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Delayed sleep phase disorder

Delayed sleep phase disorder (DSPD), more often known as delayed sleep phase syndrome and also as delayed sleep–wake phase disorder, is the delaying of a person's circadian rhythm compared to those of social norms. The disorder affects the timing of biological rhythms including sleep, peak period of alertness, core body temperature, and hormonal cycles. People with this disorder are often called "night owls". It is considered to be a category of circadian rhythm sleep disorder.

Signs and symptoms
DSPD is responsible for 7–13% 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. People with DSPD generally fall asleep some hours after midnight and have difficulty waking up in the morning. 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 4:00 am to 1:00 pm, their sleep is improved and they may not experience excessive daytime sleepiness. Comorbidity Depression In the DSPD cases reported in the literature, about half of the patients have had clinical depression or other psychological problems, about the same proportion as among patients with chronic insomnia. and states that The fact that half of DSPD patients are not depressed indicates that DSPD is not merely a symptom of depression. Sleep researcher Michael Terman has suggested that those who follow their internal circadian clocks may be less likely to have depression than those trying to live on a different schedule. DSPD patients with depression may be best served by seeking treatment for both problems. There is some evidence that effectively treating DSPD can improve the patient's mood and make antidepressants more effective. Vitamin D deficiency has been linked to depression. As it is a condition which comes from lack of exposure to sunlight, anyone who does not get enough sunlight exposure during daylight hours (about 20 to 30 minutes three times a week, depending on skin tone, latitude, and the time of year) could be at risk, without adequate dietary sources or supplements. Attention deficit hyperactivity disorder DSPD is genetically linked to attention deficit hyperactivity disorder (ADHD), according to genetic polymorphism studies that have linked genes involved in ADHD to genes involved in circadian rhythm. A high proportion of people with ADHD have DSPD. Overweight A 2019 study from Boston showed a relationship of evening chronotypes and greater social jet lag with greater body weight / adiposity in adolescent girls, but not boys, independent of sleep duration. Obsessive–compulsive disorder People with obsessive–compulsive disorder are also diagnosed with DSPD at a much higher rate than the general public. Head injury There have been several documented cases of DSPD and non-24-hour sleep–wake disorder developing after traumatic head injury. There have been cases of DSPD developing into non-24-hour sleep–wake disorder, a severe and debilitating disorder in which the individual sleeps later each day. ==Mechanism==
Mechanism
DSPD is a disorder of the body's timing system—the circadian clock. Individuals with DSPD might have an unusually long circadian cycle, might have a reduced response to the resetting effect of daylight on the body clock, or may respond overly to the delaying effects of evening light and too little to the advancing effect of light earlier in the day. In support of the increased sensitivity to evening light hypothesis, "the percentage of melatonin suppression by a bright light stimulus of 1,000 lux administered 2 hours prior to the melatonin peak has been reported to be greater in 15 DSPD patients than in 15 controls". The altered phase relationship between the timing of sleep and the circadian rhythm of body core temperature has been reported previously in DSPD patients studied in entrained conditions. That such an alteration has also been observed in temporal isolation (i.e.; in absence of all external time cues) supports the notion that the etiology of DSPD goes beyond simply a reduced capacity to achieve and maintain the appropriate phase relationship between sleep timing and the 24-hour day. Rather, the disorder may also reflect a fundamental inability of the endogenous circadian timing system to maintain normal phase relationships among physiological systems, and to properly adjust those internal relationships within the confines of the 24-hour day. In normal subjects, the phase relationship between sleep and temperature changes in temporal isolation relative to that observed under entrained conditions: in isolation, temperature minimum tends to occur toward the beginning of sleep, whereas under entrained conditions, temperature minimum occurs toward the end of the sleep period—a change in phase angle of several hours; DSPD patients may have a reduced capacity to achieve such a change in phase angle in response to entrainment. People with normal circadian systems can generally fall asleep quickly at night if they slept too little the night before. Falling asleep earlier will in turn automatically help to advance their circadian clocks due to decreased light exposure in the evening. In contrast, people with DSPD have difficulty falling asleep before their usual sleep time, even if they are sleep-deprived. Sleep deprivation does not reset the circadian clock of DSPD patients, as it does with normal people. Genetic factors Researchers in 2017 linked DSPD to at least one genetic mutation. An adolescent version may disappear in late adolescence or early adulthood; otherwise, DSPD is a lifelong condition. The best estimate of prevalence among adults is 0.13–0.17% (1 in 600). In most cases, it is not known what causes the abnormality in the biological clocks of DSPD patients. DSPD tends to run in families, and a growing body of evidence suggests that the problem is associated with the hPer3 (human period 3) gene and the CRY1 gene. may be warranted. ==Diagnosis==
Diagnosis
DSPD is diagnosed by a clinical interview, actigraphic monitoring, or a sleep diary kept by the patient for at least two weeks. When polysomnography is also used, it is primarily for the purpose of ruling out other disorders such as narcolepsy or sleep apnea. DSPD is frequently misdiagnosed or dismissed. It has been named as one of the sleep disorders most commonly misdiagnosed as a primary psychiatric disorder. DSPD is often confused with psychophysiological insomnia, depression, psychiatric disorders such as schizophrenia or ADHD, other sleep disorders, or school refusal. Practitioners of sleep medicine point out the dismally low rate of accurate diagnosis of the disorder, and have often asked for better physician education on sleep disorders. Definition 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 they usually fall 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. In the ICSD criteria, symptoms must have been present for at least three months before a diagnosis of DSPD can be made. ==Management==
Management
Treatment, a set of management techniques, is specific to DSPD. It is different from treatment of insomnia, and recognizes the patients' ability to sleep well on their own schedules, while addressing the timing problem. Success, if any, may be partial; for example, a patient who normally awakens at noon may only attain a wake time of 10 or 10:30 with treatment and follow-up. Being consistent with the treatment is paramount. Before starting DSPD treatment, patients are often asked to spend at least a week sleeping regularly, without napping, at the times when the patient is most comfortable. It is important for patients to start treatment well-rested. Non-pharmacological Techniques to shift the cycle to earlier times that do not require technology often involve gradually shifting the sleeping time earlier at a pace comfortable for the patient (melatonin may be used as an augment here). The photopigment of the retinal photosensitive ganglion cells, melanopsin, is excited by light mainly in the blue portion of the visible spectrum (absorption peaks at ~480 nanometers). A formerly popular treatment, phase delay chronotherapy, is intended to reset the circadian clock by manipulating bedtimes. It consists of going to bed two or more hours later each day for several days until the desired bedtime is reached, and it often must be repeated every few weeks or months to maintain results. Its safety is uncertain, notably because it has led to the development of non-24-hour sleep–wake disorder, a much more severe disorder. Earlier exercise and meal times can also help promote earlier sleep times. Pharmacological Aripiprazole (brand name Abilify) is an atypical antipsychotic that has been shown to be effective in treating DSPD by advancing sleep onset, sleep midpoint, and sleep offset at relatively low doses (0.5–1 mg), Agomelatine works on melatonin MT1 and MT2 receptors, alongside having antidepressant (antagonist) effects on the 5-HT2C receptor. It was used successfully in a case study of a man who acquired DSPD-like symptoms from a TBI. It is not currently approved for DSPD, and other evidence for its usage is scarce. but a decrease in exposure to light in the evening is helpful in establishing an earlier pattern. In accordance with its phase response curve (PRC), a very small dose of melatonin can also, or instead, be taken 6-8 hours before sleep onset as an aid to advancing the circadian phase; Side effects of melatonin may include sleep disturbance, nightmares, daytime sleepiness, and depression, though the current tendency to use lower doses has decreased such complaints. Large doses of melatonin can even be counterproductive: Lewy et al. provide support to "the idea that too much melatonin may spill over onto the wrong zone of the melatonin phase-response curve." The long-term effects of melatonin administration have not been examined. In some countries, the hormone is available only by prescription or not at all. In the United States, Canada and Germany, melatonin is on the shelf of most pharmacies and herbal stores. The prescription medication ramelteon (Rozerem) is a melatonin analogue that selectively binds to the melatonin MT1 and MT2 receptors, which has led to the hypothesis that it may be effective in the treatment of DSPD. The effectiveness of ramelteon has been contested, with studies often finding mixed results. A review by the US Department of Health and Human Services found little difference between melatonin and placebo for most primary and secondary sleep disorders. The one exception, where melatonin is effective, is the "circadian abnormality" DSPD. Another systematic review found inconsistent evidence for the efficacy of melatonin in treating DSPD in adults, and noted that it was difficult to draw conclusions about its efficacy because many recent studies on the subject were uncontrolled. Modafinil (brand name Provigil) is a stimulant approved in the US for treatment of shift-work sleep disorder, which shares some characteristics with DSPD. A number of clinicians prescribe it for DSPD patients, as it may improve a sleep-deprived patient's ability to function adequately during socially desirable hours. It is generally not recommended to take modafinil after noon; modafinil is a relatively long-acting drug with a half-life of 15 hours, and taking it during the later part of the day can make it harder to fall asleep at bedtime. Vitamin B12 was, in the 1990s, suggested as a remedy for DSPD, and is still recommended by some sources. Several case reports were published. However, a review for the American Academy of Sleep Medicine in 2007 concluded that no benefit was seen from this treatment. ==Prognosis==
Prognosis
The long-term course of DSPD is not well understood. Its prevalence, however, declines with age, falling from an estimated 3-7% in adolescence to <1% among adults aged 40-64. Persistence of DSPD has been associated with impaired behavioral regulation, specifically attention deficit hyperactivity disorder (ADHD), poor sleep hygiene, and gaming addiction. Adaptation to late sleeping times Working the evening or night shift, or working at home, makes DSPD less of an obstacle for some. Many of these people do not describe their pattern as a "disorder". Some DSPD individuals nap, even taking 4–5 hours of sleep in the morning and 4–5 in the evening. DSPD-friendly careers can include security work, the entertainment industry, hospitality work in restaurants, theaters, hotels, bars, call center work, manufacturing, healthcare or emergency medicine, commercial cleaning, taxi or truck driving, the media, freelance writing, translation, IT work, or medical transcription. Some other careers that have an emphasis on early morning work hours, such as bakers, coffee baristas, pilots and flight crews, teachers, mail carriers, waste collection, and farming, can be particularly difficult for people who naturally sleep later than is typical. Some careers, such as over-the-road truck drivers, firefighters, law enforcement, and nursing, can be suitable for both people with delayed sleep phase syndrome and people with the opposite condition, advanced sleep phase disorder, as these workers are needed both very early in the morning and also late at night. Some people with the disorder are unable to adapt to earlier sleeping times, even after many years of treatment. Sleep researchers Dagan and Abadi have proposed that the existence of untreatable cases of DSPD be formally recognized as a "sleep-wake schedule disorder (SWSD) disability", an invisible disability. The statute defines "disability" as a "physical or mental impairment that substantially limits one or more major life activities", and Section 12102(2)(a) itemizes sleeping as a "major life activity". Impact on patients Lack of public awareness of the disorder contributes to the difficulties experienced by people with DSPD, who are commonly stereotyped as undisciplined or lazy. Parents may be chastised for not giving their children acceptable sleep patterns, and schools and workplaces rarely tolerate chronically late, absent, or sleepy students and workers, failing to see them as having a chronic condition. As DSPD is so little-known and so misunderstood, peer support may be important for information, self-acceptance, and future research studies. People with DSPD who force themselves to follow a normal 9–5 workday "are not often successful and may develop physical and psychological complaints during waking hours, e.g., sleepiness, fatigue, headache, decreased appetite, or depressed mood. Patients with circadian rhythm sleep disorders often have difficulty maintaining ordinary social lives, and some of them lose their jobs or fail to attend school." ==Epidemiology==
Epidemiology
There have been several studies that have attempted to estimate the prevalence of DSPD. Results vary due to differences in methods of data collection and diagnostic criteria. A particular issue is where to draw the line between extreme evening chronotypes and clinical DSPD. Using the ICSD-1 diagnostic criteria (current edition ICSD-3), a study by telephone questionnaire in 1993 of 7,700 randomly selected adults (aged 18–67) in Norway estimated the prevalence of DSPD at 0.17%. A similar study in 1999 of 1,525 adults (aged 15–59) in Japan estimated its prevalence at 0.13%. A somewhat higher prevalence of 0.7% was found in a 1995 San Diego study. A 2002 study of older adults (age 40–65) in San Diego found 3.1% had complaints of difficulty falling asleep at night and waking in the morning, but did not apply formal diagnostic criteria. Actimetry readings showed only a small proportion of this sample had delays of sleep timing. A marked delay of sleep patterns is a normal feature of the development of adolescent humans. According to Mary Carskadon, both circadian phase and homeostasis (the accumulation of sleep pressure during the wake period) contribute to a DSPD-like condition in post-pubertal as compared to pre-pubertal youngsters. Adolescent sleep phase delay "is present both across cultures and across mammalian species" and "seems to be related to pubertal stage rather than age." As a result, diagnosable DSPD is much more prevalent among adolescents, with estimates ranging from 3.4% to 8.4% among high school students. ==History==
History
DSPD was first formally described in 1981 by Elliot D. Weitzman and others at Montefiore Medical Center. == See also ==
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