Obstructive sleep apnea
|Obstructive sleep apnea|
|Classification and external resources|
Obstructive sleep apnea
Obstructive sleep apnea (OSA) or obstructive sleep apnea syndrome is the most common type of sleep apnea and is caused by obstruction of the upper airway. It is characterized by repetitive pauses in breathing during sleep, despite the effort to breathe, and is usually associated with a reduction in blood oxygen saturation. These pauses in breathing, called "apneas" (literally, "without breath"), typically last 20 to 40 seconds.
The individual with OSA is rarely aware of having difficulty breathing, even upon awakening. It is recognized as a problem by others witnessing the individual during episodes or is suspected because of its effects on the body (sequelae). OSA is commonly accompanied with snoring.
Symptoms may be present for years or even decades without identification, during which time the sufferer may become conditioned to the daytime sleepiness and fatigue associated with significant levels of sleep disturbance. Sufferers who generally sleep alone are often unaware of the condition, without a regular bed-partner to notice and make them aware of their symptoms.
As the muscle tone of the body ordinarily relaxes during sleep, and the airway at the throat is composed of walls of soft tissue, which can collapse, it is not surprising that breathing can be obstructed during sleep. Although a very minor degree of OSA is considered to be within the bounds of normal sleep, and many individuals experience episodes of OSA at some point in life, a small percentage of people are afflicted with chronic, severe OSA.
Many people experience episodes of OSA for only a short period of time. This can be the result of an upper respiratory infection that causes nasal congestion, along with swelling of the throat, or tonsillitis that temporarily produces very enlarged tonsils. The Epstein-Barr virus, for example, is known to be able to dramatically increase the size of lymphoid tissue during acute infection, and OSA is fairly common in acute cases of severe infectious mononucleosis. Temporary spells of OSA syndrome may also occur in individuals who are under the influence of a drug (such as alcohol) that may relax their body tone excessively and interfere with normal arousal from sleep mechanisms.
- 1 Signs and symptoms
- 2 Risk factors
- 3 Causes
- 4 Pathophysiology
- 5 Diagnosis
- 6 Treatment
- 7 Prognosis
- 8 Epidemiology
- 9 Research
- 10 See also
- 11 References
- 12 Further reading
- 13 External links
Signs and symptoms
Common signs of OSA include unexplained daytime sleepiness, restless sleep, and loud snoring (with periods of silence followed by gasps). Less common symptoms are morning headaches; insomnia; trouble concentrating; mood changes such as irritability, anxiety and depression; forgetfulness; increased heart rate and/or blood pressure; decreased sex drive; unexplained weight gain; increased urination and/or nocturia; frequent heartburn or gastroesophageal reflux disease; and heavy night sweats.
In adults, the most typical individual with OSA syndrome suffers from obesity, with particular heaviness at the face and neck. Obesity is not always present with OSA; in fact, a significant number of adults with normal body mass indices (BMIs) have decreased muscle tone causing airway collapse and sleep apnea. The cause of this is not well understood. The hallmark symptom of OSA syndrome in adults is excessive daytime sleepiness. Typically, an adult or adolescent with severe long-standing OSA will fall asleep for very brief periods in the course of usual daytime activities if given any opportunity to sit or rest. This behavior may be quite dramatic, sometimes occurring during conversations with others at social gatherings.
The hypoxia (absence of oxygen supply) related to OSA may cause changes in the neurons of the hippocampus and the right frontal cortex. Research using neuro-imaging revealed evidence of hippocampal atrophy in people suffering from OSA. They found that in more than 25% of the OSA cases, this problem results in irreversible problems in mentally manipulating non-verbal information and in executive functions and working memory, despite years of optimal CPAP treatment.
Although this so-called "hypersomnolence" (excessive sleepiness) may also occur in children, it is not at all typical of young children with sleep apnea. Toddlers and young children with severe OSA instead ordinarily behave as if "over-tired" or "hyperactive." Adults and children with very severe OSA also differ in typical body habitus. Adults are generally heavy, with particularly short and heavy necks. Young children, on the other hand, are generally not only thin, but may have "failure to thrive", where growth is reduced. Poor growth occurs for two reasons: the work of breathing is intense enough that calories are burned at high rates even at rest, and the nose and throat are so obstructed that eating is both tasteless and physically uncomfortable. OSA in children, unlike adults, is often caused by obstructive tonsils and adenoids and may sometimes be cured with tonsillectomy and adenoidectomy.
This problem can also be caused by excessive weight in children. In this case, the symptoms are more like the symptoms adults feel: restlessness, exhaustion, etc.
Children with OSA may experience learning and memory deficits and OSA has also been linked to lowered childhood IQ scores.
Old age is often accompanied by muscular and neurological loss of muscle tone of the upper airway. Decreased muscle tone is also temporarily caused by chemical depressants; alcoholic drinks and sedative medications being the most common. Permanent premature muscular tonal loss in the upper airway may be precipitated by traumatic brain injury, neuromuscular disorders, or poor adherence to chemical and or speech-therapy treatments.
Individuals with decreased muscle tone, increased soft tissue around the airway, and structural features that give rise to a narrowed airway are at high risk for OSA. Men, in which the anatomy is typified by increased mass in the torso and neck, are at increased risk of developing sleep apnea, especially through middle age and later. Women suffer typically less frequently and to a lesser degree than do men, owing partially to physiology, but possibly also to differential levels of progesterone. Prevalence in post-menopausal women approaches that of men in the same age range. Women are at greater risk for developing OSA during pregnancy.
OSA also appears to have a genetic component; those with a family history of it are more likely to develop it themselves. Lifestyle factors such as smoking may also increase the chances of developing OSA as the chemical irritants in smoke tend to inflame the soft tissue of the upper airway and promote fluid retention, both of which can result in narrowing of the upper airway. An individual may also experience or exacerbate OSA with the consumption of alcohol, sedatives, or any other medication that increases sleepiness as most of these drugs are also muscle relaxants.
OSA and recurrent tonsillitis (RT) are fundamentally different in their pathogenesis and outcome.   Recurrent tonsillitis refers to repeated tonsil infections. Multiple repeated tonsil infections can spread to structures around the mouth resulting in severe infections and/or airway obstruction.
Most cases of OSA are believed to be caused by:
- old age (natural or premature)
- brain injury (temporary or permanent)
- decreased muscle tone
Decreased muscle tone can be caused by drugs or alcohol, or it can be caused by neurological problems or other disorders. Some people have more than one of these issues. There is also a theory that long-term snoring might induce local nerve lesions in the pharynx in the same way as long-term exposure to vibration might cause nerve lesions in other parts of the body. Snoring is a vibration of the soft tissues of the upper airways, and studies have shown electrophysiological findings in the nerves and muscles of the pharynx indicating local nerve lesions.
- increased soft tissue around the airway (sometimes due to obesity), and
- structural features that give rise to a narrowed airway.
There are patterns of unusual facial features that occur in recognizable syndromes. Some of these craniofacial syndromes are genetic, others are from unknown causes. In many craniofacial syndromes, the features that are unusual involve the nose, mouth and jaw, or resting muscle tone, and put the individual at risk for OSA syndrome.
Down syndrome is one such syndrome. In this chromosomal abnormality, several features combine to make the presence of obstructive sleep apnea more likely. The specific features in Down syndrome that predispose to obstructive sleep apnea include: relatively low muscle tone, narrow nasopharynx, and large tongue. Obesity and enlarged tonsils and adenoids, conditions that occur commonly in the western population, are much more likely to be obstructive in a person with these features than without them. Obstructive sleep apnea does occur even more frequently in people with Down syndrome than in the general population. A little over 50% of all people with Down syndrome suffer from obstructive sleep apnea, and some physicians advocate routine testing of this group.
In other craniofacial syndromes, the abnormal feature may actually improve the airway, but its correction may put the person at risk for obstructive sleep apnea after surgery, when it is modified. Cleft palate syndromes are such an example. During the newborn period, all humans are obligate nasal breathers. The palate is both the roof of the mouth and the floor of the nose. Having an open palate may make feeding difficult, but generally does not interfere with breathing, in fact, if the nose is very obstructed, then an open palate may relieve breathing. There are a number of clefting syndromes in which the open palate is not the only abnormal feature; additionally there is a narrow nasal passage - which may not be obvious. In such individuals, closure of the cleft palate – whether by surgery or by a temporary oral appliance, can cause the onset of obstruction.
Skeletal advancement in an effort to physically increase the pharyngeal airspace is often an option for craniofacial patients with upper airway obstruction and small lower jaws (mandibles). These syndromes include Treacher Collins syndrome and Pierre Robin sequence. Mandibular advancement surgery is often just one of the modifications needed to improve the airway, others may include reduction of the tongue, tonsillectomy or modified uvulopalatoplasty.
OSA can also occur as a serious post-operative complication that seems to be most frequently associated with pharyngeal flap surgery as compared to other procedures for the treatment of velopharyngeal inadequacy (VPI). In OSA, recurrent interruptions of respiration during sleep are associated with temporary airway obstruction. Following pharyngeal flap surgery, depending on size and position, the flap itself may have an "obturator" or obstructive effect within the pharynx during sleep, blocking ports of airflow and hindering effective respiration. There have been documented instances of severe airway obstruction, and reports of post-operative OSA continue to increase as healthcare professionals (i.e. physicians, speech language pathologists) become more educated about this possible dangerous condition. Subsequently, in clinical practice, concerns of OSA have matched or exceeded interest in speech outcomes following pharyngeal flap surgery.
The surgical treatment for velopalatal insufficiency may cause obstructive sleep apnea syndrome. When velopalatal insufficiency is present, air leaks into the nasopharynx even when the soft palate should close off the nose. A simple test for this condition can be made by placing a tiny mirror at the nose, and asking the subject to say "P". This p sound, a plosive, is normally produced with the nasal airway closes off - all air comes out of the pursed lips, none from the nose. If it is impossible to say the sound without fogging a nasal mirror, there is an air leak - reasonable evidence of poor palatal closure. Speech is often unclear due to inability to pronounce certain sounds. One of the surgical treatments for velopalatal insufficiency involves tailoring the tissue from the back of the throat and using it to purposefully cause partial obstruction of the opening of the nasopharynx. This may actually cause OSA syndrome in susceptible individuals, particularly in the days following surgery, when swelling occurs (see below: Special Situation: Anesthesia and Surgery).
The normal sleep/wake cycle in adults is divided into REM (rapid eye movement) sleep, non-REM (NREM) sleep, and consciousness. NREM sleep is further divided into Stages 1, 2 and 3 NREM sleep. The deepest stage (stage 3 of NREM) is required for the physically restorative effects of sleep, and in pre-adolescents this is the period of release of human growth hormone. NREM stage 2 and REM, which combined are 70% of an average person's total sleep time, are more associated with mental recovery and maintenance. During REM sleep in particular, muscle tone of the throat and neck, as well as the vast majority of all skeletal muscles, is almost completely attenuated, allowing the tongue and soft palate/oropharynx to relax, and in the case of sleep apnea, to impede the flow of air to a degree ranging from light snoring to complete collapse. In the cases where airflow is reduced to a degree where blood oxygen levels fall, or the physical exertion to breathe is too great, neurological mechanisms trigger a sudden interruption of sleep, called a neurological arousal. These arousals rarely result in complete awakening, but can have a significant negative effect on the restorative quality of sleep. In significant cases of OSA, one consequence is sleep deprivation due to the repetitive disruption and recovery of sleep activity. This sleep interruption in stage 3 (also called slow-wave sleep), and in REM sleep, can interfere with normal growth patterns, healing, and immune response, especially in children and young adults.
Diagnosis of OSA is often based on a combination of patient history and tests (lab- or home-based). These tests range, in decreasing order of cost, complexity and tethering of the patient (number and type of channels of data recorded), from lab-attended full polysomnography ("sleep study") down to single-channel home recording. In the USA, these categories are associated with insurance classification from Type I down to Type IV. Reimbursement rules vary among European countries.
Polysomnography in diagnosing OSA characterizes the pauses in breathing. As in central apnea, pauses are followed by a relative decrease in blood oxygen and an increase in the blood carbon dioxide. Whereas in central sleep apnea the body's motions of breathing stop, in OSA the chest not only continues to make the movements of inhalation, but the movements typically become even more pronounced. Monitors for airflow at the nose and mouth demonstrate that efforts to breathe are not only present, but that they are often exaggerated. The chest muscles and diaphragm contract and the entire body may thrash and struggle.
An "event" can be either an apnea, characterised by complete cessation of airflow for at least 10 seconds, or a hypopnea in which airflow decreases by 50 percent for 10 seconds or decreases by 30 percent if there is an associated decrease in the oxygen saturation or an arousal from sleep. To grade the severity of sleep apnea, the number of events per hour is reported as the apnea-hypopnea index (AHI). An AHI of less than 5 is considered normal. An AHI of 5-15 is mild; 15-30 is moderate and more than 30 events per hour characterizes severe sleep apnea.
In patients who are at high likelihood of having OSA, a randomized controlled trial found that home oximetry (a non-invasive method of monitoring blood oxygenation) may be adequate and easier to obtain than formal polysomnography. High probability patients were identified by an Epworth Sleepiness Scale (ESS) score of 10 or greater and a Sleep Apnea Clinical Score (SACS) of 15 or greater. Home oximetry, however, does not measure apneic events or respiratory event-related arousals and thus does not produce an AHI value.
Numerous treatment options are used in obstructive sleep apnea. Avoiding alcohol and smoking is recommended, as is avoiding medications that relax the central nervous system (for example, sedatives and muscle relaxants). Weight loss is recommended in those who are overweight. Continuous positive airway pressure and mandibular advancement devices are often used. Physical training, even without weight loss, improves sleep apnea. There is insufficient evidence to support widespread use of medications or surgery.
The most widely used current therapeutic intervention is positive airway pressure whereby a breathing machine pumps a controlled stream of air through a mask worn over the nose, mouth, or both. The additional pressure holds open the relaxed muscles. There are several variants:
- Continuous positive airway pressure (CPAP) is effective for both moderate and severe disease. It is the most common treatment for obstructive sleep apnea.
- (VPAP), or variable positive airway pressure, also known as bilevel or BiPAP, uses an electronic circuit to monitor the patient's breathing, and provides two different pressures, a higher one during inhalation and a lower pressure during exhalation. This system is more expensive, and is sometimes used with patients who have other coexisting respiratory problems and/or who find breathing out against an increased pressure to be uncomfortable or disruptive to their sleep.
- (APAP), or automatic positive airway pressure, also known as "Auto CPAP", is the newest form of such treatment. An APAP machine incorporates pressure sensors and a computer which continuously monitors the patient's breathing performance.
Oral appliances or splints are often preferred but may not be as effective as CPAP. This device is a mouthguard similar to those used in sports to protect the teeth. It is designed to hold the lower jaw slightly down and forward relative to the natural, relaxed position. This position holds the tongue farther away from the back of the airway, and may be enough to relieve apnea or improve breathing.
Many people benefit from sleeping at a 30 degree elevation of the upper body or higher, as if in a recliner. Doing so helps prevent the gravitational collapse of the airway. Sleeping on a side as opposed to sleeping on the back is also recommended.
Evidence is insufficient to support the use of medications to treat obstructive sleep apnea. This includes the use of fluoxetine, paroxetine, acetazolamide and tryptophan among others.
Surgical treatments to modify airway anatomy can generate controversy based on dissimilar guideline evaluations of effectiveness, which can be offset factors such as individual specific anatomy and physiology, personal preference and disease severity, as well as responsiveness and tolerabilty of alternative approaches, leaving uncertainty in what may be the best selection for a particular individual. The evidence for all types of sleep surgery is poor. There are a number of different operations that may be performed including:
- Nasal surgery, including turbinectomy (removal or reduction of a nasal turbinate), or straightening of the nasal septum, in patients with nasal obstruction or congestion which reduces airway pressure and complicates OSA.
- Tonsillectomy and/or adenoidectomy in an attempt to increase the size of the airway.
- Removal or reduction of parts of the soft palate and some or all of the uvula, such as uvulopalatopharyngoplasty (UPPP) or laser-assisted uvulopalatoplasty (LAUP). Modern variants of this procedure sometimes use radiofrequency waves to heat and remove tissue.
- Reduction of the tongue base, either with laser excision or radiofrequency ablation.
- Genioglossus advancement, in which a small portion of the lower jaw that attaches to the tongue is moved forward, to pull the tongue away from the back of the airway.
- Hyoid suspension, in which the hyoid bone in the neck, another attachment point for tongue muscles, is pulled forward in front of the larynx.
- Maxillomandibular advancement
In the morbidly obese, a major loss of weight (such as what occurs after bariatric surgery) can sometimes cure the condition.
OSA in children is sometimes due to chronically enlarged tonsils and adenoids. Tonsillectomy and adenoidectomy is curative. The operation may be far from trivial, especially in the worst apnea cases, in which growth is retarded and abnormalities of the right heart may have developed. Even in these extreme cases, the surgery tends to cure not only the apnea and upper airway obstruction, but allows normal subsequent growth and development. Once the high end-expiratory pressures are relieved, the cardiovascular complications reverse themselves. The postoperative period in these children requires special precautions (see "Surgery and obstructive sleep apnea syndrome" below).
Radiofrequency ablation (RFA), which is conceptually analogous in some ways to surgery, uses low frequency (300kHz to 1MHz) radio wave energy to target tissue, causing coagulative necrosis. RFA was initially studied in OSA in a pig model. RFA achieves its effects at 40°C to 70°C unlike other electrosurgical devices which require 400°C to 600°C for efficacy. RFA very specifically treats the targeted tissue with a precise line of demarcation, reducing collateral tissue damage, a crucial consideration in the head and neck region which has a high density of major nerves and blood vessels.
Subsequent evaluations of safety and efficacy have led to the recognition of RFA by the American Academy of Otolaryngology as a somnoplasty treatment option in selected situations for mild to moderate OSA, but the evidence was judged insufficient for routine adoption by the American College of Physicians.
Although continuous positive airway pressure (CPAP) is the gold standard therapy for sleep apnea, RFA has some potential advantages in carefully selected medical settings, such as intolerance to the CPAP device, which historically has been poor. For example, when adherence is defined as greater than four hours of nightly use, 46% to 83% of patients with obstructive sleep apnea are non-adherent with CPAP for a variety of reasons, including discomfort while sleeping, pressure requirements being too high, pressure necrosis along nasal bridge, and disruption to bed partner's sleep. A 2003 study looked in mild to moderate sleep apnea found RFA equally effective to CPAP in improving daytime sleepiness, sleep-related quality of life and global quality of life. A 2008 study found that radiofrequency ablation reduced the respiratory disturbance index (RDI) by 31% at 12 months, and this increased to 45% at 24 months. In this study, an average of approximately 4.5 procedures were performed to achieve this result, which however was less than the most frequently used benchmark definition (50%) of success in the literature.
RFA is usually performed in an outpatient setting, using either local anesthetics or conscious sedation anesthesia, the procedure itself typically lasting under 3 minutes. The targeted tissue, such as tongue or palate, is usually approached through the mouth without the need for incisions, although occasionally the target is approached through the neck using assisted imaging. If the tongue is being targeted, this can be done from either dorsal or ventral side. Complications include ulceration, infection, nerve weakness or numbness and swelling. These complications occur in less than 1% of procedures.
Many studies indicate the effect of a "fight or flight" response on the body that happens with each apneic event is what increases health risks and consequences in OSA. The fight or flight response causes many hormonal changes in the body; those changes, coupled with the low oxygen saturation level of the blood, cause damage to the body over time.
Without treatment, the sleep deprivation and lack of oxygen caused by sleep apnea increases health risks such as cardiovascular disease, high blood pressure, stroke, diabetes, clinical depression, weight gain and obesity.
The most serious consequence of untreated OSA is to the heart. Sleep apnea sufferers have a 30% higher risk of heart attack or death than those unaffected. In severe and prolonged cases, increased in pulmonary pressures are transmitted to the right side of the heart. This can result in a severe form of congestive heart failure known as cor pulmonale. One prospective study showed patients with OSA, compared with healthy controls, initially had statistically significant increases in vascular endothelial growth factor (P=.003) and significantly lower levels of nitrite-nitrate (P=.008), which might be pathogenic factors in the cardiovascular complications of OSA. These factors reversed to normal levels after 12 weeks of treatment by CPAP, but further long-term trials are needed to assess the impact of this therapy.
Elevated arterial pressure (i.e., hypertension) can be a consequence of OSA syndrome. When hypertension is caused by OSA, it is distinctive in that, unlike most cases (so-called essential hypertension), the readings do not drop significantly when the individual is sleeping. Stroke is also known to be associated with OSA.
If studied carefully in a sleep lab by polysomnography (formal "sleep study"), it is believed by some authorities that approximately 1 in 5 American adults would have at least mild OSA.
- Marfan syndrome
- Respiratory disturbance index (RDI)
- Upper airway resistance syndrome, related condition whose existence is questioned
- "Obstructive Sleep Apnea Syndrome (780.53-0)". The International Classification of Sleep Disorders. Westchester, Illinois: American Academy of Sleep Medicine. 2001. pp. 52–8. Retrieved 2010-09-11.
- Gale SD, Hopkins RO (2004). "Effects of hypoxia on the brain: neuroimaging and neuropsychological findings following carbon monoxide poisoning and obstructive sleep apnea". J Int Neuropsychol Soc 10 (1): 60–71. doi:10.1017/S1355617704101082. PMID 14751008.
- Halbower AC, Degaonkar M, Barker PB, et al. (August 2006). "Childhood obstructive sleep apnea associates with neuropsychological deficits and neuronal brain injury". PLoS Med. 3 (8): e301. doi:10.1371/journal.pmed.0030301. PMC 1551912. PMID 16933960.
- Edwards, Natalie; Sullivan, Colin E. (2008). "Sleep-Disordered Breathing in Pregnancy". Sleep Medicine Clinics 3: 81–95. doi:10.1016/j.jsmc.2007.10.010.
- Sleep Apnea: Risk Factors, Mayo Clinic, June 29, 2010, Retrieved November 4, 2010.
- Goldbart AD, Goldman JL, Li RC, Brittian KR, Tauman R, Gozal D (2004). "Differential expression of cysteinyl leukotriene receptors 1 and 2 in tonsils of children with obstructive sleep apnea syndrome or recurrent infection.". Chest 126 (1): 13–8. doi:10.1378/chest.126.1.13. PMID 15249436.
- Ezzedini R, Darabi M, Ghasemi B, Darabi M, Fayezi S, Moghaddam YJ et al. (2013). "Tissue fatty acid composition in obstructive sleep apnea and recurrent tonsillitis.". Int J Pediatr Otorhinolaryngol 77 (6): 1008–12. doi:10.1016/j.ijporl.2013.03.033. PMID 23643333.
- de Miguel-Díez J, Villa-Asensi JR, Alvarez-Sala JL (December 2003). "Prevalence of sleep-disordered breathing in children with Down syndrome: polygraphic findings in 108 children". Sleep 26 (8): 1006–9. PMID 14746382.
- Shott SR, Amin R, Chini B, Heubi C, Hotze S, Akers R (April 2006). "Obstructive sleep apnea: Should all children with Down syndrome be tested?". Arch. Otolaryngol. Head Neck Surg. 132 (4): 432–6. doi:10.1001/archotol.132.4.432. PMID 16618913.
- Sloan GM (March 2000). "Posterior pharyngeal flap and sphincter pharyngoplasty: the state of the art". Cleft Palate Craniofac. J. 37 (2): 112–22. doi:10.1597/1545-1569(2000)037<0112:PPFASP>2.3.CO;2. PMID 10749049.
- Pugh, M.B. et al. (2000). Apnea. Stedman's Medical Dictionary (27th ed.) Retrieved June 18, 2006 from STAT!Ref Online Medical Library database.[page needed]
- Liao YF, Noordhoff MS, Huang CS, et al. (March 2004). "Comparison of obstructive sleep apnea syndrome in children with cleft palate following Furlow palatoplasty or pharyngeal flap for velopharyngeal insufficiency". Cleft Palate Craniofac. J. 41 (2): 152–6. doi:10.1597/02-162. PMID 14989690.
- McWilliams, Betty Jane; Peterson-Falzone, Sally J.; Hardin-Jones, Mary A.; Karnell, Michael P. (2001). Cleft palate speech (3rd ed.). St. Louis: Mosby. ISBN 0-8151-3153-4.[page needed]
- FAQ on www.sleepeducation.com
- Fietze I, Penzel T, Alonderis A, et al. (February 2011). "Management of obstructive sleep apnea in Europe". Sleep Med. 12 (2): 190–7. doi:10.1016/j.sleep.2010.10.003. PMID 21167776.
- "Sleep-related breathing disorders in adults: recommendations for syndrome definition and measurement techniques in clinical research. The Report of an American Academy of Sleep Medicine Task Force". Sleep 22 (5): 667–89. August 1999. PMID 10450601.
- Mulgrew AT, Fox N, Ayas NT, Ryan CF (February 2007). "Diagnosis and initial management of obstructive sleep apnea without polysomnography: a randomized validation study". Annals of Internal Medicine 146 (3): 157–66. doi:10.7326/0003-4819-146-3-200702060-00004. PMID 17283346.
- Flemons WW, Whitelaw WA, Brant R, Remmers JE (November 1994). "Likelihood ratios for a sleep apnea clinical prediction rule". Am. J. Respir. Crit. Care Med. 150 (5 Pt 1): 1279–85. doi:10.1164/ajrccm.150.5.7952553. PMID 7952553.
- Friedman: Sleep Apnea and Snoring, 1st ed. 2008
- Azagra-Calero, E; Espinar-Escalona, E; Barrera-Mora, JM; Llamas-Carreras, JM; Solano-Reina, E (2012 Nov 1). "Obstructive sleep apnea syndrome (OSAS). Review of the literature.". Medicina oral, patologia oral y cirugia bucal 17 (6): e925–9. PMID 22549673.
- Qaseem, A; Holty, JE; Owens, DK; Dallas, P; Starkey, M; Shekelle, P; for the Clinical Guidelines Committee of the American College of, Physicians (2013 Sep 24). "Management of Obstructive Sleep Apnea in Adults: A Clinical Practice Guideline From the American College of Physicians.". Annals of Internal Medicine. doi:10.7326/0003-4819-159-7-201310010-00704. PMID 24061345.
- Iftikhar, IH; Kline, CE; Youngstedt, SD (2013 Sep 29). "Effects of Exercise Training on Sleep Apnea: A Meta-analysis.". Lung. doi:10.1007/s00408-013-9511-3. PMID 24077936.
- Giles, TL; Lasserson, TJ; Smith, BH; White, J; Wright, J; Cates, CJ (2006 Jul 19). "Continuous positive airways pressure for obstructive sleep apnoea in adults.". The Cochrane database of systematic reviews (3): CD001106. doi:10.1002/14651858.CD001106.pub3. PMID 16855960.
- Whitelaw WA, Brant RF, Flemons WW (January 2005). "Clinical usefulness of home oximetry compared with polysomnography for assessment of sleep apnea". Am. J. Respir. Crit. Care Med. 171 (2): 188–93. doi:10.1164/rccm.200310-1360OC. PMID 15486338. Review in: Caples SM (2005). "The accuracy of physicians in predicting successful treatment response in suspected obstructive sleep apnea did not differ between home monitoring and polysomnography". ACP J. Club 143 (1): 21. PMID 15989309.
- Littner M, Hirshkowitz M, Davila D, et al. (March 2002). "Practice parameters for the use of auto-titrating continuous positive airway pressure devices for titrating pressures and treating adult patients with obstructive sleep apnea syndrome. An American Academy of Sleep Medicine report". Sleep 25 (2): 143–7. PMID 11902424.
- Neill AM, Angus SM, Sajkov D, McEvoy RD (January 1997). "Effects of sleep posture on upper airway stability in patients with obstructive sleep apnea". Am. J. Respir. Crit. Care Med. 155 (1): 199–204. doi:10.1164/ajrccm.155.1.9001312. PMID 9001312.
- Nakano H, Ikeda T, Hayashi M, Ohshima E, Onizuka A (March 2003). "Effects of body position on snoring in apneic and nonapneic snorers". Sleep 26 (2): 169–72. PMID 12683476.
- Loord H, Hultcrantz E (August 2007). "Positioner--a method for preventing sleep apnea". Acta Otolaryngol. 127 (8): 861–8. doi:10.1080/00016480601089390. PMID 17762999.
- Szollosi I, Roebuck T, Thompson B, Naughton MT (August 2006). "Lateral sleeping position reduces severity of central sleep apnea / Cheyne-Stokes respiration". Sleep 29 (8): 1045–51. PMID 16944673.
- Mason, M; Welsh, EJ; Smith, I (2013 May 31). "Drug therapy for obstructive sleep apnoea in adults.". The Cochrane database of systematic reviews 5: CD003002. doi:10.1002/14651858.CD003002.pub3. PMID 23728641.
- Veasey SC (2003). "Serotonin agonists and antagonists in obstructive sleep apnea: therapeutic potential". Am J Respir Med 2 (1): 21–9. doi:10.1007/BF03256636. PMID 14720019.
- "Submucosal Ablation of the Tongue Base for OSAS". American Academy of Otolaryngology- Head and Neck Surgery. Retrieved 29 October 2013.
- Sleep apnea
- Farrar, J; Ryan, Olliver, Gillespie (October 2008). "Radiofrequency ablation for the treatment of obstructive sleep apnea: a meta-analysis.". The Laryngoscope 118 (10): 1878–83. doi:10.1097/MLG.0b013e31817d9cc1. PMID 18806478.
- Powell, Nelson; Riley, Troell, Blumen, Guilleminault (May 1997). "Radiofrequency Volumetric Reduction of the Tongue : A Porcine Pilot Study for the Treatment of Obstructive Sleep Apnea Syndrome". Chest Journal 111 (5): 348–1355. doi:10.1378/chest.111.5.1348.
- Eick, Olaf J (1). "Temperature Controlled Radiofrequency Ablation". Indian Pacing Electrophysiol. 3 2: 66–73. PMID 17006561.
- Bashetty, Kusum; Gururaj Nadig Sandhya Kapoor (19). "Electrosurgery in aesthetic and restorative dentistry: A literature review and case reports". Journal of Conservative Dentistry 12 (4): 139–144. doi:10.4103/0972-0707.58332. PMID PMC2879725.
- Weaver, Terri; Grunstein (2008). "Adherence to Continuous Positive Airway Pressure Therapy: The Challenge to Effective Treatment". Proceedings of the American Thoracic Society 5 (2): 173-8. doi:10.1513/pats.200708-119MG.
- Woodson, BT; Steward DL, Weaver EM, Javaheri S (2003). "A randomized trial of temperature controlled radiofrequency, continuous positive airway pressure, and placebo for obstructive sleep apnea syndrome". Otol H&N Surg 128 (6): 841–61. PMID 12825037.
- Camacho, M; Jacobson, RL; Schendel, SA. Surgical Treatment of Obstructive Sleep Apnea. Sleep Medicine Clinics 2013, December Volume 8, Issue 4: pages 495-503
- Steward, DL; Weaver, Woodson (2005). "Multilevel temperature-controlled radiofrequency for obstructive sleep apnea: extended follow-up". Otolaryngol Head Neck Surg 132 (4): 630–5. PMID 15806059.
- Weaver, Jacqueline (June 15, 2007). "Sleep apnea is linked to heart disease and diabetes". Yale Bulletin and Calendar 35 (30).
- Dyugovskaya L, Lavie P, Lavie L (April 2002). "Increased adhesion molecules expression and production of reactive oxygen species in leukocytes of sleep apnea patients". Am. J. Respir. Crit. Care Med. 165 (7): 934–9. doi:10.1164/ajrccm.165.7.2104126. PMID 11934717. Lay summary – ScienceDaily (Apr. 4, 2002).
- Botros NA, Shah N, Mohsenin V, Roux F, Yaggi HK (May 21, 2007). "Obstructive Sleep Apnea as a Risk Factor for Type II Diabetes". American Thoracic Society 2007 International Conference. Lay summary – ScienceDaily (May 21, 2007).
- Paul E. Peppard, Ph.D., Terry Young, Ph.D., Mari Palta, Ph.D., and James Skatrud, M.D. (May 11, 2000). "Prospective Study of the Association Between Sleep-Disordered Breathing and Hypertension". The New England Journal of Medicine (Massachusetts Medical Society) 342 (19). Retrieved 2013-05-29. "Conclusions: We found a dose–response association between sleep-disordered breathing at base line and the presence of hypertension four years later that was independent of known confounding factors. The findings suggest that sleep-disordered breathing is likely to be a risk factor for hypertension and consequent cardiovascular morbidity in the general population."
- Peretz Lavie, Paula Herer, Victor Hoffstein (19 February 2000). "Obstructive sleep apnoea syndrome as a risk factor for hypertension: population study". BMJ (BMJ Publishing Group) 320: 479–82. Retrieved 2013-05-29. "Conclusion: Sleep apnoea syndrome is profoundly associated with hypertension independent of all relevant risk factors."
- Schröder CM, O'Hara R (June 2005). "Depression and Obstructive Sleep Apnea (OSA)". Ann Gen Psychiatry 4: 13. doi:10.1186/1744-859X-4-13. PMC 1181621. PMID 15982424.
- N.A. Shah, M.D., N.A. Botros, M.D., H.K. Yaggi, M.D., M., V. Mohsenin, M.D., New Haven, Connecticut (May 20, 2007). "Sleep Apnea Increases Risk of Heart Attack or Death by 30%". American Thoracic Society.[dead link]
- Ciftci TU, Kokturk O, Demirtas S, Gulbahar O, Bukan N (2011). "Consequences of hypoxia-reoxygenation phenomena in patients with obstructive sleep apnea syndrome". Ann Saudi Med 31 (1): 14–8. doi:10.4103/0256-4947.75772. PMC 3101718. PMID 21245593.
- Bahammam A (2011). "Obstructive sleep apnea: from simple upper airway obstruction to systemic inflammation". Ann Saudi Med 31 (1): 1–2. doi:10.4103/0256-4947.75770. PMC 3101717. PMID 21245591.
- Silverberg DS, Iaina A, Oksenberg A (January 2002). "Treating obstructive sleep apnea improves essential hypertension and quality of life". Am Fam Physician 65 (2): 229–36. PMID 11820487.
- Grigg-Damberger M (February 2006). "Why a polysomnogram should become part of the diagnostic evaluation of stroke and transient ischemic attack". J Clin Neurophysiol 23 (1): 21–38. doi:10.1097/01.wnp.0000201077.44102.80. PMID 16514349.
- Yaggi HK, Concato J, Kernan WN, Lichtman JH, Brass LM, Mohsenin V (November 2005). "Obstructive sleep apnea as a risk factor for stroke and death". N. Engl. J. Med. 353 (19): 2034–41. doi:10.1056/NEJMoa043104. PMID 16282178.
- Shamsuzzaman AS, Gersh BJ, Somers VK (October 2003). "Obstructive sleep apnea: implications for cardiac and vascular disease". JAMA 290 (14): 1906–14. doi:10.1001/jama.290.14.1906. PMID 14532320.
- Kezirian, EJ; Boudewyns, A; Eisele, DW; Schwartz, AR; Smith, PL; Van de Heyning, PH; De Backer, WA (2010 Oct). "Electrical stimulation of the hypoglossal nerve in the treatment of obstructive sleep apnea". Sleep medicine reviews 14 (5): 299–305. doi:10.1016/j.smrv.2009.10.009. PMID 20116305.
- Puhan MA, Suarez A, Lo Cascio C, Zahn A, Heitz M, Braendli O (February 2006). "Didgeridoo playing as alternative treatment for obstructive sleep apnoea syndrome: randomised controlled trial". BMJ 332 (7536): 266–70. doi:10.1136/bmj.38705.470590.55. PMC 1360393. PMID 16377643.
- Guimarães KC, Drager LF, Genta PR, Marcondes BF, Lorenzi-Filho G (May 2009). "Effects of oropharyngeal exercises on patients with moderate obstructive sleep apnea syndrome". Am. J. Respir. Crit. Care Med. 179 (10): 962–6. doi:10.1164/rccm.200806-981OC. PMID 19234106.
- García Urbano, Jesús: Orthoapnea. Snoring and Sleep Apnea. Ed. Ripano, 2010. ISBN 978-84-937793-8-2
- Mwenge GB, Rombaux P, Dury M, Lengelé B, Rodenstein D (February 2013). "Targeted hypoglossal neurostimulation for obstructive sleep apnoea: a 1-year pilot study". Eur. Respir. J. 41 (2): 360–7. doi:10.1183/09031936.00042412. PMID 22599356.
- Zaidi FN, Meadows P, Jacobowitz O, Davidson TM (August 2012). "Tongue Anatomy and Physiology, the Scientific Basis for a Novel Targeted Neurostimulation System Designed for the Treatment of Obstructive Sleep Apnea". Neuromodulation. doi:10.1111/j.1525-1403.2012.00514.x. PMID 22938390.
- American Sleep Apnea Association
- Big Daddy Blogger: An expectant father deals with chronic sleep apnea.