The most common sleep disorders include:

- Bruxism, involuntarily grinding or clenching of the teeth while sleeping.

- Catathrenia, nocturnal groaning during prolonged exhalation.

- Delayed sleep phase disorder (DSPD), inability to awaken and fall asleep at socially acceptable times but no problem with sleep maintenance, a disorder of circadian rhythms. Other such disorders are advanced sleep phase disorder (ASPD), non-24-hour sleep–wake disorder (non-24) in the sighted or in the blind, and irregular sleep wake rhythm, all much less common than DSPD, as well as the situational shift work sleep disorder.

- Hypopnea syndrome, abnormally shallow breathing or slow respiratory rate while sleeping.

- Idiopathic hypersomnia, a primary, neurologic cause of long-sleeping, sharing many similarities with narcolepsy.

- Insomnia disorder (primary insomnia), chronic difficulty in falling asleep and/or maintaining sleep when no other cause is found for these symptoms. Insomnia can also be comorbid with or secondary to other disorders.

- Kleine–Levin syndrome, a rare disorder characterized by persistent episodic hypersomnia and cognitive or mood changes.

- Narcolepsy, including excessive daytime sleepiness (EDS), often culminating in falling asleep spontaneously but unwillingly at inappropriate times. About 70% of those who have narcolepsy also have cataplexy, a sudden weakness in the motor muscles that can result in collapse to the floor while retaining full conscious awareness.

- Night terror, "Pavor nocturnus", sleep terror disorder, an abrupt awakening from sleep with behavior consistent with terror.

- Nocturia, a frequent need to get up and urinate at night. It differs from enuresis, or bed-wetting, in which the person does not arouse from sleep, but the bladder nevertheless empties.

- Parasomnias, disruptive sleep-related events involving inappropriate actions during sleep, for example sleep walking, night-terrors and catathrenia.

- Periodic limb movement disorder (PLMD), sudden involuntary movement of arms and/or legs during sleep, for example kicking the legs. Also known as nocturnal myoclonus. See also Hypnic jerk, which is not a disorder.

- Rapid eye movement sleep behavior disorder (RBD), acting out violent or dramatic dreams while in REM sleep, sometimes injuring bed partner or self (REM sleep disorder or RSD).

- Restless legs syndrome (RLS), an irresistible urge to move legs. RLS sufferers often also have PLMD.

- Shift work sleep disorder (SWSD), a situational circadian rhythm sleep disorder. (Jet lag was previously included as a situational circadian rhythm sleep disorder, but it doesn't appear in DSM-5 (see Diagnostic and Statistical Manual of Mental Disorders)).

- Sleep apnea, obstructive sleep apnea, obstruction of the airway during sleep, causing lack of sufficient deep sleep, often accompanied by snoring. Other forms of sleep apnea are less common. When air is blocked from entering into the lungs, the individual unconsciously gasps for air and sleep is disturbed. Stops of breathing of at least ten seconds, 30 times within seven hours of sleep, classifies as apnea. Other forms of sleep apnea include central sleep apnea and sleep-related hypoventilation.

- Sleep paralysis, characterized by temporary paralysis of the body shortly before or after sleep. Sleep paralysis may be accompanied by visual, auditory or tactile hallucinations. Not a disorder unless severe. Often seen as part of narcolepsy.

- Sleepwalking or "somnambulism", engaging in activities normally associated with wakefulness (such as eating or dressing), which may include walking, without the conscious knowledge of the subject.

- Somniphobia, one cause of sleep deprivation, a dread/ fear of falling asleep or going to bed. Signs of the illness include anxiety and panic attacks before and during attempts to sleep.

Hypersomnia can be primary (of central/brain origin), or it can be secondary to any of numerous medical conditions. More than one type of hypersomnia can coexist in a single patient. Even in the presence of a known cause of hypersomnia, the contribution of this cause to the complaint of EDS needs to be assessed. When specific treatments of the known condition do not fully suppress EDS, additional causes of hypersomnia should be sought. For example, if a patient with sleep apnea is treated with CPAP (continuous positive airway pressure) which resolves their apneas but not their EDS, it is necessary to seek other causes for the EDS. Obstructive sleep apnea “occurs frequently in narcolepsy and may delay the diagnosis of narcolepsy by several years and interfere with its proper management.”

The true primary hypersomnias include these: narcolepsy (with and without cataplexy); idiopathic hypersomnia; and recurrent hypersomnias (like Klein-Levin syndrome).

There are two main characteristics of narcolepsy: excessive daytime sleepiness and abnormal REM sleep. The first, excessive daytime sleepiness (EDS), occurs even after adequate night time sleep. A person with narcolepsy is likely to become drowsy or fall asleep, often at inappropriate times and places, or just be very tired throughout the day. Narcoleptics are not able to experience the amount of restorative deep sleep that healthy people experience – they are not "over-sleeping". In fact, narcoleptics live their entire lives in a constant state of extreme sleep deprivation.

Daytime naps may occur with little warning and may be physically irresistible. These naps can occur several times a day. They are typically refreshing, but only for a few hours or less. Vivid dreams may be experienced on a regular basis, even during very brief naps. Drowsiness may persist for prolonged periods or remain constant. In addition, night-time sleep may be fragmented, with frequent awakenings. A second prominent symptom of narcolepsy is abnormal REM sleep. Narcoleptics are unique in that they enter into the REM phase of sleep in the beginnings of sleep, even when sleeping during the day.

The classic symptoms of the disorder, often referred to as the "tetrad of narcolepsy," are cataplexy, sleep paralysis, hypnagogic hallucinations, and excessive daytime sleepiness. Other symptoms may include automatic behaviors and night-time wakefulness. These symptoms may not occur in all patients.

- Cataplexy is an episodic loss of muscle function, ranging from slight weakness such as limpness at the neck or knees, sagging facial muscles, weakness at the knees often referred to as "knee buckling", or inability to speak clearly, to a complete body collapse. Episodes may be triggered by sudden emotional reactions such as laughter, anger, surprise, or fear, and may last from a few seconds to several minutes. The person remains conscious throughout the episode. In some cases, cataplexy may resemble epileptic seizures. Usually speech is slurred and vision is impaired (double vision, inability to focus), but hearing and awareness remain normal. Cataplexy also has a severe emotional impact on narcoleptics, as it can cause extreme anxiety, fear, and avoidance of people or situations that might elicit an attack. Cataplexy is generally considered to be unique to narcolepsy and is analogous to sleep paralysis in that the usually protective paralysis mechanism occurring during sleep is inappropriately activated. The opposite of this situation (failure to activate this protective paralysis) occurs in rapid eye movement behavior disorder.

- Periods of wakefulness at night

- Sleep paralysis is the temporary inability to talk or move when waking (or less often, when falling asleep). It may last a few seconds to minutes. This is often frightening but is not dangerous.

- Hypnagogic hallucinations are vivid, often frightening, dreamlike experiences that occur while dozing or falling asleep. Hypnopompic hallucinations refer to the same sensations while awakening from sleep. These hallucinations may manifest in the form of visual or auditory sensations.

- Automatic behaviors occur when a person continues to function (talking, putting things away, etc.) during sleep episodes but awakens with no memory of performing such activities. It is estimated that up to 40 percent of people with narcolepsy experience automatic behavior during sleep episodes.

In most cases, the first symptom of narcolepsy to appear is excessive and overwhelming daytime sleepiness. The other symptoms may begin alone or in combination months or years after the onset of the daytime naps. There are wide variations in the development, severity, and order of appearance of cataplexy, sleep paralysis, and hypnagogic hallucinations in individuals. Only about 20 to 25 percent of people with narcolepsy experience all four symptoms. The excessive daytime sleepiness generally persists throughout life, but sleep paralysis and hypnagogic hallucinations may not. A rare subset of narcoleptics also experience a heightened sense of taste and smell known as the supertaster phenomenon.

Many people with narcolepsy also suffer from insomnia for extended periods of time. The excessive daytime sleepiness and cataplexy often become severe enough to cause serious problems in a person's social, personal, and professional life. Normally, when an individual is awake, brain waves show a regular rhythm. When a person first falls asleep, the brain waves become slower and less regular, which is called non-rapid eye movement (NREM) sleep. After about an hour and a half of NREM sleep, the brain waves begin to show a more active pattern again, called REM sleep (rapid eye movement sleep), when most remembered dreaming occurs. Associated with the EEG-observed waves during REM sleep, muscle atonia is present called REM atonia.

In narcolepsy, the order and length of NREM and REM sleep periods are disturbed, with REM sleep occurring at sleep onset instead of after a period of NREM sleep. Also, some aspects of REM sleep that normally occur only during sleep, like lack of muscular control, sleep paralysis, and vivid dreams, occur at other times in people with narcolepsy. For example, the lack of muscular control can occur during wakefulness in a cataplexy episode; it is said that there is intrusion of REM atonia during wakefulness. Sleep paralysis and vivid dreams can occur while falling asleep or waking up. Simply put, the brain does not pass through the normal stages of dozing and deep sleep but goes directly into (and out of) rapid eye movement (REM) sleep.

As a consequence night time sleep does not include as much deep sleep, so the brain tries to "catch up" during the day, hence EDS. People with narcolepsy may visibly fall asleep at unpredicted moments (such motions as head bobbing are common). People with narcolepsy fall quickly into what appears to be very deep sleep, and they wake up suddenly and can be disoriented when they do (dizziness is a common occurrence). They have very vivid dreams, which they often remember in great detail. People with narcolepsy may dream even when they only fall asleep for a few seconds. Along with vivid dreaming, people with narcolepsy are known to have audio or visual hallucinations prior to falling asleep.

Narcoleptics can gain excess weight; children can gain 20 to 40 lb (9 to 18 kg) when they first develop narcolepsy; in adults the body-mass index is about 15% above average.

Those who suffer from idiopathic hypersomnia have recurring episodes of excessive daytime sleepiness (EDS). These occur in spite of "adequate, or more typically, extraordinary sleep amounts (e.g., greater than 10 hours per night)." Sleep is usually deep, with significant difficulty arousing from sleep, even with use of several alarm clocks. In fact, patients with IH often must develop elaborate rituals to wake, as alarm clocks and even physical attempts by friends/family to wake them may fail. Despite getting more hours of sleep than typically required by the human body, patients awake unrefreshed and may also suffer sleep inertia, known more descriptively in its severe form as sleep drunkenness (significant disorientation upon awakening). Daytime naps are generally very long (up to several hours) and are also unrefreshing, as opposed to the short refreshing naps associated with narcolepsy. Sleep paralysis and hypnagogic hallucinations may also occur, as well as motor hyper-reactivity.

Several studies have shown increased frequencies of other symptoms in patients with idiopathic hypersomnia, although it is not clear whether these symptoms are caused by the idiopathic hypersomnia. These symptoms include palpitations, digestive problems, difficulty with body temperature regulation, and cognitive problems, especially deficits in memory, attention, and concentration. Anxiety and depression are often increased in idiopathic hypersomnia, most likely as a response to chronic illness. A large case series in 2010 found that peripheral vascular symptoms, such as cold hands and feet (Raynaud’s-type phenomena) were significantly more common in people with idiopathic hypersomnia than in controls. In addition to difficulty with temperature regulation and Raynaud’s type symptoms, other symptoms associated with autonomic dysfunction were noted to occur in idiopathic hypersomnia. These included: fainting episodes (syncope); dizziness upon arising (orthostatic hypotension); and headaches (possibly migrainous in quality). Food cravings and impotence have also been reported.

Symptom intensity often varies between weeks, months, or years, and symptoms can worsen just prior to menses in women. Many patients are chronically tardy to work, school or social engagements and, over time, may lose the ability to function in family, social, occupational or other settings altogether. (See Prognosis section below).

A sleep disorder, or somnipathy, is a medical disorder of the sleep patterns of a person or animal. Some sleep disorders are serious enough to interfere with normal physical, mental, social and emotional functioning. Polysomnography and actigraphy are tests commonly ordered for some sleep disorders.

Disruptions in sleep can be caused by a variety of issues, from teeth grinding (bruxism) to night terrors. When a person suffers from difficulty falling asleep and/or staying asleep with no obvious cause, it is referred to as insomnia.

Sleep disorders are broadly classified into dyssomnias, parasomnias, circadian rhythm sleep disorders involving the timing of sleep, and other disorders including ones caused by medical or psychological conditions and sleeping sickness.

Some common sleep disorders include sleep apnea (stops in breathing during sleep), narcolepsy and hypersomnia (excessive sleepiness at inappropriate times), cataplexy (sudden and transient loss of muscle tone while awake), and sleeping sickness (disruption of sleep cycle due to infection). Other disorders include sleepwalking, night terrors and bed wetting. Management of sleep disturbances that are secondary to mental, medical, or substance abuse disorders should focus on the underlying conditions.

RBD is characterized by the dreamer acting out his or her dreams. These dreams often involve kicking, screaming, punching, grabbing, and even jumping out of bed. When awakened, people can usually recall the dream they were having, which will match the actions they were performing, but they will not be aware that they were moving. In a normal sleep cycle, REM sleep may be experienced at intervals of between 90 minutes and two hours every night, which means RBD episodes may occur up to four times a night. In a rare case, they may only happen once a week or once a month. Episodes occur more towards the morning hours because that is when REM sleep is more frequent. The actions in an episode can result in injuries to oneself or one's bed partner. People can also respond to other people while sleeping and not even know it. This causes them to be aware of things while they are sleeping, which can result in sleep deprivation.

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.

In addition to differentiating between the primary and secondary hypersomnias, the 2001 International Classification of Sleep Disorders (ICSD) further classified the primary hypersomnia syndromes. These included idiopathic hypersomnia, narcolepsy, and the recurrent hypersomnias (like Klein-Levin syndrome).

The 2001 ICSD defines idiopathic hypersomnia as "a disorder of presumed central nervous system cause that is associated with a normal or prolonged major sleep episode and excessive sleepiness consisting of prolonged (1- to 2-hour) sleep episodes of N-REM"(non-rapid eye movement sleep). The ICSD initially described two clinical forms of idiopathic hypersomnia: "1) a polysymptomatic form with nocturnal sleep and naps of abnormally long duration with ‘sleep drunkenness’ on awakening, and 2) a monosymptomatic form manifested by isolated EDS." These forms were later described as idiopathic hypersomnia with long sleep time and idiopathic hypersomnia without long sleep time, respectively.

This classification has steadily evolved, as further research has shown overlap between narcolepsy and idiopathic hypersomnia. The 3rd edition of the ICSD labels narcolepsy caused by hypocretin deficiency as "type 1 narcolepsy," which is almost always associated with cataplexy. The other hypersomnias remain subdivided based on the presence of sleep-onset rapid eye movement periods (SOREMPs). They are labeled: "type 2 narcolepsy," with 2 or more SOREMPs on mean sleep latency testing (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 the newly understood overlap of idiopathic hypersomnia and narcolepsy, the 5th edition of the Diagnostic and Statistical Manual of Mental Disorders also updated its classification of the primary hypersomnias. It reclassified both idiopathic hypersomnia with and without long sleep time as major somnolence disorder (MSD). Additionally, MSD encompasses all syndromes of hypersomnolence not explained by low hypocretin, including not only idiopathic hypersomnia, but also narcolepsy without cataplexy, and long sleepers (patients 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 felt that this subgroup might have dysfunction in multiple arousal systems. (See Causes section below).

Rapid eye movement behavior disorder (RBD) occurs when there is a loss of normal voluntary muscle atonia during REM sleep resulting in motor behavior in response to dream content. It can be caused by adverse reactions to certain drugs or during drug withdrawal; however, it is most often associated with the elderly and in those with neurodegenerative disorders such as Parkinson disease and other neurodegenerative diseases, for example multiple system atrophy and Lewy body dementia.

RBD is categorized as either idiopathic or symptomatic.

This sleep disorder frequently applies when patients report not feeling tired despite their subjective perception of not having slept. Generally, they may describe experiencing several years of no sleep, short sleep, or non-restorative sleep. Otherwise, patients appear healthy, both psychiatrically and medically. (That this condition is often asymptomatic could explain why it is relatively unreported.)

However, upon clinical observation, it is found that patients may severely overestimate the time they took to fall asleep—often reporting having slept half the amount of time indicated by polysomnogram or electroencephalography (EEG), which may record normal sleep. Observing such discrepancy between subjective and objective reports, clinicians may conclude that the perception of poor sleep is primarily illusionary.

Alternatively, some people may report excessive daytime sleepiness or chronic disabling sleepiness, while no sleep disorder has been found to exist. Methods of diagnosing sleepiness objectively, such as the Multiple Sleep Latency Test do not confirm the symptom"true" sleepiness is not observed despite the complaint. (It may be speculated that such reports of daytime sleepiness may be a result of the nocebo response —the reverse of the placebo effect—due to patient expectations of adverse effects from their subjective perception of poor sleep.)

Finally, on the opposite end of the spectrum, other patients may report feeling that they have slept much longer than is observed. It has been proposed that this experience be subclassified under sleep state misperception as "positive sleep state misperception", "reverse sleep state misperception", and "negative sleep state misperception".

A sleep diary should be kept to aid in diagnosis and for chronicling the sleep schedule during treatment. Other ways to monitor the sleep schedule are actigraphy or use of a Continuous Positive Airway Pressure (CPAP) machine that can log sleeping times

The following are possible warning signs:

- sleeping off and on in a series of naps during the day and at night, with no regular pattern but with normal total sleep time,

- difficulty getting restorative sleep, and

- excessive daytime sleepiness.

Because of the changes in sleep/wake time, and because this is a rare disorder, initially it can seem like another circadian rhythm sleep disorder such as non-24-hour sleep–wake disorder or like insomnia.

According to the International Classification of Sleep Disorders, Revised (ICSD-R, 2001), the circadian rhythm sleep disorders share a common underlying chronophysiologic basis:

Incorporating minor updates (ICSD-3, 2014), the diagnostic criteria for delayed sleep phase disorder are:

Some people with the condition adapt their lives to the delayed sleep phase, avoiding morning business hours as much as possible. The ICSD's severity criteria are:

- Mild: Two-hour delay (relative to the desired sleep time) associated with little or mild impairment of social or occupational functioning.

- Moderate: Three-hour delay associated with moderate impairment.

- Severe: Four-hour delay associated with severe impairment.

Some features of DSPD which distinguish it from other sleep disorders are:

- People with DSPD have at least a normal—and often much greater than normal—ability to sleep during the morning, and sometimes in the afternoon as well. In contrast, those with chronic insomnia do not find it much easier to sleep during the morning than at night.

- People with DSPD fall asleep at more or less the same time every night, and sleep comes quite rapidly if the person goes to bed near the time he or she usually falls asleep. Young children with DSPD resist going to bed before they are sleepy, but the bedtime struggles disappear if they are allowed to stay up until the time they usually fall asleep.

- DSPD patients usually sleep well and regularly when they can follow their own sleep schedule, e.g., on weekends and during vacations.

- DSPD is a chronic condition. Symptoms must have been present for at least three months before a diagnosis of DSPD can be made.

Often people with DSPD manage only a few hours sleep per night during the working week, then compensate by sleeping until the afternoon on weekends. Sleeping late on weekends, and/or taking long naps during the day, may give people with DSPD relief from daytime sleepiness but may also perpetuate the late sleep phase.

People with DSPD can be called "night owls". They feel most alert and say they function best and are most creative in the evening and at night. People with DSPD cannot simply force themselves to sleep early. They may toss and turn for hours in bed, and sometimes not sleep at all, before reporting to work or school. Less-extreme and more-flexible night owls are within the normal chronotype spectrum.

By the time those who have DSPD seek medical help, they usually have tried many times to change their sleeping schedule. Failed tactics to sleep at earlier times may include maintaining proper sleep hygiene, relaxation techniques, early bedtimes, hypnosis, alcohol, sleeping pills, dull reading, and home remedies. DSPD patients who have tried using sedatives at night often report that the medication makes them feel tired or relaxed, but that it fails to induce sleep. They often have asked family members to help wake them in the morning, or they have used multiple alarm clocks. As the disorder occurs in childhood and is most common in adolescence, it is often the patient's parents who initiate seeking help, after great difficulty waking their child in time for school.

The current formal name established in the third edition of the International Classification of Sleep Disorders (ICSD-3) is delayed sleep-wake phase disorder. Earlier, and still common, names include delayed sleep phase disorder (DSPD), delayed sleep phase syndrome (DSPS), and circadian rhythm sleep disorder, delayed sleep phase type (DSPT).

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.

The patient has a complaint of insomnia while sleep quality and duration are normal. Polysomnographic monitoring demonstrates normal sleep latency, a normal number of arousals and awakenings, and normal sleep duration with or without a multiple sleep latency test that demonstrates a mean sleep latency of greater than 10 minutes. No medical or mental disorder produces the complaint. Other sleep disorders producing insomnia are not present to a degree that would explain the patient’s complaint.

Nocturnal awakenings are more common in older patients and have been associated with depressive disorders, chronic pain, obstructive sleep apnea, obesity, alcohol consumption, hypertension, gastroesophageal reflux disease, heart disease, menopause, prostate problems, and bipolar disorders.

Nocturnal awakenings can be mistaken as shift work disorder.

Parasomnia disorders are classified into the following categories:

- arousal disorders

- sleep-wake transition disorders

- parasomnias associated with REM sleep

The primary symptoms of shift work sleep disorder are insomnia and excessive sleepiness associated with working (and sleeping) at non-standard times. Shift work sleep disorder is also associated with falling asleep at work. Total daily sleep time is usually shortened and sleep quality is less in those who work night shifts compared to those who work day shifts. Sleepiness is manifested as a desire to nap, unintended dozing, impaired mental acuity, irritability, reduced performance, and accident proneness. Shift work is often combined with extended hours of duty, so fatigue can be a compounding factor. The symptoms coincide with the duration of shift work and usually remit with the adoption of a conventional sleep-wake schedule. The boundary between a "normal response" to the rigors of shift work and a diagnosable disorder is not sharp.

Under DSM-5 criteria, there are 11 diagnostic groups that comprise sleep-wake disorders. These include, Insomnia disorder, Hypersomnolence disorder, Narcolepsy, Obstructive sleep apnea hypopnea, Central sleep apnea, Sleep-related hypoventilation, Circadian rhythm sleep-wake disorders, Non–rapid eye movement (NREM) sleep arousal disorders, Nightmare disorder, Rapid eye movement (REM) sleep behavior disorder, Restless legs syndrome, and substance-medication-induced sleep disorder. Sexsomnia is classified under NREM arousal parasomnia.

Narcolepsy is a long-term neurological disorder that involves a decreased ability to regulate sleep-wake cycles. Symptoms include periods of excessive daytime sleepiness that usually last from seconds to minutes and may occur at any time. About 70% of those affected also experience episodes of sudden loss of muscle strength, known as cataplexy. These spells can be brought on by strong emotions. Less commonly there may be inability to move or vivid hallucinations while falling asleep or waking up. People with narcolepsy tend to sleep about the same number of hours per day as people without, but the quality of sleep tends to be worse.

The exact cause of narcolepsy is unknown with potentially several causes. In up to 10% of cases there is a family history of the disorder. Often those affected have low levels of the neuropeptide "orexin" which may be due to an autoimmune disorder. Trauma, infections, toxins, or psychological stress may also play a role. Diagnosis is typically based on the symptoms and sleep studies, after ruling out other potential causes. Excessive daytime sleepiness can also be caused by other sleep disorders such as sleep apnea, major depressive disorder, anemia, heart failure, drinking alcohol, and not getting enough sleep. Cataplexy may be mistaken for seizures.

While there is no cure, a number of lifestyle changes and medications may help. Lifestyle changes include taking regular short naps and sleep hygiene. Medications used include modafinil, sodium oxybate, and methylphenidate. While initially effective, tolerance to the benefits may develop over time. Tricyclic antidepressants and selective serotonin reuptake inhibitors (SSRIs) may improve cataplexy.

About 0.2 to 600 per 100,000 people are affected. The condition often begins in childhood. Men and women are affected equally. Untreated narcolepsy increases the risk of motor vehicle collisions and falls. The term "narcolepsy" is from the French "narcolepsie". The French term was first used in 1880 by Jean-Baptiste-Édouard Gélineau who used the Greek νάρκη ("narkē") meaning "numbness" and λῆψις ("lepsis") meaning "attack".

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

Delayed sleep phase disorder (DSPD), more often known as delayed sleep phase syndrome and also as delayed sleep-wake phase disorder, is a chronic dysregulation of a person's circadian rhythm (biological clock), compared to the general population and relative to societal norms. The disorder affects the timing of sleep, peak period of alertness, the core body temperature rhythm, and hormonal and other daily cycles. People with DSPD generally fall asleep some hours after midnight and have difficulty waking up in the morning. People with DSPD probably have a circadian period significantly longer than 24 hours. Depending on the severity, the symptoms can be managed to a greater or lesser degree, but no cure is known, and research suggests a genetic origin for the disorder.

Affected people often report that while they do not get to sleep until the early morning, they do fall asleep around the same time every day. Unless they have another sleep disorder such as sleep apnea in addition to DSPD, patients can sleep well and have a normal need for sleep. However, they find it very difficult to wake up in time for a typical school or work day. If they are allowed to follow their own schedules, e.g. sleeping from 3:00 am to 12:00 noon, their sleep is improved and they may not experience excessive daytime sleepiness. Attempting to force oneself onto daytime society's schedule with DSPD has been compared to constantly living with jet lag; DSPD has, in fact, been referred to as "social jet lag".

Researchers in 2017 linked DSPD to at least one genetic mutation. The syndrome usually develops in early childhood or adolescence. An adolescent version may disappear in late adolescence or early adulthood; otherwise, DSPD is a lifelong condition. Prevalence among adults, equally distributed among women and men, is around 0.15%, or three in 2,000. Prevalence among adolescents is as much as 7–16%.

DSPD was first formally described in 1981 by Elliot D. Weitzman and others at Montefiore Medical Center. It is responsible for 7–10% of patient complaints of chronic insomnia. However, since many doctors are unfamiliar with the condition, it often goes untreated or is treated inappropriately; DSPD is often misdiagnosed as primary insomnia or as a psychiatric condition. DSPD can be treated or helped in some cases by careful daily sleep practices, morning light therapy, evening dark therapy, earlier exercise and meal times, and medications such as melatonin and modafinil; the former is a natural neurohormone partly responsible for the human body clock. At its most severe and inflexible, DSPD is a disability. A chief difficulty of treating DSPD is in maintaining an earlier schedule after it has been established, as the patient's body has a strong tendency to reset the sleeping schedule to its intrinsic late times. People with DSPD may improve their quality of life by choosing careers that allow late sleeping times, rather than forcing themselves to follow a conventional 9-to-5 work schedule.

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.

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.

Caffeine-induced sleep disorder is a psychiatric disorder that results from overconsumption of the stimulant caffeine. "When caffeine is consumed immediately before bedtime or continuously throughout the day, sleep onset may be delayed, total sleep time reduced, normal stages of sleep altered, and the quality of sleep decreased." Caffeine reduces slow-wave sleep in the early part of the sleep cycle and can reduce rapid eye movement sleep later in the cycle. Caffeine increases episodes of wakefulness, and high doses in the late evening can increase sleep onset latency. In elderly people, there is an association between use of medication containing caffeine and difficulty in falling asleep.

The specific criteria for this disorder in the fourth version of the "Diagnostic and Statistical Manual of Mental Disorders" (DSM-IV) include that there must be a significant inability to sleep which is caused entirely by the physiological effects of caffeine as proven by an examination; if sleeping issues can be accounted for due to a breathing-related sleep disorder, narcolepsy, a circadian rhythm sleep disorder or a mental disorder, then caffeine-induced sleep disorder is not the cause. This condition causes a notable impairment in functioning in sufferers.

Overconsumption:

Excessive ingestion of caffeine can lead to a state of intoxication. This period of intoxication is characterized by restlessness, agitation, excitement, rambling thought or speech, and even insomnia. Even doses of caffeine relating to just one cup of coffee can increase sleep latency and decrease the quality of sleep especially in non-REM deep sleep. A dose of caffeine taken in the morning can have these effects the following night, so one of the main practices of sleep hygiene a person can do is to cease the consumption of caffeine.