Early signs of neurobehavioral improvement after short-termcontinuous positive airway pressure in obstructive sleep apnea

This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).Commentary on: Ivana Rosenzweig, Martin Glasser, William R. Crum, Matthew J. Kempton, Milan Milosevic, Alison McMillan, Guy D. Leschziner, Veena Kumari, Peter Goadsby, Anita K. Simonds, Steve C.R. Williams, Mary J. Morrell. (2016) Changes in Neurocognitive Architecture in Patients with Obstructive Sleep Apnea Treated with Continuous Positive Airway Pressure EBioMedicine, Volume 7, May 2016, Pages 221-22

Obstructive Sleep Apnoea: Therapeutic Options and Challenges

Creative Commons Non Commercial CC BY-NC: This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (http://www.creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage).Obstructive sleep apnoea (OSA) is a common sleep disorder that is associated with significant negative health outcomes including cardiovascular disease, daytime sleepiness, neurocognitive deficits, and increased motor vehicle and workplace accidents. There is wide variation in OSA symptoms and other downstream effects between patients highlighting the need to individualise therapy. Continuous positive airway pressure delivered by a face mask is the gold standard treatment, but adherence to this therapy is poor and improvements in outcomes are often incomplete. A range of alternative treatments are available and may suit different patients. These include behavioural treatments such as weight loss, mandibular advancement using an oral device, sleep posture modification, upper airway surgery, and upper airway muscle stimulation. Towards individualised OSA therapy, novel phenotyping approaches are being developed to identify the specific pathophysiological causes of OSA applying to individual patients. Furthermore, research is underway to help identify patients with OSA at higher risk of daytime sleepiness and adverse cardiovascular and neurocognitive consequences and predict how individuals might respond to treatment. In this article, we review the prevalence, risk factors, and main consequences of OSA; the main treatment modalities available at present; and some new methods for phenotyping patients with OSA that hold promise for a more personalised and effective approach to screening, diagnosis, and treatment

Post-stroke sleep-disordered breathing - pathophysiology and therapy options

Note: This article was submitted to Otorhinolaryngology - Head and Neck Surgery, a section of the journal Frontiers in Surgery. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.Sleep-disordered breathing (SDB), encompassing both obstructive and central sleep apnea, is prevalent in at least 50% of stroke patients. Small studies have shown vast improvements in post-stroke functional recovery outcomes after the treatment of SDB by continuous positive airway pressure. However, compliance to this therapy is very poor in this complex patient group. There are alternative therapy options for SDB that may be more amenable for use in at least some post-stroke patients, including mandibular advancement, supine avoidance, and oxygen therapy. There are few studies, however, that demonstrate efficacy and compliance with these alternative therapies currently. Furthermore, novel SDB-phenotyping approaches may help to provide important clinical information to direct therapy selection in individual patients. Prior to realizing individualized therapy, we need a better understanding of the pathophysiology of SDB in post-stroke patients, including the role of inherent phenotypic traits, as well as the contribution of stroke size and location. This review summarizes the available literature on SDB pathophysiology and treatment in post-stroke patients, identifies gaps in the literature, and sets out areas for further research

How the chance of missing the alarm during an on-call shift affects pre-bed anxiety, sleep and next day cognitive performance

© 2018 Elsevier. This manuscript version is made available under the CC-BY-NC-ND 4.0 license: http://creativecommons.org/licenses/by-nc-nd/4.0/ This author accepted manuscript is made available following 12 month embargo from date of publication (September 2018) in accordance with the publisher’s archiving policy.This study investigated how the likelihood of missing an alarm affects pre-bed anxiety, sleep and next day cognitive performance during on-call shifts. Participants (n=24) completed one adaptation night, one control night and two on-call nights in a time-isolated sleep laboratory. On one of the on-call nights, participants were informed that they would be woken by a loud alarm that they would definitely not be able to sleep through (low likelihood of missing the alarm). On the other on-call night, participants were informed that they would be woken by a quiet alarm that they may sleep through (high likelihood of missing the alarm). The two on-call nights were counterbalanced. Pre-bed anxiety was measured using the State Trait Anxiety Inventory x-1, while sleep macro- and micro-architecture was examined via routine polysomnography and power spectral analyses respectively. Following each sleep, cognitive performance was assessed four times (0930, 1200, 1430, 1700) using the 10-min psychomotor vigilance task (PVT). Results indicated that while pre-bed anxiety was similarly increased during both high and low likelihood of missing the on-call alarm conditions compared with control, only in the high likelihood condition was total sleep time shorter and sleep efficiency lower compared with the control condition. However, more wake after sleep onset was found in the low likelihood condition compared with control. PVT data indicate that response times (mean reciprocal and mean fastest 10% of reaction time) were fastest in the low likelihood condition, indicating better performance when compared with both other conditions. However, there were significantly more lapses in the low likelihood condition compared with control. No significant EEG power spectral differences were observed. As such, it appears that there are detrimental effects of both on-call conditions on anxiety, sleep and performance, with sleep poorest when the likelihood of missing the alarm is high. The adverse impacts on sleep and performance outcomes while on-call may be mitigated by the implementation of workplace systems to reduce the likelihood of missing alarms (e.g., having two available options for contacting on-call workers).This study was funded by an Australian Research Council Discovery grant (DP 150104497). Funding for Madeline Sprajcer’s PhD scholarship was provided by this grant. Dr Grace Vincent is supported by an Early Career Fellowship at Central Queensland University

Primary care management of chronic insomnia: a qualitative analysis of the attitudes and experiences of Australian general practitioners

BACKGROUND: Chronic insomnia is a highly prevalent disorder, with ten to thirty percent of Australian adults reporting chronic difficulties falling asleep and/or staying asleep such that it causes significant daytime impairment. Current Australian general practice guidelines recommend cognitive behavioural therapy for insomnia (CBTi) as first line treatment for insomnia, however research suggests that most general practice consultations for insomnia result in a prescription for hypnotic or sedative medicines. Although the first point of contact for patients experiencing symptoms of insomnia is often general practice, little is known about the current role, experiences and capacity of Australian general practitioners to manage insomnia. This study aimed to address that gap by exploring the attitudes and opinions of general practitioners regarding insomnia management, to inform the development and implementation of new models of best practice insomnia care within general practice. METHODS: A descriptive, pragmatic qualitative study. Purposive sampling was used to recruit practising Australian general practitioners, varying in age, years of experience and geographic location. Semi-structured interviews were conducted, and data analysed using thematic analysis.  RESULTS: Twenty-eight general practitioners participated in the study. Three major themes were identified: 1) Responsibility for insomnia care; 2) Complexities in managing insomnia; and 3) Navigating treatment pathways. Whilst general practitioners readily accepted responsibility for the management of insomnia, provision of care was often demanding and difficult within the funding and time constraints of general practice. Patients presenting with comorbid mental health conditions and insomnia, and decision-making regarding long-term use of benzodiazepines presented challenges for general practitioners. Whilst general practitioners confidently provided sleep hygiene education to patients, their knowledge and experience of CBTi, and access and understanding of specialised referral pathways for insomnia was limited.  CONCLUSIONS: General practitioners report that whilst assessing and managing insomnia can be demanding, it is an integral part of general practice. Insomnia presents complexities for general practitioners. Greater clarity about funding options, targeted education about effective insomnia treatments, and referral pathways to specialist services, such as benzodiazepine withdrawal support and psychologists, would benefit insomnia management within general practice

Effect of high-risk sleep apnea on treatment-response to a tailored digital cognitive behavioral therapy for insomnia program : a quasi-experimental trial

Introduction: Therapist-delivered Cognitive Behavioral Therapy for Insomnia (CBTi) is an effective but largely inaccessible treatment for people with Co-Morbid Insomnia and Sleep Apnea (COMISA). To increase CBTi access for COMISA, we aimed to develop a self-guided interactive 5-session digital CBTi program that is appropriate for people with insomnia-alone and COMISA, and compare its effectiveness between people with insomnia-alone, vs. comorbid insomnia and high-risk sleep apnea. Methods: Data from 62 adults with insomnia symptoms were used. High-risk sleep apnea was defined as a score of ≥5 on the OSA50. Participants self-reported symptoms of insomnia (ISI), depression, anxiety, sleepiness (ESS), fatigue, and maladaptive sleep-related beliefs (DBAS-16) at baseline, 8-week, and 16-week follow-up. ESS scores were additionally assessed during each CBTi session. Intent-to-treat mixed models and complete-case chi2 analyses were used. Results: There were more participants with insomnia-alone [n = 43, age M (sd) = 51.8 (17.0), 86.1% female] than suspected COMISA [n = 19, age = 54.0 (14.8), 73.7% female]. There were no between-group differences in baseline questionnaire data, or rates of missing follow-up data. There were no significant group by time interactions on any outcomes. Main effects of time indicated moderate-to-large and sustained improvements in insomnia (d = 3.3), depression (d = 1.2), anxiety (d = 0.6), ESS (d = 0.5), fatigue (d = 1.2), and DBAS-16 symptoms (d = 1.2) at 16-weeks. ESS scores did not increase significantly during any CBTi session. Conclusion: This interactive digital CBTi program is effective in people with insomnia-alone, and people with co-morbid insomnia and high-risk sleep apnea. Further research is required to determine the effectiveness, safety and acceptability of digital CBTi in people with insomnia and confirmed sleep apnea. Clinical Trial Registration: This trial was prospectively registered on the Australian and New Zealand Clinical Trials Registry (ANZCTR, ACTRN12621001395820)

High-quality and anti-inflammatory diets and a healthy lifestyle are associated with lower sleep apnea risk

Study Objectives: Most studies on diet and sleep apnea focus on calorie restriction. Here we investigate potential associations between dietary quality (Healthy Eating Index [HEI], Dietary Inflammatory Index [DII]) and overall healthy lifestyle with sleep apnea risk. Methods: National Health and Nutrition Examination Survey data (waves 2005-2008 and 2015-2018; n = 14,210) were used to determine HEI, DII, and their quintiles, with the fifth quintile indicating highest adherence to each dietary construct. A healthy lifestyle score was determined using diet, smoking, alcohol intake, and physical activity level. The STOP-BANG questionnaire was used to define sleep apnea risk. Generalized linear regression models with binomial family and logit link were used to investigate potential associations. The models were adjusted for socioeconomic status, lifestyle factors, and chronic conditions. Results: The prevalence of high sleep apnea risk was 25.1%. Higher DII was positively associated with sleep apnea (odds ratioQuintile 5 vs Quintile 1 = 1.55; 95% confidence interval, 1.24-1.94; P for trend < .001), whereas higher HEI was associated with reduced sleep apnea risk (odds ratioQuintile 5 vs Quintile 1 = 0.72; 95% confidence interval, 0.59-0.88; P for trend = .007). Higher healthy lifestyle score was also associated with decreased odds of sleep apnea (P for trend < .001). There was a significant interaction between healthy lifestyle and sex with sleep apnea risk (P for interaction = .049) whereby females with higher healthy lifestyle scores had a lower risk of sleep apnea compared to males. Conclusions: Higher-quality and anti-inflammatory diets and a healthier overall lifestyle are associated with lower sleep apnea risk. These findings underline the importance of strategies to improve overall diet quality and promote healthy behavior, not just calorie restriction, to reduce sleep apnea risk

The effects of sleep restriction and alcohol on simulated driving and cortical function in obstructive sleep apnoea.

Obstructive sleep apnoea (OSA) is a common sleep disorder associated with neurobehavioural daytime abnormalities including poor driving simulator performance and an increased risk of motor-vehicle accidents. Treating OSA with continuous positive airway pressure (CPAP) significantly improves many of the daytime consequences of OSA. Until recently it was believed that CPAP treatment can completely resolve excessive daytime sleepiness and neurobehavioural abnormalities associated with OSA. However, recent evidence suggests that compared to results in well-matched healthy subjects, levels of daytime vigilance and cortical activation and some domains of cognitive function in OSA patients may not return to normal, even after effective OSA treatment with good treatment compliance. Sleep restriction and low-dose alcohol consumption are common “life style” factors that have a negative impact on the central nervous system and driving performance in healthy subjects. However, their impact on driving simulator performance and cortical information processing in patients with OSA has not been examined. The hypotheses tested in the work presented in this thesis were that: a) Sleep restriction and alcohol have a greater deleterious effect on driving simulator performance and cortical information processing in untreated OSA patients than in healthy subjects. b) Treatment of severe OSA with CPAP improves, but does not normalise driving simulator performance and cortical information processing. Consequently, the broad aims were: a) To compare the effects of sleep restriction and alcohol on driving simulator performance and auditory cortical event-related potentials in OSA patients and healthy age and gender-matched controls. b) To compare driving simulator performance and auditory cortical eventrelated potentials in severe OSA patients before and after 3-months of CPAP therapy and to compare these results with those of healthy, untreated subjects also studied 3-months apart. Study 1 (CHAPTER 2) compared performance during a 90-minute simulated drive in 38 patients with OSA and 20 healthy age and gender-matched control subjects under 3 conditions studied in random order: 1) normal sleep, 2) sleep restriction (4 hours in bed on the night prior to study) and 3) low-dose alcohol (blood alcohol concentration 0.05 g/dL). Compared to control subjects, OSA patients exhibited a higher crash rate, increased overall steering deviation and more steering deterioration with time-on-task. Following sleep restriction and alcohol there was a ~40% greater increase in steering deviation in OSA patients than in control subjects. Crashes were more likely to occur in patients with OSA compared with control subjects. OSA patients were more likely to crash under sleep restriction and alcohol conditions compared to the normal sleep condition. Simulator crashes were associated with behavioural and physiological evidence of increased sleepiness. The results of this study showed that compared with healthy subjects, OSA patients have worse driving simulator performance and are more vulnerable to the effects of prior alcohol and sleep restriction on various driving performance parameters. To the extent that these simulator findings may be indicative of real on-road driving performance, it may be advisable for untreated OSA patients to avoid sleep restriction and even legal doses of alcohol prior to extended driving. Study 2 (CHAPTER 3) assessed the effectiveness of ~3 months CPAP treatment in improving driving simulator performance. Eleven severe OSA patients and nine age- and gender-matched controls were studied on two occasions 3 months apart using the same protocol as in Study 1. In the intervening period OSA patients were treated with CPAP during which they showed a high level of compliance with therapy (mean ± SD, 6.0 ± 1.4 hours/night). At baseline, OSA patients demonstrated worse driving simulator performance compared to controls under all conditions, and showed greater steering decrements following sleep restriction and alcohol than control subjects. After CPAP treatment, OSA patients showed significant improvements in steering deviation under all conditions, but steering deviation did not reach the level of control subjects and crash frequency remained significantly elevated. Braking reaction time was not significantly different between groups, conditions, or treatments and there were no significant interaction effects. Taken together, these findings suggest that CPAP treatment is only partially effective in improving driving performance during simulated long and monotonous driving. To the extent that driving simulator findings may be indicative of real onroad driving performance it may be appropriate to advise patients, even after apparent optimal CPAP treatment, to be cautious when undertaking long distance driving, as they could remain at higher than normal accident risk. Given the behavioural finding of residual driving simulator impairment in CPAPtreated, severe OSA patients in studies 1 and 2, the final study (CHAPTER 4) explored whether cortical information processing during a simple attention task demonstrated similar treatment resistant abnormalities. The effects of CPAP treatment on cortical information processing in OSA patients were examined by comparing early and late components of auditory target (odd-ball) event-related potential responses in 9 patients with severe OSA and 9 healthy age- and gendermatched controls. The results showed that compared to controls, early and late auditory event related potentials were abnormal in severe OSA patients at baseline. Specifically, N2 and P3 peaks were smaller and delayed in latency, and P2 amplitude was larger. At follow-up, P3 latency was the only measure to show improvement following CPAP treatment, but remained prolonged in patients compared to control subjects despite high CPAP treatment compliance in OSA patients (mean ± SD, 6.0 ± 1.6 hours/night). None of the abnormalities in earlier components (N2 and P2) observed at baseline changed in CPAP-treated OSA patients. In summary, driving simulator performance is impaired in patients with OSA compared to healthy controls, and patients demonstrate a greater susceptibility to the detrimental effects of sleep restriction and alcohol. Driving simulator performance is only partially improved in CPAP-treated OSA patients. Thus, it may be prudent to advise patients with OSA to be cautious and avoid sleep loss or alcohol prior to long distance driving, even when optimally treated. Residual abnormalities were also evident in auditory cortical evoked responses in optimally treated OSA patients, suggesting the possibility of a permanent reduction in information processing capacity. The mechanisms underlying the observed vulnerability to additional stressors (sleep loss and alcohol) and the residual driving performance and electrophysiological abnormalities observed in CPAP-treated patients warrants further investigation. In addition, examining how these driving simulator and electrophysiological findings relate to on-road motor vehicle accident risk in patients with OSA is another important question worthy of further investigation.Thesis (Ph.D.) -- University of Adelaide, School of Medical Sciences, 201

Post-Stroke Sleep-Disordered Breathing—Pathophysiology and Therapy Options

Sleep-disordered breathing (SDB), encompassing both obstructive and central sleep apnea, is prevalent in at least 50% of stroke patients. Small studies have shown vast improvements in post-stroke functional recovery outcomes after the treatment of SDB by continuous positive airway pressure. However, compliance to this therapy is very poor in this complex patient group. There are alternative therapy options for SDB that may be more amenable for use in at least some post-stroke patients, including mandibular advancement, supine avoidance, and oxygen therapy. There are few studies, however, that demonstrate efficacy and compliance with these alternative therapies currently. Furthermore, novel SDB-phenotyping approaches may help to provide important clinical information to direct therapy selection in individual patients. Prior to realizing individualized therapy, we need a better understanding of the pathophysiology of SDB in post-stroke patients, including the role of inherent phenotypic traits, as well as the contribution of stroke size and location. This review summarizes the available literature on SDB pathophysiology and treatment in post-stroke patients, identifies gaps in the literature, and sets out areas for further research