Jump to content

Delayed sleep phase disorder: Difference between revisions

From Wikipedia, the free encyclopedia
Browse history interactively
← Previous editNext edit →
Content deleted Content added
VisualWikitext
+ wikilink
→‎DSPS and depression: + new quote & ref, and removed redundant sentence
Line 127: Line 127:
{{cquote|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 to patients with other forms of "insomnia." ... Whether DSPS results directly in clinical depression, or vice versa, is unknown, but many patients express considerable despair and hopelessness over sleeping normally again.<ref>{{cite book |author=Thorpy M |title=The International Classification of Sleep Disorders, Revised: Diagnostic and Coding Manual |origdate= |origyear= |origmonth= |url=http://www.absm.org/PDF/ICSD.pdf |format=PDF |accessdate= 2008-03-23 |year=2001 |publisher=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 |location= Chicago, Illinois, USA |isbn= 0-9657220-1-5 |oclc= |doi= |id= |pages= p.72-73 |chapter= |chapterurl= |quote= }}</ref>}}
{{cquote|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 to patients with other forms of "insomnia." ... Whether DSPS results directly in clinical depression, or vice versa, is unknown, but many patients express considerable despair and hopelessness over sleeping normally again.<ref>{{cite book |author=Thorpy M |title=The International Classification of Sleep Disorders, Revised: Diagnostic and Coding Manual |origdate= |origyear= |origmonth= |url=http://www.absm.org/PDF/ICSD.pdf |format=PDF |accessdate= 2008-03-23 |year=2001 |publisher=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 |location= Chicago, Illinois, USA |isbn= 0-9657220-1-5 |oclc= |doi= |id= |pages= p.72-73 |chapter= |chapterurl= |quote= }}</ref>}}


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.
It is conceivable that DSPS often has a major role in causing depression, because it can be such a stressful and misunderstood disorder. A recent study from [[UCSD]] found no association of [[bipolar disorder]] (history of mania) with DSPD, and it states that there may be
{{cquote|behaviorally-mediated mechanisms for comorbidity between DSPD and depression. For example, the lateness of DSPD cases and their unusual hours may lead to social opprobrium and rejection, which might be depressing...<ref>{{cite journal | last = Kripke | first = Daniel F. | coauthors = Rex K M; Ancoli-Israel S; Nievergelt C M; Klimecki W; Kelsoe J R | date = | year = 2008
| month = April | title = Delayed sleep phase cases and controls | journal = Journal of Circadian Rhythms | volume = 6 | issue = 6 | pages = | publisher = | location = | issn = | pmid = | doi = 10.1186/1740-3391-6-6 | bibcode = | oclc = | id = | url = http://www.jcircadianrhythms.com/content/pdf/1740-3391-6-6.pdf
| format = PDF | accessdate = 2008-05-01 | quote = }}</ref>}} A direct neurochemical relationship between sleep mechanisms and depression is another possibility.


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.
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.


DSPS patients who also suffer from depression may be best served by seeking 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.
DSPS patients who also suffer from depression may be best served by seeking 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.

Revision as of 18:54, 1 May 2008

Delayed sleep phase disorder
SpecialtyNeurology Edit this on Wikidata

Delayed sleep-phase syndrome (DSPS), also known as delayed sleep-phase disorder (DSPD) or delayed sleep-phase type (DSPT), is a circadian rhythm sleep disorder, a chronic disorder of the timing of sleep, peak period of alertness, core body temperature, hormonal and other daily rhythms. People with DSPS tend to fall asleep well after midnight and 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, however, they are allowed to follow their own maladjusted schedule, e.g. sleeping from 4 a.m. to noon, they sleep soundly, awaken spontaneously, and do not feel sleepy again until their next "night".

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, depending on the severity, 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 where patients complain of chronic insomnia.[3] However, as few doctors are aware of its existence, it often goes untreated or is treated inappropriately. DSPS is frequently misdiagnosed as primary insomnia or as a psychiatric condition.[4]

Definition

According to the International Classification of Sleep Disorders (ICSD),[5] 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.[5]

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".[6] 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.[7]

Prevalence

Sleepy students

About three adults of 2000 have DSPS. Using the strict ICSD diagnostic criteria, a random study in 1993 of 7700 adults (aged 18-67) in Norway estimated the prevalence of DSPS at 0.17%.[8] A similar study of 1525 adults (aged 15-59) in Japan estimated its prevalence at 0.13%.[9]

At least one study has indicated that the prevalence of DSPS among adolescents is as high as 7%. Among adolescents, boys predominate, while the gender distribution shows equal numbers of women and men in adults.[5]

Physiology

Main article: Circadian rhythm sleep disorder

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 due to decreased light exposure in the evening. 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.[10]

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. The timing of 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,[11] and a growing body of evidence suggests that the problem is associated with the hPer3 (human period 3) gene.[12][13] There have been several documented cases of DSPS and non-24 hour sleep-wake syndrome developing after traumatic head injury.[14][15]

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.[16]

Diagnosis

DSPS is diagnosed by a clinical interview, actigraphic monitoring and/or a sleep log 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.

DSPS is frequently misdiagnosed or dismissed. It has been named as one of the sleep disorders most commonly misdiagnosed as a primary psychiatric disorder.[17] 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.[18]

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.[19]

As DSPS is so little known and so misunderstood, support groups may be important for information and self-acceptance.[20]

Treatment

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. 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.

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 at the patient's usual time of spontaneous awakening or shortly before, in accordance with the Phase response curve (PRC) for light. Sunlight can also be used. Only experimentation, preferably with specialist help, will show how great an advance is possible/comfortable and for how long the treatment must continue until an earlier sleep-wake schedule is attained. For maintenance, some patients 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 a common treatment.
  • Just as bright light upon awakening should advance one's sleep-phase, bright light in the evening and night delays it (see the PRC). One might be advised to keep lights dim the last hours before bedtime and even wear goggles. 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 resets the circadian clock by manipulating bedtimes. Often, chronotherapy must be repeated every few months to maintain long-lasting results. 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. Taken this late, it does not of itself affect circadian rhythms,[21] 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; it must then be so small as to not induce sleepiness. 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 suggested as an aid to combat DSPS. However, no research has yet been done that shows cannabis works in DSPS. Sleep onset is affected by the two primary cannabinoids. THC, Δ9-Tetrahydrocannabinol, dramatically increased melatonin production in some subjects in a small study in 1986 where the authors state that "[t]hese preliminary results are difficult to interpret".[22] An older study showed that CBD, cannabidiol, was effective in helping insomniacs sleep.[23] 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, 5mg doses of THC and CBD have been shown not to have these effects.[24]
  • A treatment option which shows promise is ramelteon (Rozerem), 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. Modafinil does not deal with underlying causes of DSPS, though it may improve a 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.[25]
  • Vitamin B12 was, in the 1990s, suggested as a remedy for DSPS/DSPD, and one still sees it recommended in many sources. Several case reports were published. A review for the American Academy of Sleep Medicine in 2007 concluded that no benefit at all was seen from this treatment.[26]

Once a patient has established an earlier sleep schedule, it is essential to follow highly regular sleep/wake times and to practice good sleep hygiene. With treatment, some people with mild DSPS can sleep and function well with the early sleep schedule. Caffeine and other stimulant drugs to keep a 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 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 DSPS is extremely difficult to treat. One study of 61 DSPS patients with mean sleep onset and waking times of about 3 a.m. and 11: 30 a.m., respectively, showed, a year after a 6-week treatment, that over 90% had relapsed to pretreatment sleeping patterns within a year, 28.8% reporting that the relapse occurred within one week. The milder cases retained changes significantly longer than the more severe cases.[27]

Working the evening or night shift, or working at home, makes DSPS less of an obstacle for some. Many of these people do not describe their pattern as a "disorder." Some DSPS individuals nap, even taking 4-5 hours of sleep in the daytime and 4-5 at night. DSPS-friendly careers can include security work, work in theater, the entertainment industry, the media, freelance writing, call center work, nursing, taxi or truck driving and hospitality work in restaurants, hotels or bars.

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".

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 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.[19]

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, about the same proportion as among patients with chronic insomnia.[5] 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 to patients with other forms of "insomnia." ... Whether DSPS results directly in clinical depression, or vice versa, is unknown, but many patients express considerable despair and hopelessness over sleeping normally again.[28]

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

behaviorally-mediated mechanisms for comorbidity between DSPD and depression. For example, the lateness of DSPD cases and their unusual hours may lead to social opprobrium and rejection, which might be depressing...[29]

A direct neurochemical relationship between sleep mechanisms and depression is another possibility.

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.

DSPS patients who also suffer from depression may be best served by seeking 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

References

  • Thorpy MJ, Korman E, Spielman AJ, Glovinsky PB (1988). "Delayed sleep phase syndrome in adolescents". J Adolesc Health Care. 9 (1): 22–7. PMID 3335467.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  • "When the body clock goes wrong: delayed sleep phase syndrome". Lancet. 340 (8824): 884–5. 1992. PMID 1357304.
  • Regestein QR, Pavlova M (1995). "Treatment of delayed sleep phase syndrome". Gen Hosp Psychiatry. 17 (5): 335–45. PMID 8522148.
  • Regestein QR, Monk TH (1995). "Delayed sleep phase syndrome: a review of its clinical aspects". Am J Psychiatry. 152 (4): 602–8. PMID 7694911.

Notes

  1. ^ Dagan Y, Eisenstein M (1999). "Circadian rhythm sleep disorders: toward a more precise definition and diagnosis". Chronobiol. Int. 16 (2): 213–22. PMID 10219492.
  2. ^ 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. PMID 7247637. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
  3. ^ "Sleeplessness and Circadian Rhythm Disorder". eMedicine World Medical Library from WebMD. Retrieved 2006-06-04. Implicit in the diagnosis of circadian rhythm disorder is a desire to conform to traditionally accepted sleep-wake patterns.
  4. ^ Dagan Y (2002). "Circadian rhythm sleep disorders (CRSD)" (PDF). Sleep Med Rev. 6 (1): 45–54. PMID 12531141. Retrieved 2007-11-08. Early onset of CRSD, the ease of diagnosis, the high frequency of misdiagnosis and erroneous treatment, the potentially harmful psychological and adjustment consequences, and the availability of promising treatments, all indicate the importance of greater awareness of these disorders.
  5. ^ a b c d 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.
  6. ^ 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.
  7. ^ El-Ad, Baruch. "Delayed sleep phase syndrome". MedLink Neurology. Retrieved 2008-03-24. (Type 'delayed sleep phase' in search box.)
  8. ^ Schrader H, Bovim G, Sand T (1993). "The prevalence of delayed and advanced sleep phase syndromes". J Sleep Res. 2 (1): 51–55. PMID 10607071.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  9. ^ 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. PMID 10459707.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  10. ^ 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. doi:10.1046/j.1440-1819.1999.00481.x. PMID 10459687. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
  11. ^ 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. PMID 11763990.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  12. ^ Archer, S.N. (2003-06-15). "A length polymorphism in the circadian clock gene Per3 is linked to delayed sleep phase syndrome and extreme diurnal preference" (abstract). Sleep. 26 (4): 411. PMID 12841365. Retrieved 2008-04-21. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  13. ^ 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. doi:10.1177/0748730405281332. PMID 16275768.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  14. ^ 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. PMID 12796546.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  15. ^ Quinto C, Gellido C, Chokroverty S, Masdeu J (2000). "Posttraumatic delayed sleep phase syndrome". Neurology. 54 (1): 250–2. PMID 10636163.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  16. ^ Okawa, Masako (2007). "Clinical Review. Circadian rhythm sleep disorders: Characteristics and entrainment pathology in delayed sleep phase and non-24-h sleep-wake syndrome" (PDF). Sleep Medicine (11). Elsevier Ltd: 485–496. Retrieved 2008-04-16. Although delaying both bedtime and waking time by 3h, repeated daily until rotation around the clock can achieve the desired sleep-wake schedule, this delaying chronotherapy could lead to non-24 by allowing the system to slip around the clock and cause dangerous situations. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help)
  17. ^ Stores G (2003). "Misdiagnosing sleep disorders as primary psychiatric conditions". Advances in Psychiatric Treatment. 9: 69–77.
    See also subsequent:
    * Stores G (2007). "Clinical diagnosis and misdiagnosis of sleep disorders". J. Neurol. Neurosurg. Psychiatr. 78 (12): 1293–7. doi:10.1136/jnnp.2006.111179. PMID 18024690.
  18. ^ 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. PMID 16292119.
  19. ^ a b 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. PMID 11777076.
  20. ^ Potts, Henry W. W. ([2005]). "Online support groups: An overlooked resource for patients" (PDF). University College London. Retrieved 2008-04-14. {{cite web}}: Check date values in: |year= (help)
  21. ^ 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. doi:10.1113/jphysiol.2007.143180. PMID 18006583. Using exogenous melatonin as a sleep aid at night has minimal phase shifting effects{{cite journal}}: CS1 maint: multiple names: authors list (link)
  22. ^ Lissoni P, Resentini M, Mauri R; et al. (1986). "Effects of tetrahydrocannabinol on melatonin secretion in man". Horm. Metab. Res. 18 (1): 77–8. PMID 3005151. {{cite journal}}: |format= requires |url= (help); Explicit use of et al. in: |author= (help); Text "http://web.archive.org/web/20010401010617/www.cures-not-wars.org/effects.html" ignored (help)CS1 maint: multiple names: authors list (link)
  23. ^ Carlini EA, Cunha JM (1981). "Hypnotic and antiepileptic effects of cannabidiol". J Clin Pharmacol. 21 (8-9 Suppl): 417S–427S. PMID 7028792.
  24. ^ Nicholson AN, Turner C, Stone BM, Robson PJ (2004). "Effect of Delta-9-tetrahydrocannabinol and cannabidiol on nocturnal sleep and early-morning behavior in young adults" (PDF). J Clin Psychopharmacol. 24 (3): 305–13. PMID 15118485.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  25. ^ Nakasei S; et al. (2005). "Trazodone advanced a delayed sleep phase of an elderly male: A case report". Sleep and Biological Rhythms. 3: 169. {{cite journal}}: Explicit use of et al. in: |author= (help); Unknown parameter |month= ignored (help)
  26. ^ 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" (PDF). Sleep. 30 (11): 1484–501. PMID 18041481. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
  27. ^ 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. PMID 9562922.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  28. ^ Thorpy M (2001). The International Classification of Sleep Disorders, Revised: Diagnostic and Coding Manual (PDF). 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. pp. p.72-73. ISBN 0-9657220-1-5. Retrieved 2008-03-23. {{cite book}}: |pages= has extra text (help); Cite has empty unknown parameters: |origmonth=, |chapterurl=, and |origdate= (help)
  29. ^ Kripke, Daniel F. (2008). "Delayed sleep phase cases and controls" (PDF). Journal of Circadian Rhythms. 6 (6). doi:10.1186/1740-3391-6-6. Retrieved 2008-05-01. {{cite journal}}: Unknown parameter |coauthors= ignored (|author= suggested) (help); Unknown parameter |month= ignored (help)CS1 maint: unflagged free DOI (link)

External links

Retrieved from "https://en.wikipedia.org/w/index.php?title=Delayed_sleep_phase_disorder&oldid=209518206"