Psychology Wiki

Assessment | Biopsychology | Comparative | Cognitive | Developmental | Language | Individual differences | Personality | Philosophy | Social |
Methods | Statistics | Clinical | Educational | Industrial | Professional items | World psychology |

Cognitive Psychology: Attention · Decision making · Learning · Judgement · Memory · Motivation · Perception · Reasoning · Thinking  - Cognitive processes Cognition - Outline Index

This article is in need of attention from a psychologist/academic expert on the subject.
Please help recruit one, or improve this page yourself if you are qualified.
This banner appears on articles that are weak and whose contents should be approached with academic caution.
Sleep apnea
ICD-10 G473
ICD-9 780.57
OMIM [1]
DiseasesDB [2]
MedlinePlus [3]
eMedicine ped/2114
MeSH {{{MeshNumber}}}

Sleep apnea (or sleep apnoea in British English or obstructive sleep apnea (OSA) or Obstructive sleep apne syndrome OSAS ) is a sleep disorder characterized by pauses in breathing during sleep. Each episode, called an apnea ), lasts long enough so that one or more breaths are missed, and such episodes occur repeatedly throughout sleep.[1] The standard definition of any apneic event includes a minimum 10-second interval between breaths, with either a neurological arousal (a 3-second or greater shift in EEG frequency, measured at C3, C4, O1, or O2) or a blood oxygen desaturation of 3–4% or greater, or both arousal and desaturation. Sleep apnea is diagnosed with an overnight sleep test called a polysomnogram, or a "sleep study".

Clinically significant levels of sleep apnea are defined as five or more episodes per hour of any type of apnea (from the polysomnogram). There are three distinct forms of sleep apnea: central, obstructive, and complex (i.e., a combination of central and obstructive) constituting 0.4%, 84% and 15% of cases respectively.[2] Breathing is interrupted by the lack of respiratory effort in central sleep apnea; in obstructive sleep apnea, breathing is interrupted by a physical block to airflow despite respiratory effort. In complex (or "mixed") sleep apnea, there is a transition from central to obstructive features during the events themselves.

Regardless of type, the individual with sleep apnea is rarely aware of having difficulty breathing, even upon awakening. Sleep apnea is recognized as a problem by others witnessing the individual during episodes or is suspected because of its effects on the body (sequelae). Symptoms may be present for years (or even decades) without identification, during which time the sufferer may become conditioned to the daytime sleepiness and fatigue associated with significant levels of sleep disturbance.

Development and discovery of sleep apnea in humans

The first reports in the medical literature of what is now called obstructive sleep apnea date only from 1965, when it was independently described by French and German investigators. However, 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. "Pickwickian Syndrome" is NOT an accurate description of someone with Obstructive Sleep Apnea (OSA). The description of Joe "the fat boy" is a perfect example of a person who suffers from Obesity Hypoventilation Syndrome, sometimes referred to as "Pickwickian Syndrome". Obesity Hypoventilation causes severe OSA with periods of Central Sleep Apnea and takes on a Cheyne Stokes pattern of breathing. Obesity hypoventilators will have an increase in carbon dioxide levels (hypercapnia) and low blood oxygen levels. This in turn will cause periods of rapid breathing followed by periods of no breathing. People who have Obstructive Sleep Apnea can be any size, sex, or age. While obesity is a common occurrence in OSA, very thin people can also have OSA. In addition to obesity, OSA can be caused by anatomical problems, such as an enlarged tongue, a narrow trachea, a highly arched and narrow soft palate (roof of your mouth), a soft palate that extends into the airway, excess of tissue in the throat, or retrognathia (small recessed chin).

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. Tracheostomy was the recommended treatment and, though it could be life-saving, postoperative complications in the stoma were frequent in these very obese and short-necked individuals.

The management of obstructive sleep apnea was revolutionized with the introduction of continuous positive airway pressure (CPAP), first described in 1981 by Colin Sullivan and associates in Sydney, Australia. 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.

Prevalence and costs in the USA

It is estimated[citation needed] that 20 million Americans are affected by sleep apnea. That would represent more than 6.5%, or nearly 1 in 15 Americans, making sleep apnea as prevalent as asthma or diabetes. It is also estimated that 85-90 percent of individuals affected are undiagnosed and untreated.[3] The Wisconsin Sleep Cohort Study found that, among the middle-aged, nine percent of women and 24 percent of men had sleep apnea.[4]

The costs of untreated sleep apnea reach further than just health issues. It is estimated that the average untreated sleep apnea patient's health care costs $1,336 more than an individual without sleep apnea. If approximations are correct, 17 million untreated individuals account for $22,712 million,or almost 23 billion in health care costs.[5]

Obstructive sleep apnea

File:Wired up for a sleep study 02A.jpg

Patient wired up for a sleep study to determine degree of apnea. Sensors variously detect brain activity, snoring sounds, etc. The white bands are to determine expansion and contraction of chest and abdomen.

Main article: Obstructive sleep apnea

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 which can obstruct breathing during sleep. Mild occasional sleep apnea, such as many people experience during an upper respiratory infection, may not be important, but chronic severe obstructive sleep apnea requires treatment to prevent low blood oxygen (hypoxemia), sleep deprivation, and other complications. The most serious complication is a severe form of congestive heart failure called cor pulmonale.

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 typical sleep apnea sufferers than women and children, although it is not uncommon in the latter two.

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.

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

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[6] 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,[7][8][9] largely because the gravitational component is smaller in the lateral position. Some people benefit from various kinds of oral appliances to keep the airway open during sleep. "Breathing machines" like the continuous positive airway pressure (CPAP) may help. There are also surgical procedures to remove and tighten tissue and widen the airway.

Symptoms, signs and sequelae

As already mentioned, 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 conditions such as overweight and obesity has been found to be highly predictive of OSA risk.[10] 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. If both snoring and breathing stop while the person's chest and body try to breathe, that is literally a description of an event in obstructive sleep apnea syndrome. When breathing starts again, there is typically a deep gasp and then the resumption of snoring.

Other indicators include (but are not limited to): hypersomnolence, obesity BMI >30, large neck circumference (Template:Convert/LoffAonDbSoffTemplate:Convert/test/Aon in women, Template:Convert/LoffAonDbSoffTemplate:Convert/test/Aon 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.[11][12][13][14] 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.[15] Stroke is associated with obstructive sleep apnea.[16] Sleep apnea sufferers also have a 30% higher risk of heart attack or premature death than those unaffected.[17]

In the June 27, 2008, edition of the journal Neuroscience Letters, researchers revealed that people with OSA show tissue loss in brain regions that help store memory, thus linking OSA with memory loss.[18] Using magnetic resonance imaging (MRI), the scientists discovered that sleep apnea patients' mammillary bodies were nearly 20 percent smaller, particularly on the left side. One of the key investigators hypothesized that repeated drops in oxygen lead to the brain injury.[19]

Central sleep apnea

In pure central sleep apnea or Cheyne-Stokes respiration, the brain's respiratory control centers are imbalanced during sleep. 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 hyperpnea, 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 (hyperpnea) for a period of time, a compensatory mechanism to blow off retained waste gases and absorb more oxygen.

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. The respiratory drive is so strong that even conscious efforts to hold one's breath do not overcome it. Any sudden drop in oxygen or excess of carbon dioxide (even if tiny) strongly stimulates the brain's respiratory centers to breathe.

In central sleep apnea, 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 will drop to a lower than normal level (hypoxaemia) and the concentration of carbon dioxide will build to a higher than normal level (hypercapnia). In turn, these conditions of hypoxia and hypercapnia will trigger additional effects on the body. Brain cells need constant oxygen to live, and if the level of blood oxygen goes low enough for long enough, the consequences of brain damage and even death will occur. Fortunately, central sleep apnea is more often a chronic condition that causes much milder effects than sudden death. The exact effects of the condition will depend on how severe the apnea is and on the individual characteristics of the person having the apnea. Several examples are discussed below, and more about the nature of the condition is presented in the section on Clinical Details.

In any person, hypoxia and hypercapnia have certain common effects on the body. 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. Even in severe cases of central sleep apnea, the effects almost always result in pauses that make breathing irregular, rather than cause the total cessation of breathing.

  • 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. 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 metabolic acidosis.

Laboratory findings

AHI Rating
<5 Normal
5-15 Mild
15-30 Moderate
>30 Severe

Polysomnography of sleep apnea shows pauses in breathing that are followed by drops in blood oxygen and increases in blood carbon dioxide. In adults, a pause must last 10 seconds to be scored as an apnea. However in young children, who normally breathe at a much faster rate than adults, the pause may be many seconds shorter and still be considered apnea. The cessation of airflow in central sleep apnea has an association with no physical attempts to breathe. On polysomnograms, there is an absence of rib cage and abdominal movements while airflow ceases at the nose and lips. Obstructive sleep apnea shows pauses in breathing for at least 10 seconds causing a decrease in blood oxygen and associates with physical attempts to breathe.

Hypopneas in adults are defined as a 50% reduction in air flow for more than ten seconds, followed by a 3% desaturation, and/or arousal. The Apnea-Hypopnea Index (AHI) is expressed as the number of apneas and hypopneas per hour of sleep.

Clinical details

Any individual, no matter how healthy, who is given enough of a central respiratory depressant drug will develop apnea on a central basis. Generally, drugs that are central respiratory depressants also have sedative effects, and so the individual taking a toxic dose of such a drug is likely to be asleep, or at least in an altered state of consciousness, when breathing becomes irregular. Alcohol is such a central respiratory depressant in large doses; so are opiates, barbiturates, benzodiazepines, and many other tranquilizers. Some individuals have abnormalities that predispose them to central sleep apnea. The treatment for the condition depends on its specific cause.

Similarly, in any person who has some form of sleep apnea (including obstructive sleep apnea), breathing irregularities during sleep can be dangerously aggravated by taking one of these drugs. Quantities that are normally considered safe may cause the person with chronic sleep apnea to stop breathing altogether. Should these individuals have general anesthesia, for example, they require prolonged monitoring after initial recovery, as compared to a person with no history of sleep apnea, because apnea is likely to occur with even low levels of the drugs in their system.

Premature infants with immature brains and reflex systems are at high risk for central sleep apnea syndrome, even if these babies are otherwise healthy. Fortunately, those premature babies who have the syndrome will generally outgrow it as they mature, providing they receive careful enough monitoring and supportive care during infancy to survive. Because of the propensity toward apnea, medications that can cause respiratory drive depression are either not given to premature infants, or given under careful monitoring, with equipment for resuscitation immediately available. Such precautions are routinely taken for premature infants after general anesthesia. Caffeine has been found to help reduce apnea in preterm infants and to aid in care after general anesthesia.[20]

Sudden infant death syndrome is sometimes theorized to be attributable to sleep apnea.

Congenital Central Hypoventilation Syndrome: This rare, inborn condition involves a specific gene, PHOX2B. This homeobox gene guides maturation of the autonomic nervous system, and loss-of-function mutations lead to the failure of the brain to effectively control breathing during sleep in patients with the syndrome. There may be a recognizable pattern of facial features among individuals affected with this syndrome.[21]

Once almost uniformly fatal, congenital hypoventilation ("abnormally low ventilation") syndrome is now treatable. The children who have it must have tracheotomies and access to mechanical ventilation on respirators while sleeping, but most do not need to use a respirator while awake. The use of a diaphragmatic pacemaker may offer an alternative for some patients. When pacemakers have enabled some children to sleep without the use of a mechanical respirator, reported cases still required the tracheotomy to remain in place because the vocal cords did not move apart with inhalation. This form of central sleep apnea has been called Ondine's curse. Now that some children with the syndrome have grown up, there is particular need for their avoidance of adolescent behaviors, such as alcohol use, which can easily be lethal.[22]

Adults suffering from congestive heart failure are at risk for a form of central sleep apnea called Cheyne-Stokes respiration. This is periodic breathing with recurrent episodes of apnea alternating with episodes of rapid breathing. In those who have it, Cheyne-Stokes respirations occur while both awake and asleep. There is good evidence that replacement of the failed heart (heart transplant) cures central apnea in these patients. The use of some medications that are respiratory stimulants decrease the severity of apnea in some patients.

Section references

This article or section needs to be wikified. Please format this article according to the guidelines laid out at Psychology wiki:Guide to layout. Please remove this template after wikifying.
  1. Macey PM, Macey KE, Woo MA, Keens TG, Harper RM (April 2005). Aberrant neural responses to cold pressor challenges in congenital central hypoventilation syndrome. Pediatric Research 57 (4): 500–9.
  2. Bradley TD, Floras JS (April 2003). Sleep apnea and heart failure: Part II: central sleep apnea. Circulation 107 (13): 1822–6.
  3. Mansfield DR, Solin P, Roebuck T, Bergin P, Kaye DM, Naughton MT (November 2003). The effect of successful heart transplant treatment of heart failure on central sleep apnea. Chest 124 (5): 1675–81.
  4. Javaheri S (January 2006). Acetazolamide improves central sleep apnea in heart failure: a double-blind, prospective study. American Journal of Respiratory and Critical Care Medicine 173 (2): 234–7.

Mixed apnea and complex sleep apnea

Some people with sleep apnea have a combination of both types. When obstructive sleep apnea syndrome is severe and longstanding, episodes of central apnea sometimes develop. The exact mechanism of the loss of central respiratory drive during sleep in OSA is unknown but is most commonly related to acid-base and CO2 feedback malfunctions stemming from heart failure. There is a constellation of diseases and symptoms relating to body mass, cardiovascular, respiratory, and occasionally, neurological dysfunction that have a synergistic effect in sleep-disordered breathing. The presence of central sleep apnea without an obstructive component is a common result of chronic opiate use (or abuse) owing to the characteristic respiratory depression caused by large doses of narcotics.[citation needed]

Complex sleep apnea has recently been described by researchers as a novel presentation of sleep apnea. Patients with complex sleep apnea exhibit OSA, but upon application of positive airway pressure the patient exhibits persistent central sleep apnea. This central apnea is most commonly noted while on CPAP therapy after the obstructive component has been eliminated. This has long been seen in sleep laboratories and has historically been managed either by CPAP or BiLevel therapy. Adaptive servo-ventilation (ASV) modes of therapy have been introduced to attempt to manage this complex sleep apnea. Studies have demonstrated marginally superior performance of the adaptive servo ventilators in treating Cheyne-Stokes breathing; however, no longitudinal studies have yet been published, nor have any results been generated that suggest any differential outcomes versus standard CPAP therapy. At the AARC 2006 in Las Vegas, NV, researchers reported successful treatment of hundreds of patients on ASV therapy; however, these results have not been reported in peer-reviewed publications as of 2007Template:Dated maintenance category.

An important finding by Dernaika et al. suggests that transient central apnea produced during CPAP titration (the so-called "complex sleep apnea") is "…transient and self-limited."[23] The central apneas may in fact be secondary to sleep fragmentation during the titration process. As of 2007Template:Dated maintenance category, there has been no alternate convincing evidence produced that these central sleep apnea events associated with CPAP therapy for obstructive sleep apnea are of any significant pathophysiologic importance.

Research is ongoing, however, at the Harvard Medical School, including adding dead space to positive airway pressure for treatment of complex sleep-disordered breathing.[24]


The most common treatment for sleep apnea is the use of a continuous positive airway pressure (CPAP) device,[25] which 'splints' the patient's airway open during sleep by means of a flow of pressurized air into the throat. The CPAP machine assists only inhaling, whereas a BiPAP machine assists with both inhaling and exhaling and is used in more severe cases.[citation needed]

In addition to CPAP, dentists specializing in sleep disorders can prescribe Oral Appliance Therapy (OAT). The oral appliance is a custom-made mouthpiece that shifts the lower jaw forward, opening up the airway. OAT is usually successful in patients with mild to moderate obstructive sleep apnea.[26] OAT is a relatively new treatment option for sleep apnea in the United States, but it is much more common in Canada and Europe. Its use has led to increasing recognition of the importance of upper airway anatomy in the pathophysiology of OSA [27]

CPAP and OAT are generally effective only for obstructive and mixed sleep apnea which have a mechanical rather than a neurological cause.

In mild cases of obstructive sleep apnea, use of a specially shaped pillow or shirt may reduce sleep apnea episodes, usually by causing users to sleep on the side instead of on the back or in a reclining position instead of flat.[citation needed]

For patients who do not tolerate or fail nonsurgical measures, surgical treatment to anatomically alter the airway is available. Several levels of obstruction may be addressed, including the nasal passage, throat (pharynx), base of tongue, and facial skeleton. Surgical treatment for obstructive sleep apnea needs to be individualized in order to address all anatomical areas of obstruction. 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. Tonsillectomy and uvulopalatopharyngoplasty (UPPP or UP3) is available to address pharyngeal obstruction. Base-of-tongue advancement by means of advancing the genial tubercle of the mandible may help with the lower pharynx. A myriad of other techniques are available, including hyoid bone myotomy and suspension and various radiofrequency technologies. For patients who fail these operations, the facial skeletal may be advanced by means of a technique called maxillomandibular advancement, or two-jaw surgery (upper and lower jaws). Technically, this is accomplished by a surgery similar to orthognathic surgeries addressing an abnormal bite. The surgery involves a Lefort type one osteotomy and bilateral sagittal split mandibular osteotomies.

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.[25]

Possibly owing to changes in pulmonary oxygen stores, sleeping on one's side (as opposed to on one's back) has been found to be helpful for central sleep apnea with Cheyne-Stokes respiration (CSA-CSR).[9]

Medications like Acetazolamide[28][29] lower blood pH and encourage respiration. Low doses of oxygen are also used as a treatment for hypoxia but are discouraged due to side effects.[29][30][31]

Alternative treatments

A 2005 study in the British Medical Journal found that learning and practicing the didgeridoo helped reduce snoring and sleep apnea as well as daytime sleepiness. This appears to work by strengthening muscles in the upper airway, thus reducing their tendency to collapse during sleep.[32]

A program that uses specialized "singing" exercises to tone the throat, in particular the soft palate, tongue and nasaopharynx, is 'Singing for Snorers' by Alise Ojay.[33] Dr. Elizabeth Scott, a medical doctor living in Scotland, had experimented with singing exercises and found considerable success, as reviewed in her book The Natural Way to Stop Snoring (London: Orion 1995) but had been unable to carry out a clinical trial. Alise Ojay, a choir director singer and composer, began researching the possibility of using singing exercises to help a friend with snoring and came across Dr. Scott's work. In 1999, as an Honorary Research Fellow with the support of the Department of Complementary Medicine at the University of Exeter, Alise conducted the first trial of singing exercises to reduce snoring.[34] The results were described by Ojay as promising and after two years of investigations, she designed the 'Singing for Snorers' program in 2002.[33]

The independent nonprofit UK consumer advocacy group Which? reviewed Singing for Snorers. Their physician Dr. Williams "feels the company is ethical in 'offering aims not claims' until research is complete" and the review stated: "Combining the programme with diet and exercise, the snorer in our test couple found real improvements in the volume and frequency of his snoring after six weeks. His partner is sleeping better, too."[35] In the case of snorers who also have sleep apnea, there is anecdotal evidence from some of the users of Ojay's program, as she reports on her page,[36] as reported by an American, Charley Hupp, who flew to the UK to personally thank her, on his web page[37] and as reported by one user in the UK on the discussion forum of the British Snoring and Sleep Apnoea Association. This person reported that sleep tests before and after the program showed a significant effect: "My apnoeas had gone down from 35 to 0.8 per hour."[38]

Herbal treatments for sleep apnea are also available. In 2008 herbalist Steve Frank applied to patent an "herbal preparation for relief of sleep apnea contains lobelia and/or lobelia extract material acting as a respiratory stimulant." Other herbs counteract nausea and further increase respiration during sleep. The treatment is taken in capsule form, circumventing the need for a CPAP machine and requiring no masks or oral appliances. [39]

Benefits and risks for treatment by surgery

CPAP is functional in sleep apnea and cost-efficient for the health care system, but it is a symptomatic therapy and does not cure the disease.[40] In contrast, although not well known, surgery is more expensive and can treat directly the causes of sleep apnea: The Stanford Center for Excellence in Sleep Disorders Medicine achieved a 95% cure rate of sleep apnea patients by surgery.[41] Maxillomandibular advancement (MMA) is considered the most effective surgery for sleep apnea patients,[42] because it increases the posterior airway space (PAS).[43] The main benefit of the operation is that the oxygen saturation in the arterial blood increases.[43] In a study published in 2008, 93.3.% of surgery patients achieved an adequate quality of life based on the Functional Outcomes of Sleep Questionnaire (FOSQ).[43] Surgery led to a significant increase in general productivity, social outcome, activity level, vigilance, intimacy and sex, and the total score postoperatively was P = .0002.[43] Overall risks of MMA surgery are low: The Stanford University Sleep Disorders Center found 4 failuresTemplate:Which? in a series of 177 patients, or about one out of 44 patients.[44]

Surgery and anesthesia in patients with sleep apnea

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.[45] Use of analgesics and sedatives in these patients postoperatively should therefore be minimized or avoided.

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. Individuals with sleep apnea generally require more intensive monitoring after surgery for these reasons.

Sleep apnea patients undergoing any medical treatment must make sure his or her doctor and/or anesthetist are informed about their condition. Alternate and emergency procedures may be necessary to maintain the airway of sleep apnea patients.[46] If an individual suspects he or she may have sleep apnea, communication with their doctor about possible preprocedure screening may be in order.

See also


  1. What is Sleep Apnea?. Health and Life.[unreliable source?]
  2. Morgenthaler TI, Kagramanov V, Hanak V, Decker PA (September 2006). Complex sleep apnea syndrome: is it a unique clinical syndrome?. Sleep 29 (9): 1203–9.
  3. Young T, Peppard PE, Gottlieb DJ (May 2002). Epidemiology of obstructive sleep apnea: a population health perspective. American Journal of Respiratory and Critical Care Medicine 165 (9): 1217–39.
  4. Young T, Palta M, Dempsey J, Skatrud J, Weber S, Badr S (April 1993). The occurrence of sleep-disordered breathing among middle-aged adults. The New England Journal of Medicine 328 (17): 1230–5.
  5. Kapur V, Blough DK, Sandblom RE, et al. (September 1999). The medical cost of undiagnosed sleep apnea. Sleep 22 (6): 749–55.
  6. Neill AM, Angus SM, Sajkov D, McEvoy RD (January 1997). Effects of sleep posture on upper airway stability in patients with obstructive sleep apnea. American Journal of Respiratory and Critical Care Medicine 155 (1): 199–204.
  7. (2003). The Study Of The Influence Of Sleep Position On Sleep Apnea.
  8. Loord H, Hultcrantz E (August 2007). Positioner--a method for preventing sleep apnea. Acta Oto-laryngologica 127 (8): 861–8.
  9. 9.0 9.1 Szollosi I, Roebuck T, Thompson B, Naughton MT (August 2006). Lateral sleeping position reduces severity of central sleep apnea / Cheyne-Stokes respiration. Sleep 29 (8): 1045–51.
  10. Morris LG, Kleinberger A, Lee KC, Liberatore LA, Burschtin O (November 2008). Rapid risk stratification for obstructive sleep apnea, based on snoring severity and body mass index. Otolaryngology--Head and Neck Surgery 139 (5): 615–8.
  11. Yan-fang S, Yu-ping W (August 2009). Sleep-disordered breathing: impact on functional outcome of ischemic stroke patients. Sleep Medicine 10 (7): 717–9.
  12. Bixler EO, Vgontzas AN, Lin HM, et al. (November 2008). Blood pressure associated with sleep-disordered breathing in a population sample of children. Hypertension 52 (5): 841–6.
  13. Leung RS (2009). Sleep-disordered breathing: autonomic mechanisms and arrhythmias. Progress in Cardiovascular Diseases 51 (4): 324–38.
  14. Silverberg DS, Iaina A, Oksenberg A (January 2002). Treating obstructive sleep apnea improves essential hypertension and life. American Family Physician 65 (2): 229–36.
  15. Grigg-Damberger M (February 2006). Why a polysomnogram should become part of the diagnostic evaluation of stroke and transient ischemic attack. Journal of Clinical Neurophysiology 23 (1): 21–38.
  16. Yaggi HK, Concato J, Kernan WN, Lichtman JH, Brass LM, Mohsenin V (November 2005). Obstructive sleep apnea as a risk factor for stroke and death. The New England Journal of Medicine 353 (19): 2034–41.
  17. Template:Cite pre release
  18. Kumar R, Birrer BV, Macey PM, et al. (June 2008). Reduced mammillary body volume in patients with obstructive sleep apnea. Neuroscience Letters 438 (3): 330–4.
  19. Kumar R, Birrer BV, Macey PM, et al. (June 2008). Reduced mammillary body volume in patients with obstructive sleep apnea. Neuroscience Letters 438 (3): 330–4.
  20. Henderson-Smart DJ, Steer P (2001). Prophylactic caffeine to prevent postoperative apnea following general anesthesia in preterm infants. Cochrane Database of Systematic Reviews (4): CD000048.
  21. Todd ES, Weinberg SM, Berry-Kravis EM, et al. (January 2006). Facial phenotype in children and young adults with PHOX2B-determined congenital central hypoventilation syndrome: quantitative pattern of dysmorphology. Pediatric Research 59 (1): 39–45.
  22. Chen ML, Turkel SB, Jacobson JR, Keens TG (March 2006). Alcohol use in congenital central hypoventilation syndrome. Pediatric Pulmonology 41 (3): 283–5.
  23. Dernaika T, Tawk M, Nazir S, Younis W, Kinasewitz GT (July 2007). The significance and outcome of continuous positive airway pressure-related central sleep apnea during split-night sleep studies. Chest 132 (1): 81–7.
  24. Thomas RJ (March 2005). Effect of added dead space to positive airway pressure for treatment of complex sleep-disordered breathing. Sleep Medicine 6 (2): 177–8.
  25. 25.0 25.1 How Is Sleep Apnea Treated?. National Heart, Lung, and Blood Institute.
  26. Machado MA, Juliano L, Taga M, de Carvalho LB, do Prado LB, do Prado GF (December 2007). Titratable mandibular repositioner appliances for obstructive sleep apnea syndrome: are they an option?. Sleep & Breathing 11 (4): 225–31.
  27. Chan A, Lee R, Cistulli PA. Oral Appliances for Obstructive Sleep Apnea [Review]. Chest (In Press). 2007 Aug; 132(2):693-9
  28. White DP, Zwillich CW, Pickett CK, Douglas NJ, Findley LJ, Weil JV (October 1982). Central sleep apnea: Improvement with acetazolamide therapy. Archives of Internal Medicine 142 (10): 1816–9.
  29. 29.0 29.1 Sleep Apnea. Diagnosis Dictionary. Psychology Today.
  30. Mayos M, Hernández Plaza L, Farré A, Mota S, Sanchis J (February 2001). [The effect of nocturnal oxygen therapy in patients with sleep apnea syndrome and chronic airflow limitation]. Archivos de Bronconeumología 37 (2): 65–8.
  31. Breitenbücher A, Keller-Wossidlo H, Keller R (November 1989). [Transtracheal oxygen therapy in obstructive sleep apnea syndrome]. Schweizerische Medizinische Wochenschrift 119 (46): 1638–41.
  32. Puhan MA, Suarez A, Lo Cascio C, Zahn A, Heitz M, Braendli O (February 2006). Didgeridoo playing as alternative treatment for obstructive sleep apnoea syndrome: randomised controlled trial. BMJ 332 (7536): 266–70.
  33. 33.0 33.1 Ojay, Alise About Singing for Snorers.Template:Self-published inline
  34. Ojay A, Ernst E (September 2000). Can singing exercises reduce snoring? A pilot study. Complementary Therapies in Medicine 8 (3): 151–6.
  35. Snoring remedy user trial. Which?.
  36. inline
  37. inline
  38. Singing for Snorers. The Snoring & Sleep Apnoea Discussion Forums. British Snoring & Sleep Apnoea Association.Template:Self-published inline
  39. Patent Application 20100015261. URL accessed on 24 February 2010.
  40. Hsu AA, Lo C (December 2003). Continuous positive airway pressure therapy in sleep apnoea. Respirology 8 (4): 447–54.
  41. Li KK, Riley RW, Powell NB, Troell R, Guilleminault C (November 1999). Overview of phase II surgery for obstructive sleep apnea syndrome. Ear, Nose, & Throat Journal 78 (11): 851, 854–7.
  42. Prinsell JR (November 2002). Maxillomandibular advancement surgery for obstructive sleep apnea syndrome. Journal of the American Dental Association 133 (11): 1489–97; quiz 1539–40.
  43. 43.0 43.1 43.2 43.3 Lye KW, Waite PD, Meara D, Wang D (May 2008). Quality of life evaluation of maxillomandibular advancement surgery for treatment of obstructive sleep apnea. Journal of Oral and Maxillofacial Surgery 66 (5): 968–72.
  44. Li KK, Powell NB, Riley RW, Troell RJ, Guilleminault C (2000). Long-Term Results of Maxillomandibular Advancement Surgery. Sleep & Breathing 4 (3): 137–140.
  45. (2003) Sleep Apnea-The Phantom of the Night: Overcome Sleep Apnea Syndrome and Win Your Hidden Struggle to Breathe, Sleep, and Live, New Technology Publishing.Template:Pn

General references

  • Kalra M, Chakraborty R (March 2007). Genetic susceptibility to obstructive sleep apnea in the obese child. Sleep Medicine 8 (2): 169–75.
  • (August 1999) Sleep-related breathing disorders in adults: recommendations for syndrome definition and measurement techniques in clinical research. The Report of an American Academy of Sleep Medicine Task Force. Sleep 22 (5): 667–89.
  • Bell RB, Turvey TA (March 2001). Skeletal advancement for the treatment of obstructive sleep apnea in children. The Cleft Palate-craniofacial Journal 38 (2): 147–54.
  • Caples SM, Gami AS, Somers VK (February 2005). Obstructive sleep apnea. Annals of Internal Medicine 142 (3): 187–97.
  • Cohen MM, Kreiborg S (September 1992). Upper and lower airway compromise in the Apert syndrome. American Journal of Medical Genetics 44 (1): 90–3.
  • de Miguel-Díez J, Villa-Asensi JR, Alvarez-Sala JL (December 2003). Prevalence of sleep-disordered breathing in children with Down syndrome: polygraphic findings in 108 children. Sleep 26 (8): 1006–9.
  • Mathur R, Douglas NJ (September 1994). Relation between sudden infant death syndrome and adult sleep apnoea/hypopnoea syndrome. Lancet 344 (8925): 819–20.
  • Mortimore IL, Douglas NJ (September 1997). Palatal muscle EMG response to negative pressure in awake sleep apneic and control subjects. American Journal of Respiratory and Critical Care Medicine 156 (3 Pt 1): 867–73.
  • Perkins JA, Sie KC, Milczuk H, Richardson MA (March 1997). Airway management in children with craniofacial anomalies. The Cleft Palate-craniofacial Journal 34 (2): 135–40.
  • Sculerati N, Gottlieb MD, Zimbler MS, Chibbaro PD, McCarthy JG (December 1998). Airway management in children with major craniofacial anomalies. The Laryngoscope 108 (12): 1806–12.
  • Shepard JW, Thawley SE (May 1990). Localization of upper airway collapse during sleep in patients with obstructive sleep apnea. The American Review of Respiratory Disease 141 (5 Pt 1): 1350–5.
  • Sher AE (August 1990). Obstructive sleep apnea syndrome: a complex disorder of the upper airway. Otolaryngologic Clinics of North America 23 (4): 593–608.
  • Shott SR, Amin R, Chini B, Heubi C, Hotze S, Akers R (April 2006). Obstructive sleep apnea: Should all children with Down syndrome be tested?. Archives of Otolaryngology--Head & Neck Surgery 132 (4): 432–6.
  • Shouldice RB, O'Brien LM, O'Brien C, de Chazal P, Gozal D, Heneghan C (June 2004). Detection of obstructive sleep apnea in pediatric subjects using surface lead electrocardiogram features. Sleep 27 (4): 784–92.
  • (2001) "Disordered Breathing" Cecil essentials of medicine, 210–211, Philadelphia: W.B. Saunders.
  • Strollo PJ, Rogers RM (January 1996). Obstructive sleep apnea. The New England Journal of Medicine 334 (2): 99–104.
  • Sullivan CE, Issa FG, Berthon-Jones M, Eves L (April 1981). Reversal of obstructive sleep apnoea by continuous positive airway pressure applied through the nares. Lancet 1 (8225): 862–5.

External links

  1. REDIRECT Template:CNS diseases of the nervous system

This page uses Creative Commons Licensed content from Wikipedia (view authors).
This page uses Creative Commons Licensed content from Wikipedia (view authors).