Intervention Protocol

You have free access to this content

Positional therapy for obstructive sleep apnoea

  1. P R Srijithesh1,*,
  2. Rajeswari Aghoram2,
  3. Amit Goel3,
  4. Jayaraj Dhanya4

Editorial Group: Cochrane Airways Group

Published Online: 16 FEB 2014

DOI: 10.1002/14651858.CD010990


How to Cite

Srijithesh PR, Aghoram R, Goel A, Dhanya J. Positional therapy for obstructive sleep apnoea (Protocol). Cochrane Database of Systematic Reviews 2014, Issue 2. Art. No.: CD010990. DOI: 10.1002/14651858.CD010990.

Author Information

  1. 1

    Jawaharlal Institute of Postgraduate Medical Education and Research, Department of Neurology, Puducherry, Puducherry, India

  2. 2

    Jawaharlal Institute of Postgraduate Medical Education and Research (JIPMER), Department of Neurology, Puducherry, Puducherry, India

  3. 3

    Sanjay Gandhi Postgraduate Institute of Medical Sciences, Department of Gastroenterology, Lucknow, Uttar Pradesh, India

  4. 4

    Government Medical College, Department of Paediatrics, Calicut, Kerala, India

*P R Srijithesh, Department of Neurology, Jawaharlal Institute of Postgraduate Medical Education and Research, Dhanvanthri Nagar, Puducherry-6, Puducherry, Puducherry, India. srijitheshpr@gmail.com. srijitheshpr@rediffmail.com.

Publication History

  1. Publication Status: New
  2. Published Online: 16 FEB 2014

SEARCH

 

Background

  1. Top of page
  2. Background
  3. Objectives
  4. Methods
  5. Acknowledgements
  6. Appendices
  7. Contributions of authors
  8. Declarations of interest

Obstructive sleep apnoea (OSA) is a common condition. Its prevalence varies between 4% and 9% in women and between 9% and 24% in men, depending upon the criteria used to define the condition (Young 1993; Young 2002). OSA is known to be a risk factor for road traffic accidents and is associated with several systemic illnesses including cardiovascular disease, cognitive impairment and impaired neurological recovery after stroke (Arzt 2005; Chobanian 2003; Dumitrascu 2012; Lal 2012; Marin 2005; Marshall 2008; Martinez-Garcia 2005; Parra 2004; Peppard 2000; Shahar 2001; Yaggi 2005). For example, OSA is two to four times more common among people with systemic hypertension, stroke or coronary artery disease than in the general population (Bassetti 1999; Harbison 2002; Wessendorf 2000).

Treatment modalities for OSA include behavioural and lifestyle modifications, oral appliance devices (OAs), continuous positive airway pressure (CPAP) therapy and medicine or surgery for selected groups (Giles 2006; Lim 2004; Shneerson 2001; Smith 2002; Sundaram 2005). In patients with a new diagnosis of OSA, positional therapy may be tried before more invasive therapies are begun.

 

Description of the condition

Obstructive sleep apnoea is characterised by recurrent episodes of pharyngeal collapse leading to intermittent hypoxaemia (abnormally low oxygen level in the blood) and sleep fragmentation. Repeated sleep disturbance at night may result in non-refreshing sleep and excessive daytime sleepiness, especially in moderate to severe cases. Other clinical features include fatigue, insomnia, loud snoring, gasping, choking and breath holding during sleep. Recent studies suggest that OSA can induce oxidative stress and a state of subclinical inflammation (Schulz 2000; Shamsuzzaman 2002; Vgontzas 1997); therefore it may be linked to other systemic diseases.

The diagnosis of OSA is based on sleep-related symptoms and findings on polysomnography (PSG). This diagnosis is confirmed if the number of apnoea, hypopnoea and respiratory event–related arousals on PSG is greater than 15 per hour, or greater than five per hour in patients presenting with clinical features suggestive of OSA. The severity of OSA can be graded by the Respiratory Disturbance Index (RDI), which is defined as the number of apnoea, hypopnoea or respiratory event–related arousal events (not satisfying PSG criteria for apnoea or hypopnoea) per hour of sleep. OSA is mild when the RDI is between five and 14, moderate when it is between 15 and 30 and severe when RDI is greater than 30 (Epstein 2009).

About 50% of cases of OSA can be improved by patient positioning (Cartwright 1984; Mador 2005; Oksenberg 2009). Positional OSA is defined as a 50% reduction in Apnoea-Hypopnoea Index (AHI) score when the person is lying on his or her side (lateral recumbent position) rather than on the back (supine). In one study, Mador et al found that 49.5% of mild, 19.4% of moderate and 6.5% of severe sleep apnoea participants had positional OSA (Mador 2005).

 

Description of the intervention

Positional therapy uses devices that help patients to sleep on their side. The American Academy of Sleep Medicine (AASM) task force on adult obstructive sleep apnoea recommends positional therapy as an effective secondary therapy for patients with positional OSA (Epstein 2009). This recommendation was based on evidence of a moderate degree of clinical certainty, implying use of level II evidence or consensus of level III evidence (randomised controlled trials (RCTs) with high-beta error or consensus of evidence from non-randomised controlled studies). The European Respiratory Society task force on non-CPAP therapies in OSA states that positional therapy can yield a moderate reduction in AHI score. With a grade C recommendation (evidence based on case studies or cohort studies or extrapolation of systematic reviews of homogenous results), the task force stated that positional therapy is inferior to CPAP but may be recommended for carefully selected patients (Randerath 2011).

Currently, several devices are commercially available. Devices that have been designed for this purpose include lumbar or abdominal binders, semirigid backpacks, full-length pillows, tennis ball attached to the back of the night suit and electrical sensors with alarms that indicate change in position. Other options include support devices, pillows and T-shirts that can be used to progressively train patients to sleep on their sides. These therapies may be an attractive option because of their cost-effectiveness and possibly better patient compliance, especially in patients with mild to moderate OSA, for whom compliance with CPAP therapy is particularly poor

(Permut 2010; Zuberi 2004; Ravesloot 2013).

CPAP is the current gold standard of treatment for OSA. The AASM task force recommends positive airway pressure (PAP) as the treatment of choice for mild, moderate and severe OSA. As a consensus recommendation, this group states that CPAP should be offered to all patients with OSA (Epstein 2009). The National Institute for Health and Care Excellence (NICE) guidelines recommend CPAP as the best treatment option in cases of symptomatic moderate or severe OSA, in which compliance is also better (Sarrell 2013). In mild OSA, however, NICE considers CPAP as a treatment option only if OSA is symptomatic enough to cause impairment in quality of life. For mild OSA, NICE recommends CPAP only after lifestyle advice and other treatment options have been unsuccessful or have been found to be inappropriate (NICE 2008).

 

How the intervention might work

Sleeping in the lateral position may reduce pressure on the airway and lower the chance of sleep apnoea (Isono 2002). This can also reduce the tendency of the tongue to fall back and block the pharyngeal airway and of the pharyngeal dilator muscles to collapse because of reduced tone, thus culminating in OSA.

 

Why it is important to do this review

Although CPAP therapy is considered to be the gold standard and the most effective currently available therapy for OSA, its clinical application can be compromised by poor compliance (Kribbs 1993), as up to two-thirds of OSA patients do not routinely use their CPAP machine (Sarrell 2013). Poor compliance is more common among patients with mild to moderate OSA and largely asymptomatic disease or in patients with other co-morbidities. Furthermore, CPAP may not be a widely accessible choice in resource-poor settings because of the cost involved. Therefore, as evidence continues to emerge, a focused systematic review should explore the role of positional therapy to make clear the benefits of CPAP treatment and the patient groups for which this approach is best suited.

 

Objectives

  1. Top of page
  2. Background
  3. Objectives
  4. Methods
  5. Acknowledgements
  6. Appendices
  7. Contributions of authors
  8. Declarations of interest

To assess the effects of positional therapy on patients with obstructive sleep apnoea.

 

Methods

  1. Top of page
  2. Background
  3. Objectives
  4. Methods
  5. Acknowledgements
  6. Appendices
  7. Contributions of authors
  8. Declarations of interest
 

Criteria for considering studies for this review

 

Types of studies

We will include randomised controlled trials (RCTs) that use positional therapy for OSA regardless of blinding, language or stage of publication. Cross-over trials will be excluded.

 

Types of participants

We will include participants with OSA irrespective of their age, the severity of disease or the diagnostic criteria used to diagnose the condition. The diagnostic criteria of the AASM will be considered the standard criteria (Epstein 2009) for comparison purposes.

 

Types of interventions

We will include trials that compare positional therapy versus sham intervention/no intervention or CPAP therapy. We will use the following comparisons.

  1. Postional therapy versus CPAP.
  2. Positional therapy versus sham intervention/no intervention.

 

Types of outcome measures

 

Primary outcomes

  1. Epworth Sleepiness Scale/symptoms of excessive daytime sleepiness.
  2. Apnoea-Hypopnoea Index (AHI).
  3. Compliance rate,

 

Secondary outcomes

  1. Quality of life (assessed using appropriate scales such as Short Form-36 (SF-36) and the Functional Outcomes Sleep Questionnaire (FOSQ).
  2. Sleep quality assessed by average duration of slow wave and REM sleep periods.
  3. Respiratory Disturbance Index (RDI).
  4. Frequency of desaturation episodes per hour of sleep.
  5. Average duration of oxygen desaturations.
  6. Cognitive dysfunction (assessed using appropriate instruments such as the Psychomotor Vigilance Test and the Hospital Anxiety Depression Scale).
  7. Adverse events (back discomfort and skin irritation due to application of the positional device and facial discomfort, nasal congestion, dry mouth and skin irritation due to CPAP therapy).

 

Search methods for identification of studies

 

Electronic searches

Trials will be identified from the Specialised Register of the Cochrane Airways Group (CAGR), which is maintained by the trials search co-ordinator for the Group. The Register contains results of systematic searches of bibliographic databases including the Cochrane Central Register of Controlled Trials (CENTRAL), MEDLINE, EMBASE, CINAHL, AHMED and PsycINFO. It also contains results derived from handsearching of respiratory journals and major annual meetings abstract books (see Appendix 1 for additional details). We will use the strategy provided in Appendix 2 to identify relevant trials from the CAGR.

We will also search ClinicalTrials.gov (www.ClinicalTrials.gov) and the World Health Organization (WHO) trials portal (www.who.int/ictrp/en/). All databases will be searched from their inception to the present, with no restrictions on language of publication or publication type.

 

Searching other resources

We will search primary studies and review articles for additional references.

Additional information on ongoing trials will be accessed from manufacturers' websites.

We will check for any errata or retractions from included studies that have been published and will report them along with the date.

 

Data collection and analysis

 

Selection of studies

Abstracts of the studies will be reviewed by three review investigators (PRS, RA and JD) using the predetermined inclusion criteria. Full texts of suitable studies will be reviewed in detail. Articles for inclusion will be assessed by using a predesigned eligibility form. Disagreements will be adjudicated by a fourth review investigator (AG), who is not a member of the data extraction team. Care will be taken to check for multiple publications of the same data. Reasons for excluded studies will be documented.

The selection process will be recorded in a PRISMA flow diagram and in a 'Characteristics of excluded studies' table.

 

Data extraction and management

Two review investigators (JD and RA) will independently extract data and assess the quality of studies using data extraction forms. These investigators will independently assess the quality of studies. A third review investigator (PRS) will adjudicate if any disagreement arises between the investigators who extract data and assess the quality of studies. Data will be entered in Review Manager software and analysed. Data entry into RevMan will be done by RA. The entries will be double-checked, and a second review author (PRS) will spot-check study characteristics for accuracy.

For study characteristics and outcome data, we will use a data collection form that has been piloted by at least one study in the review. Two review authors (RA and JD) will independently extract study characteristics from included studies. We will extract the following study characteristics.

  1. Methods: study design, total duration of study, details of any 'run-in' period, country in which study was conducted, number of study centres, study setting, withdrawals and date of study.
  2. Participants: number of participants, mean age, age range, gender, severity of condition, diagnostic criteria, inclusion criteria and exclusion criteria.
  3. Interventions: intervention, comparison, concomitant medications and interventions.
  4. Outcomes: primary and secondary outcomes specified and collected and time points reported.
  5. Notes: funding for trial and notable conflicts of interest of trial authors.

 

Assessment of risk of bias in included studies

The risk of bias of all studies will be assessed by using The Cochrane Collaboration tool for assessing risk of bias (Higgins 2011). Domains assessed will include sequence generation and allocation concealment, blinding of outcome assessors (blinding of participants not possible by the very nature of the intervention), completeness of outcome data and selective outcome reporting. Other points considered will be baseline imbalances, any premature stopping of studies and commercial conflicts of interest of authors. The risk of bias analysis will be done by three review authors independently (PRS, RA and JD). If any disagreement arises, the fourth review author (AG) will adjudicate the disagreement. The risk of bias will be recorded in the risk of bias tables.

 

Assesment of bias in conducting the systematic review

Any deviation from the above mentioned protocol will be noted in the 'Differences between protocol and review' section of the systematic review.

 

Measures of treatment effect

Most of the outcome variables expected in the studies are continuous variables. Data from each study will be expressed as mean differences or standardised mean differences with 95% confidence intervals.

Dichotomous data will be expressed as odds ratios.

Meta-analysis will be conducted only if meaningful data are provided that are clinically and methodologically similar in terms of studies and participants.

Skewed data will be reported as medians and interquartile ranges.

In trials with multiple trial arms, only the relevant arms will be combined. If two comparisons are combined in the same meta-analysis, the control group will be halved to avoid double-counting.

 

Unit of analysis issues

The unit of analysis will be the participant.

 

Dealing with missing data

Data will be analysed on an intention-to-treat basis. Any missing information will be clarified by authors of the trials. When this is not possible, the risk of bias attributed to the missing data will be recorded and taken into consideration in further analysis.

 

Assessment of heterogeneity

The I² statistic will be used to measure heterogeneity among trials. If we identify substantial heterogeneity, we will report it and will explore possible causes by prespecified subgroup analysis. 

 

Assessment of reporting biases

If we are able to pool more than 10 trials, we will create and examine a funnel plot to explore possible small-study biases.

 

Data synthesis

Data analysis will be performed by using Review Manager (RevMan) software.

If we identify two or more studies, we will use RevMan software to pool the results by employing methods appropriate to the types of outcome measures. Means of outcomes will be used to obtain a mean difference pooled from all studies. Studies will be combined using a fixed-effect analysis if no significant evidence of heterogeneity is found. Otherwise, random-effects analysis will be used. If clinical or methodological differences between studies are significant, the studies will not be combined.

 

Summary of findings table

GRADEpro will be used to prepare 'Summary of findings' tables that include the following outcomes.

  1. Epworth Sleepiness Scale.
  2. Apnoea-Hypopnoea Index (AHI).
  3. Compliance with the regimen.
  4. Quality of life (assessed using appropriate scales such as SF-36 and FOSQ).
  5. Significant adverse events defined as adverse events severe enough to require temporary (> three hours) or permanent termination of the treatment regimen.
  6. Sleep quality (assessed by the average duration of slow wave and REM sleep periods).
  7. Cognitive dysfunction (assessed using appropriate instruments such as the Psychomotor Vigilance Test and the Hospital Anxiety Depression Scale).

We will justify all decisions to downgrade or upgrade the quality of studies using footnotes.

 

Subgroup analysis and investigation of heterogeneity

We plan to carry out the following subgroup analyses to look for potential sources of heterogeneity.

  1. Mild to moderate OSA versus severe OSA or asymptomatic OSA versus symptomatic OSA.
  2. Studies including only OSA participants without co-morbidities such as stroke versus studies done on populations with co-morbidities such as stroke survivors.
  3. Types of interventions used for positional therapy (e.g. mechanical restrainers vs electronic sensors with alarms with or without mechanical restrainers).

We will use the following outcomes in subgroup analyses.

  1. Epworth Sleepiness Scale/symptoms of excessive daytime sleepiness.
  2. Apnoea-Hypopnoea Index (AHI).
  3. Compliance rate.
  4. Quality of life (assessed using appropriate scales such as SF-36 and FOSQ).
  5. Cognitive dysfunction (assessed using appropriate instruments such as the Psychomotor Vigilance Test and the Hospital Anxiety Depression Scale).

Tests for subgroup interactions will be done in Review Manager.

 

Sensitivity analysis

If sufficient numbers of trials are identified, we will test the robustness of study results to various components of risk of bias. Sensitivity analysis will also be done by excluding studies in which the diagnosis of sleep apnoea is made without technician-attended overnight polysomnography (e.g. using an unattended portable respiratory monitor). We will also perform sensitivity analysis by excluding studies that have used a definition of OSA that is different from that provided in standard AASM guidelines.

 

Acknowledgements

  1. Top of page
  2. Background
  3. Objectives
  4. Methods
  5. Acknowledgements
  6. Appendices
  7. Contributions of authors
  8. Declarations of interest

We acknowledge Dr Prathap Tharyan and his team at South Asian Cochrane Network for giving us the intellectual impetus for writing this protocol.

We acknowledge Dr Emma Welsh and Mrs Elizabeth Stovold of the Cochrane Airways Group for their advice and support.

We are indebted to Dr Tamilarasu Kadiravan of the Department of Medicine, JIPMER, Pondicherry, for providing timely practical advice.

The contact editor for this protocol was Dr Jimmy Chong.

 

Appendices

  1. Top of page
  2. Background
  3. Objectives
  4. Methods
  5. Acknowledgements
  6. Appendices
  7. Contributions of authors
  8. Declarations of interest
 

Appendix 1. Sources and search methods for the Cochrane Airways Group Specialised Register (CAGR)

 

Electronic searches: core databases


DatabaseFrequency of search

CENTRALMonthly

MEDLINE (Ovid)Weekly

EMBASE (Ovid)Weekly

PsycINFO (Ovid)Monthly

CINAHL (EBSCO)Monthly

AHMED (EBSCO)Monthly



 

 

Handsearches: core respiratory conference abstracts


ConferenceYears searched

American Academy of Allergy, Asthma and Immunology (AAAAI)2001 onwards

American Thoracic Society (ATS)2001 onwards

Asia Pacific Society of Respirology (APSR)2004 onwards

British Thoracic Society Winter Meeting (BTS)2000 onwards

Chest Meeting2003 onwards

European Respiratory Society (ERS)1992, 1994, 2000 onwards

International Primary Care Respiratory Group Congress (IPCRG)2002 onwards

Thoracic Society of Australia and New Zealand (TSANZ)1999 onwards



 

 

MEDLINE search strategy used to identify trials for the CAGR

 

Sleep apnoea search

1. exp Sleep Apnea Syndromes/

2. (sleep$ adj3 (apnea$ or apnoea$)).mp.

3. (hypopnoea$ or hypopnoea$).mp.

4. OSA.mp.

5. SHS.mp.

6. OSAHS.mp.

7. or/1-6

 

Filter to identify RCTs

1. exp "clinical trial [publication type]"/

2. (randomised or randomised).ab,ti.

3. placebo.ab,ti.

4. dt.fs.

5. randomly.ab,ti.

6. trial.ab,ti.

7. groups.ab,ti.

8. or/1-7

9. Animals/

10. Humans/

11. 9 not (9 and 10)

12. 8 not 11

The MEDLINE strategy and RCT filter are adapted to identify trials in other electronic databases

 

Appendix 2. Search strategy to identify relevant trials from the CAGR

#1 SLP:MISC2

#2 MeSH DESCRIPTOR Sleep Apnea, Obstructive

#3 sleep near3 (apnea* or apnoea*)

#4 (hypopnoea* or hypopnoea*)

#5 (OSA OR SHS OR OSAHS:TI,AB)

#6 (#1 OR #2 OR #3 OR #4 OR #5)

#7 MeSH DESCRIPTOR Posture Explode All

#8 MeSH DESCRIPTOR Patient Positioning

#9 postur*

#10 position*

#11 supine*

#12 lateral*

#13 #7 or #8 or #9 or #10 or #11 or #12

#14 #6 and #13

#15 (#14) AND (INREGISTER)

[Note: In search line #1, MISC1 refers to the field in the record where the reference has been coded for condition, in this case, obstructive sleep apnoea]

 

Contributions of authors

  1. Top of page
  2. Background
  3. Objectives
  4. Methods
  5. Acknowledgements
  6. Appendices
  7. Contributions of authors
  8. Declarations of interest

The protocol was conceived by PR Srijithesh and was written in collaboration with Amit Goel.

 

Declarations of interest

  1. Top of page
  2. Background
  3. Objectives
  4. Methods
  5. Acknowledgements
  6. Appendices
  7. Contributions of authors
  8. Declarations of interest

None.

References

Additional references

  1. Top of page
  2. Abstract
  3. Background
  4. Objectives
  5. Methods
  6. Acknowledgements
  7. Appendices
  8. Contributions of authors
  9. Declarations of interest
  10. Additional references
Arzt 2005
  • Arzt M, Young T, Finn L, Skatrud JB, Bradley TD. Association of sleep-disordered breathing and the occurrence of stroke. American Journal of Respiratory and Critical Care Medicine 2005;172(11):1447-51. [PUBMED: 16141444]
Bassetti 1999
Cartwright 1984
Chobanian 2003
  • Chobanian AV, Bakris GL, Black HR, Cushman WC, Green LA, Izzo JL Jr, et al. The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: the JNC 7 report. JAMA 2003;289(19):2560-72. [PUBMED: 12748199]
Dumitrascu 2012
  • Dumitrascu R, Tiede H, Rosengarten B, Schulz R. [Obstructive sleep apnea and stroke] [Obstruktive Schlaf-Apnoe und Schlaganfall.]. Pneumologie (Stuttgart, Germany) 2012;66(8):476-9. [PUBMED: 22875731]
Epstein 2009
  • Epstein LJ, Kristo D, Strollo PJ Jr, Friedman N, Malhotra A, Patil SP, et al. Clinical guideline for the evaluation, management and long-term care of obstructive sleep apnea in adults. Journal of Clinical Sleep Medicine 2009;5(3):263-76. [PUBMED: 19960649]
Giles 2006
  • Giles TL, Lasserson TJ, Smith B, White J, Wright JJ, Cates CJ. Continuous positive airways pressure for obstructive sleep apnoea in adults. Cochrane Database of Systematic Reviews 2006, Issue 3. [DOI: 10.1002/14651858.CD001106.pub3]
Harbison 2002
Higgins 2011
  • Higgins JPT, Green S (editors). Cochrane Handbook for Systematic Reviews of Interventions Version 5.1 [updated March 2011]. The Cochrane Collaboration, 2011. www.cochrane-handbook.org.
Isono 2002
  • Isono S, Tanaka A, Nishino T. Lateral position decreases collapsibility of the passive pharynx in patients with obstructive sleep apnea. Anesthesiology 2002;97(4):780-5. [PUBMED: 12357140]
Kribbs 1993
  • Kribbs NB, Pack AI, Kline LR, Smith PL, Schwartz AR, Schubert NM, et al. Objective measurement of patterns of nasal CPAP use by patients with obstructive sleep apnea. The American Review of Respiratory Disease 1993;147(4):887-95. [PUBMED: 8466125]
Lal 2012
Lim 2004
Mador 2005
  • Mador MJ, Kufel TJ, Magalang UJ, Rajesh SK, Watwe V, Grant BJ. Prevalence of positional sleep apnea in patients undergoing polysomnography. Chest 2005;128(4):2130-7. [PUBMED: 16236865]
Marin 2005
  • Marin JM, Carrizo SJ, Vicente E, Agusti AG. Long-term cardiovascular outcomes in men with obstructive sleep apnoea-hypopnoea with or without treatment with continuous positive airway pressure: an observational study. Lancet 2005;365(9464):1046-53. [PUBMED: 15781100]
Marshall 2008
  • Marshall NS, Wong KK, Liu PY, Cullen SR, Knuiman MW, Grunstein RR. Sleep apnea as an independent risk factor for all-cause mortality: the Busselton Health Study. Sleep 2008;31(8):1079-85. [PUBMED: 18714779]
Martinez-Garcia 2005
  • Martinez-Garcia MA, Galiano-Blancart R, Roman-Sanchez P, Soler-Cataluna JJ, Cabero-Salt L, Salcedo-Maiques E. Continuous positive airway pressure treatment in sleep apnea prevents new vascular events after ischemic stroke. Chest 2005;128(4):2123-9. [PUBMED: 16236864]
NICE 2008
  • National Institute for Health and Clinical Excellence. NICE technology appraisal guidance 139. Continuous positive airway pressure for the treatment of obstructive sleep apnoea/hypopnoea syndrome. March 2008:1-25. www.nice.org.uk/TA139 (accessed 10 January 2014).
Oksenberg 2009
  • Oksenberg A, Arons E, Greenberg-Dotan S, Nasser K, Radwan H. The significance of body posture on breathing abnormalities during sleep: data analysis of 2077 obstructive sleep apnea patients. Harefuah 2009;148(5):304-9, 350, 351. [PUBMED: 19630360]
Parra 2004
  • Parra O, Arboix A, Montserrat JM, Quinto L, Bechich S, Garcia-Eroles L. Sleep-related breathing disorders: impact on mortality of cerebrovascular disease. The European Respiratory Journal 2004;24(2):267-72. [PUBMED: 15332396]
Peppard 2000
  • Peppard PE, Young T, Palta M, Skatrud J. Prospective study of the association between sleep-disordered breathing and hypertension. The New England Journal of Medicine 2000;342(19):1378-84. [PUBMED: 10805822]
Permut 2010
  • Permut I, Diaz-Abad M, Chatila W, Crocetti J, Gaughan JP, D'Alonzo GE, et al. Comparison of positional therapy to CPAP in patients with positional obstructive sleep apnea. Journal of Clinical Sleep Medicine 2010;6(3):238-43. [PUBMED: 20572416]
Randerath 2011
  • Randerath WJ, Verbraecken J, Andreas S, Bettega G, Boudewyns A, Hamans E, et al. Non-CPAP therapies in obstructive sleep apnoea. The European Respiratory Journal 2011;37(5):1000-28. [PUBMED: 21406515]
Ravesloot 2013
  • Ravesloot MJ, van Maanen JP, Dun L, de Vries N. The undervalued potential of positional therapy in position-dependent snoring and obstructive sleep apnea—a review of the literature. Sleep & Breathing = Schlaf & Atmung 2013;17(1):39-49. [PUBMED: 22441662]
Review Manager (RevMan)
  • The Nordic Cochrane Centre, The Cochrane Collaboration. Review Manager (RevMan). 5.2. Copenhagen: The Nordic Cochrane Centre, The Cochrane Collaboration, 2012.
Sarrell 2013
  • Sarrell EM, Chomsky O, Shechter D. [Treatment compliance with continuous positive airway pressure device among adults with obstructive sleep apnea (OSA): how many adhere to treatment?]. Harefuah 2013;152(3):140-4, 183, 184. [PUBMED: 23713371]
Schulz 2000
  • Schulz R, Mahmoudi S, Hattar K, Sibelius U, Olschewski H, Mayer K, et al. Enhanced release of superoxide from polymorphonuclear neutrophils in obstructive sleep apnea. Impact of continuous positive airway pressure therapy. American Journal of Respiratory and Critical Care Medicine 2000;162(2 Pt 1):566-70. [PUBMED: 10934088]
Shahar 2001
  • Shahar E, Whitney CW, Redline S, Lee ET, Newman AB, Nieto FJ, et al. Sleep-disordered breathing and cardiovascular disease: cross-sectional results of the Sleep Heart Health Study. American Journal of Respiratory and Critical Care Medicine 2001;163(1):19-25. [PUBMED: 11208620]
Shamsuzzaman 2002
  • Shamsuzzaman AS, Winnicki M, Lanfranchi P, Wolk R, Kara T, Accurso V, et al. Elevated C-reactive protein in patients with obstructive sleep apnea. Circulation 2002;105(21):2462-4. [PUBMED: 12034649]
Shneerson 2001
  • Shneerson J, Wright JJ. Lifestyle modification for obstructive sleep apnoea. Cochrane Database of Systematic Reviews 2001, Issue 1. [DOI: 10.1002/14651858.CD002875]
Smith 2002
Sundaram 2005
Vgontzas 1997
  • Vgontzas AN, Papanicolaou DA, Bixler EO, Kales A, Tyson K, Chrousos GP. Elevation of plasma cytokines in disorders of excessive daytime sleepiness: role of sleep disturbance and obesity. The Journal of Clinical Endocrinology and Metabolism 1997;82(5):1313-6. [PUBMED: 9141509]
Wessendorf 2000
Yaggi 2005
  • Yaggi HK, Concato J, Kernan WN, Lichtman JH, Brass LM, Mohsenin V. Obstructive sleep apnea as a risk factor for stroke and death. The New England Journal of Medicine 2005;353(19):2034-41. [PUBMED: 16282178]
Young 1993
  • Young T, Palta M, Dempsey J, Skatrud J, Weber S, Badr S. The occurrence of sleep-disordered breathing among middle-aged adults. The New England Journal of Medicine 1993;328(17):1230-5. [PUBMED: 8464434]
Young 2002
  • Young T, Peppard PE, Gottlieb DJ. Epidemiology of obstructive sleep apnea: a population health perspective. American Journal of Respiratory and Critical Care Medicine 2002;165(9):1217-39. [PUBMED: 11991871]
Zuberi 2004
  • Zuberi NA, Rekab K, Nguyen HV. Sleep apnea avoidance pillow effects on obstructive sleep apnea syndrome and snoring. Sleep & Breathing = Schlaf & Atmung 2004;8(4):201-7. [PUBMED: 15611895]