Impact of cystic fibrosis multidisciplinary virtual clinics on patient experience, time commitments and costs.

BACKGROUND AND AIMS: The experience of outpatient care may differ for select patient groups. This prospective study evaluates the adult patient experience of multidisciplinary outpatient cystic fibrosis (CF) care with videoconferencing through telehealth compared with face-to-face care the year prior. METHODS: People with CF without a lung transplant were recruited. Patient-reported outcomes were obtained at commencement and 12 months into the study, reflecting both their face-to-face and telehealth through videoconferencing experience, respectively. Three patient cohorts were analysed: (i) participants with a regional residence, (ii) participants with a nonregional including metropolitan residence and (iii) participants with colonised multiresistant microbiota. RESULTS: Seventy-four patients were enrolled in the study (mean age, 37 ± 11 years; 50% male; mean forced expiratory volume in the first second of expiration, 60% [standard deviation, 23]) between February 2020 and May 2021. No differences between models were observed in the participants' rating of the health care team, general and mental health rating, and their confidence in handling treatment plans at home. No between-group differences in the Cystic Fibrosis Questionnaire - Revised (CFQ-R) were observed. Travel duration and the cost of attending a clinic was significantly reduced, particularly for the regional group (4 h, AU$108 per clinic; P < 0.05). A total of 93% respondents preferred to continue with a hybrid approach. CONCLUSION: In this pilot study, participants' experience of care and quality of life were no different with face-to-face and virtual care between the groups. Time and cost-savings, particularly for patients living in regional areas, were observed. Most participants preferred to continue with a hybrid model for outpatient care.

Predictors of weight loss in obese patients with obstructive sleep apnea.

PURPOSE: Consistent predictors of weight loss outcomes with very low-energy diets (VLEDs) in obstructive sleep apnea (OSA) have not been identified. This study aimed to identify variables predictive of weight loss success in obese patients with OSA undertaking an intensive weight loss programme. METHODS: We analysed biological, psychological, and behavioural variables as potential predictors of weight loss in obese patients with OSA after a 2-month VLED followed by one of two 10-month weight loss maintenance diets. Actigraphy, in-lab polysomnography, urinary catecholamines, and various psychological and behavioural variables were measured at baseline, 2, and 12 months. Spearman's correlations analysed baseline variables with 2-month weight loss, and 2-month variables with 2-12 month-weight change. RESULTS: Forty-two patients completed the VLED and thirty-eight completed the maintenance diets. Actigraphy data revealed that late bedtime (rs = - 0.45, p = < 0.01) was correlated with 2-month weight loss. The change in the time that participants got out of bed (rise-time) from baseline to two months was also correlated with 2-month weight loss (rs = 0.36, p = 0.03). The Impact of Weight on Quality of Life-Lite questionnaire (IWQOL) Public Distress domain (rs = - 0.54, p = < 0.01) and total (rs = - 0.38, p = 0.02) scores were correlated with weight loss maintenance from 2 to 12 months. CONCLUSIONS: Results from this small patient sample reveal correlations between actigraphy characteristics and weight loss in obese patients with OSA. We suggest the IWQOL may also be a useful clinical tool to identify OSA patients at risk of weight regain after initial weight loss. CLINICAL TRIAL REGISTRATION: This clinical trial was prospectively registered on 18/02/2013 with the Australia and New Zealand Clinical Trials Registry (ACTRN12613000191796). PUBLIC REGISTRY TITLE: Sleep, Lifestyle, Energy, Eating, Exercise Program for the management of sleep apnea patients indicated for weight loss treatment: A randomised, controlled pilot study. URL: https://www.anzctr.org.au/Trial/Registration/TrialReview.aspx?id=363680.

The effect of acute morphine on sleep in male patients suffering from sleep apnea: Is there a genetic effect? An RCT Study.

Questionnaire-based studies have suggested genetic differences in sleep symptoms in chronic opioid users. The present study aims to investigate if there is a genetic effect on sleep architecture and quantitative electroencephalogram (EEG) in response to acute morphine. Under a randomized, double-blind, placebo-controlled, crossover design, 68 men with obstructive sleep apnea undertook two overnight polysomnographic studies conducted at least 1 week apart. Each night they received either 40 mg of controlled-release morphine or placebo. Sleep architecture and quantitative EEG were compared between conditions. Blood was sampled before sleep and on the next morning for genotyping and pharmacokinetic analyses. We analysed three candidate genes (OPRM1 [rs1799971, 118 A > G], ABCB1[rs1045642, 3435 C > T] and HTR3B [rs7103572 C > T]). We found that morphine decreased slow wave sleep and rapid eye movement sleep and increased stage 2 sleep. Those effects were less in subjects with HTR3B CT/TT than in those with CC genotype. Similarly, sleep onset latency was shortened in the ABCB1 CC subgroup compared with the CT/TT subgroup. Total sleep time was significantly increased in ABCB1 CC but not in CT/TT subjects. Sleep apnea and plasma morphine and metabolite concentration were not confounding factors for these genetic differences in sleep. With morphine, patients had significantly more active/unstable EEG (lower delta/alpha ratio) during sleep. No genetic effects on quantitative EEG were detected. In summary, we identified two genes (HTR3B and ABCB1) with significant variation in the sleep architecture response to morphine. Morphine caused a more active/unstable EEG during sleep. Our findings may have relevance for a personalized medicine approach to targeted morphine therapy.

Development and validation of a model for diagnosis of obstructive sleep apnoea in primary care.

BACKGROUND AND OBJECTIVE: Use of in-laboratory polysomnography (PSG) to diagnose obstructive sleep apnoea (OSA) is cost and resource intensive. Questionnaires, physical measurements and home monitors have been studied as potential simpler alternatives. This study aimed to develop a diagnostic model for OSA for use in primary care. METHODS: Primary care practitioners were trained to recognize symptoms of sleep apnoea and recruited patients based on the clinical need to investigate OSA. Assessment was by symptom questionnaires, anthropomorphic measurements, digital facial photography, and a single-channel nasal flow monitor (Flow Wizard©, DiagnoseIT, Sydney, Australia) worn at home for 3 nights. The in-laboratory PSG was the reference test, with OSA defined as apnoea-hypopnoea index (AHI) ≥10 events/h. RESULTS: In the model development phase, 25 primary care practitioners studied 315 patients in whom they suspected OSA, of which 57% had AHI≥10 and 22% had AHI≥30. Published OSA questionnaires provided low to moderate prediction of OSA (area under the curve [AUC] 0.53-0.73). The nasal flow monitor alone yielded high accuracy for predicting OSA with AUC of 0.87. Sensitivity was 0.87 and specificity 0.77 at a threshold respiratory event index (REI) of 18 events/h. A model adding age, gender, symptoms and BMI to the nasal flow monitor REI only modestly improved OSA prediction (AUC 0.89), with similar AUC (0.88) confirmed in the validation population of 114 patients. CONCLUSION: Sleep apnoea can be diagnosed in the primary care setting with a combination of clinical judgement and portable monitor test outcomes.

Sleep EEG microstructure is associated with neurobehavioural impairment after extended wakefulness in obstructive sleep apnea.

PURPOSE: Using quantitative EEG (qEEG) analysis, we investigated sleep EEG microstructure as correlates of neurobehavioural performance after 24 h of extended wakefulness in untreated OSA. METHODS: Eight male OSA patients underwent overnight polysomnography (PSG) at baseline followed by 40 h awake with repeated performance testing (psychomotor vigilance task [PVT] and AusEd driving simulator). EEG slowing during REM and spindle density during NREM sleep were calculated using power spectral analysis and a spindle detection algorithm at frontal and central electrode sites. Correlations between sleep EEG microstructure measures and performance after 24-h awake were assessed. RESULTS: Greater EEG slowing during REM sleep was associated with slower PVT reaction times (rho = - 0.79, p = 0.02), more PVT lapses (rho = 0.87, p = 0.005) and more AusEd crashes (rho = 0.73, p = 0.04). Decreased spindle density in NREM sleep was also associated with slower PVT reaction times (rho = 0.89, p = 0.007). Traditional PSG measures of disease severity were not consistent correlates of neurobehavioural performance in OSA. CONCLUSIONS: Sleep EEG microstructure measures recorded during routine PSG are associated with impaired vigilance in OSA patients after sleep deprivation. SIGNIFICANCE: Quantitative brain oscillatory (or EEG)-based measures of sleep may better reflect the deleterious effects of untreated OSA than traditional PSG metrics in at-risk individuals. Trial Registration ACTRN12606000066583.

Comparing treatment effects of a convenient vibratory positional device to CPAP in positional OSA: a crossover randomised controlled trial.

OBJECTIVES: Up to 77% of patients with obstructive sleep apnoea (OSA) have positional OSA (POSA) but traditional positional therapy (PT) methods have failed as they were poorly tolerated. New convenient vibratory PT devices have been invented but while recent studies suggest high treatment efficacy and adherence, there are no published data comparing these devices directly with continuous positive airway pressure (CPAP). Our objective is to evaluate if a convenient vibratory PT device is non-inferior to CPAP in POSA treatment. METHODS: In this crossover randomised controlled trial, we enrolled patients with POSA with significant daytime sleepiness (Epworth Sleepiness Scale (ESS)≥10). POSA diagnosis was based on: (1) total Apnoea/Hypopnoea Index (AHI)>10/hour and non-supine AHI<10/hour (2) supine AHI≥2 × non-supine AHI. Patients used their initial allocated devices (PT or CPAP) for 8 weeks before crossing to the alternative intervention after a 1 week washout. The primary aim is to measure changes in ESS between the two treatments. Secondary outcomes include sleep study parameters and patient treatment preference (ClinicalTrials.gov: NCT03125512). RESULTS: 40 patients completed the trial between April 2017 and December 2018. Difference in ESS after 8 weeks of device use (PT minus CPAP) was 2.0 (95% CI 0.68 to 3.32), exceeding our predetermined non-inferiority margin of 1.5. AHI on CPAP was lower than with PT (4.0±3.2 vs 13.0±13.8 events/hour, respectively, p=0.001), although both were lower than at baseline. Time spent supine was significantly lower with PT than CPAP (p<0.001). 60% of patients preferred CPAP, 20% preferred PT, while 20% preferred neither device. CONCLUSIONS: The non-inferiority ESS endpoint for PT compared with CPAP was not met and the results were inconclusive. Future trials with larger sample sizes or in less symptomatic patients are warranted to provide further insight into the role of these new vibratory PT devices.

Melatonin for rapid eye movement sleep behavior disorder in Parkinson's disease: A randomised controlled trial.

BACKGROUND: Melatonin may reduce REM-sleep behavior disorder (RBD) symptoms in Parkinson's disease (PD), though robust clinical trials are lacking. OBJECTIVE: To assess the efficacy of prolonged-release (PR) melatonin for RBD in PD. METHODS: Randomized, double-blind, placebo-controlled, parallel-group trial with an 8-week intervention and 4-week observation pre- and postintervention (ACTRN12613000648729). Thirty PD patients with rapid eye movement sleep behavior disorder were randomized to 4 mg of prolonged-release melatonin (Circadin) or matched placebo, ingested orally once-daily before bedtime. Primary outcome was the aggregate of rapid eye movement sleep behavior disorder incidents averaged over weeks 5 to 8 of treatment captured by a weekly diary. Data were included in a mixed-model analysis of variance (n = 15 per group). RESULTS: No differences between groups at the primary endpoint (3.4 events/week melatonin vs. 3.6 placebo; difference, 0.2; 95% confidence interval = -3.2 to 3.6; P = 0.92). Adverse events included mild headaches, fatigue, and morning sleepiness (n = 4 melatonin; n = 5 placebo). CONCLUSION: Prolonged-release melatonin 4 mg did not reduce rapid eye movement sleep behavior disorder in PD. © 2019 The Authors. Movement Disorders published by Wiley Periodicals, Inc. on behalf of International Parkinson and Movement Disorder Society.

The effect of acute morphine on obstructive sleep apnoea: a randomised double-blind placebo-controlled crossover trial.

OBJECTIVE: Anaesthesiology guidelines suggest that opioids worsen obstructive sleep apnoea (OSA) despite no randomised controlled trial evidence. We therefore conducted a randomised controlled trial to evaluate the effects of a common clinical dose of morphine on OSA, and to identify clinical phenotype and genotype vulnerability to opioid-respiratory depression. METHODS: Under a double-blind, randomised, crossover design, 60 male patients with OSA attended two visits to the hospital sleep laboratory, at least 1 week apart. Either 40 mg controlled-release oral morphine or placebo was administered. Awake ventilatory chemoreflex tests were performed post dose and prior to overnight polysomnography monitoring. Blood was sampled before sleep and the next morning for toxicology and genotype analyses. Sleep time with oxygen saturation (SpO2) <90% (T90) was the primary outcome. RESULTS: Despite a large inter-individual variability, 40 mg morphine did not worsen T90 and apnoea-hypopnoea index, and only decreased the SpO2 nadir by 1.3%. In patients with severe OSA, a lower baseline CO2ventilatory response threshold correlated with the worsening of T90, apnoea-hypopnoea index and oxygen desaturation index with morphine use. Patients with OSA and the A118G OPRM1 polymorphism of A/A and A/G had a significantly different morphine effect on awake ventilatory chemosensitivity and T90 during sleep. CONCLUSIONS: 40 mg oral controlled-release morphine did not worsen OSA in men, challenging traditional thinking that OSA will be worsened by opioids. Individual opioid response in patients with OSA may relate to baseline CO2 response threshold and OPRM1 genotype. Our study findings may pave the way for a precision medicine approach to avoid opioid-related risks. TRIAL REGISTRATION NUMBER: The Australian and New Zealand Clinical Trial Registry, ACTRN12613000858796.

Intra-individual stability of NREM sleep quantitative EEG measures in obstructive sleep apnea.

Electroencephalography is collected routinely during clinical polysomnography, but is often utilised to simply determine sleep time to calculate apnea-hypopnea indices. Quantitative analysis of these data (quantitative electroencephalogram) may provide trait-like information to predict patient vulnerability to sleepiness. Measurements of trait-like characteristics need to have high test-retest reliability. We aimed to investigate the intra-individual stability of slow-wave (delta power) and spindle frequency (sigma power) activity during non-rapid eye movement sleep in patients with obstructive sleep apnea. We recorded sleep electroencephalograms during two overnight polysomnographic recordings in 61 patients with obstructive sleep apnea (median days between studies 47, inter-quartile range 53). Electroencephalograms recorded at C3-M2 derivation were quantitatively analysed using power spectral analysis following artefact removal. Relative delta (0.5-4.5 Hz) and sigma (12-15 Hz) power during non-rapid eye movement sleep were calculated. Intra-class correlation coefficients and Bland-Altman plots were used to assess agreement between nights. Intra-class correlation coefficients demonstrated good-to-excellent agreement in the delta and sigma frequencies between nights (intra-class correlation coefficients: 0.84, 0.89, respectively). Bland-Altman analysis of delta power showed a mean difference close to zero (-0.4, 95% limits of agreement -9.4, 8.7) and no heteroscedasticity with increasing power. Sigma power demonstrated heteroscedasticity, with reduced stability as sigma power increased. The mean difference of sigma power between nights was close to zero (0.1, 95% limits -1.6, 1.8). We have demonstrated the stability of slow-wave and spindle frequency electroencephalograms during non-rapid eye movement sleep within patients with obstructive sleep apnea. The electroencephalogram profile during non-rapid eye movement sleep may be a useful biomarker for predicting vulnerability to daytime impairment in obstructive sleep apnea and responsiveness to treatment.

Nocturnal hypoxaemia is associated with adverse outcomes in interstitial lung disease.

BACKGROUND AND OBJECTIVE: Sleep-disordered breathing (SDB) has been reported as highly prevalent in idiopathic pulmonary fibrosis (IPF) and other interstitial lung disease (ILD) populations. Nocturnal oxygen desaturation (NOD), or the total sleep time spent with SpoO2 < 90% (TST < 90), can occur both with and without associated apnoeas, and is common in ILD. This study aimed to characterize abnormal SDB and extent of TST < 90 in ILD patients and evaluate relationships between TST < 90 and markers of disease severity, development of pulmonary hypertension (PH) and mortality. METHODS: Consecutive, newly referred ILD patients attending a specialist clinic underwent polysomnography (PSG). Serial lung function tests, echocardiography and other clinical variables were recorded. Predictors of PH and mortality were evaluated using logistic regression and Cox proportional hazards regression analyses. RESULTS: A total of 92 ILD patients (including 44 with IPF) underwent PSG. At least mild obstructive sleep apnoea (OSA) was observed in 65.2%, with rapid eye movement (REM)-related events occurring frequently. At least 10% TST < 90 (designated 'significant NOD') was present in 35.9% of patients, and was associated with PH at baseline echocardiography. Multiple indices of hypoxaemia during sleep, including significant NOD, predicted the development of new or worsening PH. TST < 90 predicted overall and progression-free survival. CONCLUSION: Nocturnal oxygen saturation is associated with poorer prognosis in ILD patients and may contribute towards the pathogenesis of pulmonary vascular disease.

Does Armodafinil Improve Driving Task Performance and Weight Loss in Sleep Apnea? A Randomized Trial.

RATIONALE: Patients with obstructive sleep apnea (OSA) unable to tolerate standard treatments have few alternatives. They may benefit from weight loss, but the major symptom of daytime performance impairment may remain during weight loss programs. OBJECTIVES: We hypothesized that wakefulness-promoter armodafinil would improve driving task performance over placebo in patients undergoing weight loss. METHODS: This was a placebo-controlled, double-blind, randomized trial of armodafinil versus placebo daily for 6 months in patients who were also randomized to one of two diets for 6 months with follow-up at 1 year in overweight, adult, patients with OSA who had rejected standard treatment and suffered daytime sleepiness. MEASUREMENTS AND MAIN RESULTS: Primary outcome was change in steering deviation in the final 30 minutes of a 90-minute afternoon driving task (AusED) at 6 months. Secondary outcomes were Epworth Sleepiness Scale, Functional Outcomes of Sleep Questionnaire, and fat mass measured by dual-emission X-ray absorptiometry. Armodafinil improved driving task performance over placebo at 3 months (12.9 cm; 95% confidence interval, 4.1-21.7; P = 0.004), but not the primary time point of 6 months (5.5 cm; 95% confidence interval, -3.3 to 14.3; P = 0.223). Patients on armodafinil lost 2.4 kg more fat than those on placebo at 6 months (95% confidence interval, 0.9-4.0; P = 0.002). Other secondary outcomes were not significantly improved. CONCLUSIONS: Armodafinil did not improve driving task performance at the primary endpoint of 6 months. Armodafinil might be a useful adjunctive to weight loss in patients with OSA rejecting conventional treatments but this needs to be directly tested in a specifically designed, properly powered clinical trial. Clinical trial registered with Australian and New Zealand Clinical Trials Registry (ACTRN 12611000847910).

Role of venous blood gases in hypercapnic respiratory failure chronic obstructive pulmonary disease patients presenting to the emergency department.

BACKGROUND: Many patients with acute exacerbations of chronic obstructive pulmonary disease (AECOPD) have type 2 respiratory failure (T2RF). Often arterial blood gases are not performed and correlation with venous blood gases (VBG) is controversial. The venous pH and bicarbonate (HCO3 ) are useful, but VBG pCO2 (PvCO2 ) is considered too unpredictable. AIM: To examine the utility of VBG in this cohort of patients. METHODS: A prospective study of AECOPD patients with T2RF presenting to the emergency department was performed. Patients being considered for non-invasive ventilation and who required an arterial blood gas were invited to participate. A subsequent VBG was also taken, and Bland-Altman plots were used for analysis. RESULTS: Sixty-three patients were included in this study. The limits of agreement for pH and HCO3 were narrow. Wider limits of agreement with a systematic bias of 7.7 mmHg were noted with pCO2 . CONCLUSIONS: The utility of VBG pH and HCO3 was again demonstrated. VBG pCO2 in this cohort of patients may have a role in the assessment of patients with AECOPD. Further study is needed on the possible role of VBG in the management of such patients with T2RF particularly those using non-invasive ventilation.

Parsing the craniofacial phenotype: effect of weight change in an obstructive sleep apnoea population.

PURPOSE: Craniofacial structure is an important risk factor in the development of obstructive sleep apnoea. Most craniofacial imaging methods are not feasible for large-scale studies or the clinic. Craniofacial photography is a high-throughput technique for facial phenotyping; however, derived measurements are a composite of skeletal and soft tissue craniofacial information. Weight change is a paradigm to help determine which facial measurements most relate to regional soft tissue (i.e. change with weight) versus skeletal structure (i.e. stable with weight changes). We aimed to assess the association between weight change and changes in key facial measurements from facial photography. METHODS: Calibrated frontal and profile photographs were taken of participants in weight loss studies (N = 106). Univariate linear regression was used to assess whether weight change explained changes in facial dimensions. RESULTS: Patients lost 11.7 ± 10.8 kg body weight and 2.0 ± 2.0 cm of neck circumference. Weight changes influenced face width (r = 0.3, p < 0.001), mandibular width (r = 0.4, p < 0.001) and cervicomental angle (r = 0.3, p = 0.001). Facial angles, facial heights and mandibular length were not influenced by weight change. CONCLUSIONS: A weight loss paradigm suggests that face and mandibular width and cervicomental angle most strongly reflect regional adiposity. Facial angles and heights are insensitive to weight change and could be more representative of craniofacial skeletal structure. This study informs the interpretation of facial phenotype assessed by this craniofacial photographic method which can be applied to future studies of craniofacial phenotype in OSA.

Maintenance diets following rapid weight loss in obstructive sleep apnea: a pilot 1-year clinical trial.

Very low energy diets (VLED) appear to be the most efficacious dietary-based obesity reduction treatments in obstructive sleep apnea (OSA); however, effective weight loss maintenance strategies remain untested in this condition. Our study aimed to assess the feasibility, tolerability and efficacy of two common maintenance diets during a 10-month follow-up period after rapid weight loss using a 2-month VLED. In this two-arm, single-centre, open-label pilot trial, obese adult OSA patients received a 2-month VLED before being allocated to either the Australian Guide to Healthy Eating diet (AGHE) or a low glycaemic index high-protein diet (LGHP). Outcomes were measured at 0, 2 and 12 months. We recruited 44 patients [113.1 ± 19.5 kg, body mass index (BMI): 37.2 ± 5.6 kg m-2 , 49.3 ± 9.2 years, 12 females]. Twenty-four patients were on continuous positive airway pressure (CPAP) or mandibular advancement splint (MAS) therapy for OSA. Forty-two patients completed the VLED. The primary outcome of waist circumference was reduced by 10.6 cm at 2 months [95% confidence interval (CI): 9.2-12.1], and patients lost 12.9 kg in total weight (95% CI: 11.2-14.6). There were small but statistically significant regains in waist circumference between 2 and 12 months [AGHE = 3.5 cm (1.3-5.6) and LGHP = 2.8 cm (0.6-5.0]. Other outcomes followed a similar pattern of change. After weight loss with a 2-month VLED in obese patients with OSA, a structured weight loss maintenance programme incorporating commonly used diets was feasible, tolerable and efficacious for 10 months. This programme may be deployed easily within sleep clinics; however, future research should first test its translation within general clinical practice.

Diagnostic pathways for obstructive sleep apnoea in the Australian community: observations from pharmacy-based CPAP providers.

PURPOSE: Models for the diagnosis of obstructive sleep apnoea (OSA) are evolving in many countries to meet public demand. In Australia, the unregulated sleep industry does not provide a framework to govern or review emerging pathways in the community. The objectives of this study were to (1) describe current diagnostic pathways for OSA in Australia as reported by continuous positive airway pressure (CPAP) providers in community pharmacies and (2) obtain stakeholder feedback on pathways and identify potential areas for practice improvement. METHODS: Semi-structured telephone interviews were conducted with pharmacy-based CPAP practitioners. Participants described diagnostic pathways used in their setting. Subsequently, an expert forum of stakeholders provided feedback on identified pathways during a focus group. RESULTS: Twenty-two telephone interviews were conducted, identifying six key diagnostic pathways. Pathways varied in terms of the diagnostic test used, the practitioner who initiated or interpreted the test and who discussed results with the patient and made treatment recommendations. A nine-member stakeholder group raised medical, ethical and organisational concerns over certain pathways. Concerns included diagnostic tests initiated or interpreted in the absence of an appropriately trained medical practitioner and potential conflicts of interest for CPAP providers offering both diagnostic and treatment services. A best practice framework was proposed to guide practice and translate study findings. Preliminary practice recommendations were subsequently developed. CONCLUSIONS: Diagnostic models have evolved in Australia that raise stakeholder concerns. It is important to address these concerns while still facilitating patient access to services. Development of a practice framework could promote medically appropriate, patient-centred care.

An automated algorithm to identify and reject artefacts for quantitative EEG analysis during sleep in patients with sleep-disordered breathing.

PURPOSE: Large quantities of neurophysiological electroencephalogram (EEG) data are routinely collected in the sleep laboratory. These are underutilised due to the burden of managing artefact contamination. The aim of this study was to develop a new tool for automated artefact rejection that facilitates subsequent quantitative analysis of sleep EEG data collected during routine overnight polysomnography (PSG) in subjects with and without sleep-disordered breathing (SDB). METHODS: We evaluated the accuracy of an automated algorithm to detect sleep EEG artefacts against artefacts manually scored by three experienced technologists (reference standard) in 40 PSGs. Spectral power was computed using artefact-free EEG data derived from (1) the reference standard, (2) the algorithm and (3) raw EEG without any prior artefact rejection. RESULTS: The algorithm showed a high level of accuracy of 94.3, 94.7 and 95.8% for detecting artefacts during the entire PSG, NREM sleep and REM sleep, respectively. There was good to moderate sensitivity and excellent specificity of the algorithm detection capabilities during sleep. The EEG spectral power for the reference standard and algorithm was significantly lower than that of the raw, unprocessed EEG signal. CONCLUSIONS: These preliminary findings support an automated way to process EEG artefacts during sleep, providing the opportunity to investigate EEG-based markers of neurobehavioural impairment in sleep disorders in future studies.

Modafinil improves daytime sleepiness in patients with mild to moderate obstructive sleep apnoea not using standard treatments: a randomised placebo-controlled crossover trial.

INTRODUCTION: Patients with mild to moderate obstructive sleep apnoea (OSA) commonly suffer excessive daytime sleepiness. Continuous positive airway pressure (CPAP) has limited effectiveness in reducing sleepiness in milder OSA. Modafinil is a wake-promoting drug licensed to treat residual sleepiness in CPAP-treated OSA. We hypothesised that modafinil may effectively treat sleepiness in untreated mild to moderate OSA. METHODS: Untreated sleepy men with mild to moderate OSA (age 18-70, apnoea-hypopnoea index (AHI) 5-30/h, Epworth Sleepiness Scale (ESS) ≥10) were randomised to receive 200 mg modafinil or matching placebo daily for 2 weeks before crossing over to the alternative treatment after a minimum 2-week washout. Mixed model analysis of variance was used to compare the changes on modafinil to placebo while classifying all randomised patients as random factors. RESULTS: 32 patients were randomised (mean (SD) AHI 13 (6.4)/h, age 47 (10.7) years, ESS 13.6 (3.3), body mass index 28.2 (3.6) kg/m(2)), 29 of whom (91%) completed the trial. The primary outcome (ESS) improved more on modafinil than placebo (3.6 points, 95% CI 1.3 to 5.8, p=0.003) and the secondary outcome (40-min driving simulator performance) also improved more on modafinil than placebo (steering deviation 4.7 cm, 95% CI 0.8 to 8.5, p=0.018). Psychomotor Vigilance Task reciprocal reaction time improved significantly over placebo (0.15 (1/ms), 95% CI 0.03 to 0.27, p=0.016). Improvements on the Functional Outcomes of Sleep Questionnaire were not significant (5.3 points over placebo, 95% CI -1 to 11.6, p=0.093). CONCLUSIONS: Modafinil significantly improved subjective sleepiness in patients with untreated mild to moderate OSA. The size of this effect is clinically relevant at 3-4 ESS points of improvement compared with only 1-2 points in CPAP clinical trials. Driving simulator performance and reaction time also improved on modafinil. CLINICAL TRIAL REGISTRATION: ACTRN#12608000128392.

An overview of service quality of continuous positive airway pressure services in Australian pharmacies.

BACKGROUND AND OBJECTIVE: Little is known about CPAP services offered in the Australian primary care pharmacy setting, despite the potential influence of service quality on patient adherence. The objective of this study was to provide an overview on a nationwide scale of the range and quality of CPAP and sleep apnoea-related services in Australian pharmacies. METHODS: A paper-based questionnaire was developed and mailed to all pharmacies in Australia that currently provide CPAP services (as identified by manufacturer's distributor lists or Internet search). A point system was devised to score participants on the quality of their CPAP service. Pharmacies were rated against a list of 23 criteria that were determined by consensus, with one point allocated for each criterion met, allowing for a maximum score of 23. RESULTS: The study response rate was 55% (110/199), and representation was obtained from all eight Australian states and territories. The mean number of criteria met (total score) for pharmacies was 15.7 ± 3.4 (15.7/23 = 68.3%; score range 2-22). Variability was evident in the range of services offered. Eighty-seven per cent of respondents believed that pharmacies supplying CPAP should adhere to a formalized set of professional guidelines. CONCLUSIONS: The accessibility of pharmacies may make them a valuable venue for CPAP service provision. However, models of care to guide practice and standardize the variability in services are required. Implementation of such models could improve patient access to quality treatment in the primary care setting.

Region-specific changes in brain activity and memory after continuous positive airway pressure therapy in obstructive sleep apnea: a pilot high-density electroencephalography study.

STUDY OBJECTIVES: Limited channel electroencephalography (EEG) investigations in obstructive sleep apnea (OSA) have revealed deficits in slow wave activity (SWA) and spindles during sleep and increased EEG slowing during resting wakefulness. High-density EEG (Hd-EEG) has also detected local parietal deficits in SWA (delta power) during NREM. It is unclear whether effective continuous positive airway pressure (CPAP) treatment reverses regional SWA deficits, and other regional sleep and wake EEG abnormalities, and whether any recovery relates to improved overnight memory consolidation. METHODS: A clinical sample of men with moderate-severe OSA underwent sleep and resting wake recordings with 256-channel Hd-EEG before and after 3 months of CPAP. Declarative and procedural memory tasks were administered pre- and post-sleep. Topographical spectral power maps and differences between baseline and treatment were compared using t-tests and statistical nonparametric mapping (SnPM). RESULTS: In 11 compliant CPAP users (5.2 ±â€…1.1 hours/night), total sleep time did not differ after CPAP but N1 and N2 sleep were lower and N3 was higher. Centro-parietal gamma power during N3 increased and fronto-central slow spindle activity during N2 decreased (SnPM < 0.05). No other significant differences in EEG power were observed. When averaged specifically within the parietal region, N3 delta power increased after CPAP (p = 0.0029) and was correlated with the change in overnight procedural memory consolidation (rho = 0.79, p = 0.03). During resting wakefulness, there were trends for reduced delta and theta power. CONCLUSIONS: Effective CPAP treatment of OSA may correct regional EEG abnormalities, and regional recovery of SWA may relate to procedural memory improvements in the short term.

Residual sleep-disordered breathing during autotitrating continuous positive airway pressure therapy.

Obstructive sleep apnoea (OSA) is often treated with autotitrating continuous positive airway pressure (autoCPAP) devices. Clinical and bench tests of these devices have suggested performance limitations. These studies do not indicate whether this is a failure to detect or a failure to respond to airway obstruction. In this randomised, crossover trial, 34 patients with moderate-to-severe OSA underwent polysomnography on two laboratory visits. The autoCPAP device was randomly set to a fixed subtherapeutic pressure (detection assessment) or autotitrating mode (response assessment). Airflow was measured both from the autoCPAP (autoCPAP flow) and directly from the nasal mask, and recorded on polysomnography. Apnoea/hypopnoea indices (AHIs) measured at the two sites and from the autoCPAP download report were compared. Regarding detection, the AHI measured from the nasal mask showed good agreement with the autoCPAP flow AHI, but agreement was lower with the autoCPAP report AHI. In autotitrating mode, there was significant misclassification of those with and without OSA (AHI ≥ 10 events · h(-1)) on the autoCPAP report. Regarding response, residual OSA (AHI ≥ 10 events · h(-1)) was still evident in 24% of patients during autotitration. In some patients, autoCPAP fails to detect and/or respond to sleep apnoea. Clinicians should consider limitations of each device and use caution when using autoCPAP report statistics to verify effective treatment.