Benutzer:SelbsthilfeSchlafapnoe/Schlafapnoe

Dieser Artikel (Schlafapnoe) ist im Entstehen begriffen und noch nicht Bestandteil der freien Enzyklopädie Wikipedia.
Wenn du dies liest:
Wenn du diesen Artikel überarbeitest:
  • Bitte denke daran, die Angaben im Artikel durch geeignete Quellen zu belegen und zu prüfen, ob er auch anderweitig den Richtlinien der Wikipedia entspricht (siehe Wikipedia:Artikel).
  • Nach erfolgter Übersetzung kannst du diese Vorlage entfernen und den Artikel in den Artikelnamensraum verschieben. Die entstehende Weiterleitung kannst du schnelllöschen lassen.
  • Importe inaktiver Accounts, die länger als drei Monate völlig unbearbeitet sind, werden gelöscht.

Vorlage:Short description Vorlage:Cs1 config Vorlage:Use dmy dates Vorlage:Infobox medical condition (new) Sleep apnea is a sleep-related breathing disorder in which repetitive pauses in breathing, periods of shallow breathing, or collapse of the upper airway during sleep results in poor ventilation and sleep disruption.[1][2] Each pause in breathing can last for a few seconds to a few minutes and occurs many times a night.[3] A choking or snorting sound may occur as breathing resumes.[4] Common symptoms include daytime sleepiness, snoring, and non restorative sleep despite adequate sleep time.[5] Because the disorder disrupts normal sleep, those affected may experience sleepiness or feel tired during the day.[4] It is often a chronic condition. [6]

Sleep apnea may be categorized as obstructive sleep apnea (OSA), in which breathing is interrupted by a blockage of air flow, central sleep apnea (CSA), in which regular unconscious breath simply stops, or a combination of the two.[7] OSA is the most common form.[7] OSA has four key contributors; these include a narrow, crowded, or collapsible upper airway, an ineffective pharyngeal dilator muscle function during sleep, airway narrowing during sleep, and unstable control of breathing (high loop gain).[8][9] In CSA, the basic neurological controls for breathing rate malfunction and fail to give the signal to inhale, causing the individual to miss one or more cycles of breathing. If the pause in breathing is long enough, the percentage of oxygen in the circulation can drop to a lower than normal level (hypoxaemia) and the concentration of carbon dioxide can build to a higher than normal level (hypercapnia).[10] In turn, these conditions of hypoxia and hypercapnia will trigger additional effects on the body such as Cheyne-Stokes Respiration.[11]

Some people with sleep apnea are unaware they have the condition.[4] In many cases it is first observed by a family member.[4] An in-lab sleep study overnight is the preferred method for diagnosing sleep apnea. [12] In the case of OSA, the outcome that determines disease severity and guides the treatment plan is the apnea-hypopnea index (AHI). [12] This measurement is calculated from totaling all pauses in breathing and periods of shallow breathing lasting greater than 10 seconds and dividing the sum by total hours of recorded sleep. [13][12] In contrast, for CSA the degree of respiratory effort, measured by esophageal pressure or displacement of the thoracic or abdominal cavity, is an important distinguishing factor between OSA and CSA. [14]

A systemic disorder, sleep apnea is associated with a wide array of effects, including increased risk of car accidents, hypertension, cardiovascular disease, myocardial infarction, stroke, atrial fibrillation, insulin resistance, higher incidence of cancer, and neurodegeneration.[15] The exact effects of the condition depend on how severe the apnea is and on the individual characteristics of the person having the apnea.Vorlage:Medical citation needed

Treatment may include lifestyle changes, mouthpieces, breathing devices, and surgery.[4] Effective lifestyle changes may include avoiding alcohol, losing weight, stopping smoking, and sleeping on one's side.[16] Breathing devices include the use of a CPAP machine.[17] With proper use, CPAP improves outcomes.[18] Evidence suggests that CPAP may improve sensitivity to insulin, blood pressure, and sleepiness.[19][20][21] Long term compliance, however, is an issue with more than half of people not appropriately using the device.[18][22] In 2017, only 15% of potential patients in developed countries used CPAP machines, while in developing countries well under 1% of potential patients used CPAP.[23] Without treatment, sleep apnea may increase the risk of heart attack, stroke, diabetes, heart failure, irregular heartbeat, obesity, and motor vehicle collisions.[4]

Alzheimer's disease and severe obstructive sleep apnea are connected[24] because there is an increase in the protein beta-amyloid as well as white-matter damage. These are the main indicators of Alzheimer's, which in this case comes from the lack of proper rest or poorer sleep efficiency resulting in neurodegeneration.[25][26][27] Having sleep apnea in mid-life brings a higher likelihood of developing Alzheimer's in older age, and if one has Alzheimer's then one is also more likely to have sleep apnea.[28] This is demonstrated by cases of sleep apnea even being misdiagnosed as dementia.[29] With the use of treatment through CPAP, there is a reversible risk factor in terms of the amyloid proteins. This usually restores brain structure and diminishes cognitive impairment.[30][31][32]

OSA is a common sleep disorder. A large analysis in 2019 of the estimated prevalence of OSA found that OSA affects 936 million—1 billion people between the ages of 30–69 globally, or roughly every 1 in 10 people, and up to 30% of the elderly.[33] Sleep apnea is somewhat more common in men than women, roughly a 2:1 ratio of men to women, and in general more people are likely to have it with older age and obesity.[34] Other risk factors include being overweight,[15] a family history of the condition, allergies, and enlarged tonsils.[35]

Signs and symptoms

Bearbeiten

People with sleep apnea have problems with excessive daytime sleepiness (EDS) and impaired alertness.[36] OSA may increase risk for driving accidents and work-related accidents. If OSA is not treated, people are at increased risk of other health problems, such as diabetes.Vorlage:Medical citation needed

Due to the disruption in daytime cognitive state, behavioral effects may be present. These can include moodiness, belligerence, as well as a decrease in attentiveness and energy.[37] These effects may become intractable, leading to depression.[38]

There is evidence that the risk of diabetes among those with moderate or severe sleep apnea is higher.[39] Finally, because there are many factors that could lead to some of the effects previously listed, some people are not aware that they have sleep apnea and are either misdiagnosed or ignore the symptoms altogether.[36]

Risk factors

Bearbeiten

Sleep apnea can affect people regardless of sex, race, or age.[40] However, risk factors include:[41]

Alcohol, sedatives and tranquilizers may also promote sleep apnea by relaxing throat muscles. People who smoke tobacco have sleep apnea at three times the rate of people who have never done so.[43]

Central sleep apnea is more often associated with any of the following risk factors:Vorlage:Medical citation needed

High blood pressure is very common in people with sleep apnea.[44]

Mechanism

Bearbeiten

When breathing is paused, carbon dioxide builds up in the bloodstream. Chemoreceptors in the bloodstream note the high carbon dioxide levels. The brain is signaled to awaken the person, which clears the airway and allows breathing to resume. Breathing normally will restore oxygen levels and the person will fall asleep again.[45] This carbon dioxide build-up may be due to the decrease of output of the brainstem regulating the chest wall or pharyngeal muscles, which causes the pharynx to collapse.[46] People with sleep apnea experience reduced or no slow-wave sleep and spend less time in REM sleep.[46]

Complications

Bearbeiten

OSA is a serious medical condition. Daytime fatigue and sleepiness, cardiovascular problems and eye problems are considered potential complications of OSA. OSA may also be a risk factor of COVID-19. People with OSA have a higher risk of developing severe complications of COVID-19.[47]

Diagnosis

Bearbeiten

Despite thisVorlage:Which medical consensus, the variety of apneic events (e.g., hypopnea vs apnea, central vs obstructive), the variability of patients' physiologies, and the inherent shortcomings and variability of equipment and methods, this field is subject to debate.[48] Within this context, the definition of an event depends on several factors (e.g., patient's age) and account for this variability through a multi-criteria decision rule described in several, sometimes conflicting, guidelines.[49][50]

Oximetry

Bearbeiten

Oximetry, which may be performed over one or several nights in a person's home, is a simpler, but less reliable alternative to a polysomnography. The test is recommended only when requested by a physician and should not be used to test those without symptoms.[51] Home oximetry may be effective in guiding prescription for automatically self-adjusting continuous positive airway pressure.[52][53]

Classification

Bearbeiten

There are three types of sleep apnea. OSA accounts for 84%, CSA for 0.9%, and 15% of cases are mixed.[54]

Obstructive sleep apnea

Bearbeiten
 
Screenshot of a PSG system showing an obstructive apnea
 
No airway obstruction during sleep
 
Airway obstruction during sleep

Obstructive sleep apnea (OSA) is the most common category of sleep-disordered breathing. The muscle tone of the body ordinarily relaxes during sleep, and at the level of the throat, the human airway is composed of collapsible walls of soft tissue that can obstruct breathing. Mild occasional sleep apnea, such as many people experience during an upper respiratory infection, may not be significant, but chronic severe obstructive sleep apnea requires treatment to prevent low blood oxygen (hypoxemia), sleep deprivation, and other complications.Vorlage:Medical citation needed

Individuals with low muscle-tone and soft tissue around the airway (e.g., because of obesity) and structural features that give rise to a narrowed airway are at high risk for obstructive sleep apnea. The elderly are more likely to have OSA than young people. Men are more likely to develop sleep apnea than women and children are, though it is not uncommon in the last two population groups.[55]

The risk of OSA rises with increasing body weight, active smoking and age. In addition, patients with diabetes or "borderline" diabetes have up to three times the risk of having OSA.Vorlage:Medical citation needed

Common symptoms include loud snoring, restless sleep, and sleepiness during the daytime. Diagnostic tests include home oximetry or polysomnography in a sleep clinic.Vorlage:Medical citation needed

Some treatments involve lifestyle changes, such as avoiding alcohol or muscle relaxants, losing weight, and quitting smoking. Many people benefit from sleeping at a 30-degree elevation of the upper body[56] or higher, as if in a recliner. Doing so helps prevent the gravitational collapse of the airway. Lateral positions (sleeping on a side), as opposed to supine positions (sleeping on the back), are also recommended as a treatment for sleep apnea,[57][58][59] largely because the gravitational component is smaller in the lateral position. Some people benefit from various kinds of oral appliances such as the Mandibular advancement splint to keep the airway open during sleep. Continuous positive airway pressure (CPAP) is the most effective treatment for severe obstructive sleep apnea, but oral appliances are considered a first-line approach equal to CPAP for mild to moderate sleep apnea, according to the American Academy of Sleep Medicine (AASM) parameters of care.[60] There are also surgical procedures to remove and tighten tissue and widen the airway.Vorlage:Medical citation needed

Snoring is a common finding in people with this syndrome. Snoring is the turbulent sound of air moving through the back of the mouth, nose, and throat. Although not everyone who snores is experiencing difficulty breathing, snoring in combination with other risk factors has been found to be highly predictive of OSA.[61] The loudness of the snoring is not indicative of the severity of obstruction, however. If the upper airways are tremendously obstructed, there may not be enough air movement to make much sound. Even the loudest snoring does not mean that an individual has sleep apnea syndrome. The sign that is most suggestive of sleep apneas occurs when snoring stops.Vorlage:Medical citation needed

Up to 78% of genes associated with habitual snoring also increase the risk for OSA.[62]

Other indicators include (but are not limited to): hypersomnolence, obesity (BMI ≥ 30), large neck circumference—Vorlage:Convert in women, Vorlage:Convert in men — enlarged tonsils and large tongue volume, micrognathia, morning headaches, irritability/mood-swings/depression, learning and/or memory difficulties, and sexual dysfunction.

The term "sleep-disordered breathing" is commonly used in the U.S. to describe the full range of breathing problems during sleep in which not enough air reaches the lungs (hypopnea and apnea). Sleep-disordered breathing is associated with an increased risk of cardiovascular disease, stroke, high blood pressure, arrhythmias, diabetes, and sleep deprived driving accidents.[63][64][65][66] When high blood pressure is caused by OSA, it is distinctive in that, unlike most cases of high blood pressure (so-called essential hypertension), the readings do not drop significantly when the individual is sleeping.[67] Stroke is associated with obstructive sleep apnea.[68]

Obstructive sleep apnea is associated with problems in daytime functioning, such as daytime sleepiness, motor vehicle crashes, psychological problems, decreased cognitive functioning, and reduced quality of life.[69] Other associated problems include cerebrovascular diseases (hypertension, coronary artery disease, and stroke) and diabetes.[69] These problems could be, at least in part, caused by risk factors of OSA.[69]

Central sleep apnea

Bearbeiten

Vorlage:More citations needed

 
Screenshot of a PSG system showing a central apnea

In pure central sleep apnea or Cheyne–Stokes respiration, the brain's respiratory control centers are imbalanced during sleep.[70] Blood levels of carbon dioxide, and the neurological feedback mechanism that monitors them, do not react quickly enough to maintain an even respiratory rate, with the entire system cycling between apnea and tachypnea, even during wakefulness. The sleeper stops breathing and then starts again. There is no effort made to breathe during the pause in breathing: there are no chest movements and no struggling. After the episode of apnea, breathing may be faster (tachypnea) for a period of time, a compensatory mechanism to blow off retained waste gases and absorb more oxygen.Vorlage:Medical citation needed

While sleeping, a normal individual is "at rest" as far as cardiovascular workload is concerned. Breathing is regular in a healthy person during sleep, and oxygen levels and carbon dioxide levels in the bloodstream stay fairly constant. Any sudden drop in oxygen or excess of carbon dioxide (even if tiny) strongly stimulates the brain's respiratory centers to breathe.Vorlage:Medical citation needed

In any person, hypoxia and hypercapnia have certain common effects on the body.[71] The heart rate will increase, unless there are such severe co-existing problems with the heart muscle itself or the autonomic nervous system that makes this compensatory increase impossible. The more translucent areas of the body will show a bluish or dusky cast from cyanosis, which is the change in hue that occurs owing to lack of oxygen in the blood ("turning blue"). Overdoses of drugs that are respiratory depressants (such as heroin, and other opiates) kill by damping the activity of the brain's respiratory control centers. In central sleep apnea, the effects of sleep alone can remove the brain's mandate for the body to breathe.

  • Normal Respiratory Drive: After exhalation, the blood level of oxygen decreases and that of carbon dioxide increases. Exchange of gases with a lungful of fresh air is necessary to replenish oxygen and rid the bloodstream of built-up carbon dioxide. Oxygen and carbon dioxide receptors in the blood stream (called chemoreceptors) send nerve impulses to the brain, which then signals reflex opening of the larynx (so that the opening between the vocal cords enlarges) and movements of the rib cage muscles and diaphragm. These muscles expand the thorax (chest cavity) so that a partial vacuum is made within the lungs and air rushes in to fill it.
  • Physiologic effects of central apnea: During central apneas, the central respiratory drive is absent, and the brain does not respond to changing blood levels of the respiratory gases. No breath is taken despite the normal signals to inhale. The immediate effects of central sleep apnea on the body depend on how long the failure to breathe endures. At worst, central sleep apnea may cause sudden death. Short of death, drops in blood oxygen may trigger seizures, even in the absence of epilepsy. In people with epilepsy, the hypoxia caused by apnea may trigger seizures that had previously been well controlled by medications.[72] In other words, a seizure disorder may become unstable in the presence of sleep apnea. In adults with coronary artery disease, a severe drop in blood oxygen level can cause angina, arrhythmias, or heart attacks (myocardial infarction). Longstanding recurrent episodes of apnea, over months and years, may cause an increase in carbon dioxide levels that can change the pH of the blood enough to cause a respiratory acidosis.Vorlage:Medical citation needed

Mixed apnea

Bearbeiten

Some people with sleep apnea have a combination of both types; its prevalence ranges from 0.56% to 18%. The condition is generally detected when obstructive sleep apnea is treated with CPAP and central sleep apnea emerges. The exact mechanism of the loss of central respiratory drive during sleep in OSA is unknown but is most likely related to incorrect settings of the CPAP treatment and other medical conditions the person has.[73]

Management

Bearbeiten

The treatment of obstructive sleep apnea is different than that of central sleep apnea. Treatment often starts with behavioral therapy and some people may be suggested to try a continuous positive airway pressure device. Many people are told to avoid alcohol, sleeping pills, and other sedatives, which can relax throat muscles, contributing to the collapse of the airway at night.[74] The evidence supporting one treatment option compared to another for a particular person is not clear.[75]

Changing sleep position

Bearbeiten

More than half of people with obstructive sleep apnea have some degree of positional obstructive sleep apnea, meaning that it gets worse when they sleep on their backs.[76] Sleeping on their sides is an effective and cost-effective treatment for positional obstructive sleep apnea.[76]

Continuous positive airway pressure

Bearbeiten
 
Person using a CPAP mask, covering only the nose
 
CPAP machine with two models of masks

Vorlage:See also For moderate to severe sleep apnea, the most common treatment is the use of a continuous positive airway pressure (CPAP) or automatic positive airway pressure (APAP) device.[74][77] These splint the person's airway open during sleep by means of pressurized air. The person typically wears a plastic facial mask, which is connected by a flexible tube to a small bedside CPAP machine.[74]

Although CPAP therapy is effective in reducing apneas and less expensive than other treatments, some people find it uncomfortable. Some complain of feeling trapped, having chest discomfort, and skin or nose irritation. Other side effects may include dry mouth, dry nose, nosebleeds, sore lips and gums.[78]

Whether or not it decreases the risk of death or heart disease is controversial with some reviews finding benefit and others not.[18][79][75] This variation across studies might be driven by low rates of compliance—analyses of those who use CPAP for at least four hours a night suggests a decrease in cardiovascular events.[80]

Weight loss

Bearbeiten

Excess body weight is thought to be an important cause of sleep apnea.[81] People who are overweight have more tissues in the back of their throat which can restrict the airway, especially when sleeping.[82] In weight loss studies of overweight individuals, those who lose weight show reduced apnea frequencies and improved apnoea–hypopnoea index (AHI).[81][83] Weight loss effective enough to relieve obesity hypoventilation syndrome (OHS) must be 25–30% of body weight. For some obese people, it can be difficult to achieve and maintain this result without bariatric surgery.[84]

Rapid palatal expansion

Bearbeiten

Vorlage:See also

In children, orthodontic treatment to expand the volume of the nasal airway, such as nonsurgical rapid palatal expansion is common. The procedure has been found to significantly decrease the AHI and lead to long-term resolution of clinical symptoms.[85][86]

Since the palatal suture is fused in adults, regular RPE using tooth-borne expanders cannot be performed. Mini-implant assisted rapid palatal expansion (MARPE) has been recently developed as a non-surgical option for the transverse expansion of the maxilla in adults. This method increases the volume of the nasal cavity and nasopharynx, leading to increased airflow and reduced respiratory arousals during sleep.[87][88] Changes are permanent with minimal complications.

 
Illustration of surgery on the mouth and throat

Several surgical procedures (sleep surgery) are used to treat sleep apnea, although they are normally a third line of treatment for those who reject or are not helped by CPAP treatment or dental appliances.[18] Surgical treatment for obstructive sleep apnea needs to be individualized to address all anatomical areas of obstruction.Vorlage:Medical citation needed

Nasal obstruction

Bearbeiten

Often, correction of the nasal passages needs to be performed in addition to correction of the oropharynx passage. Septoplasty and turbinate surgery may improve the nasal airway,[89] but has been found to be ineffective at reducing respiratory arousals during sleep.[90]

Pharyngeal obstruction

Bearbeiten

Tonsillectomy and uvulopalatopharyngoplasty (UPPP or UP3) are available to address pharyngeal obstruction.Vorlage:Medical citation needed

 
Uvulopalatopharyngoplasty. A) pre-operative, B) original UPPP, C) modified UPPP, and D) minimal UPPP.

The "Pillar" device is a treatment for snoring and obstructive sleep apnea; it is thin, narrow strips of polyester. Three strips are inserted into the roof of the mouth (the soft palate) using a modified syringe and local anesthetic, in order to stiffen the soft palate. This procedure addresses one of the most common causes of snoring and sleep apnea — vibration or collapse of the soft palate. It was approved by the FDA for snoring in 2002 and for obstructive sleep apnea in 2004. A 2013 meta-analysis found that "the Pillar implant has a moderate effect on snoring and mild-to-moderate obstructive sleep apnea" and that more studies with high level of evidence were needed to arrive at a definite conclusion; it also found that the polyester strips work their way out of the soft palate in about 10% of the people in whom they are implanted.[91]

Hypopharyngeal or base of tongue obstruction

Bearbeiten

Base-of-tongue advancement by means of advancing the genial tubercle of the mandible, tongue suspension, or hyoid suspension (aka hyoid myotomy and suspension or hyoid advancement) may help with the lower pharynx.Vorlage:Medical citation needed

Other surgery options may attempt to shrink or stiffen excess tissue in the mouth or throat, procedures done at either a doctor's office or a hospital. Small shots or other treatments, sometimes in a series, are used for shrinkage, while the insertion of a small piece of stiff plastic is used in the case of surgery whose goal is to stiffen tissues.[74]

Multi-level surgery

Bearbeiten

Maxillomandibular advancement (MMA) is considered the most effective surgery for people with sleep apnea, because it increases the posterior airway space (PAS).[92] However, health professionals are often unsure as to who should be referred for surgery and when to do so: some factors in referral may include failed use of CPAP or device use; anatomy which favors rather than impedes surgery; or significant craniofacial abnormalities which hinder device use.[93]

Potential complications

Bearbeiten

Several inpatient and outpatient procedures use sedation. Many drugs and agents used during surgery to relieve pain and to depress consciousness remain in the body at low amounts for hours or even days afterwards. In an individual with either central, obstructive or mixed sleep apnea, these low doses may be enough to cause life-threatening irregularities in breathing or collapses in a patient's airways.[94] Use of analgesics and sedatives in these patients postoperatively should therefore be minimized or avoided.Vorlage:Medical citation needed

Surgery on the mouth and throat, as well as dental surgery and procedures, can result in postoperative swelling of the lining of the mouth and other areas that affect the airway. Even when the surgical procedure is designed to improve the airway, such as tonsillectomy and adenoidectomy or tongue reduction, swelling may negate some of the effects in the immediate postoperative period. Once the swelling resolves and the palate becomes tightened by postoperative scarring, however, the full benefit of the surgery may be noticed.Vorlage:Medical citation needed

A person with sleep apnea undergoing any medical treatment must make sure their doctor and anesthetist are informed about the sleep apnea. Alternative and emergency procedures may be necessary to maintain the airway of sleep apnea patients.[95]

Neurostimulation

Bearbeiten

Diaphragm pacing, which involves the rhythmic application of electrical impulses to the diaphragm, has been used to treat central sleep apnea.[96][97]

In April 2014, the U.S. Food and Drug Administration granted pre-market approval for use of an upper airway stimulation system in people who cannot use a continuous positive airway pressure device. The Inspire Upper Airway Stimulation system senses respiration and applies mild electrical stimulation during inspiration, which pushes the tongue slightly forward to open the airway.[98]

Medications

Bearbeiten

There is currently insufficient evidence to recommend any medication for OSA.[99] This may result in part because people with sleep apnea have tended to be treated as a single group in clinical trials. Identifying specific physiological factors underlying sleep apnea makes it possible to test drugs specific to those causal factors: airway narrowing, impaired muscle activity, low arousal threshold for waking, and unstable breathing control.[100][101] Those who experience low waking thresholds may benefit from eszopiclone, a sedative typically used to treat insomnia.[100][102] The antidepressant desipramine may stimulate upper airway muscles and lessen pharyngeal collapsibility in people who have limited muscle function in their airways.[100][103]

There is limited evidence for medication, but 2012 AASM guidelines suggested that acetazolamide "may be considered" for the treatment of central sleep apnea; zolpidem and triazolam may also be considered for the treatment of central sleep apnea,[104] but "only if the patient does not have underlying risk factors for respiratory depression".[99][77] Low doses of oxygen are also used as a treatment for hypoxia but are discouraged due to side effects.[105][106][107]

Oral appliances

Bearbeiten

An oral appliance, often referred to as a mandibular advancement splint, is a custom-made mouthpiece that shifts the lower jaw forward and opens the bite slightly, opening up the airway. These devices can be fabricated by a general dentist. Oral appliance therapy (OAT) is usually successful in patients with mild to moderate obstructive sleep apnea.[108][109] While CPAP is more effective for sleep apnea than oral appliances, oral appliances do improve sleepiness and quality of life and are often better tolerated than CPAP.[109]

Nasal EPAP

Bearbeiten

Nasal EPAP is a bandage-like device placed over the nostrils that uses a person's own breathing to create positive airway pressure to prevent obstructed breathing.[110]

Oral pressure therapy

Bearbeiten

Oral pressure therapy uses a device that creates a vacuum in the mouth, pulling the soft palate tissue forward. It has been found useful in about 25 to 37% of people.[111][112]

Prognosis

Bearbeiten

Death could occur from untreated OSA due to lack of oxygen to the body.[78]

There is increasing evidence that sleep apnea may lead to liver function impairment, particularly fatty liver diseases (see steatosis).[37][113][114][115]

It has been revealed that people with OSA show tissue loss in brain regions that help store memory, thus linking OSA with memory loss.[116] Using magnetic resonance imaging (MRI), the scientists discovered that people with sleep apnea have mammillary bodies that are about 20% smaller, particularly on the left side. One of the key investigators hypothesized that repeated drops in oxygen lead to the brain injury.[117]

The immediate effects of central sleep apnea on the body depend on how long the failure to breathe endures. At worst, central sleep apnea may cause sudden death. Short of death, drops in blood oxygen may trigger seizures, even in the absence of epilepsy. In people with epilepsy, the hypoxia caused by apnea may trigger seizures that had previously been well controlled by medications.[72] In other words, a seizure disorder may become unstable in the presence of sleep apnea. In adults with coronary artery disease, a severe drop in blood oxygen level can cause angina, arrhythmias, or heart attacks (myocardial infarction). Longstanding recurrent episodes of apnea, over months and years, may cause an increase in carbon dioxide levels that can change the pH of the blood enough to cause a respiratory acidosis.Vorlage:Medical citation needed

Epidemiology

Bearbeiten

Vorlage:Globalize The Wisconsin Sleep Cohort Study estimated in 1993 that roughly one in every 15 Americans was affected by at least moderate sleep apnea.[118][119] It also estimated that in middle-age as many as 9% of women and 24% of men were affected, undiagnosed and untreated.[81][118][119]

The costs of untreated sleep apnea reach further than just health issues. It is estimated that in the U.S., the average untreated sleep apnea patient's annual health care costs $1,336 more than an individual without sleep apnea. This may cause $3.4 billion/year in additional medical costs. Whether medical cost savings occur with treatment of sleep apnea remains to be determined.[120]

Frequency and population

Bearbeiten

Sleep disorders including sleep apnea have become an important health issue in the United States. Twenty-two million Americans have been estimated to have sleep apnea, with 80% of moderate and severe OSA cases undiagnosed.[121]

OSA can occur at any age, but it happens more frequently in men who are over 40 and overweight.[121]

A type of CSA was described in the German myth of Ondine's curse where the person when asleep would forget to breathe.[122] The clinical picture of this condition has long been recognized as a character trait, without an understanding of the disease process. The term "Pickwickian syndrome" that is sometimes used for the syndrome was coined by the famous early 20th-century physician William Osler, who must have been a reader of Charles Dickens. The description of Joe, "the fat boy" in Dickens's novel The Pickwick Papers, is an accurate clinical picture of an adult with obstructive sleep apnea syndrome.[123]

The early reports of obstructive sleep apnea in the medical literature described individuals who were very severely affected, often presenting with severe hypoxemia, hypercapnia and congestive heart failure.Vorlage:Medical citation needed

Treatment

Bearbeiten

The management of obstructive sleep apnea was improved with the introduction of continuous positive airway pressure (CPAP), first described in 1981 by Colin Sullivan and associates in Sydney, Australia.[124] The first models were bulky and noisy, but the design was rapidly improved and by the late 1980s, CPAP was widely adopted. The availability of an effective treatment stimulated an aggressive search for affected individuals and led to the establishment of hundreds of specialized clinics dedicated to the diagnosis and treatment of sleep disorders. Though many types of sleep problems are recognized, the vast majority of patients attending these centers have sleep-disordered breathing. Sleep apnea awareness day is 18 April in recognition of Colin Sullivan.[125]

See also

Bearbeiten
Portal: Medicine – Übersicht zu Wikipedia-Inhalten zum Thema Medicine

Vorlage:Div col

Vorlage:Div col end

References

Bearbeiten

Vorlage:Reflist

Vorlage:Medical resources Vorlage:Sleep {{Authority control}} {{DEFAULTSORT:Sleep Apnea}} [[Category:Breathing abnormalities]] [[Category:Medical conditions related to obesity]] [[Category:Sleep disorders]] [[Category:Sleep physiology]] [[Category:Wikipedia medicine articles ready to translate]] [[Category:Wikipedia neurology articles ready to translate]] [[Category:Otorhinolaryngology]]

  1. Jolie L. Chang, Andrew N. Goldberg, Jeremiah A. Alt, Alzoubaidi Mohammed, Liza Ashbrook, Dennis Auckley, Indu Ayappa, Hira Bakhtiar, José E. Barrera, Bethany L. Bartley, Martha E. Billings, Maurits S. Boon, Pien Bosschieter, Itzhak Braverman, Kara Brodie: International Consensus Statement on Obstructive Sleep Apnea. In: International Forum of Allergy & Rhinology. 13. Jahrgang, Nr. 7, 13. Juli 2023, ISSN 2042-6976, S. 1061–1482, doi:10.1002/alr.23079, PMID 36068685, PMC 10359192 (freier Volltext) – (englisch).
  2. Erin Grattan Roberts, Janna R. Raphelson, Jeremy E. Orr, Jamie Nicole LaBuzetta, Atul Malhotra: The Pathogenesis of Central and Complex Sleep Apnea. In: Current Neurology and Neuroscience Reports. 22. Jahrgang, Nr. 7, 1. Juli 2022, ISSN 1534-6293, S. 405–412, doi:10.1007/s11910-022-01199-2, PMID 35588042, PMC 9239939 (freier Volltext) – (englisch, doi.org).
  3. Sleep Apnea: What Is Sleep Apnea? In: NHLBI: Health Information for the Public. U.S. Department of Health and Human Services, 10. Juli 2012, abgerufen am 18. August 2016.
  4. a b c d e f Sleep Apnea: What Is Sleep Apnea? In: NHLBI: Health Information for the Public. U.S. Department of Health and Human Services, 10. Juli 2012, abgerufen am 18. August 2016.
  5. Robert C. Stansbury, Patrick J. Strollo: Clinical manifestations of sleep apnea. In: Journal of Thoracic Disease. 7. Jahrgang, Nr. 9, 7. September 2015, ISSN 2077-6624, S. E298–310, doi:10.3978/j.issn.2072-1439.2015.09.13, PMID 26543619, PMC 4598518 (freier Volltext) – (englisch, amegroups.org).
  6. Naresh M. Punjabi: The Epidemiology of Adult Obstructive Sleep Apnea. In: Proceedings of the American Thoracic Society. 5. Jahrgang, Nr. 2, 15. Februar 2008, ISSN 1546-3222, S. 136–143, doi:10.1513/pats.200709-155MG, PMID 18250205, PMC 2645248 (freier Volltext).
  7. a b Sleep Apnea: What Is Sleep Apnea? In: NHLBI: Health Information for the Public. U.S. Department of Health and Human Services, 10. Juli 2012, abgerufen am 18. August 2016.
  8. Elie Dolgin: Treating sleep apnea with pills instead of machines. In: Knowable Magazine. 29. April 2020, doi:10.1146/knowable-042820-1 (knowablemagazine.org [abgerufen am 9. Mai 2022]).
  9. A. M. Osman, S. G. Carter, J. C. Carberry, D. J. Eckert: Obstructive sleep apnea: Current perspectives. In: Nature and Science of Sleep. 10. Jahrgang, 2018, S. 21–34, doi:10.2147/NSS.S124657, PMID 29416383, PMC 5789079 (freier Volltext).
  10. Sapan H. Majmundar, Shivani Patel: Physiology, Carbon Dioxide Retention. StatPearls Publishing, 27. Oktober 2018, PMID 29494063 (nih.gov).
  11. M. Rudrappa, P. Modi, P.C. Bollu: Cheyne Stokes Respirations. StatPearls Publishing, Treasure Island, FL 1. August 2022, PMID 28846350 (nih.gov).
  12. a b c Amal M. Osman, Sophie G. Carter, Jayne C. Carberry, Danny J. Eckert: Obstructive sleep apnea: current perspectives. In: Nature and Science of Sleep. 10. Jahrgang, 23. Januar 2018, S. 21–34, doi:10.2147/NSS.S124657, PMID 29416383, PMC 5789079 (freier Volltext) – (englisch).
  13. Jolie L. Chang, Andrew N. Goldberg, Jeremiah A. Alt, Alzoubaidi Mohammed, Liza Ashbrook, Dennis Auckley, Indu Ayappa, Hira Bakhtiar, José E. Barrera, Bethany L. Bartley, Martha E. Billings, Maurits S. Boon, Pien Bosschieter, Itzhak Braverman, Kara Brodie: International Consensus Statement on Obstructive Sleep Apnea. In: International Forum of Allergy & Rhinology. 13. Jahrgang, Nr. 7, 13. Juli 2023, ISSN 2042-6976, S. 1061–1482, doi:10.1002/alr.23079, PMID 36068685, PMC 10359192 (freier Volltext) – (englisch).
  14. M. Safwan Badr, Shahrokh Javaheri: Central Sleep Apnea: a Brief Review. In: Current Pulmonology Reports. 8. Jahrgang, Nr. 1, 13. März 2019, ISSN 2199-2428, S. 14–21, doi:10.1007/s13665-019-0221-z, PMID 31788413, PMC 6883649 (freier Volltext) – (englisch).
  15. a b Diane C. Lim, Allan I. Pack: Obstructive Sleep Apnea: Update and Future. In: Annual Review of Medicine. 68. Jahrgang, Nr. 1, 14. Januar 2017, ISSN 0066-4219, S. 99–112, doi:10.1146/annurev-med-042915-102623, PMID 27732789 (annualreviews.org [abgerufen am 10. Mai 2022]).
  16. Daniel J. Gottlieb, Naresh M. Punjabi: Diagnosis and Management of Obstructive Sleep Apnea: A Review. In: JAMA. 323. Jahrgang, Nr. 14, 14. April 2020, ISSN 0098-7484, S. 1389–1400, doi:10.1001/jama.2020.3514, PMID 32286648 (doi.org [abgerufen am 22. Oktober 2021]).
  17. How Is Sleep Apnea Treated? In: NHLBI. 10. Juli 2012, abgerufen am 18. August 2016.
  18. a b c d Spicuzza L, Caruso D, Di Maria G: Obstructive sleep apnoea syndrome and its management. In: Therapeutic Advances in Chronic Disease. 6. Jahrgang, Nr. 5, September 2015, S. 273–85, doi:10.1177/2040622315590318, PMID 26336596, PMC 4549693 (freier Volltext).
  19. Iftikhar IH, Khan MF, Das A, Magalang UJ: Meta-analysis: continuous positive airway pressure improves insulin resistance in patients with sleep apnea without diabetes. In: Annals of the American Thoracic Society. 10. Jahrgang, Nr. 2, April 2013, S. 115–20, doi:10.1513/annalsats.201209-081oc, PMID 23607839, PMC 3960898 (freier Volltext).
  20. Haentjens P, Van Meerhaeghe A, Moscariello A, De Weerdt S, Poppe K, Dupont A, Velkeniers B: The impact of continuous positive airway pressure on blood pressure in patients with obstructive sleep apnea syndrome: evidence from a meta-analysis of placebo-controlled randomized trials. In: Archives of Internal Medicine. 167. Jahrgang, Nr. 8, April 2007, S. 757–64, doi:10.1001/archinte.167.8.757, PMID 17452537.
  21. Patel SR, White DP, Malhotra A, Stanchina ML, Ayas NT: Continuous positive airway pressure therapy for treating sleepiness in a diverse population with obstructive sleep apnea: results of a meta-analysis. In: Archives of Internal Medicine. 163. Jahrgang, Nr. 5, März 2003, S. 565–71, doi:10.1001/archinte.163.5.565, PMID 12622603.
  22. Hsu AA, Lo C: Continuous positive airway pressure therapy in sleep apnoea. In: Respirology. 8. Jahrgang, Nr. 4, Dezember 2003, S. 447–54, doi:10.1046/j.1440-1843.2003.00494.x, PMID 14708553.
  23. 3 Top Medical Device Stocks to Buy Now. 18. November 2017, abgerufen am 7. März 2021.
  24. A. Andrade, O. M. Bubu, A. W. Varga, R. S. Osorio: The relationship between Obstructive Sleep Apnea and Alzheimer's Disease. In: Journal of Alzheimer's Disease. 64. Jahrgang, Suppl 1, 2018, S. S255–S270, doi:10.3233/JAD-179936, PMID 29782319, PMC 6542637 (freier Volltext).
  25. Referenzfehler: Ungültiges <ref>-Tag; kein Text angegeben für Einzelnachweis mit dem Namen Jackson et al 2020.
  26. Antoine Weihs, Stefan Frenzel, Hans J. Grabe: The Link Between Obstructive Sleep Apnoea and Neurodegeneration and Cognition. In: Current Sleep Medicine Reports. 7. Jahrgang, Nr. 3. Springer Science and Business Media LLC, 13. Juli 2021, ISSN 2198-6401, S. 87–96, doi:10.1007/s40675-021-00210-5 (dzne.de [PDF; abgerufen am 6. Februar 2024]).
  27. Min-Hee Lee, Seung Ku Lee, Soriul Kim, Regina E. Y. Kim, Hye Ryeong Nam, Ali T. Siddiquee, Robert J. Thomas, Inha Hwang, Jee-Eun Yoon, Chang-Ho Yun, Chol Shin: Association of Obstructive Sleep Apnea With White Matter Integrity and Cognitive Performance Over a 4-Year Period in Middle to Late Adulthood. In: JAMA Network Open. 5. Jahrgang, Nr. 7, 20. Juli 2022, S. e2222999, doi:10.1001/jamanetworkopen.2022.22999, PMID 35857321, PMC 9301517 (freier Volltext) – (jamanetwork.com [abgerufen am 28. Juni 2023]).
  28. Referenzfehler: Ungültiges <ref>-Tag; kein Text angegeben für Einzelnachweis mit dem Namen Owen et al 2020.
  29. When Sleep Apnea Masquerades as Dementia. 6. Oktober 2010, abgerufen am 1. März 2021.
  30. Claudio Liguori, Agostino Chiaravalloti, Francesca Izzi, Marzia Nuccetelli, Sergio Bernardini, Orazio Schillaci, Nicola Biagio Mercuri, Fabio Placidi: Sleep apnoeas may represent a reversible risk factor for amyloid-β pathology. In: Brain. 140. Jahrgang, Nr. 12, 1. Dezember 2017, S. e75, doi:10.1093/brain/awx281, PMID 29077794.
  31. Vincenza Castronovo, Paola Scifo, Antonella Castellano, Mark S. Aloia, Antonella Iadanza, Sara Marelli, Stefano F. Cappa, Luigi Ferini Strambi, Andrea Falini: White Matter Integrity in Obstructive Sleep Apnea before and after Treatment. In: Sleep. 37. Jahrgang, Nr. 9, 1. September 2014, S. 1465–1475, doi:10.5665/sleep.3994, PMID 25142557, PMC 4153061 (freier Volltext) – (aasm.org [abgerufen am 1. März 2021]).
  32. Jana R. Cooke, Liat Ayalon, Barton W. Palmer, Jose S. Loredo, Jody Corey-Bloom, Loki Natarajan, Lianqi Liu, Sonia Ancoli-Israel: Sustained Use of CPAP Slows Deterioration of Cognition, Sleep, and Mood in Patients with Alzheimer's Disease and Obstructive Sleep Apnea: A Preliminary Study. In: Journal of Clinical Sleep Medicine. 05. Jahrgang, Nr. 4. American Academy of Sleep Medicine (AASM), 15. August 2009, ISSN 1550-9389, S. 305–309, doi:10.5664/jcsm.27538.
  33. Karl A. Franklin, Eva Lindberg: Obstructive sleep apnea is a common disorder in the population—a review on the epidemiology of sleep apnea. In: Journal of Thoracic Disease. 7. Jahrgang, Nr. 8, August 2015, ISSN 2072-1439, S. 1311–1322, doi:10.3978/j.issn.2072-1439.2015.06.11, PMID 26380759, PMC 4561280 (freier Volltext).
  34. Referenzfehler: Ungültiges <ref>-Tag; kein Text angegeben für Einzelnachweis mit dem Namen ReferenceC.
  35. Who Is at Risk for Sleep Apnea? In: NHLBI. 10. Juli 2012, abgerufen am 18. August 2016.
  36. a b El-Ad B, Lavie P: Effect of sleep apnea on cognition and mood. In: International Review of Psychiatry. 17. Jahrgang, Nr. 4, August 2005, S. 277–82, doi:10.1080/09540260500104508, PMID 16194800.
  37. a b Aloia MS, Sweet LH, Jerskey BA, Zimmerman M, Arnedt JT, Millman RP: Treatment effects on brain activity during a working memory task in obstructive sleep apnea. In: Journal of Sleep Research. 18. Jahrgang, Nr. 4, Dezember 2009, S. 404–10, doi:10.1111/j.1365-2869.2009.00755.x, PMID 19765205.
  38. Sculthorpe LD, Douglass AB: Sleep pathologies in depression and the clinical utility of polysomnography. In: Canadian Journal of Psychiatry. 55. Jahrgang, Nr. 7, Juli 2010, S. 413–21, doi:10.1177/070674371005500704, PMID 20704768 (canada.ca [abgerufen am 6. Dezember 2023]).
  39. Morgenstern M, Wang J, Beatty N, Batemarco T, Sica AL, Greenberg H: Obstructive sleep apnea: an unexpected cause of insulin resistance and diabetes. In: Endocrinology and Metabolism Clinics of North America. 43. Jahrgang, Nr. 1, März 2014, S. 187–204, doi:10.1016/j.ecl.2013.09.002, PMID 24582098.
  40. Rundo JV: Obstructive sleep apnea basics. In: Cleveland Clinic Journal of Medicine. 86. Jahrgang, 9 Suppl 1, 2019, S. 2–9, doi:10.3949/ccjm.86.s1.02, PMID 31509498 (ccjm.org [abgerufen am 6. Februar 2024]).
  41. a b c d e f g h i j Sleep Apnea - Causes and Risk Factors | NHLBI, NIH. 24. März 2022, abgerufen am 6. Februar 2024.
  42. a b c d Risk Factors. Abgerufen am 6. Februar 2024.
  43. Mayo Clinic: Sleep apnea 
  44. What Is Sleep Apnea? In: Nhlbi health 
  45. Simon Green: Biological Rhythms, Sleep and Hyponosis. Palgrave Macmillan, England 2011, ISBN 978-0-230-25265-3, S. 85.
  46. a b Dale Purves: Neuroscience. Sixth Auflage. Oxford University Press, New York 2018, ISBN 978-1-60535-380-7.Vorlage:Page needed
  47. Obstructive sleep apnea - Symptoms and causes. In: Mayo Clinic. Abgerufen am 30. März 2022 (englisch).
  48. Redline S, Budhiraja R, Kapur V, Marcus CL, Mateika JH, Mehra R, Parthasarthy S, Somers VK, Strohl KP, Sulit LG, Gozal D, Wise MS, Quan SF: The scoring of respiratory events in sleep: reliability and validity. In: Journal of Clinical Sleep Medicine. 3. Jahrgang, Nr. 2, März 2007, S. 169–200, doi:10.5664/jcsm.26818, PMID 17557426.
  49. AASM Task Force: 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. In: Sleep. 22. Jahrgang, Nr. 5, August 1999, S. 667–89, doi:10.1093/sleep/22.5.667, PMID 10450601.
  50. Ruehland WR, Rochford PD, O'Donoghue FJ, Pierce RJ, Singh P, Thornton AT: The new AASM criteria for scoring hypopneas: impact on the apnea hypopnea index. In: Sleep. 32. Jahrgang, Nr. 2, Februar 2009, S. 150–7, doi:10.1093/sleep/32.2.150, PMID 19238801, PMC 2635578 (freier Volltext).
  51. AASM releases position statement on home sleep apnea testing – American Academy of Sleep Medicine – Association for Sleep Clinicians and Researchers. In: aasm.org. 13. Oktober 2017, abgerufen am 18. Oktober 2017.
  52. William A. Whitelaw, Rollin F. Brant, W. Ward Flemons: Clinical Usefulness of Home Oximetry Compared with Polysomnography for Assessment of Sleep Apnea. In: American Journal of Respiratory and Critical Care Medicine. 171. Jahrgang, Nr. 2, 15. Januar 2005, S. 188–193, doi:10.1164/rccm.200310-1360OC, PMID 15486338.
  53. Caples SM: The accuracy of physicians in predicting successful treatment response in suspected obstructive sleep apnea did not differ between home monitoring and polysomnography. In: ACP Journal Club. 143. Jahrgang, Nr. 1, 2005, S. 21, doi:10.7326/ACPJC-2005-143-1-021, PMID 15989309.
  54. Timothy I. Morgenthaler, Vadim Kagramanov, Viktor Hanak, Paul A. Decker: Complex Sleep Apnea Syndrome: Is It a Unique Clinical Syndrome? In: Sleep. 29. Jahrgang, Nr. 9, September 2006, S. 1203–1209, doi:10.1093/sleep/29.9.1203, PMID 17040008 (sciencedaily.com [abgerufen am 28. Februar 2018]).
  55. Sleep Apnea: Who Is At Risk for Sleep Apnea? In: NHLBI: Health Information for the Public. U.S. Department of Health and Human Services;
  56. Neill AM, Angus SM, Sajkov D, McEvoy RD: Effects of sleep posture on upper airway stability in patients with sleep apnea. In: American Journal of Respiratory and Critical Care Medicine. 155. Jahrgang, Nr. 1, Januar 1997, S. 199–204, doi:10.1164/ajrccm.155.1.9001312, PMID 9001312.
  57. Guo Xiheng, Wang Chen, Zhang Hongyu, Kong Weimin, An Li, Liu Li, Weng Xinzhi: Cardinal Health, 2003;.
  58. Loord H, Hultcrantz E: Positioner--a method for preventing sleep apnea. In: Acta Oto-Laryngologica. 127. Jahrgang, Nr. 8, August 2007, S. 861–8, doi:10.1080/00016480601089390, PMID 17762999.
  59. Irene Szollosi, Teanau Roebuck, Bruce Thompson, Matthew T Naughton: Lateral Sleeping Position Reduces Severity of Central Sleep Apnea / Cheyne-Stokes Respiration. In: Sleep. 29. Jahrgang, Nr. 8, August 2006, S. 1045–1051, doi:10.1093/sleep/29.8.1045, PMID 16944673.
  60. Vennelle M, White S, Riha RL, Mackay TW, Engleman HM, Douglas NJ: Randomized controlled trial of variable-pressure versus fixed-pressure continuous positive airway pressure (CPAP) treatment for patients with obstructive sleep apnea/hypopnea syndrome (OSAHS). In: Sleep. 33. Jahrgang, Nr. 2, Februar 2010, S. 267–71, doi:10.1093/sleep/33.2.267, PMID 20175411, PMC 2817914 (freier Volltext).
  61. Morris LG, Kleinberger A, Lee KC, Liberatore LA, Burschtin O: Rapid risk stratification for obstructive sleep apnea, based on snoring severity and body mass index. In: Otolaryngology–Head and Neck Surgery. 139. Jahrgang, Nr. 5, November 2008, S. 615–8, doi:10.1016/j.otohns.2008.08.026, PMID 18984252.
  62. Adrián I. Campos, Luis M. García-Marín, Enda M. Byrne, Nicholas G. Martin, Gabriel Cuéllar-Partida, Miguel E. Rentería: Insights into the aetiology of snoring from observational and genetic investigations in the UK Biobank. In: Nature Communications. 11. Jahrgang, Nr. 1, Dezember 2020, S. 817, doi:10.1038/s41467-020-14625-1, PMID 32060260, PMC 7021827 (freier Volltext), bibcode:2020NatCo..11..817C.
  63. Yan-fang S, Yu-ping W: Sleep-disordered breathing: impact on functional outcome of ischemic stroke patients. In: Sleep Medicine. 10. Jahrgang, Nr. 7, August 2009, S. 717–9, doi:10.1016/j.sleep.2008.08.006, PMID 19168390.
  64. Bixler EO, Vgontzas AN, Lin HM, Liao D, Calhoun S, Fedok F, Vlasic V, Graff G: Blood pressure associated with sleep-disordered breathing in a population sample of children. In: Hypertension. 52. Jahrgang, Nr. 5, November 2008, S. 841–6, doi:10.1161/HYPERTENSIONAHA.108.116756, PMID 18838624, PMC 3597109 (freier Volltext).
  65. Leung RS: Sleep-disordered breathing: autonomic mechanisms and arrhythmias. In: Progress in Cardiovascular Diseases. 51. Jahrgang, Nr. 4, 2009, S. 324–38, doi:10.1016/j.pcad.2008.06.002, PMID 19110134.
  66. Silverberg DS, Iaina A, Oksenberg A: Treating obstructive sleep apnea improves essential hypertension and quality of life. In: American Family Physician. 65. Jahrgang, Nr. 2, Januar 2002, S. 229–36, PMID 11820487 (aafp.org).
  67. Grigg-Damberger M: Why a polysomnogram should become part of the diagnostic evaluation of stroke and transient ischemic attack. In: Journal of Clinical Neurophysiology. 23. Jahrgang, Nr. 1, Februar 2006, S. 21–38, doi:10.1097/01.wnp.0000201077.44102.80, PMID 16514349.
  68. H. Klar Yaggi, John Concato, Walter N. Kernan, Judith H. Lichtman, Lawrence M. Brass, Vahid Mohsenin: Obstructive Sleep Apnea as a Risk Factor for Stroke and Death. In: New England Journal of Medicine. 353. Jahrgang, Nr. 19, 10. November 2005, S. 2034–2041, doi:10.1056/NEJMoa043104, PMID 16282178.
  69. a b c Terry Young: Risk Factors for Obstructive Sleep Apnea in Adults. In: JAMA. 291. Jahrgang, Nr. 16, 28. April 2004, S. 2013–6, doi:10.1001/jama.291.16.2013, PMID 15113821.
  70. Yumino D, Bradley TD: Central sleep apnea and Cheyne-Stokes respiration. In: Proceedings of the American Thoracic Society. 5. Jahrgang, Nr. 2, Februar 2008, S. 226–36, doi:10.1513/pats.200708-129MG, PMID 18250216.
  71. Sicard KM, Duong TQ: Effects of hypoxia, hyperoxia, and hypercapnia on baseline and stimulus-evoked BOLD, CBF, and CMRO2 in spontaneously breathing animals. In: NeuroImage. 25. Jahrgang, Nr. 3, April 2005, S. 850–8, doi:10.1016/j.neuroimage.2004.12.010, PMID 15808985, PMC 2962945 (freier Volltext).
  72. a b Devinsky O, Ehrenberg B, Barthlen GM, Abramson HS, Luciano D: Epilepsy and sleep apnea syndrome. In: Neurology. 44. Jahrgang, Nr. 11, November 1994, S. 2060–4, doi:10.1212/WNL.44.11.2060, PMID 7969960.
  73. Khan MT, Franco RA: Complex sleep apnea syndrome. In: Sleep Disorders. 2014. Jahrgang, 2014, S. 1–6, doi:10.1155/2014/798487, PMID 24693440, PMC 3945285 (freier Volltext).
  74. a b c d How Is Sleep Apnea Treated? National Heart, Lung, and Blood Institute;
  75. a b Ana Carolina Pereira Nunes Pinto, Aline Rocha, Luciano F Drager, Geraldo Lorenzi-Filho, Daniela V Pachito: Non-invasive positive pressure ventilation for central sleep apnoea in adults. In: Cochrane Database of Systematic Reviews. 2022. Jahrgang, Nr. 10, 24. Oktober 2022, S. CD012889, doi:10.1002/14651858.CD012889.pub2, PMID 36278514, PMC 9590003 (freier Volltext) – (englisch).
  76. a b Olabimpe Omobomi, Stuart F. Quan: Positional therapy in the management of positional obstructive sleep apnea-a review of the current literature. In: Sleep & Breathing = Schlaf & Atmung. 22. Jahrgang, Nr. 2, Mai 2018, ISSN 1522-1709, S. 297–304, doi:10.1007/s11325-017-1561-y, PMID 28852945 (harvard.edu [PDF; abgerufen am 30. Dezember 2023]).
  77. a b Aurora RN, Chowdhuri S, Ramar K, Bista SR, Casey KR, Lamm CI, Kristo DA, Mallea JM, Rowley JA, Zak RS, Tracy SL: The treatment of central sleep apnea syndromes in adults: practice parameters with an evidence-based literature review and meta-analyses. In: Sleep. 35. Jahrgang, Nr. 1, Januar 2012, S. 17–40, doi:10.5665/sleep.1580, PMID 22215916, PMC 3242685 (freier Volltext).
  78. a b Diagnosis and Treatment of Obstructive Sleep Apnea in Adults. AHRQ Effective Health Care Program, 8. August 2011, archiviert vom Original am 31. Dezember 2016;.. A 2012 surveillance update web.archive.org Fehler bei Vorlage * Parametername unbekannt (Vorlage:Webarchiv): "date"Vorlage:Webarchiv/Wartung/Parameter Fehler bei Vorlage:Webarchiv: Genau einer der Parameter 'wayback', 'webciteID', 'archive-today', 'archive-is' oder 'archiv-url' muss angegeben werden.Vorlage:Webarchiv/Wartung/Linktext_fehltVorlage:Webarchiv/Wartung/URL Fehler bei Vorlage:Webarchiv: enWP-Wert im Parameter 'url'. found no significant information to update.
  79. Yu J, Zhou Z, McEvoy RD, Anderson CS, Rodgers A, Perkovic V, Neal B: Association of Positive Airway Pressure With Cardiovascular Events and Death in Adults With Sleep Apnea: A Systematic Review and Meta-analysis. In: JAMA. 318. Jahrgang, Nr. 2, Juli 2017, S. 156–166, doi:10.1001/jama.2017.7967, PMID 28697252, PMC 5541330 (freier Volltext).
  80. Gottlieb DJ: Does Obstructive Sleep Apnea Treatment Reduce Cardiovascular Risk?: It Is Far Too Soon to Say. In: JAMA. 318. Jahrgang, Nr. 2, Juli 2017, S. 128–130, doi:10.1001/jama.2017.7966, PMID 28697240.
  81. a b c Terry Young, Paul E. Peppard, Daniel J. Gottlieb: Epidemiology of Obstructive Sleep Apnea: A Population Health Perspective. In: American Journal of Respiratory and Critical Care Medicine. 165. Jahrgang, Nr. 9, Mai 2002, S. 1217–1239, doi:10.1164/rccm.2109080, PMID 11991871.
  82. Stephanie Watson: Weight loss, breathing devices still best for treating obstructive sleep apnea In: Harvard Health Blog, 2 October 2013. Abgerufen im 21 October 2019 
  83. Tuomilehto HP, Seppä JM, Partinen MM, Peltonen M, Gylling H, Tuomilehto JO, Vanninen EJ, Kokkarinen J, Sahlman JK, Martikainen T, Soini EJ, Randell J, Tukiainen H, Uusitupa M: Lifestyle intervention with weight reduction: first-line treatment in mild obstructive sleep apnea. In: American Journal of Respiratory and Critical Care Medicine. 179. Jahrgang, Nr. 4, Februar 2009, S. 320–7, doi:10.1164/rccm.200805-669OC, PMID 19011153.
  84. Babak Mokhlesi, Juan Fernando Masa, Jan L. Brozek, Indira Gurubhagavatula, Patrick B. Murphy, Amanda J. Piper, Aiman Tulaimat, Majid Afshar, Jay S. Balachandran, Raed A. Dweik, Ronald R. Grunstein, Nicholas Hart, Roop Kaw, Geraldo Lorenzi-Filho, Sushmita Pamidi, Bhakti K. Patel, Susheel P. Patil, Jean Louis Pépin, Israa Soghier, Maximiliano Tamae Kakazu, Mihaela Teodorescu: Evaluation and Management of Obesity Hypoventilation Syndrome. An Official American Thoracic Society Clinical Practice Guideline. In: American Journal of Respiratory and Critical Care Medicine. 200. Jahrgang, Nr. 3, 1. August 2019, S. e6–e24, doi:10.1164/rccm.201905-1071ST, PMID 31368798, PMC 6680300 (freier Volltext).
  85. Maria Pia Villa, Alessandra Rizzoli, Silvia Miano, Caterina Malagola: Efficacy of rapid maxillary expansion in children with obstructive sleep apnea syndrome: 36 months of follow-up. In: Sleep and Breathing. 15. Jahrgang, Nr. 2, 1. Mai 2011, S. 179–184, doi:10.1007/s11325-011-0505-1, PMID 21437777.
  86. Almiro-José Machado-Júnior, Edilson Zancanella, Agrício-Nubiato Crespo: Rapid maxillary expansion and obstructive sleep apnea: A review and meta-analysis. In: Medicina Oral, Patología Oral y Cirugía Bucal. 21. Jahrgang, Nr. 4, 2016, S. e465–e469, doi:10.4317/medoral.21073, PMID 27031063, PMC 4920460 (freier Volltext).
  87. Qiming Li, Hongyi Tang, Xueye Liu, Qing Luo, Zhe Jiang, Domingo Martin, Jing Guo: Comparison of dimensions and volume of upper airway before and after mini-implant assisted rapid maxillary expansion. In: The Angle Orthodontist. 90. Jahrgang, Nr. 3, 1. Mai 2020, S. 432–441, doi:10.2319/080919-522.1, PMID 33378437, PMC 8032299 (freier Volltext).
  88. Jose Abdullatif, Victor Certal, Soroush Zaghi, Sungjin A. Song, Edward T. Chang, M. Boyd Gillespie, Macario Camacho: Maxillary expansion and maxillomandibular expansion for adult OSA: A systematic review and meta-analysis. In: Journal of Cranio-Maxillofacial Surgery. 44. Jahrgang, Nr. 5, 1. Mai 2016, S. 574–578, doi:10.1016/j.jcms.2016.02.001, PMID 26948172.
  89. Supriya Sundaram, Jerome Lim, Toby J Lasserson, TJ Lasserson: Surgery for obstructive sleep apnoea in adults. In: Cochrane Database of Systematic Reviews. Nr. 4, 19. Oktober 2005, S. CD001004, doi:10.1002/14651858.CD001004.pub2, PMID 16235277.
  90. Hsueh-Yu Li, Pa-Chun Wang, Yu-Pin Chen, Li-Ang Lee, Tuan-Jen Fang, Hsin-Ching Lin: Critical Appraisal and Meta-Analysis of Nasal Surgery for Obstructive Sleep Apnea. In: American Journal of Rhinology & Allergy. 25. Jahrgang, Nr. 1, Januar 2011, S. 45–49, doi:10.2500/ajra.2011.25.3558, PMID 21711978.
  91. Choi JH, Kim SN, Cho JH: Efficacy of the Pillar implant in the treatment of snoring and mild-to-moderate obstructive sleep apnea: a meta-analysis. In: The Laryngoscope. 123. Jahrgang, Nr. 1, Januar 2013, S. 269–76, doi:10.1002/lary.23470, PMID 22865236.
  92. Prinsell JR: Maxillomandibular advancement surgery for obstructive sleep apnea syndrome. In: Journal of the American Dental Association. 133. Jahrgang, Nr. 11, November 2002, S. 1489–97; quiz 1539–40, doi:10.14219/jada.archive.2002.0079, PMID 12462692.
  93. MacKay, Stuart: Treatments for snoring in adults. In: Australian Prescriber. 34. Jahrgang, Nr. 34, Juni 2011, S. 77–79, doi:10.18773/austprescr.2011.048.
  94. T. Scott Johnson, William A. Broughton, Jerry Halberstadt: Sleep Apnea – The Phantom of the Night: Overcome Sleep Apnea Syndrome and Win Your Hidden Struggle to Breathe, Sleep, and Live. New Technology Publishing, 2003, ISBN 978-1-882431-05-2 (archive.org).Vorlage:Page needed
  95. What is Sleep Apnea? In: National Heart, Lung, and Blood Institute. National Institutes of Health, 2012, abgerufen am 15. Februar 2013.
  96. Vorlage:EMedicine
  97. Yun AJ, Lee PY, Doux JD: Negative pressure ventilation via diaphragmatic pacing: a potential gateway for treating systemic dysfunctions. In: Expert Review of Medical Devices. 4. Jahrgang, Nr. 3, Mai 2007, S. 315–9, doi:10.1586/17434440.4.3.315, PMID 17488226.
  98. Inspire Upper Airway Stimulation – P130008. In: FDA.gov. Food and Drug Administration, 11. Januar 2016, abgerufen am 9. März 2016.
  99. a b Thomas Gaisl, Sarah R. Haile, Sira Thiel, Martin Osswald, Malcolm Kohler: Efficacy of pharmacotherapy for OSA in adults: A systematic review and network meta-analysis. In: Sleep Medicine Reviews. 46. Jahrgang, August 2019, S. 74–86, doi:10.1016/j.smrv.2019.04.009, PMID 31075665.
  100. a b c Elie Dolgin: Treating sleep apnea with pills instead of machines. In: Knowable Magazine. 29. April 2020, doi:10.1146/knowable-042820-1 (knowablemagazine.org [abgerufen am 9. Mai 2022]).
  101. Andrew Wellman, Danny J. Eckert, Amy S. Jordan, Bradley A. Edwards, Chris L. Passaglia, Andrew C. Jackson, Shiva Gautam, Robert L. Owens, Atul Malhotra, David P. White: A method for measuring and modeling the physiological traits causing obstructive sleep apnea. In: Journal of Applied Physiology. 110. Jahrgang, Nr. 6, Juni 2011, S. 1627–1637, doi:10.1152/japplphysiol.00972.2010, PMID 21436459, PMC 3119134 (freier Volltext).
  102. Danny J. Eckert, Robert L. Owens, Geoffrey B. Kehlmann, Andrew Wellman, Shilpa Rahangdale, Susie Yim-Yeh, David P. White, Atul Malhotra: Eszopiclone increases the respiratory arousal threshold and lowers the apnoea/hypopnoea index in obstructive sleep apnoea patients with a low arousal threshold. In: Clinical Science. 120. Jahrgang, Nr. 12, 7. März 2011, ISSN 0143-5221, S. 505–514, doi:10.1042/CS20100588, PMID 21269278, PMC 3415379 (freier Volltext) – (doi.org [abgerufen am 10. Mai 2022]).
  103. Luigi Taranto-Montemurro, Scott A. Sands, Bradley A. Edwards, Ali Azarbarzin, Melania Marques, Camila de Melo, Danny J. Eckert, David P. White, Andrew Wellman: Desipramine improves upper airway collapsibility and reduces OSA severity in patients with minimal muscle compensation. In: European Respiratory Journal. 48. Jahrgang, Nr. 5, 1. November 2016, ISSN 0903-1936, S. 1340–1350, doi:10.1183/13993003.00823-2016, PMID 27799387, PMC 5437721 (freier Volltext) – (englisch, ersjournals.com [abgerufen am 10. Mai 2022]).
  104. Mara Lambert: Updated Guidelines from AASM for the Treatment of Central Sleep Apnea Syndromes. In: American Family Physician. 86. Jahrgang, Nr. 10, 15. November 2012, ISSN 0002-838X, S. 968–971 (aafp.org [abgerufen am 10. Mai 2022]).
  105. Sleep Apnea. In: Diagnosis Dictionary. Psychology Today;
  106. M. Mayos, L. Hernández Plaza, A. Farré, S. Mota, J. Sanchis: Efecto de la oxigenoterapia nocturna en el paciente con síndrome de apnea-hipopnea del sueño y limitación crónica al flujo aéreo. (deutsch: The effect of nocturnal oxygen therapy in patients with sleep apnea syndrome and chronic airflow limitation). In: Archivos de Bronconeumología. 37. Jahrgang, Nr. 2, Januar 2001, S. 65–68, doi:10.1016/s0300-2896(01)75016-8, PMID 11181239 (spanisch).
  107. Breitenbücher A, Keller-Wossidlo H, Keller R: Transtracheale Sauerstofftherapie beim obstruktiven Schlafapnoe-Syndrom. (deutsch: Transtracheal oxygen therapy in obstructive sleep apnea syndrome). In: Schweizerische Medizinische Wochenschrift. 119. Jahrgang, Nr. 46, November 1989, OCLC 119157195, S. 1638–1641, PMID 2609134.
  108. Machado MA, Juliano L, Taga M, de Carvalho LB, do Prado LB, do Prado GF: Titratable mandibular repositioner appliances for obstructive sleep apnea syndrome: are they an option? In: Sleep & Breathing = Schlaf & Atmung. 11. Jahrgang, Nr. 4, Dezember 2007, S. 225–31, doi:10.1007/s11325-007-0109-y, PMID 17440760.
  109. a b Chen H, Lowe AA: Updates in oral appliance therapy for snoring and obstructive sleep apnea. In: Sleep & Breathing = Schlaf & Atmung. 17. Jahrgang, Nr. 2, Mai 2013, S. 473–86, doi:10.1007/s11325-012-0712-4, PMID 22562263.
  110. 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. In: Sleep Disorders. 2015. Jahrgang, 2015, S. 734798, doi:10.1155/2015/734798, PMID 26798519, PMC 4699057 (freier Volltext).
  111. Nigam G, Pathak C, Riaz M: Effectiveness of oral pressure therapy in obstructive sleep apnea: a systematic analysis. In: Sleep & Breathing = Schlaf & Atmung. 20. Jahrgang, Nr. 2, Mai 2016, S. 663–71, doi:10.1007/s11325-015-1270-3, PMID 26483265.
  112. Colrain IM, Black J, Siegel LC, Bogan RK, Becker PM, Farid-Moayer M, Goldberg R, Lankford DA, Goldberg AN, Malhotra A: A multicenter evaluation of oral pressure therapy for the treatment of obstructive sleep apnea. In: Sleep Medicine. 14. Jahrgang, Nr. 9, September 2013, S. 830–7, doi:10.1016/j.sleep.2013.05.009, PMID 23871259, PMC 3932027 (freier Volltext) – (escholarship.org [abgerufen am 7. Oktober 2018]).
  113. Ahmed MH, Byrne CD: Obstructive sleep apnea syndrome and fatty liver: association or causal link? In: World Journal of Gastroenterology. 16. Jahrgang, Nr. 34, September 2010, S. 4243–52, doi:10.3748/wjg.v16.i34.4243, PMID 20818807, PMC 2937104 (freier Volltext).
  114. Singh H, Pollock R, Uhanova J, Kryger M, Hawkins K, Minuk GY: Symptoms of obstructive sleep apnea in patients with nonalcoholic fatty liver disease. In: Digestive Diseases and Sciences. 50. Jahrgang, Nr. 12, Dezember 2005, S. 2338–43, doi:10.1007/s10620-005-3058-y, PMID 16416185.
  115. Tanné F, Gagnadoux F, Chazouillères O, Fleury B, Wendum D, Lasnier E, Lebeau B, Poupon R, Serfaty L: Chronic liver injury during obstructive sleep apnea. In: Hepatology. 41. Jahrgang, Nr. 6, Juni 2005, S. 1290–6, doi:10.1002/hep.20725, PMID 15915459.
  116. Kumar R, Birrer BV, Macey PM, Woo MA, Gupta RK, Yan-Go FL, Harper RM: Reduced mammillary body volume in patients with obstructive sleep apnea. In: Neuroscience Letters. 438. Jahrgang, Nr. 3, Juni 2008, S. 330–4, doi:10.1016/j.neulet.2008.04.071, PMID 18486338.
  117. Kumar R, Birrer BV, Macey PM, Woo MA, Gupta RK, Yan-Go FL, Harper RM: Reduced mammillary body volume in patients with obstructive sleep apnea. In: Neuroscience Letters. 438. Jahrgang, Nr. 3, Juni 2008, S. 330–4, doi:10.1016/j.neulet.2008.04.071, PMID 18486338 (newswise.com [abgerufen am 12. Juni 2008]).
  118. a b Terry Young, Mari Palta, Jerome Dempsey, James Skatrud, Steven Weber, Safwan Badr: The Occurrence of Sleep-Disordered Breathing among Middle-Aged Adults. In: New England Journal of Medicine. 328. Jahrgang, Nr. 17, 29. April 1993, S. 1230–1235, doi:10.1056/NEJM199304293281704, PMID 8464434.
  119. a b Lee W, Nagubadi S, Kryger MH, Mokhlesi B: Epidemiology of Obstructive Sleep Apnea: a Population-based Perspective. In: Expert Review of Respiratory Medicine. 2. Jahrgang, Nr. 3, Juni 2008, S. 349–364, doi:10.1586/17476348.2.3.349, PMID 19690624, PMC 2727690 (freier Volltext).
  120. Vishesh Kapur, David K. Blough, Robert E. Sandblom, Richard Hert, James B. de Maine, Sean D. Sullivan, Bruce M. Psaty: The Medical Cost of Undiagnosed Sleep Apnea. In: Sleep. 22. Jahrgang, Nr. 6, September 1999, S. 749–755, doi:10.1093/sleep/22.6.749, PMID 10505820.
  121. a b Sleep Apnea Information for Clinicians - www.sleepapnea.org. In: www.sleepapnea.org. 13. Januar 2017, abgerufen am 30. März 2022 (amerikanisches Englisch).
  122. Steven M. Yentis, Nicholas P. Hirsch, James Ip: Anaesthesia and Intensive Care A-Z: An Encyclopedia of Principles and Practice. Elsevier Health Sciences, 2013, ISBN 978-0-7020-5375-7, S. 428 (google.com [abgerufen am 11. September 2017]).
  123. Kryger MH: Fat, sleep, and Charles Dickens: literary and medical contributions to the understanding of sleep apnea. In: Clinics in Chest Medicine. 6. Jahrgang, Nr. 4, Dezember 1985, S. 555–62, doi:10.1016/S0272-5231(21)00394-4, PMID 3910333.
  124. Sullivan CE, Issa FG, Berthon-Jones M, Eves L: Reversal of obstructive sleep apnoea by continuous positive airway pressure applied through the nares. In: Lancet. 1. Jahrgang, Nr. 8225, April 1981, S. 862–5, doi:10.1016/S0140-6736(81)92140-1, PMID 6112294.
  125. Lori Sichtermann: Industry Recognizes Sleep Apnea Awareness Day 2014. Sleep Review, 19. April 2014, abgerufen am 30. April 2014.