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.

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.

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

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.

An adult who is compelled to nap repeatedly during the day may have excessive daytime sleepiness; however, it is important to distinguish between occasional daytime sleepiness and excessive daytime sleepiness, which is chronic.

A number of tools for screening for EDS have been developed. One is the Epworth Sleepiness Scale which grades the results of a questionnaire. The ESS generates a numerical score from zero (0) to 24 where a score of ten [10] or higher may indicate that the person should consult a specialist in sleep medicine for further evaluation.

Another tool is the Multiple Sleep Latency Test (MSLT), which has been used since the 1970s. It is used to measure the time it takes from the start of a daytime nap period to the first signs of sleep, called sleep latency. The test is based on the idea that the sleepier people are, the faster they will fall asleep.

The Maintenance of Wakefulness Test (MWT) is also used to quantitatively assess daytime sleepiness. This test is performed in a sleep diagnostic center. The test is similar to the MSLT. However, during this test the patient is instructed to try to stay awake.

A physician specializing in sleep medicine may ask patients about their medical history; for example: neurological problems, prescription or non-prescription medications taken, alcohol use, family history, and any other sleep problems. A thorough medical and neurological exam is indicated. The patient will be asked to complete a sleep diary, recording natural sleep and wake up times, over several weeks. Sleep rating with the Epworth Sleepiness Scale may be used.

EDS can be a symptom of a number of factors and disorders. Specialists in sleep medicine are trained to diagnose them. Some are:

- Insufficient quality or quantity of night time sleep.

- Misalignments of the body's circadian pacemaker with the environment (e.g. jet lag, shift work or other circadian rhythm sleep disorders).

- Another underlying sleep disorder, such as narcolepsy, sleep apnea, idiopathic hypersomnia or restless legs syndrome.

- Disorders such as clinical depression or atypical depression.

- Tumors, head trauma, anemia, kidney failure, hypothyroidism or an injury to the central nervous system.

- Drug abuse.

- Genetic predisposition

- Vitamin deficiency, such as Biotin deficiency

- Particular classes of prescription and OTC medication

A neurological condition or another medical problem may be suspected, in which case, blood tests, a CT scan or an MRI may be used. An overnight sleep study is usually not needed to detect this disorder, but may be indicated if other sleep disorders, such as sleep apnea and periodic limb movement disorder, seem likely. The overnight sleep study is called polysomnography. It charts brain waves, heart beat, muscle activity, and breathing during sleep. It also records arm and leg movement. It will show if there are other sleep disorders that are causing or increasing the problems with ISWD.

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.

Because a number of parasomnias may be confused with RBD, it is necessary to conduct formal sleep studies such as polysomnography (PSG) performed at sleep centers that are experienced in evaluating parasomnias in order to establish a diagnosis. In RBD, a single night of extensive monitoring of sleep, brain, and muscle activity will almost always reveal the lack of muscle paralysis during REM sleep, and it will also eliminate other causes of parasomnias.

Recently, due to the limited access to PSG, attempts have been made to identify RBD from clinical interview as well as questionnaires. Postuma et al. have validated a single-question screening tool for RBD (RBD1Q) that could be easily applied in general practice to the patient and their bed partner. A positive answer to the RBDQ1, ‘Have you ever been told or suspected yourself, that you seem to act out your dreams while asleep (for example, punching, flailing your arms in the air, making running movement etc.)?’ should encourage the medical practitioner to consider the diagnosis of RBD as it offers good sensitivity (94%) and specificity (87%). Other questionnaires, such as the Rapid Eye Movement (REM) sleep Behavior Disorder Screening Questionnaire (RBDSQ) or the REM Sleep Behavior Questionnaires – Hong-Kong are available for more detailed characterisation.

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.

Sleeping in a more upright position seems to lessen catathrenia (as well as sleep apnea). Performing regular aerobic exercise, where steady breathing is necessary (running, cycling etc.) may lessen catathrenia. Strength exercise, on the other hand, may worsen catathrenia because of the tendency to hold one's breath while exercising. Yoga and/or meditation focused on steady and regular breathing may lessen catathrenia.

Diagnosis is relatively easy when all the symptoms of narcolepsy are present, but if the sleep attacks are isolated and cataplexy is mild or absent, diagnosis is more difficult. It is also possible for cataplexy to occur in isolation. Three tests that are commonly used in diagnosing narcolepsy are the polysomnogram, the multiple sleep latency test (MSLT), and administration of the Epworth Sleepiness Scale. These tests are usually performed by a sleep specialist. The polysomnogram involves continuous recording of sleep brain waves and a number of nerve and muscle functions during night time sleep. When tested, people with narcolepsy fall asleep rapidly, enter REM sleep early, and may often awaken during the night. The polysomnogram also helps to detect other possible sleep disorders that could cause daytime sleepiness.

The Epworth Sleepiness Scale is a brief questionnaire that is administered to determine the likelihood of the presence of a sleep disorder, including narcolepsy. For the multiple sleep latency test, a person is given a chance to sleep every 2 hours during normal wake times. The patient is taken in usually for an overnight sleep study. The following day the patient will have multiple tests where they will be told to nap after a full nights sleep (usually eight hours). Observations are made of the time taken to reach various stages of sleep (sleep onset latency). This test measures the degree of daytime sleepiness and also detects how soon REM sleep begins. Again, people with narcolepsy fall asleep rapidly and enter REM sleep early. Occasionally, a multiple sleep latency test can result in a false-negative for a narcoleptic.

The system which regulates sleep, arousal, and transitions between these states in humans is composed of three interconnected subsystems: the orexin projections from the lateral hypothalamus, the reticular activating system, and the ventrolateral preoptic nucleus. In narcoleptic individuals, these systems are all associated with impairments due to a greatly reduced number of hypothalamic orexin projection neurons and significantly fewer orexin neuropeptides in cerebrospinal fluid and neural tissue, compared to non-narcoleptic individuals. Those with narcolepsy generally experience the REM stage of sleep within five minutes of falling asleep, while people who do not have narcolepsy (unless they are significantly sleep deprived) do not experience REM until after a period of slow-wave sleep, which lasts for about the first hour or so of a sleep cycle.

Measuring orexin levels in a person's cerebrospinal fluid sampled in a spinal tap may help in diagnosing narcolepsy, with abnormally low levels serving as an indicator of the disorder. This test can be useful when MSLT results are inconclusive or difficult to interpret.

Idiopathic hypersomnia has historically been "difficult to diagnose at an early stage," especially because many other disorders can cause symptoms of excessive daytime sleepiness (EDS). Therefore, "at the time of presentation, most patients have had the disorder for many years."

Further complicating the diagnostic process, idiopathic hypersomnia lacks a clearly defining clinical feature. Whereas narcolepsy is associated with cataplexy and sleep-onset REM episodes, and Kleine-Levin syndrome is associated with megaphagia (compulsive food cravings) and hypersexuality, idiopathic hypersomnia has no such dramatic associated features, except perhaps sleep drunkenness. "Consequently there has been an unfortunate tendency to label all difficult-to-classify cases of excessive daytime sleepiness as idiopathic hypersomnia." For example, upper airway resistance syndrome and delayed sleep phase disorder were formerly confused with idiopathic hypersomnia, but now that they have been more clearly defined, doctors can more carefully exclude these causes of EDS in order to more correctly diagnose idiopathic hypersomnia. However, "even in the presence of other specific causes of hypersomnia, one should carefully assess the contribution of these etiological factors to the complaint of EDS and when specific treatments of these conditions fail to suppress EDS, the [additional] diagnosis of idiopathic hypersomnia should be considered."

The severity of EDS can be quantified by subjective scales, such as the Epworth sleepiness scale and the Stanford sleepiness scale (SSS), and also by objective tests, like the multiple sleep latency test (MSLT)."

In 2001, the ICSD (International Classification of Sleep Disorders) updated their criteria for the diagnosis of idiopathic hypersomnia. Essentially, EDS must be present for at least 6 months, sleep studies (polysomnography and multiple sleep latency test) must show certain characteristics, and all other known causes for long sleep time and EDS must be considered (see hypersomnia). For the patient, this diagnostic process is often tedious, expensive and time-consuming, as other than the sleep studies, it is still basically a diagnosis of exclusion.

In patients with idiopathic hypersomnia, polysomnography typically shows short sleep latency, increased mean slow wave sleep, and a high mean sleep efficiency. "Latency to REM sleep and percentages of light sleep and REM sleep were normal, compared with normal ranges." Despite this, one study has found increased sleep fragmentation in patients with idiopathic hypersomnia without long sleep time, suggesting multiple possible presentations.

It is important to note that although sleep latencies are typically short in idiopathic hypersomnia, the clinical severity may not correlate closely with the MSLT results. In fact, "latencies above 5 minutes are not uncommon in patients with clinically severe hypersomnia." When sleep latency is below 10 minutes, the presence of sleep-onset REM periods (SOREMPs) in two or more of the MSLT naps suggests a diagnosis of narcolepsy, whereas sleep periods lacking rapid eye movement (NREM sleep) in the various naps suggests a diagnosis of idiopathic hypersomnia. However, the importance of this differentiation between REM and NREM has been called into question. (see Classification)

Although the MSLT is currently the best available test to diagnose EDS in general, the MSLT protocol lacks the ability to document the extended, unrefreshing daytime naps that often occur in idiopathic hypersomnia. Complicating the matter, several groups of researchers have found normal MSLT results in patients who otherwise seem to have idiopathic hypersomnia. Therefore, when idiopathic hypersomnia is suspected, researchers suggest appending a 24-hour continuous polysomnography to the standard overnight/MSLT study in order to record total sleep time. Alternatively, an assay of the patient's cerebrospinal fluid (CSF) can be performed in order to test for an adequate level of hypocretin (to exclude narcolepsy with cataplexy) and to determine whether the patient’s CSF abnormally boosts GABA receptor sensitivity (thought to underlie many cases of idiopathic hypersomnia and narcolepsy without cataplexy). Globally, there are very few labs capable of performing the CSF assays referenced above.

It is also important to note that whereas narcolepsy is strongly associated with the HLA-DQB1*0602 genotype, "HLA typing is of no help in the positive diagnosis of idiopathic hypersomnia." This is "despite some reports that suggest an increase frequency of HLA Cw2 and DRS in idiopathic hypersomnia subjects."

The 2001 International Classification of Sleep Disorders (ICSD) divides primary hypersomnia syndromes between narcolepsy, idiopathic hypersomnia, and the recurrent hypersomnias (like Klein-Levin syndrome); it further divides narcolepsy into that with cataplexy and that without cataplexy. This ICSD version defines narcolepsy as a disorder of unknown cause "that is characterized by excessive sleepiness that typically is associated with cataplexy and other REM-sleep phenomena, such as sleep paralysis and hypnagogic hallucinations". It also establishes baseline categorical standards for diagnosis of narcolepsy, through 2 sets of well defined criteria, as follows.

Minimal narcolepsy diagnostic criteria set #2:

- A "complaint of excessive sleepiness or sudden muscle weakness."

- Associated features that include: sleep paralysis; disrupted major sleep episode; hypnagogic hallucinations; automatic behaviors.

- Polysomnography with one or more of the following: "sleep latency less than 10 minutes;" "REM sleep latency less than 20 minutes;" an MSLT with a mean sleep latency less than 5 minutes; "two or more sleep-onset REM periods" (SOREMPs).

- "No medical or mental disorder accounts for the symptoms." (see hypersomnia differential diagnosis)

In the absence of clear cataplexy, it becomes much more difficult to make a firm diagnosis of narcolepsy. “Various terms, such as essential hypersomnia, primary hypersomnia, ambiguous narcolepsy, atypical narcolepsy, etc., have been used to classify these patients, who may be in the developing phase of narcolepsy.”

Since the 2001 ICSD, the classification of primary hypersomnias has been steadily evolving, as further research has shown more overlap between narcolepsy and idiopathic hypersomnia. The 3rd edition of the ICSD is currently being finalized, and its new classification will label narcolepsy caused by orexin deficiency as “type 1 narcolepsy,” which is almost always associated with cataplexy. The other primary hypersomnias will remain subdivided based on the presence of SOREMPs. They will be labeled: “type 2 narcolepsy,” with 2 or more SOREMPs on MSLT; and “idiopathic hypersomnia,” with less than 2 SOREMPS.

However, “there is no evidence that the pathophysiology or therapeutic response is substantially different for hypersomnia with or without SOREMPs on the MSLT.” Given this currently understood overlap of idiopathic hypersomnia and narcolepsy, the 5th edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-V) is also updating its classification of the primary hypersomnias. It reclassifies narcolepsy without cataplexy as major somnolence disorder (MSD). Additionally, MSD will encompass all syndromes of hypersomnolence not explained by low orexin concentrations, including idiopathic hypersomnia (with and without long sleep time) and long sleepers (people requiring >10 hours sleep/day).

Further complicating these updated classification schemes, overlap between narcolepsy "with" cataplexy and idiopathic hypersomnia has also been reported. A subgroup of narcoleptics with long sleep time, comprising 18% of narcoleptics in one study, had symptoms of both narcolepsy with cataplexy and idiopathic hypersomnia (long sleep time and unrefreshing naps). It is believed that this subgroup might have dysfunction in multiple arousal systems, including orexin and GABA (see idiopathic hypersomnia causes).

Several circumstances have been identified that are associated with an increased risk of sleep paralysis. These include insomnia, sleep deprivation, an erratic sleep schedule, stress, and physical fatigue. It is also believed that there may be a genetic component in the development of RISP, because there is a high concurrent incidence of sleep paralysis in monozygotic twins. Sleeping in the supine position has been found an especially prominent instigator of sleep paralysis.

Sleeping in the supine position is believed to make the sleeper more vulnerable to episodes of sleep paralysis because in this sleeping position it is possible for the soft palate to collapse and obstruct the airway. This is a possibility regardless of whether the individual has been diagnosed with sleep apnea or not. There may also be a greater rate of microarousals while sleeping in the supine position because there is a greater amount of pressure being exerted on the lungs by gravity.

While many factors can increase risk for ISP or RISP, they can be avoided with minor lifestyle changes. By maintaining a regular sleep schedule and observing good sleep hygiene, one can reduce chances of sleep paralysis. It helps subjects to reduce the intake of stimulants and stress in daily life by taking up a hobby or seeing a trained psychologist who can suggest coping mechanisms for stress. However, some cases of ISP and RISP involve a genetic factor—which means some people may find sleep paralysis unavoidable. Practicing meditation regularly might also be helpful in preventing fragmented sleep, and thus the occurrence of sleep paralysis. Research has shown that long-term meditation practitioners spend more time in slow wave sleep, and as such regular meditation practice could reduce nocturnal arousal and thus possibly sleep paralysis.

Sleep paralysis is mainly diagnosed via clinical interview and ruling out other potential sleep disorders that could account for the feelings of paralysis. The main disorder that is checked for is narcolepsy due to the high prevalence of narcolepsy in conjunction with sleep paralysis. The availability of a genetic test for narcolepsy makes this an easy disorder to rule out. Several measures are available to reliably diagnose (e.g., the "fearful isolated sleep paralysis interview") or screen ("Munich Parasomnia Screening") for recurrent isolated sleep paralysis.

In general, there are two broad classes of treatment, and the two may be combined: psychological (cognitive-behavioral) and pharmacological. In situations of acute distress such as a grief reaction, pharmacologic measures may be most appropriate. With primary insomnia, however, initial efforts should be psychologically based, including discussion of good sleep hygiene. Other specific treatments are appropriate for some of the disorders, such as ingestion of the hormone melatonin, correctly timed bright light therapy and correctly timed dark therapy or light restriction for the circadian rhythm sleep disorders. Specialists in sleep medicine are trained to diagnose and treat these disorders, though many specialize in just some of them.

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.

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.

DSPD is diagnosed by a clinical interview, actigraphic monitoring, and/or a sleep diary kept by the patient for at least two weeks. When polysomnography is also used, it is primarily for the purpose of ruling out other disorders such as narcolepsy or sleep apnea. If a person can adjust to a normal daytime schedule on her/his own, with just the help of alarm clocks and will-power, the diagnosis is not given.

DSPD is frequently misdiagnosed or dismissed. It has been named as one of the sleep disorders most commonly misdiagnosed as a primary psychiatric disorder. DSPD is often confused with: psychophysiological insomnia; depression; psychiatric disorders such as schizophrenia, ADHD or ADD; other sleep disorders; or school refusal. Practitioners of sleep medicine point out the dismally low rate of accurate diagnosis of the disorder, and have often asked for better physician education on sleep disorders.

The primary treatment for children is the removal of enlarged tonsils and adenoids via a tonsillectomy and adenoidectomy. Orthodontic treatment is frequently recommended and CPAP may also be necessary for children with UARS.

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.

Statistics on snoring are often contradictory, but at least 30% of adults and perhaps as many as 50% of people in some demographics snore. One survey of 5,713 American residents identified habitual snoring in 24% of men and 13.8% of women, rising to 60% of men and 40% of women aged 60 to 65 years; this suggests an increased susceptibility to snoring with age.

Middle-of-the-night insomnia is often treated with medication, although currently Intermezzo (zolpidem tartrate sublingual tablets) is the only Food and Drug Administration-approved medication specifically for treating MOTN awakening. Because most medications usually require 6–8 hours of sleep to avoid lingering effects the next day, these are often used every night at bedtime to prevent awakenings. Medication may not be prescribed in some cases, especially if the cause turns out to be the patient ingesting too much fluid during the day or just before they go to sleep.

Sleep restriction therapy and stimulus control therapy as described in insomnia have shown significance in treating middle of night insomnia.

Some studies have shown that zaleplon, which has a short elimination half-life, may be suitable for middle-of-the-night administration because it does not impair next day performance.