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.

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.

There is some evidence that a predisposition to night terrors and other parasomnias may be congenital. Individuals frequently report that past family members have had either episodes of sleep terrors or sleepwalking. In some studies, a ten-fold increase in the prevalence of night terrors in first-degree biological relatives has been observed—however, the exact link to inheritance is not known. Familial aggregation has been found suggesting that there is an autosomal mode of inheritance. In addition, some laboratory findings suggest that sleep deprivation and having a fever can increase the likelihood of a night terror episode occurring. Other contributing factors include nocturnal asthma, gastroesophageal reflux, and central nervous system medications. Special consideration must be used when the subject suffers from narcolepsy, as there may be a link. There have been no findings that show a cultural difference between manifestations of night terrors, though it is thought that the significance and cause of night terrors differ within cultures. Evidence suggests that nightmares are more common among women than men.

Also, older children and adults provide highly detailed and descriptive images associated with their sleep terrors compared to younger children, who either cannot recall or only vaguely remember. Sleep terrors in children are also more likely to occur in males than females; in adults, the ratio between sexes is equal. A longitudinal study examined twins, both identical and fraternal, and found that a significantly higher concordance rate of night terror was found in identical twins than in fraternal.

Though the symptoms of night terrors in adolescents and adults are similar, their causes, prognoses, and treatments are qualitatively different. There is some evidence that suggests that night terrors can occur if the sufferer does not eat a proper diet, does not get the appropriate amount or quality of sleep (e.g., because of sleep apnea), or is enduring stressful events. Adults who have experienced sexual abuse are more likely to receive a diagnosis of sleep disorders, including night terrors. Overall, though, adult night terrors are much less common and often respond best to treatments that rectify causes of poor quality or quantity of sleep.

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.

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.

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

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:

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.

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.

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.

Night terrors typically occur in children between the ages of three and twelve years, with a peak onset in children aged three and a half years old.

An estimated 1–6% of children experience night terrors. Boys and girls of all ethnic backgrounds are affected equally. In children younger than three and a half years old, peak frequency of night terrors is at least one episode per week. Among older children, peak frequency of night terrors is one or two episodes per month. The children will most likely have no recollection of the episode the next day. Pediatric evaluation may be sought to exclude the possibility that the night terrors are caused by seizure disorders or breathing problems. Most children will outgrow sleep terrors.

Sexsomnia affects individuals of all age groups and backgrounds but present as an increased risk for individuals who possess the following:

- coexisting sleep disorders

- sleep disruption secondary to obstructive sleep apnea

- sleep related epilepsy

- certain medications

Behaviors of pelvic thrusting, sexual arousal, and orgasms are often attributed to sleep related epilepsy disorder. In some cases, physical contact with a partner in bed acted as a trigger to initiate sexsomia behaviors.

Medications, such as the commonly prescribed treatment for insomnia, Ambien, have been shown to induce symptoms commonly associated with sexsomnia.

Like sleep-related eating disorders, sexsomnia presents more commonly in adults than children. However, these individuals usually have a history of parasomnias that began during childhood.

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.

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.

Symptoms of sexsomnia can be caused by or be associated with:

- stress factors

- sleep deprivation

- Consumption of alcohol or other drugs

- Pre-existing parasomnia behaviors

Sleep deprivation is known to have negative effects on the brain and behavior. Extended periods of sleep deprivation often results in the malfunctioning of neurons, directly effecting an individual's behavior. While muscles are able to regenerate even in the absence of sleep, neurons are incapable of this ability. Specific stages of sleep are responsible for the regeneration of neurons while others are responsible for the generation of new synaptic connections, the formation of new memories, etc.

Zolpidem, the widely known sedative Ambien, is used as common treatment for insomnia and has been seen to result in sexsomnia as an adverse effect.

Sexsomnia can also be triggered by physical contact initiated by a partner, or an individual sharing the same bed.

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.

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.

Waking up in the middle of the night, or nocturnal awakening, is the most frequently reported insomnia symptom, with approximately 35% of Americans over 18 reporting waking up three or more times per week. Of those who experience nocturnal awakenings, 43% report difficulty in resuming sleep after waking, while over 90% report the condition persisting for more than six months. Greater than 50% contend with MOTN conditions for more than five years.

A 2008 "Sleep in America" poll conducted by the National Sleep Foundation found that 42% of respondents awakened during the night at least a few nights a week, and 29% said they woke up too early and couldn’t get back to sleep. Other clinical studies have reported between 25% and 35% of people experience nocturnal awakenings at least three nights a week.

The primary genetic factor that has been strongly implicated in the development of narcolepsy involves an area of chromosome 6 known as the human leukocyte antigen (HLA) complex. Specific variations in HLA genes are strongly correlated with the presence of narcolepsy; however, these variations are not required for the condition to occur and sometimes occur in individuals without narcolepsy. These genetic variations in the HLA complex are thought to increase the risk of an auto-immune response to orexin-releasing neurons in the lateral hypothalamus.

The allele HLA-DQB1*06:02 of the human gene HLA-DQB1 was reported in more than 90% of patients, and alleles of other HLA genes such as HLA-DQA1*01:02 have been linked. A 2009 study found a strong association with polymorphisms in the TRAC gene locus (dbSNP IDs rs1154155, rs12587781, and rs1263646). A 2013 review article reported additional but weaker links to the loci of the genes TNFSF4 (rs7553711), Cathepsin H (rs34593439), and P2RY11-DNMT1 (rs2305795).

Another gene locus that has been associated with narcolepsy is EIF3G (rs3826784).

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.

One of these disorders is extrinsic (from Latin "extrinsecus", from without, on the outside) or circumstantial:

- Shift work sleep disorder, which affects people who work nights or rotating shifts.

Formerly, jet lag, too, was classified as an extrinsic type circadian rhythm disorder.

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.

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).

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.

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.