Psychology Wiki

Assessment | Biopsychology | Comparative | Cognitive | Developmental | Language | Individual differences | Personality | Philosophy | Social |
Methods | Statistics | Clinical | Educational | Industrial | Professional items | World psychology |

Clinical: Approaches · Group therapy · Techniques · Types of problem · Areas of specialism · Taxonomies · Therapeutic issues · Modes of delivery · Model translation project · Personal experiences ·

Delayed sleep phase disorder
Classification and external resources
ICD-10 G472
ICD-9 327.31
eMedicine neuro/655
MeSH D021081

Delayed sleep-phase disorder (DSPD), also known as delayed sleep-phase syndrome (DSPS) or delayed sleep-phase type (DSPT), is a circadian rhythm sleep disorder affecting the timing of sleep, peak period of alertness, the core body temperature rhythm, hormonal and other daily rhythms, compared to the general population and relative to societal requirements. People with DSPD fall asleep some hours after midnight and have difficulty waking up in the morning.[1]

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, however, they are allowed to follow their own schedules, e.g. sleeping from 4 a.m. to noon (04:00 to 12:00), they sleep soundly, awaken spontaneously, and do not experience excessive daytime sleepiness.[citation needed]

The syndrome usually develops in early childhood or adolescence.[2] An adolescent version disappears in adolescence or early adulthood; otherwise DSPD is a lifelong condition. Depending on the severity, the symptoms can be managed to a greater or lesser degree, but there is no all-encompassing cure. Prevalence among adults, equally distributed among women and men, is approximately 0.15%, or 3 in 2,000.

DSPD is also genetically linked to ADHD by findings of polymorphism in genes in common between those apparently involved in ADHD and those involved in the circadian rhythm[3][4] and a high proportion of DSPD among those with ADHD.[5][6]

DSPD was first formally described in 1981 by Dr. Elliot D. Weitzman and others at Montefiore Medical Center.[7] It is responsible for 7–10% of patient complaints of chronic insomnia.[8] However, as few doctors are aware of it, it often goes untreated or is treated inappropriately; DSPD is often misdiagnosed as primary insomnia or as a psychiatric condition.[9] DSPD can be treated or helped in some cases by careful daily sleep practices, light therapy, and medications such as melatonin and modafinil (Provigil); the former is a natural neurohormone responsible partly and in tiny amounts for the human body clock. At its most severe and inflexible, DSPD is a disability.[10]


According to the International Classification of Sleep Disorders (ICSD),[11] the circadian rhythm sleep disorders share a common underlying chronophysiologic basis:

The major feature of these disorders is a misalignment between the patient's sleep pattern and the sleep pattern that is desired or regarded as the societal norm... In most circadian rhythm sleep disorders, the underlying problem is that the patient cannot sleep when sleep is desired, needed or expected.

The ICSD (page 128-133) diagnostic criteria for delayed sleep-phase disorder are:

  1. There is an intractable delay in the phase of the major sleep period in relation to the desired clock time, as evidenced by a chronic or recurrent complaint of inability to fall asleep at a desired conventional clock time together with the inability to awaken at a desired and socially acceptable time.
  2. When not required to maintain a strict schedule, patients will exhibit normal sleep quality and duration for their age and maintain a delayed, but stable, phase of entrainment to local time.
  3. Patients have little or no reported difficulty in maintaining sleep once sleep has begun.
  4. Patients have a relatively severe to absolute inability to advance the sleep phase to earlier hours by enforcing conventional sleep and wake times.
  5. Sleep-wake logs and/or actigraphy monitoring for at least two weeks document a consistent habitual pattern of sleep onsets, usually later than 2 a.m., and lengthy sleeps.
  6. Template:AnchorsOccasional noncircadian days may occur (i.e., sleep is "skipped" for an entire day and night plus some portion of the following day), followed by a sleep period lasting 12 to 18 hours.
  7. The symptoms do not meet the criteria for any other sleep disorder causing inability to initiate sleep or excessive sleepiness.
  8. If any of the following laboratory methods is used, it must demonstrate a delay in the timing of the habitual sleep period: 1) Twenty-four-hour polysomnographic monitoring (or by means of two consecutive nights of polysomnography and an intervening multiple sleep latency test), 2) Continuous temperature monitoring showing that the time of the absolute temperature nadir is delayed into the second half of the habitual (delayed) sleep episode.[11]

Some people with the condition adapt their lives to the delayed sleep phase, avoiding common business hours (e.g., 9 a.m. to 5 p.m.) as much as possible. The ICSD's severity criteria, all of them "over at least a one-month period", are:

  • Mild: Two-hour delay 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 can 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 one month before a diagnosis of DSPD can be made.

Template:AnchorsAttempting to force oneself onto daytime society's schedule with DSPD has been compared to constantly living with 6 hours of jet lag; DSPD has, in fact, been referred to as "social jet lag".[12] Often people with DSPD manage only a few hours sleep a night during the working week, then compensate by sleeping until the afternoon on weekends. Sleeping in 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, and indeed morning larks, 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 several 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 second edition of the International Classification of Sleep Disorders is circadian rhythm sleep disorder, delayed sleep phase type; the preferred common name is delayed sleep-phase disorder.[13][14]


About 0.15% of adults, three in 2,000, have DSPD. Using the strict ICSD diagnostic criteria, a random study in 1993 of 7700 adults (aged 18–67) in Norway estimated the prevalence of DSPD at 0.17%.[15] A similar study of 1525 adults (aged 15–59) in Japan estimated its prevalence at 0.13%.[16]

File:Sleeping students.jpg

Sleepy students

Template:AnchorsDSPD is not uncommon among teenagers;[17] at least one study has indicated that the prevalence of DSPD among adolescents is as high as 7%. Among adolescents, boys predominate; in adults, the gender distribution shows equal numbers of women and men.[11]

Template:AnchorsA 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 adolescents.[18] Adolescent sleep phase delay "is present both across cultures and across mammalian species" and "it seems to be related to pubertal stage rather than age."[19]


Main article: Circadian rhythm sleep disorder

DSPD is a disorder of the body's timing system—the biological clock. Individuals with DSPD might have an unusually long circadian cycle, might have a reduced response to the re-setting effect of daylight on the body clock and/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."[20]

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 are unable to fall 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.[21]

People with the disorder who try to live on a normal schedule cannot fall asleep at a "reasonable" hour and have extreme difficulty waking because their biological clocks are not in phase with that schedule. Non-DSPD people who do not adjust well to working a night shift have similar symptoms (diagnosed as shift-work sleep disorder, SWSD).

In most cases, it is not known what causes the abnormality in the biological clocks of DSPD patients. DSPD tends to run in families,[22] and a growing body of evidence suggests that the problem is associated with the hPer3 (human period 3) gene.[23][24] There have been several documented cases of DSPD and non-24-hour sleep-wake syndrome developing after traumatic head injury.[25][26]

There have been a few cases of DSPD developing into non-24-hour sleep-wake syndrome, a more severe and debilitating disorder in which the individual sleeps later each day.[27] It has been suggested that, instead of (or perhaps in addition to) a reduced reaction to light in the morning, an abnormal over-sensitivity to light in the late evening might contribute to the odd non-circadian pattern.[28]


File:Sleep diary.jpg

A sleep diary with nighttime in the middle and the weekend in the middle, the better to notice trends

DSPD is diagnosed by a clinical interview, actigraphic monitoring and/or a sleep diary kept by the patient for at least three weeks. When polysomnography is also used, it is primarily for the purpose of ruling out other disorders such as narcolepsy or sleep apnea. If a person can, on her/his own with just the help of alarm clocks and will-power, adjust to a daytime schedule, the diagnosis is not given.

DSPD is frequently misdiagnosed or dismissed. It has been named as one of the sleep disorders most commonly misdiagnosed as a primary psychiatric disorder.[29] DSPD is often confused with: psychophysiological insomnia; depression; psychiatric disorders such as schizophrenia, ADHD or ADD; 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.[30]


Treatment, a set of management techniques, is specific to DSPD. It is different from the 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.

Several treatments that have been reported in the medical literature.


Light therapy (phototherapy) with a full spectrum lamp or portable visor, usually 10,000 lux for 30–90 minutes at the patient's usual time of spontaneous awakening, or shortly before (but not long before), which is in accordance with the phase response curve (PRC) for light. The use of an LED light therapy device can reduce this to 15–30 minutes. Sunlight can also be used. Only experimentation, preferably with specialist help, will show how great an advance is possible and comfortable. For maintenance, some patients must continue the treatment indefinitely, some may reduce the daily treatment to 15 minutes, others may use the lamp, for example, just a few days a week or just every third week. Whether the treatment is successful is highly individual. Light therapy generally requires adding some extra time to the patient's morning routine. Patients with a family history of macular degeneration are advised to consult with an eye doctor. The use of exogenous melatonin administration (see below) in conjunction with light therapy is common.

Light restriction in the evening, sometimes called darkness therapy. Just as bright light upon awakening should advance one's sleep-phase, bright light in the evening and night delays it (see the PRC). It is suspected that DSPS patients may be overly sensitive to evening light.[31] Thus, one might be advised to keep lights dim the last hours before bedtime and even wear sunglasses or amber-colored (blue-blocking) goggles. 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[32]).

Attaining an earlier sleep onset, in a dark room with eyes closed, effectively blocks a period of phase-delaying light. An understanding of this is a motivating factor in treatment.

Chronotherapy, which is intended to reset the circadian clock by manipulating bedtimes. Often, chronotherapy must be repeated every few months to maintain results, and its safety is uncertain.[33] It can be one of two types. The most common consists of going to bed two or more hours later each day for several days until the desired bedtime is reached. A modified chronotherapy (Thorpy, 1988) is called controlled sleep deprivation with phase advance, SDPA. One stays awake one whole night and day, then goes to bed 90 minutes earlier than usual and maintains the new bedtime for a week. This process is repeated weekly until the desired bedtime is reached.


Melatonin taken an hour or so before usual bedtime may induce sleepiness.


Phase response curves for light and for melatonin administration

Taken this late, it does not, of itself, affect circadian rhythms,[34] 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 some hours earlier as an aid to resetting the body clock;[35] it must then be so small as to not induce excessive sleepiness.

Side effects of melatonin may include disturbance of sleep, 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.[36] 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 and Canada, melatonin is on the shelf of most drug and herbal stores. The prescription drug Rozerem (ramelteon) is a melatonin analogue that selectively binds to the melatonin MT1 and MT2 receptors and, hence, has the possibility of being effective in the treatment of DSPD.

A review by a US government agency 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.[37]

Modafinil (Provigil) is approved in the US for treatment of shift-work sleep disorder, which shares some characteristics with DSPD. A number of clinicians are prescribing it for DSPS patients as it may improve a sleep-deprived patient's ability to function adequately during socially desirable hours. Taking modafinil less than 12 hours before the desired sleep onset time will likely exacerbate the symptoms by delaying sleep.Template:Medical citation needed

Trazodone successfully treated DSPD in one elderly man.[38]

Vitamin B12 was, in the 1990s, suggested as a remedy for DSPD, and can still be found to be recommended by many 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.[39]

A strict schedule and good sleep hygiene are essential in maintaining any good effects of treatment. With treatment, some people with mild DSPD may sleep and function well with an early sleep schedule. Caffeine and other stimulant drugs to keep a person awake during the day may not be necessary and should be avoided in the afternoon and evening, in accordance with good sleep hygiene. A chief difficulty of treating DSPD is in maintaining an earlier schedule after it has been established. Inevitable events of normal life, such as staying up late for a celebration or having to stay in bed with an illness, tend to reset the sleeping schedule to its intrinsic late times.


Adaptation to late sleeping times

Long-term success rates of treatment have seldom been evaluated. However, experienced clinicians acknowledge that DSPD is extremely difficult to treat. One study of 61 DSPD patients with mean sleep onset at about 3 a.m. and mean waking time of about 11:30 a.m., was followed up with questionnaires to the subjects a year later. Good effect was seen during the 6-week treatment with a daily, very large dose (5 mg), of melatonin. Follow-up showed that over 90% had relapsed to pretreatment sleeping patterns within the year, 28.8% reporting that the relapse occurred within one week. The milder cases retained changes significantly longer than the more severe cases.[40]

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, work in theater, the entertainment industry, hospitality work in restaurants, hotels or bars, call center work, nursing, emergency medicine, taxi or truck driving, the media, and freelance writing, translation, IT work, or medical transcription.

Some people with the disorder are unable to adapt to earlier sleeping times, even after many years of treatment. Sleep researchers have proposed that the existence of untreatable cases of DSPD be formally recognized as a "sleep-wake schedule disorder disability", an invisible disability.

Rehabilitation for DSPD patients includes acceptance of the condition and choosing a career that allows late sleeping times or running a home business with flexible hours. In a few schools and universities, students with DSPD have been able to arrange to take exams at times of day when their concentration levels may be good.

Patients suffering from SWSD disability should be encouraged to accept the fact that they suffer from a permanent disability, and that their quality of life can only be improved if they are willing to undergo rehabilitation. It is imperative that physicians recognize the medical condition of SWSD disability in their patients and bring it to the notice of the public institutions responsible for vocational and social rehabilitation.[10]

In the United States, the Americans with Disabilities Act requires that employers make reasonable accommodations for employees with sleeping disorders. In the case of DSPD, this may require that the employer accommodate later working hours for jobs normally performed on a "9 to 5" work schedule.[41]

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 illness.

By the time DSPD sufferers receive an accurate diagnosis, they often have been misdiagnosed or labeled as lazy and incompetent workers or students for years. Misdiagnosis of circadian rhythm sleep disorders as psychiatric conditions causes considerable distress to patients and their families, and leads to some patients being inappropriately prescribed psychoactive drugs. For many patients, the diagnosis of DSPD is itself a life-changing breakthrough.[10]

As DSPD is so little-known and so misunderstood, support groups may be important for information and self-acceptance.[42]

People with DSPD who force themselves to live on a normal 9-5 day "are not often successful and may develop physical and psychological complaints during waking hours, i.e. 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."[12]


In the DSPD cases reported in the literature, about half of the patients have suffered from clinical depression or other psychological problems, about the same proportion as among patients with chronic insomnia.[11] According to the ICSD:

Although some degree of psychopathology is present in about half of adult patients with DSPD, there appears to be no particular psychiatric diagnostic category into which these patients fall. Psychopathology is not particularly more common in DSPD patients compared to patients with other forms of "insomnia." ... Whether DSPD results directly in clinical depression, or vice versa, is unknown, but many patients express considerable despair and hopelessness oversleeping normally again.[43]

A direct neurochemical relationship between sleep mechanisms and depression is another possibility. DSPD may cause excessive or inappropriate production of melatonin. Serotonin, a mood regulator, is a precursor to melatonin. As a result, increased endogenous melatonin production can deplete serotonin levels and may cause depression.

It is conceivable that DSPD often has a major role in causing depression because it can be such a stressful and misunderstood disorder. A recent study from the University of California, San Diego found no association of bipolar disorder (history of mania) with DSPD, and it states that there may be

behaviorally-mediated mechanisms for comorbidity between DSPS and depression. For example, the lateness of DSPS cases and their unusual hours may lead to social opprobrium and rejection, which might be depressing...[44]

The fact that half of DSPD patients are not depressed indicates that DSPD is not merely a symptom of depression. Sleep researcher M. Terman has suggested that those who follow their internal circadian clocks may be less likely to suffer from depression than those trying to live on a different schedule.

DSPD patients who also suffer from 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 the daylight hours could be at risk.

Persons with obsessive-compulsive disorder are also diagnosed with DSPD at a much higher rate than the general public.[45]


United States

According to the Americans with Disabilities Act of 1990, "disability" is defined as a "physical or mental impairment that substantially limits one or more major life activities". "Sleeping" is defined as a "major life activity" in § 12102(2)(a) of the statute.[46]

See also


  1. Hirshkowitz, Max (2004). "Chapter 10, Neuropsychiatric Aspects of Sleep and Sleep Disorders (pp. 315-340)" Stuart C. Yudofsky and Robert E. Hales, editors Essentials of neuropsychiatry and clinical neurosciences (Google Books preview includes entire chapter 10), 4, 324–325, Arlington, Virginia, USA: American Psychiatric Publishing. URL accessed 2009-12-06. "Individuals with delayed sleep phase are more alert in the evening and early nighttime, stay up later, and are more tired in the morning."
  2. Dagan Y, Eisenstein M (1999). Circadian rhythm sleep disorders: toward a more precise definition and diagnosis. Chronobiol. Int. 16 (2): 213–22.
  3. A polymorphism at the 3′-untranslated region of the CLOCK gene is associated with adult attention-deficit hyperactivity disorder: American Journal of Medical Genetics Part B: Neuropsychiatric Genetics, Volume 147B, Issue 3, pages 333–338, 5 April 2008
  4. “Adult attention-deficit hyperactivity disorder is associated with alterations in circadian rhythms at the behavioural, endocrine and molecular levels” - Molecular Psychiatry , (22 November 2011) | doi:10.1038/mp.2011.149 (PubMed ID: 22105622 pre pub)
  5. Van der Heijden KB, Smits MG, Van Someren EJ, Gunning WB (2005). Idiopathic chronic sleep onset insomnia in attention-deficit/hyperactivity disorder: a circadian rhythm sleep disorder. Chronobiology International 22 (3): 559–70.
  6. - “About three-fourths of all adults with ADHD report inability to ‘shut off my mind so I can fall asleep at night’.”
  7. Weitzman ED, Czeisler CA, Coleman RM, et al. (1981). Delayed sleep phase syndrome. A chronobiological disorder with sleep-onset insomnia. Arch. Gen. Psychiatry 38 (7): 737–46.
  8. Sleeplessness and Circadian Rhythm Disorder. eMedicine World Medical Library from WebMD. URL accessed on 2006-06-04.
  9. Dagan Y (2002). Circadian rhythm sleep disorders (CRSD). Sleep Med Rev 6 (1): 45–54.
  10. 10.0 10.1 10.2 Dagan Y, Abadi J (2001). Sleep-wake schedule disorder disability: a lifelong untreatable pathology of the circadian time structure. Chronobiol. Int. 18 (6): 1019–27.
  11. 11.0 11.1 11.2 11.3 American College of Physicians--American Society of Internal Medicine (2005). International Classification of Sleep Disorders: Diagnostic & Coding Manual (PDF: full text, 2001 version), Amer Academy of Sleep Medicine.
  12. 12.0 12.1 Okawa M, Uchiyama M (2007). Circadian rhythm sleep disorders: characteristics and entrainment pathology in delayed sleep phase and non-24-h sleep-wake syndrome. Sleep Med Rev 11 (6): 485–96.
  13. El-Ad, Baruch Delayed sleep phase syndrome. MedLink Neurology. URL accessed on 2008-03-24.
  14. International Classification of Sleep Disorders – Second Edition (ICSD-2), 298 pages. ©2005 American Academy of Sleep Medicine, ISBN 0965722023 ISBN 978-0965722025
  15. Schrader H, Bovim G, Sand T (1993). The prevalence of delayed and advanced sleep phase syndromes. J Sleep Res 2 (1): 51–55.
  16. Yazaki M, Shirakawa S, Okawa M, Takahashi K (1999). Demography of sleep disturbances associated with circadian rhythm disorders in Japan. Psychiatry Clin. Neurosci. 53 (2): 267–8.
  18. Carskadon, Mary A. (2008). Circadian and Homeostatic Regulation of Sleep in Adolescent Humans. (PDF, abstract) conference presentations, p. 44. Society for Research on Biological Rhythms. URL accessed on 2008-05-14.
  19. doi = 10.1016/jsleep.2011.10.024
  20. Billiard, Michel; Angela Kent (2003). Sleep: Physiology, Investigations and Medicine (Page view, Google books), 495–97, New York: Springer. URL accessed 2009-08-03.
  21. Uchiyama M, Okawa M, Shibui K, et al. (1999). Poor recovery sleep after sleep deprivation in delayed sleep phase syndrome. Psychiatry Clin. Neurosci. 53 (2): 195–7.
  22. Ancoli-Israel S, Schnierow B, Kelsoe J, Fink R (2001). A pedigree of one family with delayed sleep phase syndrome. Chronobiol. Int. 18 (5): 831–40.
  23. Archer SN, Robilliard DL, Skene DJ, Smits M, Williams A, Arendt J, von Schantz M. (June 2003). A length polymorphism in the circadian clock gene Per3 is linked to delayed sleep phase syndrome and extreme diurnal preference. Sleep 26 (4): 413–5.
  24. Nadkarni NA, Weale ME, von Schantz M, Thomas MG (2005). Evolution of a length polymorphism in the human PER3 gene, a component of the circadian system. J. Biol. Rhythms 20 (6): 490–9.
  25. Boivin DB, James FO, Santo JB, Caliyurt O, Chalk C (2003). Non-24-hour sleep-wake syndrome following a car accident. Neurology 60 (11): 1841–3.
  26. Quinto C, Gellido C, Chokroverty S, Masdeu J (2000). Posttraumatic delayed sleep phase syndrome. Neurology 54 (1): 250–2.
  27. Okawa, Masako, Uchiyama, Makoto (2007). Clinical Review. Circadian rhythm sleep disorders: Characteristics and entrainment pathology in delayed sleep phase and non-24-h sleep-wake syndrome. Sleep Medicine (11): 485–496.
  28. Aoki H, Ozeki Y, Yamada N (March 2001). Hypersensitivity of melatonin suppression in response to light in patients with delayed sleep phase syndrome. Chronobiol. Int. 18 (2): 263–71.
  29. Stores G (2003). Misdiagnosing sleep disorders as primary psychiatric conditions. Advances in Psychiatric Treatment 9 (1): 69–77.
    See also subsequent:
    * Stores G (2007). Clinical diagnosis and misdiagnosis of sleep disorders. J. Neurol. Neurosurg. Psychiatr. 78 (12): 1293–7.
  30. Dagan Y, Ayalon L (2005). Case study: psychiatric misdiagnosis of non-24-hours sleep-wake schedule disorder resolved by melatonin. J Am Acad Child Adolesc Psychiatry 44 (12): 1271–5.
  31. Dodson, Ehren R.; Zee, Phyllis C.. Therapeutics for Circadian Rhythm Sleep Disorders. URL accessed on 2012-08-08.
  32. DOI:10.1007/s00424-007-0242-2 10.1007/s00424-007-0242-2
    This citation will be automatically completed in the next few minutes. You can jump the queue or expand by hand
  33. Morgenthaler, TI, Lee-Chiong T; Alessi C; Friedman L; Aurora N; Boehlecke B; Brown T; Chesson AL; Kapur V; Maganti R; Owens J; Pancer J; Swick TJ; Zak R (November 2007). Standards of Practice Committee of the AASM. Practice Parameters for the Clinical Evaluation and Treatment of Circadian Rhythm Sleep Disorders. SLEEP 30 (11): 1445–59.
  34. Burgess HJ, Revell VL, Eastman CI (2008). A three pulse phase response curve to three milligrams of melatonin in humans. J. Physiol. (Lond.) 586 (2): 639–47.
  35. Mundey, K, Benloucif S, Harsanyi K, Dubocovich ML, Zee PC (October 2005). Phase-dependent treatment of delayed sleep phase syndrome with melatonin. Sleep 28 (10): 1214–6.
  36. Lewy AJ, Emens JS, Sack RL, Hasler BP, Bernert RA (2002). Low, but not high, doses of melatonin entrained a free-running blind person with a long circadian period. Chronobiol Int. 19 (3): 649–58.
  37. Buscemi N., Vandermeer B., Pandya R., et al. Melatonin for Treatment of Sleep Disorders. Summary, Evidence Report/Technology Assessment: Number 108. AHRQ Publication Number 05-E002-1, November 2004. Agency for Healthcare Research and Quality, Rockville, MD.
  38. Nakasei S et al. (October 2005). Trazodone advanced a delayed sleep phase of an elderly male: A case report. Sleep and Biological Rhythms 3 (3): 169.
  39. Sack RL, Auckley D, Auger RR, et al. (2007). Circadian rhythm sleep disorders: part II, advanced sleep phase disorder, delayed sleep phase disorder, free-running disorder, and irregular sleep-wake rhythm. An American Academy of Sleep Medicine review. Sleep 30 (11): 1484–501.
  40. Dagan Y, Yovel I, Hallis D, Eisenstein M, Raichik I (1998). Evaluating the role of melatonin in the long-term treatment of delayed sleep phase syndrome (DSPS). Chronobiol. Int. 15 (2): 181–90.
  41. You may need to offer flex schedule as ADA accommodation. Business Management Daily.
  42. Potts, Henry W.W. ([2005]). Online support groups: An overlooked resource for patients. (PDF: full text) University College London. URL accessed on 2008-04-14.
  43. Thorpy M (2001). The International Classification of Sleep Disorders, Revised: Diagnostic and Coding Manual (PDF: full text), 72–73, Chicago, Illinois, USA: The American Academy of Sleep Medicine in association with the European Sleep Research Society, the Japanese Society of Sleep Research and the Latin American Sleep Society. URL accessed 2008-03-23.
  44. Kripke, Daniel F., Rex K.M.; Ancoli-Israel S.; Nievergelt C.M.; Klimecki W.; Kelsoe J.R. (April 2008). Delayed sleep phase cases and controls. Journal of Circadian Rhythms 6 (6).
  46. Americans with Disabilities Act of 1990. URL accessed on 2010-01-20.


  • Thorpy MJ, Korman E, Spielman AJ, Glovinsky PB (1988). Delayed sleep phase syndrome in adolescents. J Adolesc Health Care 9 (1): 22–7.
  • (1992). When the body clock goes wrong: delayed sleep phase syndrome. Lancet 340 (8824): 884–5.
  • Regestein QR, Pavlova M (1995). Treatment of delayed sleep phase syndrome. Gen Hosp Psychiatry 17 (5): 335–45.
  • Regestein QR, Monk TH (1995). Delayed sleep phase syndrome: a review of its clinical aspects. Am J Psychiatry 152 (4): 602–8.
  • Terman, Michael (2010-04-19). Sleeping (or Not) by the Wrong Clock. New York Times.

External links


This page uses Creative Commons Licensed content from Wikipedia (view authors).