Delayed sleep phase syndrome

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Delayed sleep phase syndrome
ICD-10 G47.2
ICD-9 327.31

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]


Delayed sleep-phase syndrome (DSPS), also known as delayed sleep-phase disorder or as circadian rhythm sleep disorder delayed sleep-phase type (DSPT), is a chronic disorder of sleep timing. People with DSPS tend to fall asleep at very late times, and also have difficulty waking up in the morning.

Often, people with the disorder report that they cannot sleep until early morning, but they fall asleep at about the same time every "night", no matter what time they go to bed. Unless they have another sleep disorder such as sleep apnea in addition to DSPS, patients can sleep well, and have a normal need for sleep. Therefore, they find it very difficult to wake up in time for a typical school or work day if they have only slept for a few hours. However, they sleep soundly, wake up spontaneously, and do not feel sleepy again until their next "night" if they are allowed to follow their own late schedule, e.g. sleeping from 4 a.m. to noon.

The syndrome usually develops in early childhood or adolescence,[1] and sometimes disappears in adolescence or early adulthood. It can be to a greater or lesser degree treatable, but cannot be cured.

DSPS was first formally described in 1981 by Dr. Elliot D. Weitzman and others at Montefiore Medical Center.[2] It is responsible for 7 -10% of cases of chronic insomnia.[3] However, as few doctors are aware of its existence, it often goes untreated or is treated inappropriately. DSPS is often frequently misdiagnosed as primary insomnia or as a psychiatric condition.


According to the International Classification of Sleep Disorders (ICSD),[4] 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 Syndrome 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. Occasional 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.[4]

Some people with the abnormality adapt their lives to the delayed sleep phase, avoiding the 9–5 society as much as possible. They have the disorder, but for them it is not a disability. 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 DSPS which distinguish it from other sleep disorders are:

  • People with DSPS 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 DSPS 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 DSPS 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.
  • DSPS patients can sleep well and regularly when they can follow their own sleep schedule, e.g. on weekends and during vacations.
  • DSPS is a chronic condition. Symptoms must have been present for at least one month before a diagnosis of DSPS can be made.

Attempting to force oneself through 9–5 life with DSPS has been compared to constantly living with 6 hours of jet lag; the disorder has, in fact, been referred to as "social jet lag".[5] Often, sufferers 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, gives people with the disorder relief from daytime sleepiness but also perpetuates the late sleep phase.

People with DSPS tend to be extreme night owls. They feel most alert and say they function best and are most creative in the evening and at night. DSPS patients 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 DSPS patients seek medical help, they usually have tried many times to change their sleeping schedule. Failed tactics to sleep at earlier times may include relaxation techniques, early bedtimes, hypnosis, alcohol, sleeping pills, dull reading, and home remedies. DSPS 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 syndrome 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.[6]


Using the strict ICSD diagnostic criteria, a random study in 1993 of 10,000 adults in Norway estimated the prevalence of DSPS at 0.17%.[7] A similar study with 1525 adults in Japan estimated its prevalence at 0.13%.[8] Other studies have indicated that the prevalence of DSPS among adolescents is as high as 7%.[4]


DSPS is a disorder of the body's timing system - the biological clock. Individuals with DSPS might have an unusually long circadian cycle, or might have a reduced response to the re-setting effect of light on the body clock.

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 advance their circadian clocks. In contrast, people with DSPS are unable to fall asleep before their usual sleep time, even if they are sleep-deprived. Research has shown that sleep deprivation does not reset the circadian clock of DSPS patients, as it does with normal people.[9]

People with the disorder who try to live on a normal schedule have difficulty falling asleep and difficulty waking because their biological clocks are not in phase with that schedule. Normal people who do not adjust well to working a night shift have similar symptoms.

People with the disorder also show delays in other circadian markers, such as melatonin-secretion and the core body temperature minimum, that correspond to the delay in the sleep/wake cycle. Sleepiness, spontaneous awakening, and these internal markers are all delayed by the same number of hours. Non-dipping blood pressure patterns are also associated with the disorder when present in conjunction with socially unacceptable sleeping and waking times.

In most cases, it is not known what causes the abnormality in the biological clocks of DSPS patients. DSPS tends to run in families[10] and a growing body of evidence suggests that the problem is associated with the hPer3 (human period 3) gene.[11] There have been several documented cases of DSPS and non-24 hour sleep-wake syndrome developing after traumatic head injury.[12][13]

There have been a few cases of DSPS developing into non 24-hour sleep-wake syndrome, a more severe and debilitating disorder in which the individual sleeps later each day.


DSPS is diagnosed by a clinical interview, actigraphic monitoring and/or a sleep log kept by the patient for at least three weeks.

DSPS is frequently misdiagnosed or dismissed. It has been named as one of the sleep disorders most commonly misdiagnosed as a primary psychiatric disorder.[14] DSPS is often confused with psychophysiological insomnia, depression, psychiatric disorders such as schizophrenia, ADHD or ADD, other sleep disorders, or willful behaviour such as 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.[15]

Impact on patients

Lack of public awareness of the disorder contributes to the difficulties experienced by DSPS patients, who are commonly stereotyped as undisciplined or lazy. Parents may be chastised for not giving their children acceptable sleep patterns, and schools rarely tolerate chronically late, absent, or sleepy students and fail to see them as having a chronic illness.

By the time DSPS sufferers receive an accurate diagnosis, they often have been misdiagnosed or labelled 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, diagnosis of DSPS is itself a life-changing breakthrough.[16]


Treatment for DSPS is specific. It is different from treatment of insomnia, and recognizes the patient's ability to sleep well while addressing the timing problem.

Before starting DSPS treatment, patients are often asked to spend 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.

Treatments that have been reported in the medical literature include:

  • Light therapy (phototherapy) with a full spectrum lamp or portable visor, usually 10000 lux for 30-90 minutes in the morning. Sunlight can also be used. Light therapy generally requires adding some extra time to the patient's morning routine. It takes from a few days to two weeks to take effect, with occasional use thereafter to help maintain the schedule. Avoidance of bright light in the evening may also help.
  • Chronotherapy, which resets the circadian clock by manipulating bedtimes. 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.
  • A small (~1mg) melatonin supplement taken an hour or so before bedtime may be helpful in establishing an earlier pattern, especially in conjunction with bright light therapy at the time of spontaneous awakening. However, some suggest taking melatonin at sunset to mimic natural endogenous secretion of melatonin. Rather than taking melatonin as a sedative, it is used in this way as a natural way to reset the circadian clock. Side effects of melatonin may include disturbance of sleep, nightmares, daytime sleepiness and depression. The long-term effects of melatonin administration have not been examined and production is unregulated. In some countries the hormone is available only by prescription or not at all. In the United States and Canada, melatonin is freely available as a dietary supplement.
  • Cannabis has been successfully used as a sleeping aid to combat DSPS. Sleep onset is affected by the two primary cannabinoids, Δ9-Tetrahydrocannabinol (THC) dramatically increases melatonin production[17] and Cannabidiol (CBD) has been shown to be effective in helping insomniacs sleep[18]. Heavy cannabis use can lead to decreased levels of REM sleep and increased levels of slow-wave sleep along with reduced mental function the next morning however this is heavily dependent on dose, 5mg doses of THC and CBD have been shown not to have these effects[19]. Anecdotal evidence suggests that the Indica strain is particularly effective.
  • Some claim that large doses of vitamin B12 help normalize the onset of sleepiness, but little is known of the effectiveness of the treatment.
  • A treatment option which shows promise is Ramelteon, a recently-approved drug which in some ways acts as melatonin does. Production of ramelteon is as regulated as any other prescription medicine, so it avoids any possible problem of variable purity with melatonin supplements.
  • Modafinil is approved in the USA for treatment of Shift-work sleep disorder, which shares some characteristics with DSPS, and a number of clinicians are prescribing it for DSPS patients. However, modafinil does not deal with underlying causes of DSPS, it merely improves sleep deprived patient's quality of life. Taking modafinil less than 12 hours before the desired sleep onset time will actually exacerbate the symptoms by pushing back the sleep/wake cycle.
  • There has been one documented case in which a person with DSPS was successfully treated with trazodone.[20]

See Also: Phase response curve

Once the patient has established an earlier sleep schedule, following highly regular sleep/wake times and practicing good sleep hygiene are essential. DSPS patients are counselled to not go to bed if they are not sleepy, as doing so generally does not result in earlier sleep times. They are also advised to avoid alcohol and caffeine before bedtime.

With treatment, some people with DSPS can sleep and function well with the early sleep schedule. Stimulant drugs (including caffeine) to keep the person awake during the day may not be necessary. A chief difficulty of treating DSPS 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 person's sleeping schedule to late times again.

Adaptation to late sleeping times

Long-term success rates of treatment have not been evaluated. However, experienced clinicians acknowledge that DSPS is extremely difficult to treat.

Working the evening or night shift, or working at home, make DSPS less of an obstacle for some. Many of these people do not think of describing their pattern as a "disorder." Some DSPS individuals nap, even taking four hours of sleep a day and four at night. Some DSPS-friendly careers include security work, work in theatre and the media, work in hospitality such as restaurants and hotels, freelance writing, call center work, nursing, and taxi or truck driving.

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 DSPS be formally recognized as a "sleep-wake schedule disorder disability".

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.[16]

Rehabilitation for DSPS patients includes acceptance of the condition, and choosing a career that allows late sleeping times. In a few schools and universities, students with DSPS have been able to arrange to take exams at times when their concentration is good.

DSPS and depression

In the DSPS cases reported in the literature, about half of the patients have suffered from clinical depression or other psychological problems. The relationship between DSPS and depression is unclear. The fact that half of DSPS patients are not depressed indicates that DSPS is not merely a symptom of depression. Even in depressed patients, treatment methods such as chronotherapy can be effective without directly treating the depression.

According to the ICSD, "Although some degree of psychopathology is present in about half of adult patients with DSPS, there appears to be no particular psychiatric diagnostic category into which these patients fall. Psychopathology is not particularly more common in DSPS patients" compared with others complaining of "insomnia".[4]

It is conceivable that DSPS often has a major role in causing depression, because it can be such a stressful and misunderstood disorder. A direct neurochemical relationship between sleep mechanisms and depression is another possibility.

DSPS patients who also suffer from depression should seek treatment for both problems. There is some evidence that effectively treating DSPS can improve the patient's mood and make antidepressants more effective. In addition, treatment for depression can make patients more able to successfully follow DSPS treatments.

See also


  1. Dagan Y; Eisenstein M Circadian rhythm sleep disorders: toward a more precise definition and diagnosis. Chronobiol Int 1999 Mar;16(2):213-22
  2. *Weitzman, E.D., Czeisler, CA; et al. (1981). "Delayed sleep phase syndrome: a chronobiological disorder with sleep-onset insomnia". Archives of General Psychiatry. 38: 737–746.
  3. "Sleeplessness and Circadian Rhythm Disorder". eMedicine World Medical Library from WebMD. Retrieved 2006-06-04.
  4. 4.0 4.1 4.2 4.3 American College of Physicians--American Society of Internal Medicine (2005). International Classification of Sleep Disorders: Diagnostic & Coding Manual (PDF). Amer Academy of Sleep Medicine. ISBN 0-9657220-2-3.
  5. Okawa M, Uchiyama M (2007). "Circadian rhythm sleep disorders: characteristics and entrainment pathology in delayed sleep phase and non-24-h sleep-wake syndrome" (PDF). Sleep Med Rev. 11 (6): 485–96. doi:10.1016/j.smrv.2007.08.001. PMID 17964201. Retrieved 2008-03-13.
  6. El-Ad, Baruch. "Delayed sleep phase syndrome". MedLink Neurology. Retrieved 2008-03-24. (Type 'delayed sleep phase' in search box.)
  7. Schrader H, Bovim G, Sand T. The prevalence of delayed and advanced sleep phase syndromes. J Sleep Res. 1993 Mar;2(1):51-55.
  8. Yazaki, Mikako et al. Demography of sleep disturbances associated with circadian rhythm disorders in Japan Psychiatry and Clinical Neurosciences Volume 53 Issue 2 Page 267 April 1999
  9. Uchiyama, Makoto et al. Poor recovery sleep after sleep deprivation in delayed sleep phase syndrome Psychiatry and Clinical Neurosciences Volume 53 Issue 2 Page 195 - 197 April 1999
  10. Ancoli-Israel S, Schnierow B, Kelsoe J, Fink R. (2001). "A pedigree of one family with delayed sleep phase syndrome". Chronobiology International. 18 (5): 831&ndash, 840.
  11. Evolution of a length polymorphism in the human PER3 Gene, Nadakarni et al.JOURNAL OF BIOLOGICAL RHYTHMS / December 2005.
  12. Boivin, D.B. et al. Non-24-hour sleep–wake syndrome following a car accident Neurology 2003;60:1841-1843
  13. Quinto, Christine et al. Posttraumatic delayed sleep phase syndrome Neurology 2000;54:250
  14. Stores, Gregory. Misdiagnosing sleep disorders as primary psychiatric conditions. Advances in Psychiatric Treatment 2003, vol.9, 69-77
  15. Dagan, Yaron M.D., D.Sc.; Ayalon, Liat Ph.D. Case Study: Psychiatric Misdiagnosis of Non-24-Hours Sleep-Wake Schedule Disorder Resolved by Melatonin. Journal of the American Academy of Child & Adolescent Psychiatry. December 2005;44(12):1271-1275.
  16. 16.0 16.1 Dagan, Yaron and Abadi, Judith Sleep-Wake Schedule Disorder Disability: A lifelong untreatable pathology of the circadian time structure. Chronobiology International 2001; Volume 18, Number 6 Pages: 1019 - 1027
  17. *WP. Lissori, M. Resentini; et al. (1986). "Effects of Tetra-hydrocannabinol on Melatonin Secretion in Man". Hormone and Metabolic Research. 18: 77–78. External link in |title= (help)
  18. *E.A. Carlini and J.M. Cunha (1981). "Hypnotic and Antiepileptic Effects of Cannabidiol". Journal of Clinical Pharmacology. 21: 4175–274.
  19. *AN Nicholson, C Turner; et al. (2004). "Effect of Tetrahydrocannabinol and Cannabidiol on Nocturnal Sleep and Early-Morning Behavior in Young Adults.". Journal of Clinical Psychopharmacology. 24(3): 305–313. External link in |title= (help)
  20. Nakasei, Shinji et al. Trazodone advanced a delayed sleep phase of an elderly male: A case report Sleep and Biological Rhythms Volume 3 Page 169 - October 2005


  • Thorpy, M.J.; et al. (1988). "Delayed sleep phase syndrome in adolescents". Journal of Adolescent Health Care. 9: 22–27.
  • "When the body clock goes wrong: delayed sleep phase syndrome". Lancet. 340: 884. 1992.
  • Regestein, Q.; et al. (1995). "Treatment of delayed sleep phase syndrome". General Hospital Psychiatry. 17: 335–345.
  • Regestein, Q. and Monk, TH (1995). "Delayed sleep phase syndrome: a review of its clinical aspects". American Journal of Psychiatry. 152: 602–608.

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