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Parker JL, Vakulin A, Melaku YA, et al. Nat Sci Sleep. 2023;15:389–406. The authors advise that the funding section on page 404 is incorrect. The funding statement should read as follows: Funding This study was funded by a National Health and Medical Research Council of Australia Project Grant (627227) 2010-12, The Hospital Research Foundation, and The Freemasons Foundation Centre for Male Health and Wellbeing. Financial support for the conduct of sleep studies (2011) and quantitative EEG analysis was obtained from the ResMed Foundation, California, USA. The authors apologize for this error.

The termination of obstructive respiratory events is typically associated with arousal from sleep. The ventilatory response to arousal may be an important determinant of subsequent respiratory stability/instability and therefore may be involved in perpetuating obstructive respiratory events. In healthy subjects arousal is associated with brief hyperventilation followed by more prolonged hypoventilation on return to sleep. This study was designed to assess whether elevated sleeping upper airway resistance (R(UA)) alters the ventilatory response to arousal and subsequent breathing on return to sleep in patients with obstructive sleep apnoea (OSA). Inspired minute ventilation (V(I)), R(UA) and end-tidal CO(2) pressure (P(ET,CO(2))) were measured in 22 patients (11 men, 11 women) with OSA (mean +/-s.e.m., apnoea-hypopnoea index (AHI) 48.9 +/- 5.9 events h(-1)) during non-rapid eye movement (NREM) sleep with low R(UA) (2.8 +/- 0.3 cmH(2)O l(-1) s; optimal continuous positive airway pressure (CPAP) = 11.3 +/- 0.7 cmH(2)O) and with elevated R(UA) (17.6 +/- 2.8 cmH(2)O l(-1) s; sub-optimal CPAP = 8.4 +/- 0.8 cmH(2)O). A single observer, unaware of respiratory data, identified spontaneous and tone-induced arousals of 3-15 s duration preceded and followed by stable NREM sleep. V(I) was compared between CPAP levels before and after spontaneous arousal in 16 subjects with tone-induced arousals in both conditions. During stable NREM sleep at sub-optimal CPAP, P(ET,CO(2)) was mildly elevated (43.5 +/- 0.8 versus 42.5 +/- 0.8 Torr). However, baseline V(I) (7.8 +/- 0.3 versus 8.0 +/- 0.3 l min(-1)) was unchanged between CPAP conditions. For the first three breaths following arousal, V(I) was higher for sub-optimal than optimal CPAP (first breath: 11.2 +/- 0.9 versus 9.3 +/- 0.6 l min(-1)). The magnitude of hypoventilation on return to sleep was not affected by the level of CPAP and both obstructive and central respiratory events were rare following arousal. Similar results occurred after tone-induced arousals which led to larger responses than spontaneous arousals. V(I) for the first breath following arousal under optimal CPAP was greater in men than women (11.0 +/- 0.4 versus 7.6 +/- 0.6 l min(-1)). These results demonstrate that the ventilatory response to arousal is influenced by pre-arousal airway resistance and gender. Whether this contributes to the perpetuation of respiratory events and the pathogenesis of OSA is unclear.

Background: To address the growing burden of disease and long waiting lists for sleep services, a simplified two-stage model was developed and validated for identifying obstructive sleep apnoea (OSA) in primary care using a screening questionnaire followed by home sleep monitoring. Methods: 157 patients aged 25–70 years attending their primary care physician for any reason at six primary care clinics in rural and metropolitan regions of South Australia participated. The first 79 patients formed the development group and the next 78 patients the validation group. A screening questionnaire was developed from factors identified from sleep surveys, demographic and anthropometric data to be predictive of moderate to severe OSA. Receiver operating characteristic (ROC) curve analysis was used to validate the two-channel ApneaLink device against full polysomnography. The diagnostic accuracy of the overall two-stage model was then evaluated. Results: Snoring, waist circumference, witnessed apnoeas and age were predictive of OSA and incorporated into a screening questionnaire (ROC area under curve (AUC) 0.84, 95% CI 0.75 to 0.94, p

Study Objectives: Obstructive sleep apnea (OSA) is associated with driving impairment and road crashes. However, daytime function varies widely between patients presenting a clinical challenge when assessing crash risk. This study aimed to determine the proportion of patients showing “normal” versus “abnormal” driving simulator performance and examine whether anthropometric, clinical, and neurobehavioral measures predict abnormal driving. Methods: Thirty-eight OSA patients performed a 90-min simulated driving task under 3 conditions: normal sleep, restricted sleep (4 h in bed), and normal sleep + alcohol (BAC~0.05 g/dL). Patients were classifi ed as “resilient” drivers if, under all 3 experimental conditions their mean steering deviation fell within 2 standard deviations of the mean steering deviation of 20 controls driving under baseline normal sleep conditions, or a “vulnerable” driver if mean steering deviation was outside this range in at least one experimental condition. Potentially predictive baseline anthropometric, clinical, neurocognitive, and cortical activation measures were examined. Results: Of the 38 OSA patients examined, 23 (61%) and 15 (39%) were classifi ed as resilient and vulnerable drivers, respectively. There were no differences in baseline measures between the groups, although the proportion of females was greater and self-reported weekly driving exposure was less among vulnerable drivers (p < 0.05). On univariate analysis gender, weekly driving hours, and auditory event related potential P2 amplitude were weakly associated with group status. Multivariate analysis showed weekly driving hours (OR 0.69, 95%CI, 0.51-0.94, p = 0.02) and P2 amplitude (OR 1.34, 95%CI 1.02-1.76, p = 0.035) independently predicted vulnerable drivers. Conclusions: Most OSA patients demonstrated normal simulated driving performance despite exposure to further sleep loss or alcohol. Most baseline measures did not differentiate between resilient and vulnerable drivers, although prior driving experience and cortical function were predictive. Novel measures to assist identifi cation of OSA patients at risk of driving impairment and possibly accidents are needed. Trial Registration: Data presented in this manuscript was collected as part of a clinical trial “Experimental Investigations of Driving Impairment in Obstructive Sleep Apnea.” Trial ID: ACTRN12610000009011, URL: http://www.anzctr.org.au/trial_

Due to rising demand for sleep services, there has been growing interest in ambulatory models of care for obstructive sleep apnea (OSA). With appropriate training and simplified management tools, primary care physicians (PCPs) are ideally positioned to take on a greater role in the diagnosis and treatment of OSA. Objective: To compare the clinical efficacy and cost-effectiveness of a simplified model of diagnosis and care for OSA in primary care relative to that in specialist sleep centres. Design: A randomised, controlled, non-inferiority study. Setting: Primary care practices in metropolitan Adelaide and 3 rural regions of South Australia and a university hospital sleep medicine centre in Adelaide, Australia. Patients: A total of 155 patients with OSA (identified by screening questionnaire and home oximetry) and Epworth Sleepiness Scale (ESS) ≥8 or resistant hypertension were randomised into the study between September 2008 to June 2010. 81 patients were randomly assigned to the primary care arm and 74 patients to the specialist arm., The study was funded by the National Health and Medical Research Council of Australia (Project Grant 426744) and a small grant from the Flinders Medical Centre Foundation. Research scholarship support was provided to Dr Chai-Coetzer by the Flinders Medical Centre Clinicians Trust. Equipment donations were received from ResMed (ApneaLink oximetry monitors and CPAP machines), Philips Respironics (CPAP machines) and SomnoMed (mandibular advancement splints).