In patients who are at high likelihood of having OSA, a randomized controlled trial found that home oximetry (a non-invasive method of monitoring blood oxygenation) may be adequate and easier to obtain than formal polysomnography. High probability patients were identified by an Epworth Sleepiness Scale (ESS) score of 10 or greater and a Sleep Apnea Clinical Score (SACS) of 15 or greater. Home oximetry, however, does not measure apneic events or respiratory event-related arousals and thus does not produce an AHI value.

Polysomnograms can be used to help diagnose UARS. Patient who have UARS typically show multiple EEG arousals during the sleep study and little to no polygraphic evidence of obstructive sleep apnea or decreased levels of oxygen. UARS arousals, or respiratory-effort related arousals, typically last for one to three breaths. These arousals may be due to snoring, but patients do not need to snore in order to have UARS. Polysomnogram patterns must exhibit no evidence of apneas or hypopneas in order to be lead to a diagnosis of UARS. Even with polysomnography, diagnosis of UARS may be difficult because of insufficient means of measuring changes in airflow. This lack of sensitivity in detection may lead to misdiagnosis, as minor undetectable changes in airflow may still be responsible for the arousals. In order to definitively diagnose UARS, there must be a demonstrated pattern of greater negative esophageal pressures which are then followed by a rapid change to a more positive level with a sleep arousal. This can be confirmed with invasive polysomnography that uses an esophageal balloon transducer and full pneumotachograph.

Based on symptoms, patients are commonly misdiagnosed with chronic fatigue syndrome, fibromyalgia, or a psychiatric disorder such as ADHD or depression.

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 only recommended when requested by a physician and should not be used to test those without symptoms. Home oximetry may be effective in guiding prescription for automatically self-adjusting continuous positive airway pressure.

Polysomnography in diagnosing OSA characterizes the pauses in breathing. As in central apnea, pauses are followed by a relative decrease in blood oxygen and an increase in the blood carbon dioxide. Whereas in central sleep apnea the body's motions of breathing stop, in OSA the chest not only continues to make the movements of inhalation, but the movements typically become even more pronounced. Monitors for airflow at the nose and mouth demonstrate that efforts to breathe are not only present but that they are often exaggerated. The chest muscles and diaphragm contract and the entire body may thrash and struggle.

An "event" can be either an apnea, characterised by complete cessation of airflow for at least 10 seconds, or a hypopnea in which airflow decreases by 50 percent for 10 seconds or decreases by 30 percent if there is an associated decrease in the oxygen saturation or an arousal from sleep. To grade the severity of sleep apnea, the number of events per hour is reported as the apnea-hypopnea index (AHI). An AHI of less than 5 is considered normal. An AHI of 5-15 is mild; 15-30 is moderate and more than 30 events per hour characterizes severe sleep apnea.

Nasal steroids may be prescribed in order to ease nasal allergies and other obstructive nasal conditions that could cause UARS.

Among the natural remedies are exercises to increase the muscle tone of the upper airway, and one medical practitioner noting anecdotally that professional singers seldom snore, but there have been no medical studies to fully link the two.

Excess body weight is thought to be an important cause of sleep apnea. In weight loss studies of obese and overweight individuals, those who lose weight show reduced apnea frequencies and improved Apnoea–Hypopnoea Index (AHI) compared to controls.

An open label non-randomized study in 30 patients found benefit from pseudoephedrine, domperidone, and the combination in the treatment of severe snoring.

One treatment for obstructive hypopnea is continuous positive airway pressure (CPAP). CPAP is a treatment in which the patient wears a mask over the nose and/or mouth. An air blower forces air through the upper airway. The air pressure is adjusted so that it is just enough to maintain the oxygen saturation levels in the blood. Another treatment is sometimes a custom fitted oral appliance. The American Academy of Sleep Medicine's protocol for obstructive sleep apnea (OSA) recommends oral appliances for those who prefer them to CPAP and have mild to moderate sleep apnea or those that do not respond to/cannot wear a CPAP. Severe cases of OSA may be treated with an oral appliance if the patient has had a trial run with a CPAP. Oral Appliances should be custom made by a dentist with training in dental sleep medicine. Mild obstructive hypopnea can often be treated by losing weight or by avoiding sleeping on one's back. Also quitting smoking, and avoiding alcohol, sedatives and hypnotics (soporifics) before sleep can be quite effective. Surgery is generally a last resort in hypopnea treatment, but is a site-specific option for the upper airway. Depending on the cause of obstruction, surgery may focus on the soft palate, the uvula, tonsils, adenoids or the tongue. There are also more complex surgeries that are performed with the adjustment of other bone structures - the mouth, nose and facial bones.

People with neuromuscular disorders or hypoventilation syndromes involving failed respiratory drive experience central hypoventilation. The most common treatment for this form is the use of non-invasive ventilation such as a BPAP machine.

The most effective diagnostic strategy is to perform laryngoscopy during an episode, at which time abnormal movement of the cords, if present, can be observed. If the endoscopy is not performed during an episode, it is likely that the vocal folds will be moving normally, a 'false negative' finding.

Spirometry may also be useful to establish the diagnosis of VCD when performed during a crisis or after a nasal provocation test. With spirometry, just as the expiratory loop may show flattening or concavity when expiration is affected in asthma, so may the Inspiratory loop show truncation or flattening in VCD. Of course, testing may well be negative when symptoms are absent.

The symptoms of VCD are often inaccurately attributed to asthma, which in turn results in the unnecessary and futile intake of corticosteroids, bronchodilators and leukotriene modifiers, although there are instances of comorbidity of asthma and VCD.

The differential diagnosis for vocal cord dysfunction includes vocal fold swelling from allergy, asthma, or some obstruction of the vocal folds or throat. Anyone suspected of this condition should be evaluated and the vocal folds (voice box) visualized. In individuals who experience a persistent difficulty with inhaling, consideration should be given to a neurological cause such as brain stem compression, cerebral palsy, etc.

The main difference between VCD and asthma is the audible stridor or wheezing that occurs at different stages of the breath cycle: VCD usually causes stridor on the inhalation, while asthma results in wheezing during exhalation. Patients with asthma usually respond to the usual medication and see their symptoms resolve. Clinical measures that can be done to differentiate VCD from asthma include:

- rhinolaryngoscopy: A patient with asthma will have normal vocal cord movement, while one with VCD will display vocal cord abduction during inhalation

- spirometry: A change in the measure following the administration of a bronchodilator is suggestive of asthma rather than VCD

- chest radiography: The presence of hyperinflation and peribronchial thickening are indicative of asthma, as patients with VCD will show normal results.

Although "there has been no cure of chronic hypersomnia", there are several treatments that may improve patients' quality of life, depending on the specific cause or causes of hypersomnia that are diagnosed.

The physician will ask some questions about the baby’s health problems and may recommend a flexible laryngoscopy to further evaluate the infant's condition.

Secondary hypersomnias are extremely numerous.

Hypersomnia can be secondary to disorders such as clinical depression, multiple sclerosis, encephalitis, epilepsy, or obesity. Hypersomnia can also be a symptom of other sleep disorders, like sleep apnea. It may occur as an adverse effect of taking certain medications, of withdrawal from some medications, or of drug or alcohol abuse. A genetic predisposition may also be a factor. In some cases it results from a physical problem, such as a tumor, head trauma, or dysfunction of the autonomic or central nervous system.

Sleep apnea is the most frequent cause of secondary hypersomnia, affecting up to 4% of middle-aged adults, mostly men. Upper airway resistance syndrome (UARS) is a clinical variant of sleep apnea that can also cause hypersomnia. Just as other sleep disorders (like narcolepsy) can coexist with sleep apnea, the same is true for UARS. There are many cases of UARS in which EDS persists after CPAP treatment, indicating an additional cause, or causes, of the hypersomnia and requiring further evaluation.

Sleep movement disorders, such as restless legs syndrome (RLS) and periodic limb movement disorder (PLMD or PLMS) can also cause secondary hypersomnia. Although RLS does commonly cause EDS, PLMS does not. There is no evidence that PLMS plays "a role in the etiology of daytime sleepiness. In fact, two studies showed no correlation between PLMS and objective measures of EDS. In addition, EDS in these patients is best treated with psychostimulants and not with dopaminergic agents known to suppress PLMS."

Neuromuscular diseases and spinal cord diseases often lead to sleep disturbances due to respiratory dysfunction causing sleep apnea, and they may also cause insomnia related to pain. "Other sleep alterations, such as periodic limb movement disorders in patients with spinal cord disease, have also been uncovered with the widespread use of polysomnography."

Primary hypersomnia in diabetes, hepatic encephalopathy, and acromegaly is rarely reported, but these medical conditions may also be associated with the secondary hypersomnias sleep apnea and periodic limb movement disorder (PLMD).

Chronic fatigue syndrome and fibromyalgia can also be associated with hypersomnia. Regarding chronic fatigue syndrome, it is "characterized by persistent or relapsing fatigue that does not resolve with sleep or rest. Polysomnography shows reduced sleep efficiency and may include alpha intrusion into sleep EEG. It is likely that a number of cases labeled as chronic fatigue syndrome are unrecognized cases of upper airway resistance syndrome" or other sleep disorders, such as narcolepsy, sleep apnea, PLMD, etc.

Similarly to chronic fatigue syndrome, fibromyalgia also may be associated with anomalous alpha wave activity (typically associated with arousal states) during NREM sleep. Also, researchers have shown that disrupting stage IV sleep consistently in young, healthy subjects causes a significant increase in muscle tenderness similar to that experienced in "neurasthenic musculoskeletal pain syndrome". This pain resolved when the subjects were able to resume their normal sleep patterns.

Chronic kidney disease is commonly associated with sleep symptoms and excessive daytime sleepiness. For those on dialysis, approximately 80% have sleep disturbances. Sleep apnea can occur 10 times as often in uremic patients than in the general population and can affect up to 30-80% of patients on dialysis, though nighttime dialysis can improve this. About 50% of dialysis patients have hypersomnia, as severe kidney disease can cause uremic encephalopathy, increased sleep-inducing cytokines, and impaired sleep efficiency. About 70% of dialysis patients are affected by insomnia, and RLS and PLMD affect 30%, though these may improve after dialysis or kidney transplant.

Most forms of cancer and their therapies can cause fatigue and disturbed sleep, affecting 25-99% of patients and often lasting for years after treatment completion. "Insomnia is common and a predictor of fatigue in cancer patients, and polysomnography demonstrates reduced sleep efficiency, prolonged initial sleep latency, and increased wake time during the night." Paraneoplastic syndromes can also cause insomnia, hypersomnia, and parasomnias.

Autoimmune diseases, especially lupus and rheumatoid arthritis are often associated with hypersomnia, as well. Morvan's syndrome is an example of a more rare autoimmune illness that can also lead to hypersomnia. Celiac disease is another autoimmune disease associated with poor sleep quality (which may lead to hypersomnia), "not only at diagnosis but also during treatment with a gluten-free diet." There are also some case reports of central hypersomnia in celiac disease. And RLS "has been shown to be frequent in celiac disease," presumably due to its associated iron deficiency.

Hypothyroidism and iron deficiency with or without (iron-deficiency anemia) can also cause secondary hypersomnia. Various tests for these disorders are done so they can be treated. Hypersomnia can also develop within months after viral infections such as Whipple's disease, mononucleosis, HIV, and Guillain–Barré syndrome.

Behaviorally induced insufficient sleep syndrome must also be considered in the differential diagnosis of secondary hypersomnia. This disorder occurs in individuals who fail to get sufficient sleep for at least three months. In this case, the patient has chronic sleep deprivation although he or she is not necessarily aware of it. This situation is becoming more prevalent in western society due to the modern demands and expectations placed upon the individual.

Many medications can also lead to secondary hypersomnia. Therefore, a patient's complete medication list should be carefully reviewed for sleepiness or fatigue as side effects. In these cases, careful withdrawal from the possibly offending medication(s) is needed; then, medication substitution can be undertaken.

Mood disorders, like depression, anxiety disorder and bipolar disorder, can also be associated with hypersomnia. The complaint of EDS in these conditions is often associated with poor sleep at night. "In that sense, insomnia and EDS are frequently associated, especially in cases of depression." Hypersomnia in mood disorders seems to be primarily related to "lack of interest and decreased energy inherent in the depressed condition rather than an increase in sleep or REM sleep propensity". In all cases with these mood disorders, the MSLT is normal (not too short and no SOREMPs).

First-generation antihistamine has been suggested as first-line therapy to treat post-nasal drip.

Although this is a congenital lesion, airway sounds typically begin at age 4–6 weeks. Until that age, inspiratory flow rates may not be high enough to generate the sounds. Symptoms typically peak at age 6–8 months and remit by age 2 years.

Late-onset laryngomalacia may be a distinct entity, which can present after age of 2 years

Providers such as pediatricians and dentists can provide information to parents and caregivers about what food and toys are appropriate by age to prevent choking. The American Academy of Pediatricians recommends waiting until 6 months of age before introducing solid foods to infants. Caregivers can supervise children while eating or playing. Also, caregivers can avoid giving children younger than 5 foods that pose a high risk of choking such as hot dog pieces, cheese sticks, cheese chunks, hard candy, nuts, grapes, marshmallows, or popcorn. Parents, teachers, child care providers, and other caregivers for children get training in choking first aid and cardiopulmonary resuscitation (CPR).

In the US, manufacturers of children's toys and products must follow requirements to prevent choking and include appropriate warning labels. However, toys that are resold may not be marked with warning labels. Caregivers can try to prevent choking by considering the features of a toy (such as size, shape, consistency, small parts) before giving it to a child. Children's products that are found to pose a choking risk can be recalled.

The American Heart Association recommends chest thrusts rather than abdominal thrusts for pregnant or obese persons who are choking.

Chest thrusts are performed in a similar to the abdominal thrusts, but with a change in hand placement of the rescuer. The hands are placed on the lower part of the choking victim's chest, at the base of the breastbone or sternum, rather than over the middle of the abdomen, as in traditional abdominal thrusts. Strong inward thrusts are then applied.

The risk may be reduced by administering a non-particulate antacid (e.g. Sodium Citrate) or an H-antagonist like Ranitidine.

Airway obstruction may cause obstructive pneumonitis or post-obstructive pneumonitis.

PND is suggested to be a cause of extra-oral halitosis, especially when a sinus infection is also present. Acid reflux or heartburn is believed to aggravate and in some cases cause post-nasal drip. Post-nasal drip can be a cause of laryngeal inflammation and hyperresponsiveness, leading to symptoms of vocal cord dysfunction (VCD).

Lower airway obstruction is mainly caused by increased resistance in the bronchioles (usually from a decreased radius of the bronchioles) that reduces the amount of air inhaled in each breath and the oxygen that reaches the pulmonary arteries. It is different from airway restriction (which prevents air from diffusing into the pulmonary arteries because of some kind of blockage in the lungs). Diseases that cause lower airway obstruction are termed obstructive lung diseases.

Lower airway obstruction can be measured using spirometry. A decreased FEV1/FVC ratio (versus the normal of about 80%) is indicative of an airway obstruction, as the normal amount of air can no longer be exhaled in the first second of expiration. An airway restriction would not produce a reduced FEV1/FVC ratio, but would reduce the vital capacity. The ventilation is therefore affected leading to a ventilation perfusion mismatch and hypoxia.

Reactive airways dysfunction syndrome (RADS) is a term proposed by Stuart M. Brooks and colleagues in 1985

It can also manifest in adults with exposure to high levels of chlorine, ammonia, acetic acid or sulphur dioxide, creating symptoms like asthma. These symptoms can vary from mild to fatal, and can even create long-term airway damage depending on the amount of exposure and the concentration of chlorine. Some experts classify RADS as occupational asthma. Those with exposure to highly irritating substances should receive treatment to mitigate harmful effects.

Pulmonary aspiration resulting in pneumonia, in some patients, particularly those with physical limitations, can be fatal.