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*[[Chronotherapy]], which consists of resetting the circadian clock by going to bed several hours ''later'' each day for several days.
*[[Chronotherapy]], which consists of resetting the circadian clock by going to bed several hours ''later'' each day for several days.
*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 United States and Canada, melatonin is freely available as a dietary supplement.
*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 United States and Canada, melatonin is freely available as a dietary supplement.
*[[Cannabis]] has been successfully used as a sleeping aid to combat DSPD. Sleep onset is affected by the two primary [[cannabinoids]], [[Tetrahydrocannabinol|Δ9-Tetrahydrocannabinol]] (THC) dramatically increases melatonin production<ref name=Lissori_1986>*{{cite journal | author=WP. Lissori, M. Resentini et al. | title=[http://web.archive.org/web/20010401010617/www.cures-not-wars.org/effects.html Effects of Tetra-hydrocannabinol on Melatonin Secretion in Man] | journal=Hormone and Metabolic Research | volume=18 | year=1986 | pages=77-78 }}</ref> and [[Cannabidiol]] (CBD) has been shown to be effective in helping insomniacs sleep<ref name=Carlini_1981>*{{cite journal | author=E.A. Carlini and J.M. Cunha | title=Hypnotic and Antiepileptic Effects of Cannabidiol | journal=Journal of Clinical Pharmacology | volume=21 | year=1981 | pages=4175-274 }}</ref>. 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<ref name=Nicholson_2004>*{{cite journal | author=AN Nicholson, C Turner, et al. | title=[http://www.cantodiem.org/PDF/Nicholson_CBME_Sleep.pdf Effect of Tetrahydrocannabinol and Cannabidiol on Nocturnal Sleep and Early-Morning Behavior in Young Adults.] | journal=Journal of Clinical Psychopharmacology | volume=24(3) | year=2004 | pages=305-313 }}</ref>. Anecdotal evidence suggests that the [[Cannabis|Indica strain]] is particularly effective.
*[[Cannabis]] has been successfully used as a sleeping aid to combat DSPD. Sleep onset is affected by the two primary [[cannabinoids]], [[Tetrahydrocannabinol|Δ9-Tetrahydrocannabinol]] (THC) dramatically increases melatonin production<ref name=Lissori_1986>*{{cite journal | author=WP. Lissori, M. Resentini et al. | title=[http://web.archive.org/web/20010401010617/www.cures-not-wars.org/effects.html Effects of Tetra-hydrocannabinol on Melatonin Secretion in Man] | journal=Hormone and Metabolic Research | volume=18 | year=1986 | pages=77-78 }}</ref> and [[Cannabidiol]] (CBD) has been shown to be effective in helping insomniacs sleep<ref name=Carlini_1981>*{{cite journal | author=E.A. Carlini and J.M. Cunha | title=Hypnotic and Antiepileptic Effects of Cannabidiol | journal=Journal of Clinical Pharmacology | volume=21 | year=1981 | pages=4175-274 }}</ref>. 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<ref name=Nicholson_2004>*{{cite journal | author=AN Nicholson, C Turner, et al. | title=[http://www.cantodiem.org/PDF/Nicholson_CBME_Sleep.pdf Effect of Tetrahydrocannabinol and Cannabidiol on Nocturnal Sleep and Early-Morning Behavior in Young Adults.] | journal=Journal of Clinical Psychopharmacology | volume=24(3) | year=2004 | pages=305-313 }}</ref>. Anecdotal evidence suggests that the [[Cannabis|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.
*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 a synthetic melatonin. Production of ramelteon is as regulated as any other prescription medicine, so it avoids the problems of variable purity and dosage with melatonin supplements.
*A treatment option which shows promise is [[Ramelteon]], a recently-approved drug which in some ways acts as a synthetic melatonin. Production of ramelteon is as regulated as any other prescription medicine, so it avoids the problems of variable purity and dosage with melatonin supplements.

Revision as of 18:13, 7 June 2007

Delayed sleep phase disorder
SpecialtyNeurology Edit this on Wikidata

Delayed sleep-phase Disorder (formerly Delayed sleep-phase Syndrome (DSPD or DSPS) is a chronic disorder of sleep timing. People with DSPD tend to fall asleep at very late times, and also have difficulty waking up in the morning.

Often, DSPD individuals 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 DSPD, 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 is usually treatable, but cannot be cured.

DSPD (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. DSPD is often frequently misdiagnosed as primary insomnia or as a psychiatric condition.

Definition

According to the International Classification of Sleep Disorders (ICSD), the key characteristics of DSPD (formerly DSPS) are:

  1. Sleep-onset and wake times that are intractably later than desired
  2. Actual sleep-onset times at nearly the same daily clock hour
  3. Little or no reported difficulty in maintaining sleep once sleep has begun
  4. Extreme difficulty awakening at the desired time in the morning
  5. A relatively severe to absolute inability to advance the sleep phase to earlier hours by enforcing conventional sleep and wake times.[4]

The following features of DSPD distinguish it from other sleep disorders:

  • 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. A diagnosis of DSPD is generally not given unless symptoms have been present for at least a month.

Attempting to force oneself through 9–5 life with DSPD has been compared to constantly living with 6 hours of jet lag. 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 the DSPD patient relief from daytime sleepiness but also perpetuates the late sleep phase.

People with DSPD 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. DSPD 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.

By the time DSPD 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. 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 syndrome is most common in adolescence, it is often the patient's parents who initiate seeking help, after great difficulty waking their child or teenager in time for school.

As of May 2007, the new International Classification of Sleep Disorders has changed the name from Delayed Sleep Phase Syndrome to Delayed Sleep Phase Disorder.

Prevalence

Using the strict ICSD diagnostic criteria, a random study of 10,000 adults in Norway estimated the prevalence of DSPD at 0.17%.[5] A similar study with 1525 adults in Japan estimated its prevalence at 0.13%.[6] Other studies have indicated that the prevalence of DSPD among adolescents is as high as 7%.

Physiology

Main article: Circadian rhythm sleep disorder

DSPD is a disorder of the body's timing system - the biological clock. It is believed to be caused by a reduced ability to reset the body's daily sleep/wake clock. Individuals with DSPD 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 did not have enough sleep the night before. Falling asleep earlier will in turn automatically advance their circadian clocks. In contrast, people with DSPD 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 DSPD patients, as it does with normal people.[7]

DSPD patients 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 DSPD 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 DSPD 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 DSPD patients. DSPD tends to run in families[8] and a growing body of evidence suggests that the problem is associated with the hPer3 (human period 3) gene.[9] There have been several documented cases of DSPD and non-24 hour sleep-wake syndrome developing after traumatic head injury.[10][11]

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.

Diagnosis

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

DSPD is frequently misdiagnosed or dismissed. It has been named as one of the sleep disorders most commonly misdiagnosed as a primary psychiatric disorder.[12] DSPD 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 DSPD diagnosis, and have often asked for better physician education on sleep disorders.[13]

Impact on patients

Lack of public awareness of the disorder contributes to the difficulties experienced by DSPD 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.

At a 2004 World Health Organization meeting on the effects of sleep on health, sleep experts noted that:

medium and long term effects... are known especially in DSPD. Affected individuals suffer from chronic sleep deprivation and from behavioral and cognitive consequences of sleep debt. There is increased abuse of alcohol and other substances, and some young subjects show criminal leanings. A striking relationship has been found between circadian rhythms and psychiatric disorders, particularly seasonal affective disorder, primary depression, and bipolar affective disorder.[14]

By the time DSPD 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 DSPD is itself a life-changing breakthrough.[15]

Treatment

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

Mild cases of DSPD can be controlled by waking up and going to bed 15 minutes earlier every day until the desired sleep schedule is reached. More severe cases are treated by the methods discussed below.

Before starting DSPD 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 consists of resetting the circadian clock by going to bed several hours later each day for several days.
  • 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 United States and Canada, melatonin is freely available as a dietary supplement.
  • Cannabis has been successfully used as a sleeping aid to combat DSPD. Sleep onset is affected by the two primary cannabinoids, Δ9-Tetrahydrocannabinol (THC) dramatically increases melatonin production[16] and Cannabidiol (CBD) has been shown to be effective in helping insomniacs sleep[17]. 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[18]. 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 a synthetic melatonin. Production of ramelteon is as regulated as any other prescription medicine, so it avoids the problems of variable purity and dosage with melatonin supplements.
  • Modafinil is approved in the USA for treatment of Shift-work sleep disorder, which shares some characteristics with DSPD, and a number of clinicians are prescribing it for DSPD patients. However, modafinil does not deal with underlying causes of DSPD, 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 DSPD was successfully treated with trazodone.[19]

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. DSPD 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.

If treated successfully, a person with DSPD can sleep and function as well with the early sleep schedule as with a late one. Stimulant drugs (including caffeine) to keep the person awake during the day should not be necessary. The chief difficulty of treating DSPD is in maintaining the 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 DSPD is difficult to treat.

Working the evening or night shift, or working at home, make DSPD less of an obstacle for some who have it. Many of these individuals do not think of describing their pattern as a "disorder." Some DSPD individuals nap, even taking four hours of sleep a day and four at night, although long daytime naps tend to promote nighttime sleeplessness. Some DSPD-friendly careers include security work, work in theatre and the media, freelance writing, call center work, nursing, and taxi or truck driving.

Some people with DSPD 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".

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.[15]

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

DSPD and depression

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

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

  • In one Calvin and Hobbes comic strip Calvin says as he is awakened, "No! No! No! I need more sleep!" He can hardly keep his eyes open in school that day, but while being dragged upstairs that evening by his mother, screams, "Bed?! Already?? But I'm wide awake!" In the last panel of the strip, Calvin says, "My internal clock is on Tokyo time."[20]

See also

Notes

  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. {{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.
  4. ^ American Academy of Sleep Medicine International Classification of Sleep Disorders, Revised Edition 2001.
  5. ^ Schrader H, Bovim G, Sand T. The prevalence of delayed and advanced sleep phase syndromes. J Sleep Res. 1993 Mar;2(1):51-55.
  6. ^ 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
  7. ^ 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
  8. ^ Ancoli-Israel S, Schnierow B, Kelsoe J, Fink R. (2001). "A pedigree of one family with delayed sleep phase syndrome". Chronobiology International. 18 (5): 831–840.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  9. ^ Evolution of a length polymorphism in the human PER3 Gene, Nadakarni et al.JOURNAL OF BIOLOGICAL RHYTHMS / December 2005.
  10. ^ Boivin, D.B. et al. Non-24-hour sleep–wake syndrome following a car accident Neurology 2003;60:1841-1843
  11. ^ Quinto, Christine et al. Posttraumatic delayed sleep phase syndrome Neurology 2000;54:250
  12. ^ Stores, Gregory. Misdiagnosing sleep disorders as primary psychiatric conditions. Advances in Psychiatric Treatment 2003, vol.9, 69-77
  13. ^ 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.
  14. ^ WHO Technical meeting on sleep and health - meeting report, accessed August 12 2006
  15. ^ a b 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 Cite error: The named reference "Dagan_SWSD_disability" was defined multiple times with different content (see the help page).
  16. ^ *WP. Lissori, M. Resentini; et al. (1986). "Effects of Tetra-hydrocannabinol on Melatonin Secretion in Man". Hormone and Metabolic Research. 18: 77–78. {{cite journal}}: Explicit use of et al. in: |author= (help); External link in |title= (help)
  17. ^ *E.A. Carlini and J.M. Cunha (1981). "Hypnotic and Antiepileptic Effects of Cannabidiol". Journal of Clinical Pharmacology. 21: 4175–274.
  18. ^ *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. {{cite journal}}: Explicit use of et al. in: |author= (help); External link in |title= (help)
  19. ^ 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
  20. ^ http://picayune.uclick.com/comics/ch/1995/ch950103.gif

References

  • Thorpy, M.J.; et al. (1988). "Delayed sleep phase syndrome in adolescents". Journal of Adolescent Health Care. 9: 22–27. {{cite journal}}: Explicit use of et al. in: |author= (help)
  • "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. {{cite journal}}: Explicit use of et al. in: |author= (help)
  • Regestein, Q. and Monk, TH (1995). "Delayed sleep phase syndrome: a review of its clinical aspects". American Journal of Psychiatry. 152: 602–608.{{cite journal}}: CS1 maint: multiple names: authors list (link)
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