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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 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.
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.
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.
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).
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.
Four of them are intrinsic (from Latin "intrinsecus", on the inside, inwardly), "built-in":
- Advanced sleep phase disorder (ASPD), a.k.a. advanced sleep phase syndrome (ASPS), characterized by difficulty staying awake in the evening and difficulty staying asleep in the morning
- Delayed sleep phase disorder (DSPD), a.k.a. delayed sleep phase syndrome (DSPS), characterized by a much later than normal timing of sleep onset and offset and a period of peak alertness in the middle of the night
- Irregular sleep–wake rhythm, which presents as sleeping at very irregular times, and usually more than twice per day (waking frequently during the night and taking naps during the day) but with total time asleep typical for the person's age
- Non-24-hour sleep–wake disorder (non-24, a.k.a. hypernychthemeral syndrome), in which the affected individual's sleep occurs later and later each day, with the period of peak alertness also continuously moving around the clock from day to day.
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.
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".
Symptoms reported by patients forced into a 24-hour schedule are similar to those of sleep deprivation and can include:
- Apraxia including ideational apraxia, ideomotor apraxia, kinetic apraxia, limb apraxia, verbal apraxia
- Cognitive dysfunction
- Difficulties concentrating
- Confusion
- Depressed mood
- Diarrhea
- Extreme nausea
- Extreme fatigue
- Hair loss
- Headaches
- Impaired balance
- Photosensitivity
- Joint pain
- Loss of muscle coordination (ataxia)
- Menstrual irregularities
- Muscle pain
- Suicidal thoughts
- Weight gain
- Hallucinations
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.
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".
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.
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.
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.
Sleep state misperception is classified as an intrinsic dyssomnia. While SSM is regarded a sub-type of insomnia, it is also established as a separate sleep-condition, with distinct pathophysiology. Nonetheless, the value of distinguishing this type of insomnia from other types is debatable due to the relatively low frequency of SSM being reported.
Sleep state misperception can also be further broken down into several types, by patients who—
- report short sleep (subjective insomnia complaint without objective findings)
- or no sleep at all (subjective "total" insomnia)
- report excessive daytime sleepiness (subjective sleepiness complaint without objective findings)
- report sleeping too much (subjective hypersomnia without objective findings)
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).
Dyssomnias are a broad classification of sleeping disorders involving difficulty getting to sleep, remaining asleep, or of excessive sleepiness.
Dyssomnias are primary disorders of initiating or maintaining sleep or of excessive sleepiness and are characterized by a disturbance in the amount, quality, or timing of sleep.
Patients may complain of difficulty getting to sleep or staying asleep, intermittent wakefulness during the night, early morning awakening, or combinations of any of these. Transient episodes are usually of little significance. Stress, caffeine, physical discomfort, daytime napping, and early bedtimes are common factors.
Parasomnia disorders are classified into the following categories:
- arousal disorders
- sleep-wake transition disorders
- parasomnias associated with REM sleep
Non-24-hour sleep–wake disorder (non-24), is one of several chronic circadian rhythm sleep disorders (CRSDs). It is defined as a "chronic steady pattern comprising [...] daily delays in sleep onset and wake times in an individual living in society." Symptoms result when the non-entrained (free-running) endogenous circadian rhythm drifts out of alignment with the light/dark cycle in nature.
The sleep pattern can be quite variable. People with a circadian rhythm that is quite near to 24 hours may be able to sleep on a conventional, socially acceptable schedule, that is, at night. Others, with a "daily" cycle upwards of 25 hours or more may need to adopt a sleep pattern that is congruent with their free-running circadian clock, shifting their sleep times daily, thereby often obtaining satisfactory sleep but suffering social and occupational consequences.
The majority of people with non-24 are totally blind, and the failure of entrainment is explained by an absence of photic input to the circadian clock. These people's brains may have normal "body clocks", but the clocks do not receive input from the eyes about environmental light levels, as that requires a functioning retina, optic nerve and visual processing center.
The disorder also occurs in sighted people for reasons that are not well understood. Their circadian rhythms are not normal, often running to more than 25 hours. Their visual systems may function normally but their brains are incapable of making the large adjustment to a 24-hour schedule.
Though often referred to as non-24, for example by the FDA, the disorder is also known by the following terms:
- Non-24-hour sleep–wake syndrome
- Non-24-hour sleep–wake disorder
- Non-24-hour sleep-wake rhythm disorder
- Free running disorder (FRD)
- Hypernychthemeral disorder
- Circadian rhythm sleep disorder – free-running type
- Circadian rhythm sleep disorder – nonentrained type
- N24HSWD
- Non-24-hour circadian rhythm disorder
The disorder in its extreme form is an invisible disability that can be "extremely debilitating in that it is incompatible with most social and professional obligations".
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:
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.
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.
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).
An adult who is compelled to nap repeatedly during the day may have excessive daytime sleepiness; however, it is important to distinguish between occasional daytime sleepiness and excessive daytime sleepiness, which is chronic.
A number of tools for screening for EDS have been developed. One is the Epworth Sleepiness Scale which grades the results of a questionnaire. The ESS generates a numerical score from zero (0) to 24 where a score of ten [10] or higher may indicate that the person should consult a specialist in sleep medicine for further evaluation.
Another tool is the Multiple Sleep Latency Test (MSLT), which has been used since the 1970s. It is used to measure the time it takes from the start of a daytime nap period to the first signs of sleep, called sleep latency. The test is based on the idea that the sleepier people are, the faster they will fall asleep.
The Maintenance of Wakefulness Test (MWT) is also used to quantitatively assess daytime sleepiness. This test is performed in a sleep diagnostic center. The test is similar to the MSLT. However, during this test the patient is instructed to try to stay awake.