阻塞型睡眠呼吸暂停：修订间差异

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'''阻塞性睡眠呼吸暂停'''([[英語]]：{{lang|en|'''O'''bstructive '''S'''leep '''A'''pnea, '''OSA'''}})，是[[睡眠呼吸暂停]]中的最常见形式，它是[[呼吸道|上呼氣道]]受阻所引起的。它的特点是在[[睡眠]]时重复性的[[呼吸中止]]，尽管有在尝试[[呼吸]]，这通常会伴随[[血氧饱和度]]的降低。通常会持续20到40秒。<ref name='AASM2001'>{{cite book |chapter=Obstructive Sleep Apnea Syndrome (780.53-0) |title=The International Classification of Sleep Disorders |publisher=American Academy of Sleep Medicine |year=2001 |location=Westchester, Illinois |pages=52–8 |url=http://www.esst.org/adds/ICSD.pdf |accessdate=2010-09-11 |deadurl=yes |archiveurl=https://web.archive.org/web/20110726034931/http://www.esst.org/adds/ICSD.pdf |archivedate=2011-07-26 }}</ref>
'''阻塞性睡眠呼吸暂停'''([[英語]]：{{lang|en|'''O'''bstructive '''S'''leep '''A'''pnea, '''OSA'''}})，是[[睡眠呼吸暂停]]中的最常见形式，它是[[呼吸道|上呼氣道]]{{tsl|en|airway obstruction|受阻}}所引起的。它的特点是在[[睡眠]]时重复性的[[呼吸中止]]，尽管有在尝试[[呼吸]]，这通常会伴随[[血氧饱和度]]的降低。通常会持续20到40秒。<ref name='AASM2001'>{{cite book |chapter=Obstructive Sleep Apnea Syndrome (780.53-0) |title=The International Classification of Sleep Disorders |publisher=American Academy of Sleep Medicine |year=2001 |location=Westchester, Illinois |pages=52–8 |url=http://www.esst.org/adds/ICSD.pdf |accessdate=2010-09-11 |deadurl=yes |archiveurl=https://web.archive.org/web/20110726034931/http://www.esst.org/adds/ICSD.pdf |archivedate=2011-07-26 }}</ref>


'''Obstructive sleep apnea''' ('''OSA''') is the most common type of [[sleep apnea]] and is caused by complete or partial [[airway obstruction|obstructions]] of the [[respiratory tract#Upper respiratory tract|upper airway]]. It is characterized by repetitive episodes of shallow or paused [[breathing]] during [[sleep]], despite the effort to breathe, and is usually associated with a reduction in [[oxygen saturation|blood oxygen saturation]]. These episodes of decreased breathing, called "[[apnea]]s" (literally, "without breath"), typically last 20 to 40 seconds.<ref name="AASM2001">{{cite book |chapter=Obstructive Sleep Apnea Syndrome (780.53-0) |title=The International Classification of Sleep Disorders |publisher=American Academy of Sleep Medicine |year=2001 |location=Westchester, Illinois |pages=52–8 |url=http://www.esst.org/adds/ICSD.pdf |accessdate=2010-09-11}}</ref>
{{trans H}}
Individuals with OSA are rarely aware of difficulty breathing, even upon awakening. It is often recognized as a problem by others who observe the individual during episodes or is suspected because of its effects on the body. OSA is commonly accompanied with [[snoring]]. Some use the terms '''obstructive sleep apnea syndrome''' or '''obstructive sleep apnea–hypopnea syndrome''' to refer to OSA which is associated with symptoms during the daytime.<ref name=Barnes2009>{{cite book|last=Barnes L (editor)|title=Surgical pathology of the head and neck|year=2009|publisher=Informa healthcare|location=New York|isbn=9781420091632|edition=3rd}}{{rp|226}}</ref> Symptoms may be present for years or even decades without identification, during which time the individual may become conditioned to the daytime sleepiness and [[Fatigue (medical)|fatigue]] associated with significant levels of sleep disturbance. Individuals 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 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 have chronic, severe OSA.

Many people experience episodes of OSA for only a short period. 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 [[Ethanol|alcohol]]) that may relax their body tone excessively and interfere with normal arousal from sleep mechanisms.

==Signs and symptoms==
Common symptoms 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 (mood)|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.

===Adults===
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 (medical)|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 [[continuous positive airway pressure]] (CPAP) treatment.<ref name="pmid14751008">{{cite journal |vauthors=Gale SD, Hopkins RO |title=Effects of hypoxia on the brain: neuroimaging and neuropsychological findings following carbon monoxide poisoning and obstructive sleep apnea |journal=J Int Neuropsychol Soc |volume=10 |issue=1 |pages=60–71 |year=2004 |pmid=14751008 |doi=10.1017/S1355617704101082 |url=http://journals.cambridge.org/abstract_S1355617704101082 }}</ref>

Diagnosis of obstructive sleep apnea is significantly more common among people in relationships, who are alerted to their condition by being informed by their sleeping partner since individuals with obstructive sleep apnea are often unaware of the condition. There is a stigma associated with loud snoring, and it is not considered a feminine trait. Consequently, females are less likely to be told by their partners that they snore, or to admit it to themselves or doctors. Furthermore, CPAP is also perceived negatively by females, and less likely to be utilized to its full extent in this group.<ref>{{cite journal|last=Henry|first=D|author2=Rosenthal, L|title="Listening for his breath:" the significance of gender and partner reporting on the diagnosis, management, and treatment of obstructive sleep apnea.|journal=Social science & medicine (1982)|date=Feb 2013|volume=79|pages=48–56|pmid=22770968|doi=10.1016/j.socscimed.2012.05.021}}</ref>

===Children===
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 "[[hyperactivity|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 [[tonsil]]s and [[adenoid]]s 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 such as restlessness, exhaustion, etc.

Children with OSA may experience learning and memory deficits and OSA has also been linked to lowered childhood IQ scores.<ref>{{cite journal |vauthors=Halbower AC, Degaonkar M, Barker PB, etal |title=Childhood obstructive sleep apnea associates with neuropsychological deficits and neuronal brain injury |journal=PLoS Med. |volume=3 |issue=8 |pages=e301 |date=August 2006 |pmid=16933960 |pmc=1551912 |doi=10.1371/journal.pmed.0030301 |url=http://dx.plos.org/10.1371/journal.pmed.0030301}}</ref>

==Causes==
Most cases of OSA are believed to be caused by:
* old age (natural or premature)
* brain injury (temporary or permanent)
* decreased muscle tone. This 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.

In adults, most individuals with OSA syndrome are [[obesity|obese]], however, obesity is not always present. Adults with normal body mass indices (BMIs) often have decreased muscle tone causing airway collapse and sleep apnea. The cause of this is not well understood.

OSA and recurrent [[tonsillitis]] (RT) are different in their mechanism and outcome.<ref name="pmid23643333">{{cite journal |vauthors=Ezzedini R, Darabi M, Ghasemi B, Darabi M, Fayezi S, Moghaddam YJ, etal | title=Tissue fatty acid composition in obstructive sleep apnea and recurrent tonsillitis. | journal=Int J Pediatr Otorhinolaryngol | year= 2013 | volume= 77| issue= 6| pages= 1008–12| pmid=23643333 | doi=10.1016/j.ijporl.2013.03.033 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23643333 }}</ref>

===Risk factors===
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. The 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 and 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 [[menopause|post-menopausal]] women approaches that of men in the same age range. Women are at greater risk for developing OSA during [[pregnancy]].<ref>{{cite journal |doi=10.1016/j.jsmc.2007.10.010 |title=Sleep-Disordered Breathing in Pregnancy |year=2008 |last1=Edwards |first1=Natalie |last2=Sullivan |first2=Colin E. |journal=Sleep Medicine Clinics |volume=3 |pages=81–95}}</ref>

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.<ref>[http://www.mayoclinic.com/health/sleep-apnea/DS00148/DSECTION=risk-factors Sleep Apnea: Risk Factors], Mayo Clinic, June 29, 2010, Retrieved November 4, 2010.</ref>

===Craniofacial syndromes===
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 [[chromosome|chromosomal]] abnormality, several features combine to make the presence of obstructive sleep apnea more likely. The specific features of 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,<ref>{{cite journal |vauthors=de Miguel-Díez J, Villa-Asensi JR, Alvarez-Sala JL |title=Prevalence of sleep-disordered breathing in children with Down syndrome: polygraphic findings in 108 children |journal=Sleep |volume=26 |issue=8 |pages=1006–9 |date=December 2003 |pmid=14746382}}</ref> and some physicians advocate routine testing of this group.<ref>{{cite journal |vauthors=Shott SR, Amin R, Chini B, Heubi C, Hotze S, Akers R |title=Obstructive sleep apnea: Should all children with Down syndrome be tested? |journal=Arch. Otolaryngol. Head Neck Surg. |volume=132 |issue=4 |pages=432–6 |date=April 2006 |pmid=16618913 |doi=10.1001/archotol.132.4.432}}</ref>

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 breathing|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 [[human pharynx|pharyngeal]] airspace is often an option for craniofacial patients with upper airway obstruction and small lower jaws ([[Human mandible|mandible]]s). 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]].

=== Post-operative complication ===
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).<ref name=Sloan>{{cite journal |author=Sloan GM |title=Posterior pharyngeal flap and sphincter pharyngoplasty: the state of the art |journal=Cleft Palate Craniofac. J. |volume=37 |issue=2 |pages=112–22 |date=March 2000 |pmid=10749049 |doi=10.1597/1545-1569(2000)037<0112:PPFASP>2.3.CO;2}}</ref> In OSA, recurrent interruptions of [[Respiration (physiology)|respiration]] during sleep are associated with temporary [[airway obstruction]]. Following pharyngeal flap surgery, depending on size and position, the flap itself may have an "[[wikt:obturator|obturator]]" or obstructive effect within the [[human pharynx|pharynx]] during sleep, blocking ports of airflow and hindering effective [[Respiration (physiology)|respiration]].<ref name=Pugh>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|date=May 2013}}</ref><ref name=Liao2004>{{cite journal |vauthors=Liao YF, Noordhoff MS, Huang CS, etal |title=Comparison of obstructive sleep apnea syndrome in children with cleft palate following Furlow palatoplasty or pharyngeal flap for velopharyngeal insufficiency |journal=Cleft Palate Craniofac. J. |volume=41 |issue=2 |pages=152–6 |date=March 2004 |pmid=14989690 |doi=10.1597/02-162}}</ref> There have been documented instances of severe airway obstruction, and reports of post-operative OSA continues to increase as healthcare professionals (i.e. physicians, [[Speech and language pathology|speech language pathologists]]) become more educated about this possible dangerous condition.<ref name=PetersonFalzone>{{cite book |author1=McWilliams, Betty Jane |author2=Peterson-Falzone, Sally J. |author3=Hardin-Jones, Mary A. |author4=Karnell, Michael P. |title=Cleft palate speech |publisher=Mosby |location=St. Louis |year=2001 |isbn=0-8151-3153-4 |edition=3rd}}{{page needed|date=May 2013}}</ref> Subsequently, in clinical practice, concerns of OSA have matched or exceeded interest in speech outcomes following pharyngeal flap surgery.{{citation needed|date=May 2013}}

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 on 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).

Finally, patients with OSA are at an increased risk of many perioperative complications when they are present for surgery, even if the planned procedure is not on the head and neck. Guidelines intended to reduce the risk of perioperative complications have been published.<ref>{{cite journal|last=Gross|first=JB |author2=Bachenberg, KL |author3=Benumof, JL |author4=Caplan, RA |author5=Connis, RT |author6=Coté, CJ |author7=Nickinovich, DG |author8=Prachand, V |author9=Ward, DS |author10=Weaver, EM |author11=Ydens, L |author12=Yu, S |author13=American Society of Anesthesiologists Task Force on Perioperative Management |title=Practice guidelines for the perioperative management of patients with obstructive sleep apnea: a report by the American Society of Anesthesiologists Task Force on Perioperative Management of patients with obstructive sleep apnea.|journal=Anesthesiology|date=May 2006|volume=104|issue=5|pages=1081–93; quiz 1117–8|pmid=16645462|url=http://journals.lww.com/anesthesiology/Fulltext/2006/05000/Practice_Guidelines_for_the_Perioperative.26.aspx|doi=10.1097/00000542-200605000-00026}}</ref>

==Pathophysiology==
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.{{citation needed|date=May 2013}}

==Diagnosis==
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.<ref>[http://www.sleepeducation.com/Topic.aspx?id=80 FAQ on www.sleepeducation.com]</ref> Reimbursement rules vary among European countries.<ref>{{cite journal |vauthors=Fietze I, Penzel T, Alonderis A, etal |title=Management of obstructive sleep apnea in Europe |journal=Sleep Med. |volume=12 |issue=2 |pages=190–7 |date=February 2011 |pmid=21167776 |doi=10.1016/j.sleep.2010.10.003}}</ref> In a systematic review of published evidence, the United State Preventive Services Task Force in 2017 concluded that there was uncertainty about the accuracy or clinical utility of all potential screening tools for OSA,<ref>{{cite journal|last1=Jonas|first1=Daniel E|last2=Amick|first2=Halle R.|last3=Feltner|first3=Cynthia|last4=Weber|first4=Rachel P|last5=Arvanitis|first5=Marina|last6=Stine|first6=A|last7=Lux|first7=L|last8=Harris|first8=Russell P|title=Screening for Obstructive Sleep Apnea in Adults Evidence Report and Systematic Review for the US Preventive Services Task Force|journal=JAMA|date=2017|volume=317|issue=4|pages=415–433|doi=10.1001/jama.2016.19635|url=http://jamanetwork.com/journals/jama/fullarticle/2598777|accessdate=24 January 2017}}</ref> and recommended that current evidence is insufficient to assess the balance of benefits and harms of screening for OSA in asymptomatic adults.<ref>{{cite journal|last1=US Preventive Services Task Force|title=Screening for Obstructive Sleep Apnea in Adults US Preventive Services Task Force Recommendation Statement|journal=JAMA|date=2017|volume=317|issue=4|pages=407–414|doi=10.1001/jama.2016.20325|ref=http://jamanetwork.com/journals/jama/fullarticle/2598778}}</ref>

===Polysomnography===
{| class="wikitable" align="right" style="margin: 1em 1em "
! [[Apnea-hypopnea index|AHI]]||Rating
|-
| <5||Normal
|-
| 5-15||Mild
|-
| 15-30||Moderate
|-
| >30||Severe
|}

<!-- Deleted image removed: [[Image:Apnea2Min.jpg|thumb|200px|right|Two minute epoch representing continuous OSA. Click on this image for larger version.]] -->
[[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 [[Thoracic diaphragm|diaphragm]] contract and the entire body may thrash and struggle.{{citation needed|date=May 2013}}

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.<ref>{{cite journal |title=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 |journal=Sleep |volume=22 |issue=5 |pages=667–89 |date=August 1999 |pmid=10450601 |url=http://www.journalsleep.org/ViewAbstract.aspx?pid=24156}}</ref> 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.

===Home oximetry===
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.<ref name="pmid17283346">{{cite journal |vauthors=Mulgrew AT, Fox N, Ayas NT, Ryan CF |title=Diagnosis and initial management of obstructive sleep apnea without polysomnography: a randomized validation study |journal=Annals of Internal Medicine |volume=146 |issue=3 |pages=157–66 |date=February 2007 |pmid=17283346 |doi=10.7326/0003-4819-146-3-200702060-00004}}</ref> 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.<ref name="pmid7952553">{{cite journal |vauthors=Flemons WW, Whitelaw WA, Brant R, Remmers JE |title=Likelihood ratios for a sleep apnea clinical prediction rule |journal=Am. J. Respir. Crit. Care Med. |volume=150 |issue=5 Pt 1 |pages=1279–85 |date=November 1994 |pmid=7952553 |doi=10.1164/ajrccm.150.5.7952553}}</ref> Home oximetry, however, does not measure apneic events or respiratory event-related arousals and thus does not produce an AHI value.

==Treatment ==
Numerous treatment options are used in obstructive sleep apnea.<ref name="Friedman2008">Friedman: Sleep Apnea and Snoring, 1st ed. 2008</ref> Avoiding alcohol and smoking is recommended,<ref name=Aza2012/> 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]] (CPAP) and [[mandibular advancement device]]s are often used and found to be equally effective.<ref name=Qa2013/><ref name=Brat2015>{{cite journal|last1=Bratton|first1=DJ|last2=Gaisl|first2=T|last3=Wons|first3=AM|last4=Kohler|first4=M|title=CPAP vs Mandibular Advancement Devices and Blood Pressure in Patients With Obstructive Sleep Apnea: A Systematic Review and Meta-analysis.|journal=JAMA|date=1 December 2015|volume=314|issue=21|pages=2280–93|pmid=26624827|doi=10.1001/jama.2015.16303}}</ref> Physical training, even without weight loss, improves sleep apnea.<ref>{{cite journal|last=Iftikhar|first=IH|author2=Kline, CE |author3=Youngstedt, SD |title=Effects of Exercise Training on Sleep Apnea: A Meta-analysis.|journal=Lung|date=Sep 29, 2013|pmid=24077936|doi=10.1007/s00408-013-9511-3|volume=192|pages=175–184|pmc=4216726}}</ref> There is insufficient evidence to support widespread use of medications or surgery.<ref name=Qa2013/>

=== Physical intervention ===
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.<ref name=Gil2006/> It is the most common treatment for obstructive sleep apnea.
* [[Variable positive airway pressure]] (VPAP) (also known as bilevel (BiPAP or BPAP)) 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.
* [[Nasal EPAP]], which is a bandage-like device placed over the nostrils that utilizes a person's own breathing to create positive airway pressure to prevent obstructed breathing.<ref name=Riaz2015rev>{{cite journal|last1=Riaz|first1=M|last2=Certal|first2=V|last3=Nigam|first3=G|last4=Abdullatif|first4=J|last5=Zaghi|first5=S|last6=Kushida|first6=CA|last7=Camacho|first7=M|title=Nasal Expiratory Positive Airway Pressure Devices (Provent) for OSA: A Systematic Review and Meta-Analysis.|journal=Sleep disorders|date=2015|volume=2015|pages=734798|pmid=26798519|doi=10.1155/2015/734798|pmc=4699057}}</ref>
* [[Automatic positive airway pressure]], or ''automatic positive airway pressure'', also known as "Auto CPAP", incorporates pressure sensors and monitors the person's breathing.<ref name="pmid15486338">{{cite journal |vauthors=Whitelaw WA, Brant RF, Flemons WW |title=Clinical usefulness of home oximetry compared with polysomnography for assessment of sleep apnea |journal=Am. J. Respir. Crit. Care Med. |volume=171 |issue=2 |pages=188–93 |date=January 2005 |pmid=15486338 |doi=10.1164/rccm.200310-1360OC}} Review in: {{cite journal |author=Caples SM |title=The accuracy of physicians in predicting successful treatment response in suspected obstructive sleep apnea did not differ between home monitoring and polysomnography |journal=ACP J. Club |volume=143 |issue=1 |pages=21 |year=2005 |pmid=15989309}}</ref><ref name="pmid11902424">{{cite journal |vauthors=Littner M, Hirshkowitz M, Davila D, etal |title=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 |journal=Sleep |volume=25 |issue=2 |pages=143–7 |date=March 2002 |pmid=11902424}}</ref>
* A 5% reduction in weight among those with moderate to severe OSA may decrease symptoms similarly to CPAP.<ref>{{Cite journal|last=McNicholas|first=Walter T.|last2=Bonsignore|first2=Maria R.|last3=Lévy|first3=Patrick|last4=Ryan|first4=Silke|date=2016-05-27|title=Mild obstructive sleep apnoea: clinical relevance and approaches to management|journal=The Lancet Respiratory Medicine|doi=10.1016/S2213-2600(16)30146-1|issn=2213-2619|pmid=27245915|volume=4|pages=826–834}}</ref>

''Oral appliances'' or splints are often preferred but may not be as effective as CPAP.<ref name=Gil2006>{{cite journal|last=Giles|first=TL|author2=Lasserson, TJ |author3=Smith, BH |author4=White, J |author5=Wright, J |author6= Cates, CJ |title=Continuous positive airways pressure for obstructive sleep apnoea in adults.|journal=The Cochrane database of systematic reviews|date=Jul 19, 2006|issue=3|pages=CD001106|pmid=16855960|doi=10.1002/14651858.CD001106.pub3}}</ref> 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<ref>{{cite journal|vauthors=Neill AM, Angus SM, Sajkov D, McEvoy RD |title=Effects of sleep posture on upper airway stability in patients with obstructive sleep apnea |journal=Am. J. Respir. Crit. Care Med. |volume=155 |issue=1|pages=199–204 |date=January 1997 |pmid=9001312 |doi=10.1164/ajrccm.155.1.9001312}}</ref> or higher, as if in a [[recliner]]. Doing so helps prevent the gravitational collapse of the airway. [[Human anatomical terms#Anatomical directions|Sleeping on a side]] as opposed to [[supine position|sleeping on the back]] is also recommended.<ref>{{cite journal |vauthors=Nakano H, Ikeda T, Hayashi M, Ohshima E, Onizuka A |title=Effects of body position on snoring in apneic and nonapneic snorers |journal=Sleep|volume=26 |issue=2 |pages=169–72 |date=March 2003 |pmid=12683476}}</ref><ref>{{cite journal|vauthors=Loord H, Hultcrantz E |title=Positioner--a method for preventing sleep apnea |journal=Acta Otolaryngol. |volume=127 |issue=8 |pages=861–8 |date=August 2007 |pmid=17762999|doi=10.1080/00016480601089390}}</ref><ref>{{cite journal |vauthors=Szollosi I, Roebuck T, Thompson B, Naughton MT |title=Lateral sleeping position reduces severity of central sleep apnea / Cheyne-Stokes respiration |journal=Sleep |volume=29 |issue=8 |pages=1045–51 |date=August 2006|pmid=16944673}}</ref>

Some studies have suggested that ''playing a [[wind instrument]]'': may reduce snoring and apnea incidents.<ref>[http://www.medicaldaily.com/learning-play-wind-instrument-could-lower-your-risk-obstructive-sleep-apnea-329582 Learning To Play A Wind Instrument Could Lower Your Risk For Obstructive Sleep Apnea]</ref> This may be especially true of [[double reed instrument]]s.<ref>{{cite journal | pmc = 3365082 | pmid=22701381 | doi=10.5664/jcsm.1906 | volume=8 | title=Risk of obstructive sleep apnea lower in double reed wind musicians |vauthors=Ward CP, York KM, McCoy JG | journal=J Clin Sleep Med | pages=251–5}}</ref>

=== Surgery ===
Surgical treatments to modify airway anatomy, known as [[sleep surgery]], are varied and must be tailored to the specific airway obstruction needs of a patient. Surgery is not considered a frontline treatment for obstructive sleep apnea, as prospective, randomized, comparative clinical evidence against current front line treatments is lacking.<ref name=Qa2013/><ref name="AAO2013"/> For those obstructive sleep apnea sufferers unable or unwilling to comply with front line treatment, a properly selected surgical intervention will be the result of considering an individual's specific anatomy and physiology, personal preference and disease severity.<ref name="Friedman2008"/> There is little randomized clinical trial evidence for all types of [[sleep surgery]].<ref name=Qa2013/>

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]]<ref>[http://www.umm.edu/patiented/articles/what_surgical_procedures_sleep_apnea_000065_10.htm Sleep apnea<!-- Bot generated title -->]</ref>

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 are 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).

=== Neurostimulation ===
For patients who cannot use a continuous positive airway pressure device, the U.S. Food and Drug Administration in 2014 granted pre-market approval for an upper airway stimulation system that senses respiration and delivers mild electrical stimulation to the hypoglossal nerve in order to increase muscle tone at the back of the tongue so it will not collapse over the airway. The device includes a handheld patient controller to allow it to be switched on before sleep and is powered by an implantable pulse generator, similar to one used for cardiac rhythm management. Approval for this active implantable [[Neuromodulation (medicine)|neuromodulation]] device was preceded by a clinical trial whose results were published in the ''[[New England Journal of Medicine]]''.<ref>http://www.accessdata.fda.gov/scripts/cdrh/cfdocs/cfPMA/pma.cfm?id=18437. FDA "Premarket Approval (PMA) Inspire II Upper Airway Stimulation System" U.S. Food and Drug Administration. April 30, 2014.</ref><ref>{{cite journal |author=Strollo PJ Jr, Soose RJ, Maurer JT, de Vries N, Cornelius J, Froymovich O, Hanson RD, Padhya TA, Steward DL, Gillespie MB, Woodson BT, Van de Heyning PH, Goetting MG, Vanderveken OM, Feldman N, Knaack L, Strohl KP; STAR Trial Group |title=Upper-airway stimulation for obstructive sleep apnea |journal=New England Journal of Medicine |volume=370 |issue=2 |pages=139–49 |date=January 9, 2014|pmid=24401051 |doi=10.1056/nejmoa1308659}}</ref>

=== Radiofrequency ablation ===
[[Radiofrequency ablation]] (RFA), which is conceptually analogous in some ways to surgery, uses low frequency (300&nbsp;kHz to 1&nbsp;MHz)<ref name="Farrar2008"/> [[radio wave]] energy to target [[tissue (biology)|tissue]], causing [[coagulative necrosis]]. RFA achieves its effects at 40&nbsp;°C to 70&nbsp;°C<ref name="Eick2002"/> unlike other electrosurgical devices which require 400&nbsp;°C to 600&nbsp;°C for efficacy.<ref name="Bashetty2009"/>

Subsequent evaluations of safety and efficacy have led to the recognition of RFA by the [[American Academy of Otolaryngology – Head and Neck Surgery|American Academy of Otolaryngology]]<ref name="AAO2013"/> 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.<ref name=Qa2013/>

RFA has some potential advantages in carefully selected [[medicine|medical]] settings, such as intolerance to the CPAP device. 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<ref name="Weaver2008"/> for a variety of reasons, including discomfort while sleeping.

RFA is usually performed in an [[outpatient]] setting, using either [[local anesthetic]]s or [[anesthesia awareness|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.<ref name="Steward2005"/> If the tongue is being targeted, this can be done from either [[Dorsum (anatomy)|dorsal]] or [[ventral]] side. Complications include [[ulceration]], [[infection]], nerve weakness or numbness and swelling. These complications occur in less than 1% of procedures.<ref name="Farrar2008"/>

=== Medications ===
Evidence is insufficient to support the use of medications to treat obstructive sleep apnea.<ref name=Qa2013>{{cite journal|last=Qaseem|first=A|author2=Holty, JE |author3=Owens, DK |author4=Dallas, P |author5=Starkey, M |author6=Shekelle, P |author7= for the Clinical Guidelines Committee of the American College of, Physicians |title=Management of Obstructive Sleep Apnea in Adults: A Clinical Practice Guideline From the American College of Physicians.|journal=Annals of Internal Medicine|date=Sep 24, 2013|pmid=24061345|doi=10.7326/0003-4819-159-7-201310010-00704 |volume=159 |pages=471–83}}</ref><ref>{{cite journal|last=Mason|first=M|author2=Welsh, EJ |author3=Smith, I |title=Drug therapy for obstructive sleep apnoea in adults.|journal=The Cochrane database of systematic reviews|date=May 31, 2013|volume=5|pages=CD003002|pmid=23728641|doi=10.1002/14651858.CD003002.pub3}}</ref> This includes the use of [[fluoxetine]], [[paroxetine]], [[acetazolamide]] and [[tryptophan]] among others.<ref name=Qa2013/><ref name=Vea2003>{{cite journal |author=Veasey SC |title=Serotonin agonists and antagonists in obstructive sleep apnea: therapeutic potential |journal=Am J Respir Med |volume=2|issue=1 |pages=21–9 |year=2003 |pmid=14720019 |doi=10.1007/BF03256636}}</ref>

==Prognosis==
Many studies indicate the effect of a "[[Fight-or-flight response|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.<ref>{{cite journal |url=http://www.yale.edu/opa/arc-ybc/v35.n30/story17.html |first=Jacqueline |last=Weaver |date=June 15, 2007 |volume=35 |issue=30 |title=Sleep apnea is linked to heart disease and diabetes |journal=Yale Bulletin and Calendar}}</ref><ref>{{cite journal |vauthors=Dyugovskaya L, Lavie P, Lavie L |title=Increased adhesion molecules expression and production of reactive oxygen species in leukocytes of sleep apnea patients |journal=Am. J. Respir. Crit. Care Med. |volume=165 |issue=7 |pages=934–9 |date=April 2002 |pmid=11934717 |doi=10.1164/ajrccm.165.7.2104126 |laysummary=http://www.sciencedaily.com/releases/2002/04/020403025512.htm |laysource=ScienceDaily |laydate=Apr 4, 2002}}</ref><!--<ref>http://www.schlaflabor-breisgau.de/Bild_gif/Peppard.pdf</ref> broken link --><ref>{{cite conference |url=http://www-archive.thoracic.org/sections/publications/press-releases/conference/articles/2007/abstracts/Obstructive_Sleep_Apnea_as_a_Risk_Factor_for_Type_II_Diabetes_1898.pdf |title=Obstructive Sleep Apnea as a Risk Factor for Type II Diabetes |vauthors=Botros NA, Shah N, Mohsenin V, Roux F, Yaggi HK |date=May 21, 2007 |conference=American Thoracic Society 2007 International Conference |laysummary=http://www.sciencedaily.com/releases/2007/05/070520183530.htm |laysource=ScienceDaily |laydate=May 21, 2007}}</ref>

Without treatment, the [[sleep deprivation]] and lack of oxygen caused by sleep apnea increases health risks such as [[cardiovascular disease]], aortic disease (e.g. [[aortic aneurysm]]),<ref>{{Cite journal|title = The impact of obstructive sleep apnoea on the aorta|journal = The European Respiratory Journal|date = 2015-08-01|issn = 1399-3003|pmid = 26113685|pages = 532–544|volume = 46|issue = 2|doi = 10.1183/09031936.00029315|first = Thomas|last = Gaisl|first2 = Daniel J.|last2 = Bratton|first3 = Malcolm|last3 = Kohler}}</ref> [[high blood pressure]],<ref>{{cite journal |url=http://www.schlaflabor-breisgau.de/images/stories/schlaflabor/Peppard.pdf |title=Prospective Study of the Association Between Sleep-Disordered Breathing and Hypertension |authors=Paul E. Peppard, Ph.D., Terry Young, Ph.D., Mari Palta, Ph.D., and James Skatrud, M.D. |volume=342 |date=May 11, 2000 |issue=19 |journal=[[The New England Journal of Medicine]] |publisher=[[Massachusetts Medical Society]] |accessdate=2013-05-29 |doi=10.1056/nejm200005113421901 |quote='''''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. |pages=1378–1384}}</ref><ref>{{cite journal |url=http://www.schlaflabor-breisgau.de/images/stories/schlaflabor/lavie.pdf |title=Obstructive sleep apnoea syndrome as a risk factor for hypertension: population study |authors=Peretz Lavie, Paula Herer, Victor Hoffstein |volume=320 |date=19 February 2000 |pages=479–82|journal=[[BMJ]] |publisher=BMJ Publishing Group |accessdate=2013-05-29 |quote='''''Conclusion''''': Sleep apnoea syndrome is profoundly associated with hypertension independent of all relevant risk factors. |doi=10.1136/bmj.320.7233.479}}</ref> [[stroke]],<ref>{{cite journal |vauthors=Yaggi HK, Concato J, Kernan WN, Lichtman JH, Brass LM, Mohsenin V |title=Obstructive sleep apnea as a risk factor for stroke and death |journal=N. Engl. J. Med. |volume=353 |issue=19 |pages=2034–41 |date=November 2005 |pmid=16282178 |doi=10.1056/NEJMoa043104}}</ref> [[diabetes]], [[clinical depression]],<ref name="pmid15982424">{{cite journal |vauthors=Schröder CM, O'Hara R |title=Depression and Obstructive Sleep Apnea (OSA) |journal=Ann Gen Psychiatry |volume=4 |issue= |pages=13 |date=June 2005 |pmid=15982424 |pmc=1181621 |doi=10.1186/1744-859X-4-13}}</ref> weight gain and [[obesity]].<ref>{{cite news|title=Women with sleeping problems at higher risk for Type 2 diabetes|url=https://www.sleepassociation.org/2016/01/29/women-with-sleeping-problems-at-higher-risk-for-type-2-diabetes/|accessdate=30 January 2016|work=American Sleep Association}}</ref>

The most serious consequence of untreated OSA is to the heart. Persons with sleep apnea have a 30% higher risk of [[heart attack]] or death than those unaffected.<ref>{{cite web|url=http://www.thoracic.org/sections/publications/press-releases/conference/articles/2007/press-releases/sleep-apnea-increases-risk-of-heart-attack-or-death-by-30.html |title=Sleep Apnea Increases Risk of Heart Attack or Death by 30% |last=N.A. Shah, M.D., N.A. Botros, M.D., H.K. Yaggi, M.D., M., V. Mohsenin, M.D., New Haven, Connecticut |date=May 20, 2007 |work=American Thoracic Society |deadurl=yes |archiveurl=https://web.archive.org/web/20090524193435/http://www.thoracic.org/sections/publications/press-releases/conference/articles/2007/press-releases/sleep-apnea-increases-risk-of-heart-attack-or-death-by-30.html |archivedate=May 24, 2009 }}</ref> 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]]''. Dyastolic function of the heart also becomes affected.<ref name=" pmid = 24445697 ">{{cite journal | author = Sun Y | title = Cardiac structural and functional changes in old elderly patients with obstructive sleep apnoea-hypopnoea syndrome. | journal = J Int Med Res | volume = 42 | issue = 2|date=Apr 2014 | pmid = 24445697 | url = http://imr.sagepub.com/cgi/pmidlookup?view=long&pmid=24445697 | pages = 395–404 | doi=10.1177/0300060513502890}}</ref> 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.<ref name="pmid21245593">{{cite journal |vauthors=Ciftci TU, Kokturk O, Demirtas S, Gulbahar O, Bukan N |title=Consequences of hypoxia-reoxygenation phenomena in patients with obstructive sleep apnea syndrome |journal=Ann Saudi Med |volume=31 |issue=1 |pages=14–8 |year=2011 |pmid=21245593 |pmc=3101718 |doi=10.4103/0256-4947.75772}}</ref> 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.<ref name="pmid21245591">{{cite journal |author=Bahammam A |title=Obstructive sleep apnea: from simple upper airway obstruction to systemic inflammation |journal=Ann Saudi Med |volume=31 |issue=1 |pages=1–2 |year=2011 |pmid=21245591 |pmc=3101717 |doi=10.4103/0256-4947.75770}}</ref>

Elevated arterial pressure (i.e., [[hypertension]]) can be a consequence of OSA syndrome.<ref name="Sleep Apnea">{{cite journal |vauthors=Silverberg DS, Iaina A, Oksenberg A |title=Treating obstructive sleep apnea improves essential hypertension and quality of life |journal=Am Fam Physician |volume=65 |issue=2 |pages=229–36 |date=January 2002 |pmid=11820487}}</ref> 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 (non-dipper) or even increase (inverted dipper).<ref>{{cite journal |author=Grigg-Damberger M |title=Why a polysomnogram should become part of the diagnostic evaluation of stroke and transient ischemic attack |journal=J Clin Neurophysiol |volume=23 |issue=1 |pages=21–38 |date=February 2006 |pmid=16514349 |doi=10.1097/01.wnp.0000201077.44102.80}}</ref>

==Epidemiology==
OSA accompanied by daytime sleepiness is estimated to affect 3% to 7% of men and 2% to 5% of women, and the disease is common in both developed and developing countries.<ref>{{cite journal|last1=Punjabi|first1=N. M.|title=The Epidemiology of Adult Obstructive Sleep Apnea|journal=Proceedings of the American Thoracic Society|date=15 February 2008|volume=5|issue=2|pages=136–143|doi=10.1513/pats.200709-155MG}}</ref> It is most commonly diagnosed in middle-aged males.<ref name=Aza2012>{{cite journal|last=Azagra-Calero|first=E|author2=Espinar-Escalona, E |author3=Barrera-Mora, JM |author4=Llamas-Carreras, JM |author5= Solano-Reina, E |title=Obstructive sleep apnea syndrome (OSAS). Review of the literature.|journal=Medicina oral, patologia oral y cirugia bucal|date=Nov 1, 2012|volume=17|issue=6|pages=e925-9|pmid=22549673|doi=10.4317/medoral.17706 |pmc=3505711}}</ref>

If studied carefully in a sleep lab by polysomnography (formal "sleep study"), it is believed that approximately 1 in 5 American adults would have at least mild OSA.<ref name="facial phenotype">{{cite journal |vauthors=Shamsuzzaman AS, Gersh BJ, Somers VK |title=Obstructive sleep apnea: implications for cardiac and vascular disease |journal=JAMA |volume=290 |issue=14 |pages=1906–14|date=October 2003 |pmid=14532320 |doi=10.1001/jama.290.14.1906}}</ref>

==Research==
[[Neurostimulation]] is currently being studied as a method of treatment;<ref>{{cite journal|last=Kezirian|first=EJ |author2=Boudewyns, A |author3=Eisele, DW |author4=Schwartz, AR |author5=Smith, PL |author6=Van de Heyning, PH |author7=De Backer, WA |title=Electrical stimulation of the hypoglossal nerve in the treatment of obstructive sleep apnea|journal=Sleep medicine reviews|date=October 2010|volume=14|issue=5|pages=299–305|pmid=20116305|doi=10.1016/j.smrv.2009.10.009}}</ref> an implanted hypoglossal nerve stimulation system received European CE Mark (Conformité Européenne) approval in March 2012.<ref>{{cite news|last=Editors|title=ImThera aura6000 System for Sleep Apnea Gets a Go in Europe|url=http://www.medgadget.com/2012/03/imthera-aura6000-system-for-sleep-apnea-gets-a-go-in-europe.html|accessdate=15 January 2014|newspaper=Medgadget|date=15 March 2012}}</ref> Also being studied are exercises of the muscles around the mouth and [[pharynx|throat]] through activities such as playing the [[didgeridoo]].<ref>{{cite journal |vauthors=Puhan MA, Suarez A, Lo Cascio C, Zahn A, Heitz M, Braendli O |title=Didgeridoo playing as alternative treatment for obstructive sleep apnoea syndrome: randomised controlled trial |journal=BMJ |volume=332 |issue=7536 |pages=266–70 |date=February 2006|pmid=16377643 |pmc=1360393 |doi=10.1136/bmj.38705.470590.55}}</ref><ref name="Guimaraes KC, Drager LF, Genta PR, Marcondes BF, Lorensi-Filhol G 2009 962–966">{{cite journal |vauthors=Guimarães KC, Drager LF, Genta PR, Marcondes BF, Lorenzi-Filho G |title=Effects of oropharyngeal exercises on patients with moderate obstructive sleep apnea syndrome |journal=Am. J. Respir. Crit. Care Med. |volume=179 |issue=10|pages=962–6 |date=May 2009 |pmid=19234106 |doi=10.1164/rccm.200806-981OC}}</ref>
{{trans F}}
==相關條目==
==相關條目==
*[[睡眠呼吸中止症]]
*[[睡眠呼吸中止症]]

2017年7月27日 (四) 04:24的版本

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Obstructive sleep apnea
同义词Obstructive sleep apnoea
阻塞性睡眠呼吸暂停示意圖
类型睡眠呼吸暂停
診斷方法Stop-Bang questionnaire[*]
分类和外部资源
醫學專科Sleep medicine
ICD-117A41
ICD-10G47.3
ICD-9-CM327.23
OMIM107650
DiseasesDB9135
MedlinePlus000811
eMedicineped/2114
MeSHD012891
[编辑此条目的维基数据]

阻塞性睡眠呼吸暂停(英語：Obstructive Sleep Apnea, OSA)，是睡眠呼吸暂停中的最常见形式，它是上呼氣道受阻（英语：airway obstruction）所引起的。它的特点是在睡眠时重复性的呼吸中止，尽管有在尝试呼吸，这通常会伴随血氧饱和度的降低。通常会持续20到40秒。[1]

Obstructive sleep apnea (OSA) is the most common type of sleep apnea and is caused by complete or partial obstructions of the upper airway. It is characterized by repetitive episodes of shallow or paused breathing during sleep, despite the effort to breathe, and is usually associated with a reduction in blood oxygen saturation. These episodes of decreased breathing, called "apneas" (literally, "without breath"), typically last 20 to 40 seconds.[1]

相關條目

參考文獻

神经系统（中枢神经系统疾病）病理学（G04–G47，323–349）
炎症
同时／伴发
脑部
脑病
间歇式发作
其他
脊髓/
脊髓病變
混合／伴有
描述
疾病
治療
  1. ^ 1.0 1.1 Obstructive Sleep Apnea Syndrome (780.53-0). The International Classification of Sleep Disorders (PDF). Westchester, Illinois: American Academy of Sleep Medicine. 2001: 52–8 [2010-09-11]. （原始内容 (PDF)存档于2011-07-26）.  引用错误：带有name属性“AASM2001”的<ref>标签用不同内容定义了多次
  2. ^ Barnes L (editor). Surgical pathology of the head and neck 3rd. New York: Informa healthcare. 2009. ISBN 9781420091632. :226
  3. ^ Gale SD, Hopkins RO. Effects of hypoxia on the brain: neuroimaging and neuropsychological findings following carbon monoxide poisoning and obstructive sleep apnea. J Int Neuropsychol Soc. 2004, 10 (1): 60–71. PMID 14751008. doi:10.1017/S1355617704101082. 
  4. ^ Henry, D; Rosenthal, L. "Listening for his breath:" the significance of gender and partner reporting on the diagnosis, management, and treatment of obstructive sleep apnea.. Social science & medicine (1982). Feb 2013, 79: 48–56. PMID 22770968. doi:10.1016/j.socscimed.2012.05.021. 
  5. ^ Halbower AC, Degaonkar M, Barker PB, et al. Childhood obstructive sleep apnea associates with neuropsychological deficits and neuronal brain injury. PLoS Med. August 2006, 3 (8): e301. PMC 1551912 可免费查阅. PMID 16933960. doi:10.1371/journal.pmed.0030301. 
  6. ^ Ezzedini R, Darabi M, Ghasemi B, Darabi M, Fayezi S, Moghaddam YJ, et al. Tissue fatty acid composition in obstructive sleep apnea and recurrent tonsillitis.. Int J Pediatr Otorhinolaryngol. 2013, 77 (6): 1008–12. PMID 23643333. doi:10.1016/j.ijporl.2013.03.033. 
  7. ^ Edwards, Natalie; Sullivan, Colin E. Sleep-Disordered Breathing in Pregnancy. Sleep Medicine Clinics. 2008, 3: 81–95. doi:10.1016/j.jsmc.2007.10.010. 
  8. ^ Sleep Apnea: Risk Factors, Mayo Clinic, June 29, 2010, Retrieved November 4, 2010.
  9. ^ de Miguel-Díez J, Villa-Asensi JR, Alvarez-Sala JL. Prevalence of sleep-disordered breathing in children with Down syndrome: polygraphic findings in 108 children. Sleep. December 2003, 26 (8): 1006–9. PMID 14746382. 
  10. ^ Shott SR, Amin R, Chini B, Heubi C, Hotze S, Akers R. Obstructive sleep apnea: Should all children with Down syndrome be tested?. Arch. Otolaryngol. Head Neck Surg. April 2006, 132 (4): 432–6. PMID 16618913. doi:10.1001/archotol.132.4.432. 
  11. ^ Sloan GM. Posterior pharyngeal flap and sphincter pharyngoplasty: the state of the art. Cleft Palate Craniofac. J. March 2000, 37 (2): 112–22. PMID 10749049. doi:10.1597/1545-1569(2000)037<0112:PPFASP>2.3.CO;2. 
  12. ^ Pugh, M.B. et al. (2000). Apnea. Stedman's Medical Dictionary (27th ed.) Retrieved June 18, 2006 from STAT!Ref Online Medical Library database.[页码请求]
  13. ^ Liao YF, Noordhoff MS, Huang CS, et al. Comparison of obstructive sleep apnea syndrome in children with cleft palate following Furlow palatoplasty or pharyngeal flap for velopharyngeal insufficiency. Cleft Palate Craniofac. J. March 2004, 41 (2): 152–6. PMID 14989690. doi:10.1597/02-162. 
  14. ^ McWilliams, Betty Jane; Peterson-Falzone, Sally J.; Hardin-Jones, Mary A.; Karnell, Michael P. Cleft palate speech 3rd. St. Louis: Mosby. 2001. ISBN 0-8151-3153-4. [页码请求]
  15. ^ Gross, JB; Bachenberg, KL; Benumof, JL; Caplan, RA; Connis, RT; Coté, CJ; Nickinovich, DG; Prachand, V; Ward, DS; Weaver, EM; Ydens, L; Yu, S; American Society of Anesthesiologists Task Force on Perioperative Management. Practice guidelines for the perioperative management of patients with obstructive sleep apnea: a report by the American Society of Anesthesiologists Task Force on Perioperative Management of patients with obstructive sleep apnea.. Anesthesiology. May 2006, 104 (5): 1081–93; quiz 1117–8. PMID 16645462. doi:10.1097/00000542-200605000-00026. 
  16. ^ FAQ on www.sleepeducation.com
  17. ^ Fietze I, Penzel T, Alonderis A, et al. Management of obstructive sleep apnea in Europe. Sleep Med. February 2011, 12 (2): 190–7. PMID 21167776. doi:10.1016/j.sleep.2010.10.003. 
  18. ^ Jonas, Daniel E; Amick, Halle R.; Feltner, Cynthia; Weber, Rachel P; Arvanitis, Marina; Stine, A; Lux, L; Harris, Russell P. Screening for Obstructive Sleep Apnea in Adults Evidence Report and Systematic Review for the US Preventive Services Task Force. JAMA. 2017, 317 (4): 415–433 [24 January 2017]. doi:10.1001/jama.2016.19635. 
  19. ^ US Preventive Services Task Force. Screening for Obstructive Sleep Apnea in Adults US Preventive Services Task Force Recommendation Statement. JAMA. 2017, 317 (4): 407–414. doi:10.1001/jama.2016.20325. 
  20. ^ 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. August 1999, 22 (5): 667–89. PMID 10450601. 
  21. ^ Mulgrew AT, Fox N, Ayas NT, Ryan CF. Diagnosis and initial management of obstructive sleep apnea without polysomnography: a randomized validation study. Annals of Internal Medicine. February 2007, 146 (3): 157–66. PMID 17283346. doi:10.7326/0003-4819-146-3-200702060-00004. 
  22. ^ Flemons WW, Whitelaw WA, Brant R, Remmers JE. Likelihood ratios for a sleep apnea clinical prediction rule. Am. J. Respir. Crit. Care Med. November 1994, 150 (5 Pt 1): 1279–85. PMID 7952553. doi:10.1164/ajrccm.150.5.7952553. 
  23. ^ 23.0 23.1 Friedman: Sleep Apnea and Snoring, 1st ed. 2008
  24. ^ 24.0 24.1 Azagra-Calero, E; Espinar-Escalona, E; Barrera-Mora, JM; Llamas-Carreras, JM; Solano-Reina, E. Obstructive sleep apnea syndrome (OSAS). Review of the literature.. Medicina oral, patologia oral y cirugia bucal. Nov 1, 2012, 17 (6): e925–9. PMC 3505711 可免费查阅. PMID 22549673. doi:10.4317/medoral.17706. 
  25. ^ 25.0 25.1 25.2 25.3 25.4 25.5 25.6 Qaseem, A; Holty, JE; Owens, DK; Dallas, P; Starkey, M; Shekelle, P; for the Clinical Guidelines Committee of the American College of, Physicians. Management of Obstructive Sleep Apnea in Adults: A Clinical Practice Guideline From the American College of Physicians.. Annals of Internal Medicine. Sep 24, 2013, 159: 471–83. PMID 24061345. doi:10.7326/0003-4819-159-7-201310010-00704. 
  26. ^ Bratton, DJ; Gaisl, T; Wons, AM; Kohler, M. CPAP vs Mandibular Advancement Devices and Blood Pressure in Patients With Obstructive Sleep Apnea: A Systematic Review and Meta-analysis.. JAMA. 1 December 2015, 314 (21): 2280–93. PMID 26624827. doi:10.1001/jama.2015.16303. 
  27. ^ Iftikhar, IH; Kline, CE; Youngstedt, SD. Effects of Exercise Training on Sleep Apnea: A Meta-analysis.. Lung. Sep 29, 2013, 192: 175–184. PMC 4216726 可免费查阅. PMID 24077936. doi:10.1007/s00408-013-9511-3. 
  28. ^ 28.0 28.1 Giles, TL; Lasserson, TJ; Smith, BH; White, J; Wright, J; Cates, CJ. Continuous positive airways pressure for obstructive sleep apnoea in adults.. The Cochrane database of systematic reviews. Jul 19, 2006, (3): CD001106. PMID 16855960. doi:10.1002/14651858.CD001106.pub3. 
  29. ^ Riaz, M; Certal, V; Nigam, G; Abdullatif, J; Zaghi, S; Kushida, CA; Camacho, M. Nasal Expiratory Positive Airway Pressure Devices (Provent) for OSA: A Systematic Review and Meta-Analysis.. Sleep disorders. 2015, 2015: 734798. PMC 4699057 可免费查阅. PMID 26798519. doi:10.1155/2015/734798. 
  30. ^ Whitelaw WA, Brant RF, Flemons WW. Clinical usefulness of home oximetry compared with polysomnography for assessment of sleep apnea. Am. J. Respir. Crit. Care Med. January 2005, 171 (2): 188–93. PMID 15486338. doi:10.1164/rccm.200310-1360OC.  Review in: Caples SM. 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. 2005, 143 (1): 21. PMID 15989309. 
  31. ^ Littner M, Hirshkowitz M, Davila D, et al. 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. March 2002, 25 (2): 143–7. PMID 11902424. 
  32. ^ McNicholas, Walter T.; Bonsignore, Maria R.; Lévy, Patrick; Ryan, Silke. Mild obstructive sleep apnoea: clinical relevance and approaches to management. The Lancet Respiratory Medicine. 2016-05-27, 4: 826–834. ISSN 2213-2619. PMID 27245915. doi:10.1016/S2213-2600(16)30146-1. 
  33. ^ Neill AM, Angus SM, Sajkov D, McEvoy RD. Effects of sleep posture on upper airway stability in patients with obstructive sleep apnea. Am. J. Respir. Crit. Care Med. January 1997, 155 (1): 199–204. PMID 9001312. doi:10.1164/ajrccm.155.1.9001312. 
  34. ^ Nakano H, Ikeda T, Hayashi M, Ohshima E, Onizuka A. Effects of body position on snoring in apneic and nonapneic snorers. Sleep. March 2003, 26 (2): 169–72. PMID 12683476. 
  35. ^ Loord H, Hultcrantz E. Positioner--a method for preventing sleep apnea. Acta Otolaryngol. August 2007, 127 (8): 861–8. PMID 17762999. doi:10.1080/00016480601089390. 
  36. ^ Szollosi I, Roebuck T, Thompson B, Naughton MT. Lateral sleeping position reduces severity of central sleep apnea / Cheyne-Stokes respiration. Sleep. August 2006, 29 (8): 1045–51. PMID 16944673. 
  37. ^ Learning To Play A Wind Instrument Could Lower Your Risk For Obstructive Sleep Apnea
  38. ^ Ward CP, York KM, McCoy JG. Risk of obstructive sleep apnea lower in double reed wind musicians. J Clin Sleep Med: 251–5. PMC 3365082 可免费查阅. PMID 22701381. doi:10.5664/jcsm.1906. 
  39. ^ 39.0 39.1 引用错误：没有为名为AAO2013的参考文献提供内容
  40. ^ Sleep apnea
  41. ^ http://www.accessdata.fda.gov/scripts/cdrh/cfdocs/cfPMA/pma.cfm?id=18437. FDA "Premarket Approval (PMA) Inspire II Upper Airway Stimulation System" U.S. Food and Drug Administration. April 30, 2014.
  42. ^ Strollo PJ Jr, Soose RJ, Maurer JT, de Vries N, Cornelius J, Froymovich O, Hanson RD, Padhya TA, Steward DL, Gillespie MB, Woodson BT, Van de Heyning PH, Goetting MG, Vanderveken OM, Feldman N, Knaack L, Strohl KP; STAR Trial Group. Upper-airway stimulation for obstructive sleep apnea. New England Journal of Medicine. January 9, 2014, 370 (2): 139–49. PMID 24401051. doi:10.1056/nejmoa1308659. 
  43. ^ 43.0 43.1 引用错误：没有为名为Farrar2008的参考文献提供内容
  44. ^ 引用错误：没有为名为Eick2002的参考文献提供内容
  45. ^ 引用错误：没有为名为Bashetty2009的参考文献提供内容
  46. ^ 引用错误：没有为名为Weaver2008的参考文献提供内容
  47. ^ 引用错误：没有为名为Steward2005的参考文献提供内容
  48. ^ Mason, M; Welsh, EJ; Smith, I. Drug therapy for obstructive sleep apnoea in adults.. The Cochrane database of systematic reviews. May 31, 2013, 5: CD003002. PMID 23728641. doi:10.1002/14651858.CD003002.pub3. 
  49. ^ Veasey SC. Serotonin agonists and antagonists in obstructive sleep apnea: therapeutic potential. Am J Respir Med. 2003, 2 (1): 21–9. PMID 14720019. doi:10.1007/BF03256636. 
  50. ^ Weaver, Jacqueline. Sleep apnea is linked to heart disease and diabetes. Yale Bulletin and Calendar. June 15, 2007, 35 (30). 
  51. ^ Dyugovskaya L, Lavie P, Lavie L. Increased adhesion molecules expression and production of reactive oxygen species in leukocytes of sleep apnea patients. Am. J. Respir. Crit. Care Med. April 2002, 165 (7): 934–9. PMID 11934717. doi:10.1164/ajrccm.165.7.2104126. 简明摘要 – ScienceDaily (Apr 4, 2002). 
  52. ^ Botros NA, Shah N, Mohsenin V, Roux F, Yaggi HK. Obstructive Sleep Apnea as a Risk Factor for Type II Diabetes (PDF). American Thoracic Society 2007 International Conference. May 21, 2007. 简明摘要 – ScienceDaily (May 21, 2007). 
  53. ^ Gaisl, Thomas; Bratton, Daniel J.; Kohler, Malcolm. The impact of obstructive sleep apnoea on the aorta. The European Respiratory Journal. 2015-08-01, 46 (2): 532–544. ISSN 1399-3003. PMID 26113685. doi:10.1183/09031936.00029315. 
  54. ^ Paul E. Peppard, Ph.D., Terry Young, Ph.D., Mari Palta, Ph.D., and James Skatrud, M.D. Prospective Study of the Association Between Sleep-Disordered Breathing and Hypertension (PDF). The New England Journal of Medicine (Massachusetts Medical Society). May 11, 2000, 342 (19): 1378–1384 [2013-05-29]. doi:10.1056/nejm200005113421901. 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. 
  55. ^ Peretz Lavie, Paula Herer, Victor Hoffstein. Obstructive sleep apnoea syndrome as a risk factor for hypertension: population study (PDF). BMJ (BMJ Publishing Group). 19 February 2000, 320: 479–82 [2013-05-29]. doi:10.1136/bmj.320.7233.479. Conclusion: Sleep apnoea syndrome is profoundly associated with hypertension independent of all relevant risk factors. 
  56. ^ Yaggi HK, Concato J, Kernan WN, Lichtman JH, Brass LM, Mohsenin V. Obstructive sleep apnea as a risk factor for stroke and death. N. Engl. J. Med. November 2005, 353 (19): 2034–41. PMID 16282178. doi:10.1056/NEJMoa043104. 
  57. ^ Schröder CM, O'Hara R. Depression and Obstructive Sleep Apnea (OSA). Ann Gen Psychiatry. June 2005, 4: 13. PMC 1181621 可免费查阅. PMID 15982424. doi:10.1186/1744-859X-4-13. 
  58. ^ Women with sleeping problems at higher risk for Type 2 diabetes. American Sleep Association. [30 January 2016]. 
  59. ^ N.A. Shah, M.D., N.A. Botros, M.D., H.K. Yaggi, M.D., M., V. Mohsenin, M.D., New Haven, Connecticut. Sleep Apnea Increases Risk of Heart Attack or Death by 30%. American Thoracic Society. May 20, 2007. （原始内容存档于May 24, 2009）. 
  60. ^ Sun Y. Cardiac structural and functional changes in old elderly patients with obstructive sleep apnoea-hypopnoea syndrome.. J Int Med Res. Apr 2014, 42 (2): 395–404. PMID 24445697. doi:10.1177/0300060513502890. 
  61. ^ Ciftci TU, Kokturk O, Demirtas S, Gulbahar O, Bukan N. Consequences of hypoxia-reoxygenation phenomena in patients with obstructive sleep apnea syndrome. Ann Saudi Med. 2011, 31 (1): 14–8. PMC 3101718 可免费查阅. PMID 21245593. doi:10.4103/0256-4947.75772. 
  62. ^ Bahammam A. Obstructive sleep apnea: from simple upper airway obstruction to systemic inflammation. Ann Saudi Med. 2011, 31 (1): 1–2. PMC 3101717 可免费查阅. PMID 21245591. doi:10.4103/0256-4947.75770. 
  63. ^ Silverberg DS, Iaina A, Oksenberg A. Treating obstructive sleep apnea improves essential hypertension and quality of life. Am Fam Physician. January 2002, 65 (2): 229–36. PMID 11820487. 
  64. ^ Grigg-Damberger M. Why a polysomnogram should become part of the diagnostic evaluation of stroke and transient ischemic attack. J Clin Neurophysiol. February 2006, 23 (1): 21–38. PMID 16514349. doi:10.1097/01.wnp.0000201077.44102.80. 
  65. ^ Punjabi, N. M. The Epidemiology of Adult Obstructive Sleep Apnea. Proceedings of the American Thoracic Society. 15 February 2008, 5 (2): 136–143. doi:10.1513/pats.200709-155MG. 
  66. ^ Shamsuzzaman AS, Gersh BJ, Somers VK. Obstructive sleep apnea: implications for cardiac and vascular disease. JAMA. October 2003, 290 (14): 1906–14. PMID 14532320. doi:10.1001/jama.290.14.1906. 
  67. ^ Kezirian, EJ; Boudewyns, A; Eisele, DW; Schwartz, AR; Smith, PL; Van de Heyning, PH; De Backer, WA. Electrical stimulation of the hypoglossal nerve in the treatment of obstructive sleep apnea. Sleep medicine reviews. October 2010, 14 (5): 299–305. PMID 20116305. doi:10.1016/j.smrv.2009.10.009. 
  68. ^ Editors. ImThera aura6000 System for Sleep Apnea Gets a Go in Europe. Medgadget. 15 March 2012 [15 January 2014]. 
  69. ^ Puhan MA, Suarez A, Lo Cascio C, Zahn A, Heitz M, Braendli O. Didgeridoo playing as alternative treatment for obstructive sleep apnoea syndrome: randomised controlled trial. BMJ. February 2006, 332 (7536): 266–70. PMC 1360393 可免费查阅. PMID 16377643. doi:10.1136/bmj.38705.470590.55. 
  70. ^ Guimarães KC, Drager LF, Genta PR, Marcondes BF, Lorenzi-Filho G. Effects of oropharyngeal exercises on patients with moderate obstructive sleep apnea syndrome. Am. J. Respir. Crit. Care Med. May 2009, 179 (10): 962–6. PMID 19234106. doi:10.1164/rccm.200806-981OC. 
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