Overview
Obstructive sleep apnea is caused by repeated collapse of the upper airway during sleep, which often leads to a decrease in oxygen saturation and disrupts sleep, with clinical manifestations including snoring, apnea and somnolence.
The incidence of the disease is on the rise, and its pathogenesis varies. Predisposing factors include narrowing of the upper airway, unstable respiratory control, low arousal threshold, small lung volume and dysfunction of the upper airway dilator muscle. Risk factors include obesity, masculinity, age, menopause, fluid retention, tonsillar adenoid hypertrophy, and smoking.
Obstructive sleep apnea may lead to drowsiness, airway obstruction, and systemic hypertension. It may also be associated with myocardial infarction, congestive heart failure, stroke and diabetes mellitus. Continuous positive airway pressure ventilation is the treatment of choice for obstructive sleep apnea, with an adherence rate of approximately 60-70%. Bi-level positive airway pressure ventilation or matched servo-ventilation can be used in patients who cannot tolerate continuous positive airway pressure ventilation. Other treatments include oral correction, surgery, and weight loss.
Background
Obstructive sleep apnea is a common disorder due to repeated pharyngeal collapse during sleep. Pharyngeal collapse may be complete (causing apnea) or partial (resulting in hypoventilation). Obstructive sleep apnea interferes with gas exchange, leading to decreased oxygen saturation, hypercapnia and sleep disruption, and may cause serious consequences such as cardiovascular, metabolic and cognitive dysfunction.
The current epidemic of obesity has led to a rising trend in the number of people with a tendency to pharyngeal collapse as well as obstructive sleep apnea. Several existing treatments often result in poor tolerance or only partial relief of symptoms. Therefore, there is a need to improve existing treatments and develop new ones (or combinations of them).
In 1993 Wisconsin et al. conducted a landmark cohort study to examine the prevalence of obstructive sleep apnea. reported that obstructive sleep apnea is commonly defined as >5 pauses per hour of sleep, or hypoventilation during sleep and excessive daytime sleepiness.
The prevalence in middle age (30-60 years) is 4% in men and 2% in women. Subsequent studies have shown that the prevalence in high-income countries is higher than this, at 10% for women and 20% for men, possibly as a result of malignant obesity and technological developments. However, obstructive sleep apnea is a global health problem, and the same problem exists in Brazil and some Asian countries.
Diagnosis and definition
Clinical manifestations of obstructive sleep apnea include snoring, visible apnea, awakening due to asphyxia and excessive sleepiness. Other common symptoms include non-restorative sleep, difficulty entering or maintaining sleep, fatigue or tiredness and morning headache. Rubrics include family history of disease, physical obstructive sleep apnea (e.g., narrow oropharyngeal airway), and obesity (e.g., large neck circumference).
The best way to detect obstructive sleep apnea is to perform a full night test in the laboratory using polysomnography, the main measure of which is the apnea hypoventilation index (number of sleep apnea per hour plus hypoventilation). This method allows simultaneous monitoring of sleep and breathing.
The sleep-wake state is monitored by EEG, right and left electrooculogram and electromyography recordings. Respiratory recordings include: monitoring of respiratory function (using respiratory induction volume tracing with tracing strips placed on the chest and abdomen); monitoring of airflow via nasal air pressure and thermal airflow sensors; and arterial oxygen saturation monitoring.
Because many patients have location-specific obstructive sleep apnea, physical activity may sometimes alter the patient’s sleep stage, breathing, and physical status, and this can usually be assessed using anterior tibial muscle EMG.
Differences in the current definition of hypoventilation may lead to discrepancies between the apnea hypoventilation indices measured between laboratories. Ruehland et al. found that the sleep apnea hypoventilation index could be derived using three different criteria, with results of 25.1, 8.3, or 14.9, respectively.
The criteria for defining apnea also vary around the world, but are based on a consensus on the subject. Differences in definitions can have implications for patients (e.g., reported severity can affect a patient’s eligibility for government-funded treatment) and for the interpretation of study results.
While standardization of definitions may improve the consistency and reproducibility of studies, fixed definitions of the apnea hypoventilation index may also have limitations. Obstructive sleep apnea affects different systems and organs differently, so a fixed definition is unlikely to predict all negative outcomes.
For example, different parts of the polysomnogram are the best predictors of different consequences of obstructive sleep apnea (e.g., a 4% or more decrease in pulse oximetry predicts hypertension, a 2% unsaturation predicts fasting hyperglycemia, wake frequency predicts memory integration, etc.).
Thus, different definitions of hypoventilation can also predict different consequences of obstructive sleep apnea. Nasal pressure testing is a recent addition to polysomnography. Nasal pressure detection of hypoventilation is more sensitive than thermistor, so the reported apnea hypoventilation index (or range of normal values) may also increase. Therefore, physicians should be aware that subtle differences in definition criteria between laboratories may have a significant impact on the study-reported apnea hypoventilation index.
Although polysomnography can often confirm the diagnosis of obstructive sleep apnea, the procedure is cumbersome, expensive, and time-consuming. As a result, a growing number of studies point to home diagnosis and treatment. Randomized controlled trials have shown that home-based diagnosis and treatment for some patients is no less effective than laboratory-based treatment.
However, the major relevant studies have excluded patients with underlying complexities (e.g., with pulmonary disease, heart failure, or neuromuscular disease), emphasizing that home-based diagnosis and treatment is not applicable to all patients. For some patients with obstructive sleep apnea, a well-designed home course can provide timely and cost-effective management of the patient. A number of ongoing studies focusing on clinical outcomes will also help to develop optimal management of obstructive sleep apnea.
Pathophysiology and risk factors
It is commonly believed that obstructive sleep apnea is primarily caused by anatomical problems in the upper airway, where craniofacial structures or body fat make the lumen of the pharyngeal airway smaller, leading to an increased likelihood of pharyngeal collapse.
In the awake state, the highly active upper airway dilator muscles keep the airway open, but during sleep the muscle activity decreases, making the airway prone to collapse. In addition to this, there are several other factors that may trigger obstructive sleep apnea. The importance of these non-anatomic and non-neuromuscular factors is that obstructive sleep apnea can still develop in patients with normal upper airway anatomy and normal sensitivity or activity of the upper airway dilator muscles.
1. Respiratory control system
The stability of the respiratory control system is an important variable. When the central respiratory output is abnormal, the activity of the upper airway dilator muscle changes accordingly. Low central respiratory control system drive causes reduced activity of upper airway dilator muscles, elevated airway resistance, and easy to cause airway collapse. Therefore, unstable respiratory control may be a causative factor for some patients with obstructive sleep apnea.
2.Tendency to wake up from sleep
Another potentially important factor is the tendency to wake up from sleep (wakefulness threshold). Upon awakening, most people will experience a brief period of forceful breathing, which will result in central apnea if the CO2 concentration in the blood is below the apnea chemical threshold due to hyperventilation.
In the case of mild hypocapnia, the respiratory drive drops to slightly below the normal level of breathing during the sleep state. Hypocapnia decreases upper airway dilator muscle activity and may lead to airway collapse. Apnea and arousal events are usually significantly associated with hyperventilation, as a large increase in respiratory drive can cause hypocapnia in some patients. ,.
Individuals with low arousal thresholds may also have elevated respiratory drive before the dilator muscle reopens the airway. If the upper airway muscles are fully responsive to airway stimulation to stabilize airflow prior to arousal, the use of non-muscle relaxant sedatives to delay arousal may be helpful. The reason this approach is necessary is that sedation may prolong respiratory events in some patients (those who are unable to reopen their airway without awakening).
3. Lung volume
Lung volume may also be a causative factor. In animals and humans, the cross-sectional area of the upper airway increases when lung volume increases (natural or passive increase in functional residual air volume). Conversely, when lung volume decreases, it is more likely to cause airway narrowing and collapse.
Because the upper and lower airways are mechanically connected, increased lung volume or mediastinal distraction can lead to dilatation of the pharyngeal airway. Increasing lung volume also stabilizes the respiratory control system by increasing 02 and C02 reserves and buffering blood gases by altering ventilation.
The sleep-related collapse in obstructive sleep apnea may be related to the decrease in functional residual air volume between sleep and wakefulness in individuals of normal weight. However, functional residual air volume tends to decrease to pulmonary residual air volume levels in obese individuals even when they are even awake, especially in the supine position. Therefore, it remains unclear whether there is a further decrease in lung volume between wakefulness and sleep in obese patients with obstructive sleep apnea.
4. Upper airway anatomy or muscle function
Any factor that causes damage to the anatomy or muscle function of the upper airway, such as dysfunction of the upper airway dilator muscles, predisposes to obstructive sleep apnea. The largest airway dilator muscle most commonly studied is the lingual muscle, which makes up the majority of the tongue. Adequate contractility of the lingual muscles is necessary to keep the upper airway open during sleep. Fatigue, nerve damage and myopathy may lead to dysfunction of the lingual muscles thereby triggering obstructive sleep apnea. Pharyngeal sensory deficits may also lead to collapse of the upper airway.
5.Fluid retention
Fluid retention and the movement of body fluids from the lower extremities to the neck at night can also have an effect on airway mechanics. Excess extracellular fluid can produce edema, causing heart failure, end-stage renal disease, and hypertension. Redistribution of fluid by diuretics or mechanical methods of treatment may improve obstructive sleep apnea. Fluid retention may narrow the lumen of the pharyngeal airway and may be a therapeutic target for some patients.
6, male and obesity
Men and obesity are the main risk factors for obstructive sleep apnea. Obesity may directly affect the anatomical structure of the upper airway, such as fat deposition. mri studies show that fat deposition in the tongue may weaken the function of the chin tongue muscle and increase the possibility of airway collapse. Obesity may also increase the risk of obstructive sleep apnea by affecting lung volume and thus the stability of respiratory control.
The reasons for men’s susceptibility to obstructive sleep apnea are not known. Men are more likely to be centripetal obese than women, and this pattern may lead to more fat accumulation in the upper airway structures. Anatomical studies have shown that the pharyngeal airway cross-sectional area is similar to or larger in men than in women, suggesting that differences in fat deposition may not significantly affect airway anatomy. Several studies have shown that men have longer airways than women and are not dependent on height, which may explain why men are more prone to airway collapse.
Passive pharyngeal airway collapse pressure may provide an overall measure of upper airway anatomy and its interactions, but not neuromuscular reflexes. For a given body mass index, passive pharyngeal airway collapse pressure is generally higher in men than in women, indicating that men experience more pharyngeal collapse than women.
Women responded better than men to respiratory load (e.g., higher ventilation per minute during inspiration). Finally, centripetal fat distribution in men is more likely to cause a reduction in lung volume when body mass index is certain.
7. Age
Age is another important risk factor. Older adults have reduced lung capacity and therefore upper airway volume, due to loss of elasticity in the lungs. And they are also more likely to develop airway collapse due to their poorer quality of sleep, which causes collagen deficiency or a lower excitation threshold. Finally, the function of the upper airway dilator muscle decreases with age.
8.Other
Other risk factors for obstructive sleep apnea include genetic factors and ethnic characteristics that affect craniofacial anatomy, obesity, and possibly lung volume.
Menopause (not dependent on age and body mass index) is also a risk factor. Menopause may be associated with a redistribution of body fat to central areas and a decrease in muscle function (increased fat percentage).
Smoking is also frequently associated with obstructive sleep apnea. The exact mechanism of this association is unknown and may include increased upper respiratory infections, nasal congestion, decreased respiratory sensitivity, lowered arousal thresholds, or frequent awakenings due to inability to fall asleep.
A more comprehensive understanding of obstructive sleep apnea, its risk factors, and pathogenesis will likely lead to new approaches to treat or prevent the disorder.
Clinical outcomes
Randomized trials have shown that obstructive sleep apnea causes drowsiness and that continuous positive airway pressure ventilation significantly improves its symptoms. People with obstructive sleep apnea have up to a 7-fold higher incidence of accidents compared to those without the disease. The risk of accidents is reduced in some patients after treatment. Obstructive sleep apnea affects quality of life, and continuous positive airway pressure ventilation improves the health status of patients, especially those with collapsed airways.
1. Systemic hypertension
Obstructive sleep apnea can lead to systemic hypertension. Animal studies have shown that induction produces sleep apnea, systemic blood pressure increases, and blood pressure decreases after apnea relief.
Large cross-sectional and longitudinal epidemiological randomized trials have shown that treatment of obstructive sleep apnea can reduce systemic blood pressure. Continuous positive airway pressure (CPAP) ventilation lowers blood pressure, although to a lesser extent than antihypertensive medication, by 2-3 mm Hg. In addition to hypertension, continuous positive airway pressure ventilation also resulted in an improvement in patient symptoms. The results of the meta-analysis identified predictors of improved blood pressure with continuous positive airway pressure ventilation, including collapse, younger age, baseline blood pressure (a large decrease in blood pressure in hypertensive patients), daytime sleepiness (a large decrease in blood pressure in sleepy patients), and severe obstructive sleep apnea.
Proponents of the central regulation of blood pressure theory argue that if continuous positive airway pressure ventilation only reduces vasoconstricted blood, it is unlikely to cause large changes in blood pressure and that various feedback regulatory mechanisms (e.g., pressure-sensing reflexes) will maintain blood pressure stability, at least in the short term.
However, some patients do experience significant improvement in blood pressure after the administration of continuous positive airway pressure ventilation, and the nocturnal blood pressure fluctuations associated with obstructive sleep apnea are reduced. The association between obstructive sleep apnea and hypertension is still controversial. Some studies have shown that the association is attenuated when covariates are fully considered.
2. Severe cardiovascular events
The association between severe cardiovascular events and obstructive sleep apnea has also not been confirmed. a prospective observational cohort study by Marin et al. showed that untreated severe obstructive sleep apnea led to a significant increase in the incidence of fatal and nonfatal cardiovascular events.
Although the results are consistent with the hypothesis that cardiovascular events are prevented by treating obstructive sleep apnea, it is also possible that this is caused by treatment bias. That is, patients who adhere to continuous positive airway pressure ventilation may also be proactive in adhering to diet and exercise, and medication.
Other epidemiological studies have found that obstructive sleep apnea is associated with myocardial infarction, congestive heart failure, and stroke. Subgroup analyses have shown that obstructive sleep apnea has a greater impact on cardiovascular events in younger men compared to older men. However, asymptomatic patients often fail to adhere to treatment, so there has not been much progress in terms of randomized trials. Some observational studies have evaluated the impact of obstructive sleep apnea on overall mortality and cancer risk, but large randomized controlled clinical trials are needed to reach definitive conclusions.
In patients with heart failure, continuous positive airway pressure ventilation improves cardiac function. However, there are no clear data showing that continuous positive airway pressure ventilation prevents myocardial infarction, congestive heart failure, or stroke, and studies in high-risk patients are still needed to confirm whether obstructive sleep apnea may increase the odds of cardiovascular events. Evaluation of alternative outcome methods or biological markers is also important.
3. Diabetes mellitus
Obstructive sleep apnea is associated with diabetes mellitus. Foster et al. found that 87% of obese type 2 diabetic patients had clinically significant obstructive sleep apnea. Although obesity is a common risk factor for obstructive sleep apnea and diabetes, but the relationship between the two may only be relevant.
Diabetes can cause neuromyopathy, which in turn may impair upper airway reflexes and increase the likelihood of obstructive sleep apnea. However, there is little data to support this point. In addition, because obstructive apnea promotes feedback-regulated hormone release, this group of diabetic patients may have worse than expected glycemic control if they are not treated promptly. However, most data show that even in patients treated for obstructive sleep apnea, their glycemic control is not greatly improved. This finding may be related to adherence to continuous positive airway pressure ventilation.
A study from India showed that adherence to continuous positive airway pressure ventilation improved metabolic symptoms. In addition, since the standard of care for type 2 diabetes requires good glycemic control, it is unlikely that continuous positive airway pressure ventilation would result in gains beyond the standard.
Obstructive sleep apnea and obesity and their role with glucose regulation can be quite complex. Obstructive sleep apnea and diabetes can affect vascular function through different pathways, so treating obstructive sleep apnea may improve vascular-related outcomes in patients with diabetes. Standard therapeutic targets for diabetes, such as hypercholesterolemia, blood pressure and glucose control, are well exploited, thus suggesting that new targets are needed to treat diabetes. Studies are currently evaluating the effects of continuous positive airway pressure ventilation in diabetic patients.
Patients with symptoms will benefit from continuous positive airway pressure ventilation. Patients with poor compliance will not have a significant benefit. It is difficult to conduct a randomized controlled trial of continuous positive airway pressure ventilation because of ethical and procedural issues, but it is feasible to conduct studies on treatment options (e.g., continuous positive airway pressure ventilation vs. orthodontic appliances). However, the identification of the population with the greatest benefit from continuous positive airway pressure ventilation (or a combination of treatment options) still needs to be improved to obtain definitive data.
Treatment advances
1. Continuous positive airway pressure (CPAP) ventilation
Continuous positive airway pressure (CPAP) ventilation is the treatment of choice for adults with obstructive sleep apnea and was first reported in 1981 as an effective means of preventing collapse of the pharyngeal airway. The mechanism of continuous positive airway pressure ventilation remains controversial and may involve the maintenance of positive pharyngeal transmural pressure, thereby allowing intraluminal pressure to exceed the surrounding pressure.
Continuous positive airway pressure ventilation may also increase end-expiratory lung volume and bring the upper airway to a steady state by traction. Possible symptom relief measures and cardiovascular protection should be discussed in detail with the patient prior to the administration of continuous positive airway pressure ventilation.
Continuous positive airway pressure ventilation can benefit some patients, with compliance rates of approximately 60-70%, similar to those of patients with asthma on inhalation therapy, patients with epilepsy on anticonvulsants, and patients with diabetes maintaining good glycemic control. Its effect on neurocognitive and cardiovascular sequelae is also highly cost-effective.
Patients with severe snoring, severe sleep apnea, and excessive daytime sleepiness are more likely to adhere to long-term therapy. Short-term treatment and observable early benefit are the best predictors of long-term outcomes, so it is best to take steps to optimize adherence before or soon after treatment initiation. Management of patients who have difficulty adhering to continuous positive airway pressure ventilation should be managed with the following in mind.
First, several studies have shown that patients can benefit from intensive supportive therapy. Providing education and support can improve patient adherence: making patients aware of the benefits of treatment and helping them to solve their problems can lead to a more positive response.
Secondly, some patients have nasal disease that limits their tolerance of continuous positive airway pressure ventilation via the nose. Nasal decongestants, heating, and moistening may benefit such patients. In rare cases, nasal surgery may also improve patient compliance.
Third, although randomized trials have not shown which type of breathing mask is better,, some patients prefer a complete breathing mask, while others prefer a nasal pillow mask.
Fourth, some patients who experience insomnia or frequent awakenings while using continuous positive airway pressure ventilation may respond to hypnotherapy. Some data support the administration of dextrozopiclone to patients who are initiated on continuous positive airway pressure ventilation. Our clinical experience suggests that complete sleep (stable, avoiding sleep interruptions) helps to enhance patient compliance. Once patients become accustomed to the new device, continued use of hypnotherapy is no longer necessary.
In addition, sedation should be used with caution in patients with obstructive sleep apnea.
There are several options available for patients who have failed to respond to continuous positive airway pressure ventilation. For example, bi-level positive airway pressure ventilation, although randomized trials have shown no greater benefit than continuous positive airway pressure ventilation, may be preferred in some patients with expiratory distress.
Airway pressure relief ventilation may also improve symptoms of respiratory distress in some patients, such as C-Flex or EPR, and most data suggest that this approach is not significantly different from standard continuous positive airway pressure ventilation.
Self-regulating positive airway pressure ventilation can be used to vary the pressure to maintain stable ventilation. Some patients who require the use of different external pressures (e.g., changes based on body position or sleep stage) may benefit from this by lowering the external pressure at the appropriate time. Most randomized trials have also shown that adherence to auto-adjustment ventilation also does not provide a significant improvement over standard continuous positive airway pressure ventilation, and even some data suggest that auto-adjustment positive airway pressure ventilation has poorer outcomes and may lead to arousal and hemodynamic instability because of altered intrathoracic pressures.
Thus, there is not sufficient evidence to support that the use of new technologies improves patient compliance, but their clinical benefit does occasionally become visible.
2. Oral appliances and surgery
Alternative treatments for those with failed positive airway pressure ventilation include: oral appliances, upper airway surgery, positioning therapy, and other conservative measures. Different oral appliances work in different ways, but the general mechanism is to apply pressure to the jaw to prevent tongue collapse. For some patients, especially those with mild to moderate obstructive sleep apnea, oral appliances are the best option for their continuous positive airway pressure ventilation.
However, the efficacy of the oral appliance is uncertain, and there are few data on the outcome of continuous positive airway pressure ventilation. The device also requires multiple visits to the dentist to make gradual adjustments, and the results can only be judged after 6-9 months. Although the cost of the device and repeated visits can be expensive, this approach may be economically beneficial if it is successful in treating obstructive sleep apnea.
Some simple soft palate procedures (sleep correction, laser-assisted uvulopalatopharyngoplasty, etc.) may also be used as alternative treatments, but are less useful in improving symptoms. Less than 50% of patients have significant improvement in apnea hypoventilation index after uvulopalatopharyngoplasty, so many physicians do not recommend this procedure.
However, some investigators have recommended surgical treatment because it avoids patient compliance problems. More complex surgical treatments, such as maxillary mandibular advancement – may be more effective than simple surgery, but many patients with obstructive sleep apnea would prefer to avoid major surgery.
Tracheotomy can eliminate obstructive sleep apnea, but it greatly reduces quality of life. There are few studies to predict which patients will benefit from specific procedures. Although some relevant studies are underway, definitive data are still not available. Therefore, further research is needed to determine the best treatment options for obstructive sleep apnea.
3. Conservative treatment
Patients may benefit from conservative treatment. For example, sedatives, including substances such as alcohol that may aggravate symptoms, should be avoided; sleeping 7-8 hours at night may reduce drowsiness; and avoiding supine positions may also help improve apnea caused by sleeping positions.
Because it is difficult to monitor sleep position therapy performed at home, its clinical outcomes are inconsistent. Sleep position therapy can also be used as an adjunct in combination with other methods if the patient does not respond well to oral appliances or surgical treatment.
Diet and exercise for weight loss can also be helpful in relieving symptoms. Few patients achieve sustained weight loss over time, so patient education and support may be helpful.
There are data showing that patients gain weight after continuous positive airway pressure ventilation, so the need for diet control and exercise should be emphasized in all patients. Epidemiological data suggest that exercise has benefits beyond weight loss for patients with obstructive sleep apnea, but the mechanism of improvement is not yet clear. Similarly, neuromuscular exercise can benefit some patients, but the mechanism is not clear.
Even with continuous positive airway pressure ventilation, some patients remain drowsy, which may be related to the irreversible consequences of apnea. Efforts should be made to improve compliance and sleep management in this group of patients. Results of randomized trials have shown that stimulants such as modafinil have an ameliorating effect on residual drowsiness in patients who adhere to continuous positive airway pressure ventilation. Therefore, patient education is important, and stimulants can be used as adjunctive therapy to improve drowsiness, but not for apnea, where adherence to continuous positive airway pressure ventilation is necessary.
Central apnea, also known as complex apnea, occurs in approximately 10% of patients who are treated with continuous positive airway pressure ventilation as initial therapy. The mechanism is unclear. Most studies have shown that these patients with central apnea resolve on their own with continuous positive airway pressure ventilation.
Even so, some researchers advocate the use of new devices, such as adaptive servo-ventilation, to treat this type of apnea. If the patient’s symptoms resolve spontaneously over time, it may not be reasonable to use an expensive new device. Conversely, if a patient’s first experience with continuous positive airway pressure ventilation is unpleasant (central apnea is likely to be recurrent), compliance with subsequent long-term adherence to treatment may be poor. Therefore, early intervention in patients with central apnea may improve their long-term compliance with continuous positive airway pressure ventilation.
Prevention
Patients may benefit from avoiding risk factors for obstructive sleep apnea, losing weight (diet control and exercise), quitting smoking, abstaining from alcohol, and avoiding some other muscle relaxant medications.
Randomized controlled trials have shown that a 10 kg reduction in body weight can reduce the apnea hypoventilation index by about 5 events/hour, and that 63% of patients with mild disease experience relief, while only 13% of patients with severe obstructive sleep apnea experience relief.
Although bariatric surgery is highly effective in reducing weight, it does not necessarily eliminate apnea in the long term. Studies have shown that obstructive sleep apnea symptoms can persist or recur after surgical or non-surgical weight loss.
Outlook
Because the etiology of obstructive sleep apnea varies from patient to patient, future treatment for obstructive sleep apnea may have different options for the etiology.
For patients with a low wakefulness threshold, sedative or hypnotic medications may be used. For patients with unstable ventilatory control, oxygen or acetazolamide may improve their symptoms. For patients with anatomical abnormalities at the level of the pharyngeal palate, epiglottic surgery may help to resolve the problem. And for those with upper airway muscle dysfunction, sublingual nerve stimulation, muscle training, or increasing sublingual nerve output may be effective.
Obstructive sleep apnea is a multifactorial disorder, thus necessitating combination therapy. New treatment options should be geared toward further research into disease mechanisms. The ultimate goal is to develop new drugs that can be used to prevent the onset of apnea, alleviate its symptoms, and reduce the clinical consequences.