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.

There are an estimated 140,000 people with N24 – both sighted and blind – in the European Union, a total prevalence of approximately 3 per 10,000, or 0.03%. It is unknown how many individuals with this disorder do not seek medical attention, so incidence may be higher. The European portal for rare diseases, Orphanet, lists Non-24 as a rare disease by their definition: fewer than 1 affected person for every 2000 population. The US National Organization for Rare Disorders (NORD) lists Non-24 as a rare disease by its definition.

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.

As of 2005, there had been fewer than 100 cases of sighted people with non-24 reported in the scientific literature.

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.

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.

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.

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.

A survey of 1.1 million residents in the United States found that those that reported sleeping about 7 hours per night had the lowest rates of mortality, whereas those that slept for fewer than 6 hours or more than 8 hours had higher mortality rates. Getting 8.5 or more hours of sleep per night was associated with a 15% higher mortality rate. Severe insomnia – sleeping less than 3.5 hours in women and 4.5 hours in men – is associated with a 15% increase in mortality.

With this technique, it is difficult to distinguish lack of sleep caused by a disorder which is also a cause of premature death, versus a disorder which causes a lack of sleep, and the lack of sleep causing premature death. Most of the increase in mortality from severe insomnia was discounted after controlling for co-morbid disorders. After controlling for sleep duration and insomnia, use of sleeping pills was also found to be associated with an increased mortality rate.

The lowest mortality was seen in individuals who slept between six and a half and seven and a half hours per night. Even sleeping only 4.5 hours per night is associated with very little increase in mortality. Thus, mild to moderate insomnia for most people is associated with increased longevity and severe insomnia is associated only with a very small effect on mortality. It is unclear why sleeping longer than 7.5 hours is associated with excess mortality.

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.

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.

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.

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.

Circadian rhythm sleep disorders (CRSD) are a family of sleep disorders affecting (among other bodily processes) the timing of sleep. People with circadian rhythm sleep disorders are unable to go to sleep and awaken at the times commonly required for work and school as well as social needs. They are generally able to get enough sleep if allowed to sleep and wake at the times dictated by their "body clocks". The quality of their sleep is usually normal unless they also have another sleep disorder.

Humans, like most living organisms, have various biological rhythms. Circadian rhythms, often referred to as the body clock or the biological clock, control processes that re-occur daily, e.g. body temperature, alertness, and hormone secretion as well as sleep timing. Due to the circadian clock, sleepiness does not continuously increase throughout the day; a person's desire and ability to fall asleep is influenced both by the length of time since the person woke from an adequate sleep and by internal circadian rhythms. Thus, a person's body is ready for sleep and for wakefulness at relatively specific times of the day.

Sleep researcher Yaron Dagan states that "[t]hese disorders can lead to harmful psychological and functional difficulties and are often misdiagnosed and incorrectly treated doctors are unaware of their existence".

There is currently a great deal of active research on various aspects of circadian rhythm; this often occurs at major universities in conjunction with sleep research clinics at major hospitals. An example is the program with Harvard Medical School and Brigham and Women's Hospital. This research includes programs that are staffed by researchers from various departments at the university, including psychiatry, neurology, chemistry, biology. Other major sleep research centers are in Tel Aviv in Israel, Munich in Germany and in Japan.

A wide variety of sleep disorders are actively being researched. Measuring body temperature or melatonin levels may be used. Some hospitals do blood tests for melatonin levels. Saliva tests for melatonin are now available for online purchase; its metabolites can also be tested in urine.

According to one meta-analysis, the two most prevalent sleep disorders among children are confusional arousals and sleep walking. An estimated 17.3% of kids between 3 and 13 years old experience confusional arousals. About 17% of children sleep walk, with the disorder being more common among boys than girls. The peak ages of sleep walking are from 8 to 12 years old. A different systematic review offers a high range of prevalence rates of sleep bruxism for children. Between 15.29 and 38.6% of preschoolers grind their teeth at least one night a week. All but one of the included studies reports decreasing bruxist prevalence as age increased as well as a higher prevalence among boys than girls.

Another systematic review noted 7-16% of young adults suffer from delayed sleep phase disorder. This disorder reaches peak prevalence when people are in their 20's. Between 20 and 26% of adolescents report a sleep onset latency of >30 minutes. Also, 7-36% have difficulty initiating sleep. Asian teens tend to have a higher prevalence of all of these adverse sleep outcomes than their North American and European counterparts.

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.

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).

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.

Somniloquy or sleep-talking is a parasomnia that refers to talking aloud while asleep. It can be quite loud, ranging from simple mumbling sounds to loud shouts and long, frequently inarticulate speeches, and can occur many times during a sleep cycle. As with sleepwalking and night terrors, sleeptalking usually occurs during delta-wave NREM sleep stages or during temporary arousals therefrom.

It can also occur during the REM sleep stage, at which time it represents what sleep therapists call a "motor breakthrough" (see sleep paralysis) of dream speech: words spoken in a dream are spoken out loud. Depending on its frequency, this may or may not be considered pathological. All motor functions are typically disabled during REM sleep thus, motoric, i.e., verbal elaboration of dream content, could be considered an REM behavior disorder (see below).

Sleep-talking can occur by itself or as a feature of another sleep disorder such as:

- Rapid eye movement behavior disorder (RBD) – loud, emotional or profane sleep talking

- Sleepwalking

- Night terrors – intense fear, screaming, shouting

- Sleep-related eating disorder (SRED)

Sleep-talking is very common and is reported in 50% of young children, with most of them outgrowing it by puberty, although in rare cases it may persist into adulthood (about 4% of adults are reported to talk in their sleep). It appears to run in families. In 1966, researchers worked to find links between heredity and somniloquy. Their research suggests the following:

- Sleep-talking parents are more likely to have children who sleep-talk

- Sleep talking can still occur, though much less commonly, when neither parent has a history of sleep talking

- A large portion of parents begin to sleep-talk later in life without any prior history of sleep-talking during childhood or adolescence

Sleep-talking by itself is typically harmless; however, it can wake others and cause them consternation—especially when misinterpreted as conscious speech by an observer. If the sleep-talking is dramatic, emotional, or profane it may be a sign of another sleep disorder (see above). Sleep-talking can be monitored by a partner or by using an audio recording device; devices which remain idle until detecting a sound wave are ideal for this purpose. Polysomnography (sleep recording) shows episodes of sleep talking that can occur in any stage of sleep.

In 1999, Louis Ptáček's and Ying-Hui Fu's research group at the University of California, San Francisco reported findings of a human circadian rhythm disorder showing a familial tendency. The disorder was characterized by a lifelong pattern of sleep onset around 7:30 p.m. and offset around 4:30 a.m. Among three lineages, 29 people were identified as affected with this familial advanced sleep-phase disorder (FASPD), and 46 were considered unaffected. The pedigrees demonstrated FASPD to be a highly penetrant, autosomal dominant trait.

Two years after reporting the finding of FASPD, Ptáček's and Fu's groups published results of genetic sequencing analysis on a family with FASPD. They genetically mapped the FASPD locus to chromosome 2q where very little human genome sequence was then available. Thus, they identified and sequenced all the genes in the critical interval. One of these was Period2 (Per2). Sequencing of the hPer2 gene revealed a serine-to-glycine point mutation in the CKI binding domain of the hPER2 protein that resulted in hypophosphorylation of Per2 in vitro.

In 2005, Fu's and Ptáček's labs reported discovery of a different mutation causing FASPD. This time, CKIδ was implicated, demonstrating an A-to-G missense mutation that resulted in a threonine-to-alanine alteration in the protein. The evidence for both of these reported causes of FASPD is strengthened by the absence of said mutations in all tested control subjects and by demonstration of functional consequences of the respective mutations in vitro. Fruit flies and mice engineered to carry the human mutation also demonstrated abnormal circadian phenotypes although the mutant flies had a long circadian period while the mutant mice had a shorter period. The differences between flies and mammals that account for this difference are not known. Most recently, Ptáček and Fu reported additional studies of the human Per2 S662G mutation and generation of mice carrying the human mutation. These mice had a circadian period almost 2 hours shorter than wild-type animals. Genetic dosage studies of CKIδ on the Per2 S662G mutation revealed that CKIδ is having opposite effects on Per2 levels depending on the sites on Per2 that CKIδ is phosphorylating.

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