stress.ObjectiveTo investigate whether IH causes hemorheological alterations viaoxidative stress.MethodsWistar rats were exposed to normoxia (n=7) or IH (n=8) for 14 days. Twenty-three moderate-to-severe OSA patients were assessed at three time points: baseline, after randomisation to either 2 weeks of nocturnal oxygen (n=13) or no treatment (n=10), and after 1-month of CPAP treatment (n=17). Further, an OSA-free control group (n=13) was assessed at baseline and after time-matched follow-up.MeasurementsWe measured hemorheological parameters [hematocrit, blood viscosity, plasma viscosity (rats only), erythrocyte aggregation and deformability (humans only)] and redox balance (SOD, GPX, protein oxidation [AOPP] and lipid peroxidation [MDA]). We also tested erythrocytes hemorheological sensitivity to reactive oxygen species (ROS) in our human participants using the oxidant t-butyl hydroperoxide (TBHP).ResultsIn rats, IH increased blood viscosity by increasing hematocrit without altering erythrocytes hemorheological properties. IH also reduced SOD activity and increased AOPP. In humans, baseline hemorheological properties were similar between patients and controls, and properties were unaltered following oxygen and CPAP, except erythrocyte deformability was reduced following oxygen therapy. Redox balance was comparable between patients and controls. At baseline, TBHP induced a greater reduction of erythrocyte deformability in patients while CPAP reduced TBHP-induced increase in aggregation strength.ConclusionIH and OSA per se do not cause hemorheological alterations despite the presence of oxidative stress or higher sensitivity to ROS, respectively.