A link between GlaxoSmithKline's H1N1 flu vaccine Pandemrix and childhood narcolepsy was investigated due to increased prevalence of narcolepsy in Irish, Finnish and Swedish children after vaccinations. Finland's National Institute of Health and Welfare recommended that Pandemrix vaccinations be suspended pending further investigation into 15 reported cases of children developing narcolepsy. In Finland in mid-November 2010, 37 cases of children's narcolepsy had been reported by doctors. This can be compared to the normal average of 3 cases of children's narcolepsy per year. "The incidence of narcolepsy with cataplexy in children/adolescents in the Swedish population increased during the pandemic and vaccination period, with a rapid decline in incidence during the post pandemic period." They concluded that these results "provide strengthened evidence that vaccination with Pandemrix during the pandemic period could be associated with an increase in the risk for narcolepsy with cataplexy in predisposed children/adolescents 19 years and younger." In 2013, the link between Pandemrix and narcolepsy was confirmed by a registry study by the Swedish Medical Products Agency, with a three-fold increase in risk for people under the age of 20.

DSPD is genetically linked to attention deficit hyperactivity disorder by findings of polymorphism in genes in common between those apparently involved in ADHD and those involved in the circadian rhythm and a high proportion of DSPD among those with ADHD.

Idiopathic hypersomnia is a lifelong disorder (with only rare spontaneous remissions) whose symptoms typically begin in adolescence or young adulthood. It is initially progressive, but may stabilize, and its main consequences are professional and social.

Idiopathic hypersomnia profoundly affects work, education, and quality of life. Patients are often too sleepy to work or attend school regularly, and they are predisposed "to develop serious performance decrements in multiple areas of function as well as to potentially life-threatening domestic, work-related and driving accidents." Furthermore, these risks are higher for idiopathic hypersomnia patients than for those with sleep apnea or severe insomnia. In fact, "the most severe cases of daytime somnolence are found in patients affected by narcolepsy or idiopathic hypersomnia." And idiopathic hypersomnia is often as, if not more, disabling than narcolepsy; surprisingly, excessive daytime sleepiness is even more handicapping than the cataplectic attacks of narcolepsy.

Due to the consequences of their profound EDS, both idiopathic hypersomnia and narcolepsy can often result in unemployment. Several studies have shown a high rate of unemployment in narcoleptics (from 30-59%), which was felt to be related to the severe symptoms of their illness.

Sleep apnea can affect people regardless of sex, race, or age. However, risk factors include:

- being male

- excessive weight

- an age above 40

- large neck size (greater than 16–17 inches)

- enlarged tonsils or tongue

- small jaw bone

- gastroesophageal reflux

- allergies

- sinus problems

- a family history of sleep apnea

- deviated septum

Alcohol, sedatives and tranquilizers may also promote sleep apnea by relaxing throat muscles. Smokers have sleep apnea at three times the rate of people who have never smoked.

Central sleep apnea is more often associated with any of the following risk factors:

- being male

- an age above 65

- having heart disorders such as atrial fibrillation or atrial septal defects such as PFO

- stroke

High blood pressure is very common in people with sleep apnea.

Histamine plays a role in wakefulness in the brain. An allergic reaction over produces histamine causing wakefulness and inhibiting sleep Sleep problems are common in people with allergic rhinitis. A study from the N.I.H. found that sleep is dramatically impaired by allergic symptoms and that the degree of impairment is related to the severity of those symptoms s Treatment of allergies has also been shown to help sleep apnea.

The exact cause of narcolepsy is unknown, and it may be caused by several distinct factors. Part of the mechanism involves the loss of orexin-releasing neurons within the lateral hypothalamus. In up to 10% of cases there is a family history of the disorder. There is a strong link with certain genetic variants. In addition to genetic factors, low levels of orexin peptides have been correlated with a past history of infection, diet, contact with toxins such as pesticides, and brain injuries due to brain tumors or strokes.

There have been many studies suggesting health risks associated with shift work. For example, a 2007 study led by the IARC (International Agency for Research on Cancer) showed that shiftwork has been associated with cancer. Other studies have reported that night workers have an increased incidence of heart disease, digestive disorders and menstrual irregularities. Because a formal diagnosis of SWSD was not typically made in these studies, it remains unclear whether the reported risks apply to the subset of shiftworkers who qualify for a diagnosis of SWSD or apply to all shiftworkers.

The most comprehensive assessment so far has estimated RBD prevalence to be about 0.5% in individuals aged 15 to 100. It is far more common in males: most studies report that only about a tenth of sufferers are female. This may partially be due to a referral bias, as violent activity carried out by men is more likely to result in harm and injury and is more likely to be reported than injury to male bed partners by women, or it may reflect a true difference in prevalence as a result of genetic or androgenic factors. The mean age of onset is estimated to be about 60 years.

Various conditions are very similar to RBD in that sufferers exhibit excessive sleep movement and potentially violent behavior. Such disorders include sleepwalking and sleep terrors, which are associated with other stages of sleep, nocturnal seizures and obstructive sleep apnea which can induce arousals from REM sleep associated with complex behaviors. Because of the similarities between the conditions, polysomnography plays an important role in confirming RBD diagnosis.

It is now apparent that RBD appears in association with a variety of different conditions. Narcolepsy has been reported as a related disorder. Both RBD and narcolepsy involve dissociation of sleep states probably arising from a disruption of sleep control mechanisms. RBD has also been reported following cerebrovascular accident and neurinoma (tumor), indicating that damage to the brain stem area may precipitate RBD. RBD is usually chronic. However, it may be acute and sudden in onset if associated with drug treatment or withdrawal (particularly with alcohol withdrawal). 60% of RBD is idiopathic. This includes RBD that is found in association with conditions such as Parkinson's disease and dementia with Lewy bodies, where it is often seen to precede the onset of neurodegenerative disease. Monoamine oxidase inhibitors, tricyclic antidepressants, Selective serotonin reuptake inhibitors, and noradrenergic antagonists can induce or aggravate RBD symptoms and should be avoided in patients with RBD.

Abnormally low levels of acylcarnitine have been observed in patients with narcolepsy. These same low levels have been associated with primary hypersomnia in general in mouse studies. "Mice with systemic carnitine deficiency exhibit a higher frequency of fragmented wakefulness and rapid eye movement (REM) sleep, and reduced locomotor activity." Administration of acetyl-L-carnitine was shown to improve these symptoms in mice. A subsequent human trial found that narcolepsy patients given L-carnitine spent less total time in daytime sleep than patients who were given placebo.

A systematic review found that traumatic childhood experiences (such as family conflict or sexual trauma) significantly increases the risk for a number of sleep disorders in adulthood, including sleep apnea, narcolepsy, and insomnia. It is currently unclear whether or not moderate alcohol consumption increases the risk of obstructive sleep apnea.

In addition, an evidence-based synopses suggests that the sleep disorder, idiopathic REM sleep behavior disorder (iRBD), may have a hereditary component to it. A total of 632 participants, half with iRBD and half without, completed self-report questionnaires. The results of the study suggest that people with iRBD are more likely to report having a first-degree relative with the same sleep disorder than people of the same age and sex that do not have the disorder. More research needs to be conducted to gain further information about the hereditary nature of sleep disorders.

A population susceptible to the development of sleep disorders is people who have experienced a traumatic brain injury (TBI). Because many researchers have focused on this issue, a systematic review was conducted to synthesize their findings. According to their results, TBI individuals are most disproportionately at risk for developing narcolepsy, obstructive sleep apnea, excessive daytime sleepiness, and insomnia. The study's complete findings can be found in the table below:

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).

Persons with obsessive-compulsive disorder are also diagnosed with DSPD at a much higher rate than the general public.

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 Wisconsin Sleep Cohort Study estimated in 1993 that roughly one in every 15 Americans was affected by at least moderate sleep apnea. It also estimated that in middle-age as many as nine percent of women and 24 percent of men were affected, undiagnosed and untreated.

The costs of untreated sleep apnea reach further than just health issues. It is estimated that in the U.S. the average untreated sleep apnea patient's annual health care costs $1,336 more than an individual without sleep apnea. This may cause $3.4 billion/year in additional medical costs. Whether medical cost savings occur with treatment of sleep apnea remains to be determined.

Insomnia and wake-time sleepiness are related to misalignment between the timing of the non-standard wake–sleep schedule and the endogenous circadian propensity for sleep and wake. In addition to circadian misalignment, attempted sleep at unusual times can be interrupted by noise, social obligations, and other factors. Finally, there is an inevitable degree of sleep deprivation associated with sudden transitions in sleep schedule.

SSM is poorly understood. As of 2008, there is little to no information regarding risk factors or prevention, though it is believed to be most prevalent among young to middle aged adults.

Distribution among the general population and by gender is unknown. About 5% of the clinical population may be affected, though that figure is subject to sampling bias.

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.

What is considered objective insomnia, unlike SSM, can easily be confirmed empirically through clinical testing, such as by polysomnogram. Those who experience SSM may believe that they have not slept for extended periods of time, when they in fact do sleep but without perceiving it. For example, while patients who claim little or no sleep may usually acknowledge impaired job performance and daytime drowsiness, sleep state misperceivers often do not.

Cases of objective total insomnia are extremely rare. The few that have been recorded have predominantly been ascribed to a rare incurable genetic disorder called fatal familial insomnia, which patients rarely survive for more than 26 months after the onset of illness—often much less. While rarer cases of objective total insomnia lasting for decades have been reported, such as with the American Al Herpin and the Vietnamese Thai Ngoc, they have not been studied extensively in a clinical setting.

ISWD has various causes, including neurological disorders such as dementia (particularly Alzheimer's Disease), brain damage, or mental retardation. It is thought that sufferers have a weak circadian clock. The risk for the disorder increases with age, but only due to increased prevalence of co-morbid medical disorders.

There are over 30 recognized kinds of dyssomnias. Major groups of dyssomnias include:

- Intrinsic sleep disorders – 12 disorders recognized, including

- idiopathic hypersomnia,

- narcolepsy,

- periodic limb movement disorder,

- restless legs syndrome,

- sleep apnea,

- sleep state misperception.

- Extrinsic sleep disorders – 13 disorders recognized, including

- alcohol-dependent sleep disorder,

- food allergy insomnia,

- inadequate sleep routine.

- Circadian rhythm sleep disorders, both intrinsic and extrinsic – 6 disorders recognized, including

- advanced sleep phase syndrome,

- delayed sleep phase syndrome,

- jetlag,

- shift work sleep disorder.

Symptomatic RBD is the more characteristically seen disorder. This category of RBD is strongly associated with neurodegenerative diseases. About 15% of Parkinson's patients also have RBD, 70% of multiple system atrophy patients also have RBD, and about 85% of Lewy body dementia patients also have RBD. Other reported neurological associations include Shy–Drager syndrome, olivopontocerebellar atrophy, multiple sclerosis, vascular encephalopathies, Tourette's syndrome, and Guillain–Barré syndrome. It is uncertain whether RBD precedes these neurodegenerative disorders, whether they coincide, or whether it follows these disorders. However, Mayo Clinic researchers have characterized RBD as the strongest predictor of whether a male patient is developing Lewy body dementia.

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

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.

The current formally correct name of the disorder is Circadian Rhythm Sleep Disorder: Irregular Sleep Wake Rhythm Type. This disorder has been referred to by many other terms, including: Irregular Sleep Wake Pattern, irregular sleep wake syndrome, Irregular Sleep Wake Rhythm (ISWRD), Irregular Sleep Wake Cycle, Irregular Sleep Wake Schedule and Irregular Sleep Wake Disorder (ISWD). Sometimes the words sleep and wake are hyphenated (sleep–wake). Sometimes the words are capitalized and sometimes they are not.

Excessive daytime sleepiness (EDS) is characterized by persistent sleepiness and often a general lack of energy, even during the day after apparently adequate or even prolonged nighttime sleep. EDS can be considered as a broad condition encompassing several sleep disorders where increased sleep is a symptom, or as a symptom of another underlying disorder like narcolepsy, sleep apnea or a circadian rhythm sleep disorder.

Some persons with EDS, including those with hypersomnias like narcolepsy and idiopathic hypersomnia, are compelled to nap repeatedly during the day; fighting off increasingly strong urges to sleep during inappropriate times such as while driving, while at work, during a meal, or in conversations. As the compulsion to sleep intensifies, the ability to complete tasks sharply diminishes, often mimicking the appearance of intoxication. During occasional unique and/or stimulating circumstances, a person with EDS can sometimes remain animated, awake and alert, for brief or extended periods of time. EDS can affect the ability to function in family, social, occupational, or other settings. A proper diagnosis of the underlying cause and ultimately treatment of symptoms and/or the underlying cause can help mitigate such complications.