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Study Objectives: To evaluate long-term safety and maintenance of efficacy of solriamfetol treatment for excessive daytime sleepiness in narcolepsy and obstructive sleep apnea (OSA)., Methods: Participants with narcolepsy or OSA who completed a prior solriamfetol study were eligible. A 2-week titration period was followed by a maintenance phase (up to 50 weeks). Efficacy was assessed by Epworth Sleepiness Scale (ESS) and Patient and Clinical Global Impression of Change (PGI-C and CGI-C, respectively). After approximately 6 months of treatment, a subgroup entered a 2-week placebo-controlled randomized withdrawal (RW) phase. Change in ESS from beginning to end of the RW phase was the primary endpoint; PGI-C and CGI-C were secondary endpoints. Safety was assessed throughout the study., Results: In the maintenance phase, solriamfetol-treated participants demonstrated clinically meaningful improvements on ESS, PGI-C, and CGI-C. In the RW phase, least squares mean change on ESS was 1.6 in participants continuing solriamfetol versus 5.3 in participants switched to placebo (p < .0001). For both secondary endpoints, higher percentages of participants receiving placebo were reported as worse at the end of the RW phase versus solriamfetol (p < .0001). Common treatment-emergent adverse events (TEAEs) with solriamfetol were headache, nausea, nasopharyngitis, insomnia, dry mouth, anxiety, decreased appetite, and upper respiratory tract infection; 27 (4.2%) participants experienced at least one serious TEAE, and 61 (9.5%) withdrew because of TEAEs., Conclusions: This study demonstrated long-term maintenance of efficacy of solriamfetol under open-label and double-blind, placebo-controlled conditions. Safety profile of solriamfetol was consistent with previous 12-week studies; no new safety concerns were identified., Trial Registration: NCT02348632., (© Sleep Research Society 2019. Published by Oxford University Press [on behalf of the Sleep Research Society].)

Study Objectives: To evaluate changes in muscle and cerebral oxygenation during intermittent hypoxia (IH)., Methods: Fifteen healthy subjects were exposed to 45-min IH (2-min cycles). Arterial blood oxygen saturation (SpO2), prefrontal cortex and brachial biceps muscle oxygenation (assessed by near-infrared spectroscopy), heart rate, and ventilation were continuously recorded., Results: During 2-min IH cycles, changes in SpO2 (9.2% ± 3.3%) were associated with significant changes in cortex oxygenation (3.2% ± 1.8%), minute ventilation, and heart rate, but no change in muscle oxygenation (0.2% ± 1.0%)., Conclusions: Fluctuations of blood oxygen levels comparable to severe obstructive sleep apnea translate into distinct pattern of oxygenation changes in the muscle and cortex., (© 2016 Associated Professional Sleep Societies, LLC.)

Study Objectives: To test the hypothesis that greater resting sympathetic activity in obstructive sleep apnea (OSA) syndrome would not induce a lesser sympathetic neurovascular transduction., Design: Case-controlled cohort study., Participants: 33 patients with newly diagnosed OSA without comorbidities and 14 healthy controls., Interventions: 6 months of continuous positive airway pressure (CPAP) treatment for OSA patients and follow-up for 9 healthy controls., Measurements and Results: We assessed resting sympathetic outflow and sympathetic neurovascular transduction. Sympathetic activity was directly measured (microneurography) at rest and in response to sustained isometric handgrip exercise. Neurovascular transduction was derived from the relationship of sympathetic activity and blood pressure to leg blood flow during exercise. Despite an elevated sympathetic activity of ∼50% in OSA compared to controls, neurovascular transduction was not different (i.e., absence of tachyphylaxis). After six months of CPAP, there were significant declines in diastolic pressure, averaging ∼4 mm Hg, and in sympathetic activity, averaging ∼20% with no change in transduction., Conclusions: Greater sympathetic activity in obstructive sleep apnea does not appear to be associated with lesser neurovascular transduction. Hence, elevated sympathetic outflow without lesser transduction may underlie the prevalent development of hypertension in this population that is well controlled by continuous positive airway pressure treatment., (© 2015 Associated Professional Sleep Societies, LLC.)

Study Objectives: Obstructive sleep apnea (OSA) is known as a major cardiovascular risk factor, and high prevalence of OSA has been reported in patients with thoracic aortic dissection. The aim of our study was to assess the relationship between OSA, its vascular consequences, and aortic root size., Design/patients: 156 newly diagnosed apneic patients free of cardiovascular disease and medication were included. Patients underwent cardiac ultrasound for measuring aortic root diameter, polysomnography, office and 24-h ambulatory blood pressure (BP) measurements, baroreflex sensitivity (BRS), and arterial stiffness evaluation by carotid-to-femoral pulse wave velocity (PWV)., Measurements and Results: In univariate analysis, greater aortic root size was associated with older age (P = 0.03) and severity of OSA as expressed by mean nocturnal oxygen saturation (SpO2) (P = 0.015). Moreover, greater aortic root size was associated with higher diastolic BP, measured both clinically (P = 0.0005) or by 24-h ambulatory BP monitoring (P = 0.02), and PWV (P = 0.03). Mean nocturnal SpO(2) was correlated with BRS (P = 0.0008), thus potentially influencing BP values and arterial stiffness. In multivariate stepwise regression analysis, diastolic BP was the only significant factor for aortic root size (P = 0.0003)., Conclusions: In OSA patients, nocturnal hypoxemia decreased BRS and increased diastolic BP, which was the main factor influencing aortic root size.

We have previously described impairments of cognitive executive functions in 17 patients with OSAS in comparison with 17 normal controls, as assessed by various frontal-lobe-related tests. In the present study, 10 of these OSAS patients treated with continuous positive airway pressure (CPAP) were reevaluated after 4-6 months of treatment. Neuropsychological tasks explored attention, short-term memory span, learning abilities, planning capacities, categorizing activities, and verbal fluency. Patients were found to have normalized most of their cognitive executive and learning disabilities, but all the short-term memory tests remained unchanged. These findings are discussed in light of the contribution of the frontal-lobe-related systems to short-term memory functions, and the eventual pathogenic role played by sleep fragmentation and nocturnal hypoxemia, which are related to the occurrence of apneic and hypopneic events. In conclusion, short-term memory impairment was persistent in OSAS patients despite CPAP treatment for 4-6 months.