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.

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.

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.

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.

After a patient receives a diagnosis, the diagnosing physician can provide different options for treatment.

- Mechanical regulation of airflow and/or airway pressure:

- An experimental pacemaker for the diaphragm has shown promising results in overcoming central sleep apnea.

A diagnosis of sleep apnea requires determination by a physician. The examination may require a study of an individual in a sleep lab, although the AAST has said a two belt IHT (In Home Test) will replace a PSG for diagnosing obstructive apnea. There, the patient will be monitored while at rest, and the periods when breathing ceases will be measured with respect to length and frequency. During a PSG (polysomnography) (a sleep study), a person with sleep apnea shows breathing interruptions followed by drops/reductions in blood oxygen and increases in blood carbon dioxide level.

- 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, shorter pauses may still be considered apneas.

- Hypopneas in adults are defined as a 30% reduction in air flow for more than ten seconds, followed by oxygen-saturation declines of at least 3% or 4% per the AASM stndards. and/or EEG arousal. The Apnea-Hypopnea Index (AHI) is expressed as the number of apneas or hypopneas per hour of sleep.

As noted above, in central sleep apnea, the cessation of airflow is associated with the absence of physical attempts to breathe; specifically, polysomnograms reveal correlation between absence of rib cage and abdominal movements and cessation of airflow at the nose and lips. By contrast, in obstructive sleep apnea, pauses are not correlated with the absence of attempts to breathe and may even be correlated with more effortful breathing in an instinctive attempt to overcome the pressure on the sufferer's airway. If the majority of a sleep-apnea sufferer's apneas/hypopneas are central, his condition is classified as central; likewise, if the majority are obstructive, his condition is classified as obstructive.

There are three types of sleep apnea. OSA accounts for 84%, CSA for 0.4%, and 15% of cases are mixed.

Formal criteria for diagnosis of OHS are:

- Body mass index over 30 kg/m (a measure of obesity, obtained by taking one's weight in kilograms and dividing it by one's height in meters squared)

- Arterial carbon dioxide level over 45 mmHg or 6.0 kPa as determined by arterial blood gas measurement

- No alternative explanation for hypoventilation, such as use of narcotics, severe obstructive or interstitial lung disease, severe chest wall disorders such as kyphoscoliosis, severe hypothyroidism (underactive thyroid), neuromuscular disease or congenital central hypoventilation syndrome

If OHS is suspected, various tests are required for its confirmation. The most important initial test is the demonstration of elevated carbon dioxide in the blood. This requires an arterial blood gas determination, which involves taking a blood sample from an artery, usually the radial artery. Given that it would be complicated to perform this test on every patient with sleep-related breathing problems, some suggest that measuring bicarbonate levels in normal (venous) blood would be a reasonable screening test. If this is elevated (27 mmol/l or higher), blood gasses should be measured.

To distinguish various subtypes, polysomnography is required. This usually requires brief admission to a hospital with a specialized sleep medicine department where a number of different measurements are conducted while the subject is asleep; this includes electroencephalography (electronic registration of electrical activity in the brain), electrocardiography (same for electrical activity in the heart), pulse oximetry (measurement of oxygen levels) and often other modalities. Blood tests are also recommended for the identification of hypothyroidism and polycythemia.

To distinguish between OHS and various other lung diseases that can cause similar symptoms, medical imaging of the lungs (such as a chest X-ray or CT/CAT scan), spirometry, electrocardiography and echocardiography may be performed. Echo- and electrocardiography may also show strain on the right side of the heart caused by OHS, and spirometry may show a restrictive pattern related to obesity.

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.

Obesity hypoventilation syndrome is associated with a reduced quality of life, and people with the condition incur increased healthcare costs, largely due to hospital admissions including observation and treatment on intensive care units. OHS often occurs together with several other disabling medical conditions, such as asthma (in 18–24%) and type 2 diabetes (in 30–32%). Its main complication of heart failure affects 21–32% of patients.

Those with abnormalities severe enough to warrant treatment have an increased risk of death reported to be 23% over 18 months and 46% over 50 months. This risk is reduced to less than 10% in those receiving treatment with PAP. Treatment also reduces the need for hospital admissions and reduces healthcare costs.

Polysomnography is also used to aid in the diagnosis of other sleep disorders such as obstructive sleep apnea (OSA), narcolepsy, and restless leg syndrome (RLS). Normal test results show little to no episodes of sleep apnea and normal electrical activity in the individual's brain and muscles during sleep.

Polysomnography is a study conducted while the individual being observed is asleep. A polysomnograph (PSG) is a recording of an individual's body functions as they sleep. Complete sleep studies are most commonly facilitated at a designated sleep center. Specialized electrodes and monitors are connected to the individual and remain in place throughout study. Video cameras can be used in certain cases to record physical behaviors occurring while the individual is asleep. Typically the unwanted sexual behaviors do not present on film, therefore the majority of information is taken from a sleep study.

According to one meta-analysis, the mean prevalence rate for North America and Western Europe is estimated to be 14.5±8.0%. Specifically in the United States, the prevalence of restless leg syndrome is estimated to be between 5 and 15.7% when using strict diagnostic criteria. RLS is over 35% more prevalent in American women than their male counterparts.

Treatments for sleep disorders generally can be grouped into four categories:

- Behavioral and psychotherapeutic treatment

- Rehabilitation and management

- Medication

- Other somatic treatment

None of these general approaches is sufficient for all patients with sleep disorders. Rather, the choice of a specific treatment depends on the patient's diagnosis, medical and psychiatric history, and preferences, as well as the expertise of the treating clinician. Often, behavioral/psychotherapeutic and pharmacological approaches are not incompatible and can effectively be combined to maximize therapeutic benefits. Management of sleep disturbances that are secondary to mental, medical, or substance abuse disorders should focus on the underlying conditions.

Medications and somatic treatments may provide the most rapid symptomatic relief from some sleep disturbances. Certain disorders like narcolepsy, are best treated with prescription drugs such as Modafinil. Others, such as chronic and primary insomnia, may be more amenable to behavioral interventions, with more durable results.

Chronic sleep disorders in childhood, which affect some 70% of children with developmental or psychological disorders, are under-reported and under-treated. Sleep-phase disruption is also common among adolescents, whose school schedules are often incompatible with their natural circadian rhythm. Effective treatment begins with careful diagnosis using sleep diaries and perhaps sleep studies. Modifications in sleep hygiene may resolve the problem, but medical treatment is often warranted.

Special equipment may be required for treatment of several disorders such as obstructive apnea, the circadian rhythm disorders and bruxism. In these cases, when severe, an acceptance of living with the disorder, however well managed, is often necessary.

Some sleep disorders have been found to compromise glucose metabolism.

Transfusion therapy lowers the risk for a new silent stroke in children who have both abnormal cerebral artery blood flow velocity, as detected by transcranial Doppler, and previous silent infarct, even when the initial MRI showed no abnormality. A finding of elevated TCD ultrasonographic velocity warrants MRI of the brain, as those with both abnormalities who are not provided transfusion therapy are at higher risk for developing a new silent infarct or stroke than are those whose initial MRI showed no abnormality.

Preventive measures that can be taken to avoid sustaining a silent stroke are the same as for stroke. Smoking cessation is the most immediate step that can be taken, with the effective management of hypertension the major medically treatable factor.

The Great Imitator (also The Great Masquerader) is a phrase used for medical conditions that feature nonspecific symptoms and may be confused with a number of other diseases. Most great imitators are systemic in nature. Diseases sometimes referred to with this name include:

- Various cancers

- Intravascular large B-cell lymphoma

- Various rheumatic conditions, including:

- Fibromyalgia

- Psoriatic arthritis

- Lupus erythematosus

- Systemic lupus erythematosus

- Sarcoidosis

- Multiple sclerosis

- Celiac disease

- Addison's Disease

- Pulmonary embolism

- Various infectious diseases, including:

- Syphilis

- Lyme disease

- Nocardiosis

- Tuberculosis

- Brucellosis

- Malaria

- Breathing-related sleep disorders (chiefly sleep apnea/hypopnea and upper-airway resistance syndrome).

Peripheral neuropathy may first be considered when an individual reports symptoms of numbness, tingling, and pain in feet. After ruling out a lesion in the central nervous system as a cause, diagnosis may be made on the basis of symptoms, laboratory and additional testing, clinical history, and a detailed examination.

During physical examination, specifically a neurological examination, those with generalized peripheral neuropathies most commonly have distal sensory or motor and sensory loss, although those with a pathology (problem) of the nerves may be perfectly normal; may show proximal weakness, as in some inflammatory neuropathies, such as Guillain–Barré syndrome; or may show focal sensory disturbance or weakness, such as in mononeuropathies. Classically, ankle jerk reflex is absent in peripheral neuropathy.

A physical examination will involve testing the deep ankle reflex as well as examining the feet for any ulceration. For large fiber neuropathy, an exam will usually show an abnormally decreased sensation to vibration, which is tested with a 128-Hz tuning fork, and decreased sensation of light touch when touched by a nylon monofilament.

Diagnostic tests include electromyography (EMG) and nerve conduction studies (NCSs), which assess large myelinated nerve fibers. Testing for small-fiber peripheral neuropathies often relates to the autonomic nervous system function of small thinly- and unmyelinated fibers. These tests include a sweat test and a tilt table test. Diagnosis of small fiber involvement in peripheral neuropathy may also involve a skin biopsy in which a 3 mm-thick section of skin is removed from the calf by a punch biopsy, and is used to measure the skin intraepidermal nerve fiber density (IENFD), the density of nerves in the outer layer of the skin. Reduced density of the small nerves in the epidermis supports a diagnosis of small-fiber peripheral neuropathy.

Laboratory tests include blood tests for vitamin B-12 levels, a complete blood count, measurement of thyroid stimulating hormone levels, a comprehensive metabolic panel screening for diabetes and pre-diabetes, and a serum immunofixation test, which tests for antibodies in the blood.

Many health conditions can cause autonomic neuropathy. Some common causes of autonomic neuropathy include:

- Diabetes, which is the most common cause of autonomic neuropathy, can gradually cause nerve damage throughout the body.

- Injury to nerves caused by surgery or radiation to the neck.

- Treatment with certain medications, including some drugs used in cancer chemotherapy.

- Abnormal protein buildup in organs (amyloidosis), which affects the organs and the nervous system.

- Other chronic illnesses, such as Parkinson's disease, multiple sclerosis and some types of dementia.

- Autonomic neuropathy may also be caused by an abnormal attack by the immune system that occurs as a result of some cancers (paraneoplastic syndrome).

- Certain infectious diseases. Some viruses and bacteria, such as botulism, Lyme disease and HIV, can cause autonomic neuropathy.

- Inherited disorders. Certain hereditary disorders can cause autonomic neuropathy.

- Autoimmune diseases, in which the immune system attacks and damages parts of the body, including the nerves. Examples include Sjogren's syndrome, systemic lupus erythematosus, rheumatoid arthritis and celiac disease. Guillain-Barre syndrome is an autoimmune disease that happens rapidly and can affect autonomic nerves.

Autonomic neuropathy (also AN or AAN) is a form of polyneuropathy that affects the non-voluntary, non-sensory nervous system (i.e., the autonomic nervous system), affecting mostly the internal organs such as the bladder muscles, the cardiovascular system, the digestive tract, and the genital organs. These nerves are not under a person's conscious control and function automatically. Autonomic nerve fibers form large collections in the thorax, abdomen, and pelvis outside the spinal cord. They have connections with the spinal cord and ultimately the brain, however. Most commonly autonomic neuropathy is seen in persons with long-standing diabetes mellitus type 1 and 2. In most—but not all—cases, autonomic neuropathy occurs alongside other forms of neuropathy, such as sensory neuropathy.

Autonomic neuropathy is one cause of malfunction of the autonomic nervous system (referred to as dysautonomia), but not the only one; some conditions affecting the brain or spinal cord also may cause autonomic dysfunction, such as multiple system atrophy, and therefore, may cause similar symptoms to autonomic neuropathy.

The treatment of peripheral neuropathy varies based on the cause of the condition, and treating the underlying condition can aid in the management of neuropathy. When peripheral neuropathy results from diabetes mellitus or prediabetes, blood sugar management is key to treatment. In prediabetes in particular, strict blood sugar control can significantly alter the course of neuropathy. In peripheral neuropathy that stems from immune-mediated diseases, the underlying condition is treated with intravenous immunoglobulin or steroids. When peripheral neuropathy results from vitamin deficiencies or other disorders, those are treated as well.