Functional magnetic resonance imaging was used to map cerebral activation in 16 patients with obstructive sleep-disordered breathing (OSDB) and 16 healthy subjects, during the performance of a 2-back verbal working memory task. Six patients with OSDB were reimaged after a minimum period of 8 wk of treatment with positive airway pressure. Working memory speed in OSDB was significantly slower than in healthy subjects, and a group average map showed absence of dorsolateral prefrontal activation, regardless of nocturnal hypoxia. After treatment, resolution of subjective sleepiness contrasted with no significant change in behavioral performance, persistent lack of prefrontal activation, and partial recovery of posterior parietal activation. These findings suggest that working memory may be impaired in OSDB and that this impairment is associated with disproportionate impairment of function in the dorsolateral prefrontal cortex. Nocturnal hypoxia may not be a necessary determinant of cognitive dysfunction, and sleep fragmentation may be sufficient. There may be dissociations between respiratory vs. cortical recovery and objective vs. subjective recovery. Hypofrontality may provide a plausible biological mechanism for a clinical overlap with disorders of mood and attention.

Complex sleep apnea is defined as sleep disordered breathing secondary to simultaneous upper airway obstruction and respiratory control dysfunction. The objective of this study was to assess the utility of an electrocardiogram (ECG)-based cardiopulmonary coupling technique to distinguish obstructive from central or complex sleep apnea. Analysis of archived polysomnographic datasets. A laboratory for computational signal analysis. None. The PhysioNet Sleep Apnea Database, consisting of 70 polysomnograms including single-lead ECG signals of approximately 8 hours duration, was used to train an ECG-based measure of autonomic and respiratory interactions (cardiopulmonary coupling) to detect periods of apnea and hypopnea, based on the presence of elevated low-frequency coupling (e-LFC). In the PhysioNet BIDMC Congestive Heart Failure Database (ECGs of 15 subjects), a pattern of “narrow spectral band” e-LFC was especially common. The algorithm was then applied to the Sleep Heart Health Study—I dataset, to select the 15 records with the highest amounts of broad and narrow spectral band e-LFC. The latter spectral characteristic seemed to detect not only periods of central apnea, but also obstructive hypopneas with a periodic breathing pattern. Applying the algorithm to 77 sleep laboratory split-night studies showed that the presence of narrow band e-LFC predicted an increased sensitivity to induction of central apneas by positive airway pressure. ECG-based spectral analysis allows automated, operatorindependent characterization of probable interactions between respiratory dyscontrol and upper airway anatomical obstruction. The clinical utility of spectrographic phenotyping, especially in predicting failure of positive airway pressure therapy, remains to be more thoroughly tested.

To define the clinical and polysomnographic features of a distinct variant of obstructive sleep-disordered breathing that is remarkably mild during rapid eye movement (REM) sleep. Observational study and evaluation of polysomnographic and clinical records. American Academy of Sleep Medicine-accredited multidisciplinary sleep disorders center and laboratory. 35 medication-free subjects with clinical and polysomnographic severe obstructive sleep-disordered breathing selected for dominance of 1 of 2 disordered breathing patterns. Positive airway pressure titration. Nasal pressure was used to score respiratory events. Sleep was scored by both the standard criteria and cyclic alternating pattern (CAP), and the distribution of respiratory events was tabulated and analyzed. A distinct clinical and polysomnographic syndrome emerged, CAP-dominant sleep-disordered breathing, characterized by severe relatively short cycle obstructive events during non-REM sleep that were mild in REM sleep. Characteristics include lower body mass index, fewer apneas, and a lower hypoxic burden as reflected by frequency and severity of nocturnal oxygen saturation. During positive pressure titration, a remarkable respiratory instability emerged selectively during CAP, in contrast to stability during REM sleep. This partial treatment failure was associated with persistent clinical symptoms. This variant of sleep apnea may reflect a dominant component of respiratory instability and periodic breathing coupled with upperairway obstruction. Its existence questions the conventional practice of calculating global respiratory indexes. Besides positive airway pressure, measures to treat periodic breathing may be required.

Ambulatory tracking of sleep and sleep pathology is rapidly increasing with the introduction of wearable devices. The objective of this study was to evaluate a wearable device which used novel computational analysis of the electrocardiogram (ECG), collected over multiple nights, as a method to track the dynamics of sleep quality in health and disease. This study used the ECG as a primary signal, a wearable device, the M1, and an analysis of cardiopulmonary coupling to estimate sleep quality. The M1 measures trunk movements, the ECG, body position, and snoring vibrations. Data from three groups of patients were analyzed: healthy participants and people with sleep apnea and insomnia, obtained from multiple nights of recording. Analysis focused on summary measures and night-to-night variability, specifically the intraclass coefficient. Data were collected from 10 healthy participants, 18 people with positive pressure–treated sleep apnea, and 20 people with insomnia, 128, 65, and 121 nights, respectively. In any participant, all nights were consecutive. High-frequency coupling (HFC), the signal biomarker of stable breathing and stable sleep, showed high intraclass coefficients (ICCs) in healthy participants and people with sleep apnea (0.83, 0.89), but only 0.66 in people with insomnia. The only statistically significant difference between weekday and weekend in healthy subjects was HFC duration: 242.8 ± 53.8 vs. 275.8 ± 57.1 minutes (89 vs. 39 total nights), F_(1,126) = 9.86, p = .002. The M1 and similar wearable devices provide new opportunities to measure sleep in dynamic ways not possible before. These measurements can yield new biological insights and aid clinical management.

To assess the efficacy of added carbon dioxide as adjunctive therapy to positive airway pressure-refractory mixed obstructive and central sleep-disordered breathing, using a prototype device—the positive airway pressure gas modulator. Open-label evaluation of low concentrations of carbon dioxide added to a positive airway pressure circuit. Physician-attended polysomnographic titration in a free-standing sleep laboratory with end-tidal and transcutaneous carbon-dioxide monitoring. Six adult men (age 54 ± 5.7 years) with severe poorly controlled mixed sleep-disordered breathing in the absence of renal or heart failure. Flow-independent addition of incremental concentrations of carbon dioxide during sleep. The respiratory disturbance index before treatment was 66 ± 14.5 events per hour of sleep, with a nocturnal desaturation low of 84.6% ± 10.1%. Residual respiratory disturbance index on best treatment was 43 ± 9 events per hour of sleep. There was an immediate (< 1 minute) response to the addition of 0.5% to 1% carbon dioxide, and minimal changes were required to be made across the night. There was no discomfort, shortness of breath, palpitations, headache, or significant increase in respiratory or heart rate. The residual respiratory disturbance index on carbon dioxide, scored irrespective of desaturations, was in the normal range (< 5 / hour of sleep). Two subjects had a second night at the concentration of carbon dioxide determined to be efficacious, with no required concentration change. No adverse effects on overall sleep architecture were noted. Low concentrations of carbon dioxide added to conventional positive airway pressure effectively control severe treatment-resistant mixed obstructive and central sleep-disordered breathing.