Advanced sleep-wake phase disorder …

Tresa Zacharias MD

Sleep Disorders

Updated 09.04.2023
Released 11.22.1993
Expires For CME 09.04.2026

Advanced sleep-wake phase disorder

Author: Tresa Zacharias MD

See Contributor Disclosures

Editor: Bradley V Vaughn MD

Advanced sleep-wake phase disorder

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Introduction

Overview

In this article, the author discusses the pathophysiology and treatment of this circadian rhythm sleep disorder. Hallmarks of this disorder include an advance in the habitual bedtime and wake time by several hours. The early morning awakening seen in this disorder may be mistaken for insomnia or depression. This is the first circadian rhythm sleep disorder for which a genetic cause was demonstrated. Current treatment primarily depends on the use of evening light therapy. Timed melatonin may theoretically be efficacious, but further trials are needed.

Key points

	• Advanced sleep-wake phase disorder consists of stable, advanced, habitual sleep and waking times, which can be seen more frequently in elderly individuals.
	• Several large kindreds with autosomal dominant familial advanced sleep-wake phase disorder have been described.
	• In some families, various missense mutations in clock genes were found.
	• This is the first hereditary circadian rhythm variant described in humans.
	• Treatment is largely empirical; timed light and melatonin may be tried.

Historical note and terminology

This disorder was initially referred to as advanced sleep phase syndrome, then was later classified as circadian rhythm sleep disorder, an advanced sleep phase type. Throughout this article the formal name advanced sleep-wake phase disorder, established in the third edition of the International Classification of Sleep Disorders, will be used (01). The preferred common name is advanced sleep phase disorder.

Clinical manifestations

Presentation and course

	• Advanced sleep-wake phase disorder is characterized by habitual sleep-wake times advanced in relation to conventional or socially acceptable time and is present for at least 3 months.
	• Symptoms of advanced sleep-wake phase disorder include evening sleepiness, early sleep onset, and early morning awakenings.
	• The prognosis of advanced sleep phase syndrome is uncertain.
	• The main complications of advanced sleep-wake disorder include restriction of social activities and evening driving.

Patients with advanced sleep-wake phase disorder have their habitual sleep-wake times advanced in relation to the conventional or socially acceptable time; this results in symptoms of evening sleepiness, early sleep onset, and early-morning awakening (01). The symptoms must be present for at least three months. Despite efforts to delay sleep to later hours, sleep onset routinely occurs between 6:00 PM and 9:00 PM. During this time window, the patient may fall asleep at social gatherings or while driving. Patients routinely curtail or avoid evening activities due to the need to go to bed earlier than the social norm. Final awakening is much earlier in the morning than is desired or necessary to meet social or occupational obligations, typically well before dawn between 2:00 AM and 5:00 AM. Delaying evening sleep onset and extending sleep later into the morning are intractably difficult for these patients; however, if patients are able to sleep during their biologically preferred time window, sleep duration and quality are normal. Unlike other disorders with prominent early morning awakening, eg, depression, the early morning awakening in advanced sleep phase syndrome occurs after a normal amount of relatively consolidated sleep, and there is no major mood disturbance during waking hours.

Prognosis and complications

The prognosis of advanced sleep phase syndrome is uncertain. Restriction of normal social activities due to the need to retire early is the main complication of advanced sleep phase syndrome. Evening driving may be dangerous due to sleepiness.

Clinical vignette

A 69-year-old woman slept well and led an active social life until three years before she came into the clinic. Being an avid concert fan, she found it progressively difficult to stay awake during the evening performances and had to give up her season tickets. She thought something was the matter with her sleep at night because she would arise early (about 5:00 AM) although she would feel alert at that time. Her past medical history included coronary artery disease; she had undergone coronary artery bypass graft six years previously; arterial hypertension was treated with beta-blockers and diuretics. Polysomnography revealed a mild sleep-related breathing disorder that was judged to be not clinically significant. Actigraphy showed a relatively consolidated nocturnal sleep episode with average bedtime and waking time at 9:00 PM and 4:30 AM hours, respectively. The patient was treated with bright light exposure at 7:30 PM. The treatment delayed the habitual bedtime and waking time to about 10:30 PM and 6:00 AM, respectively. The patient was able to stay awake later and resumed her favorite evening activities.

Biological basis

	• Nearly every cell in an organism has molecular oscillators that regulate circadian gene expression in response to various time cues.
	• The paired suprachiasmatic nuclei of the hypothalamus is the central mammalian circadian oscillator and is the “master clock” that regulates peripheral molecular oscillators by transmission of circadian timing signals.
	• The biological clocks of normal humans have a natural endogenous cycle of about 24.2 hours.
	• The 24-hour cycle is maintained by daily synchronization of internal clocks with the shorter environmental cycle through a phase advancement of a fixed time period daily.
	• Light is the main zeitgeber of endogenous clocks in humans.
	• The circadian neuronal system is activated by darkness and suppressed by light.
	• The daily rhythm of melatonin secretion is controlled by the endogenous master pacemaker. Timing in the suprachiasmatic nucleus is regulated by melatonin. Light for entrainment is only effective a few hours before or after the core body temperature nadir. Light exposure before the core body temperature minimum delays the phase. Light exposure after the core body temperature minimum advances it. The amount of maximal daily resetting by light is limited to 1 to 3 hours.
	• Dim light melatonin onset is currently the most commonly utilized marker of the circadian phase.
	• Melatonin plays a modulatory role in the human circadian system.
	• Exogenous melatonin can shift circadian phase, exhibiting a phase-response curve that roughly mirrors the phase-response curve of light. Peak phase advance occurs prior to the time of dim-light melatonin secretion onset, whereas peak phase delay occurs about 12 hours later.
	• Sleep propensity is governed by the interaction of an oscillating circadian process that promotes sleepiness at night and a steadily increasing homeostatic process that reflects prior sleep deprivation.
	• The etiology of advanced sleep-wake phase disorder is unknown in the majority of cases.
	• Advanced sleep-wake phase disorder increases in prevalence with age.
	• Several mutations in CLOCK, BMAL1, PER, CRY, CKI-delta, and TIMELESS genes have been identified in familial cases of advanced sleep-wake phase disorder.

Etiology and pathogenesis

Normal circadian physiology in humans. Almost every cell in the organism has active molecular oscillators that regulate circadian gene expression in response to various time cues, including light and chemical changes induced by feeding and temperature changes. In the absence of a central master clock, the myriad peripheral pacemakers would produce a cacophony of rhythms that would make a coordinated circadian behavior impossible.

The paired suprachiasmatic nuclei of the hypothalamus have been established as the site of the central mammalian circadian oscillator. This grouping of about 10,000 anterior ventromedial hypothalamic neurons manifests a high amplitude circadian pattern of firing both in intact, freely behaving animals and in vitro. This suprachiasmatic nuclei “master clock” is composed of multiple single-cell circadian oscillators that, when synchronized, generate a coordinated circadian output that regulates peripheral “clocks” by transmission of circadian timing signals. This regulation is achieved by means of direct and indirect projections to other regulatory brain areas, primarily in the hypothalamus, modulating in turn their circadian outputs and coordinating other overt rhythms (eg, arousal, hormonal secretion, temperature, feeding, etc.). Daily behavioral, vegetative, and circadian firing rhythms of other brain regions desynchronize if the suprachiasmatic nuclei are lesioned.

The biological clocks of normal humans of all ages have a natural endogenous circadian cycle of slightly more than 24 hours, generally about 24.2 hours. If all temporal cues (zeitgeber, German for “time givers”) are removed, the internal rhythms are progressively phase delayed relative to the external clock time. Keeping the basic 24-hour cycle involves daily synchronizing of the internal clocks with the shorter environmental cycle following external zeitgebers (a process known as entraining, a control of one oscillating process by another). This circadian correction is achieved by advancing the internal clocks by a fixed time period (about 0.2 hours) every day. The ability to phase-advance is normally limited.

Light is the main zeitgeber of endogenous clocks in humans, as it is in other animals and plants. The human circadian system is more sensitive to short-wave blue-green light than to the long-wave red-spectrum light. The major afferent input to the suprachiasmatic nucleus consists of a melanopsin-containing subset of photosensitive retinal ganglion cells whose axons depart the optic chiasm to synapse on SCN cells.

Human circadian system outline

Melatonin (upper right inset) is produced in the pineal gland. The production and secretion of melatonin is mediated largely by postganglionic retinal nerve fibers that pass through the retinohypothalamic tract to the suprachiasma...

There are three fundamental characteristics of the resetting capacity of the human circadian clock by light. First, the maximal response to a specific stimulus only occurs at a specific circadian time, which is stimulus dependent. As an example, light is generally only effective a few hours before or after the core body temperature nadir (between 3:00 AM to 5:00 AM in normally entrained humans). Stimuli applied during most of the daylight period have less effect on circadian phase timing, although there is some evidence that the human circadian pacemaker may be sensitive to bright light throughout the day. Second, the direction of resetting (advance or delay) is dependent on the circadian time at which the exposure occurs; light exposure before the core body temperature minimum delays the phase, whereas exposure after the core body temperature minimum advances it. Third, the amount of maximal daily resetting is limited to 1 to 3 hours. Plots of the magnitude and the direction of response (phase change) against the circadian time of light stimulus application (phase-response curve) reveal increasing amounts of delay from dusk to about halfway through the dark period, which roughly coincides with the nadir in core body temperature.

Phase-response curve to light and to exogenous melatonin

The y-axis shows the direction and relative magnitude of the phase shift produced by the administration of light (blue line) and melatonin (red line) at various times that are shown on the x-axis. The two x-axes show the time of m...

The direction of phase change then rapidly switches to maximal phase advances when the stimulus is applied near the beginning of the second half of the dark period, after which the advance response declines as the light stimulus moves closer to subjective dawn (30). The daily phase-advance in humans that keeps pace with the 24-hour day is a process that occurs immediately following arising in the morning and exposing the eyes to sufficient light.

The circadian clock phase (location of a certain event in the near 24-hour cycle), amplitude, and period cannot be measured directly by noninvasive means. Core body temperature varies predictably under circadian influence, even without the masking effect of sleep (which lowers the body temperature regardless of the circadian phase); it may, thus, serve as a circadian marker, but necessitates cumbersome rectal probes and constant routines regarding food intake, activity, and sleep. The rhythm of the pineal hormone melatonin is an easier measure marker of the endogenous circadian rhythm. Melatonin levels in fractional saliva specimens correlate well with plasma melatonin and are less markedly influenced by sleep and posture, although they can be affected by light exposure. This technique has been validated in the home environment (05).

The melatonin circadian rhythm is highly robust, has low intra-individual but high inter-individual variability, and is appreciably masked by light. The dynamics of the daily duration of melatonin secretion is significant in seasonal and reproductive physiology in animals; longer nights characteristic of the winter photoperiod are signaled by longer melatonin secretion duration. Dim light melatonin onset (DLMO) is currently the most commonly utilized marker of the circadian phase (23).

The role of melatonin in the human circadian cycle is modulatory. The suprachiasmatic nucleus exhibits a dense population of melatonin receptors, presumably establishing a feedback mechanism. Exogenous melatonin can shift circadian phase, exhibiting a phase-response curve that is roughly a mirror image of the phase-response curve of light. The direction and the magnitude of the shift depend on the circadian time at which the light or melatonin are applied. Bright light in the evening delays the phase of the circadian clock, whereas bright light in the morning advances the clock; exogenous melatonin does the opposite. With exogenous melatonin, peak phase advance occurs prior to the time of dim-light melatonin secretion onset (about 8:00 PM) and peak phase delay about 12 hours later.

Melatonin also affects other endogenous rhythms, including temperature, cortisol secretion, and the sleep-wake cycle. Appropriately timed light exposure and melatonin may reinforce a desired effect (09); indeed, it is possible that the physiological role of the nocturnal melatonin secretion is to reinforce the daily resetting of the endogenous clock by the morning light and to provide additional fine-tuning (28). Mutually reinforcing timed application of light and exogenous melatonin may be used in treating circadian rhythm sleep disorders (25).

The sleep-wake cycle is a major overt manifestation of the circadian rhythm, possibly through the SCN’s direct and indirect projections to wake- and sleep-promoting brain regions. However, compared to other endogenous rhythms like core body temperature or melatonin, it is more loosely associated with the circadian pacemaker and is also influenced by noncircadian homeostatic factors (eg, prior sleep deprivation). Sleep propensity is governed at any time by the interaction of two processes: (1) an oscillating circadian process coupled to other circadian rhythms (eg, melatonin secretion and core body temperature rhythms) that promote sleepiness at night and contribute to the afternoon napping “siesta” period; and (2) a steadily increasing homeostatic process reflecting prior sleep deprivation that discharges during sleep. The detailed description of the interaction of these processes is beyond the scope of this review; the classic two-process interaction model is an abstraction, and the net result of sleep-alertness is much more than the algebraic sum of the two processes. A significant, partially genetically determined, inter-individual variability exists, which determines, among other factors, the degree to which a person is an evening or morning type (14).

Pathophysiology of advanced sleep-wake phase disorder. Although in some cases genetic mutations have been identified, the etiology is unknown in the majority of cases.

The basic pattern of advanced sleep-wake phase disorder is presumably a phase-advance of the circadian pacemaker coupled with a similar phase-advance of the sleep-wake cycle (24). Advanced sleep-wake phase disorder increases in prevalence with age. Age-related changes in the circadian sleep-wake pattern are frequently observed. There seems to be a consensus about the tendency for circadian phase-advancement, sleep phase-advancement, and less consolidated sleep in healthy elderly. However, opinions vary as to whether this is due to a reduction in the output of the circadian pacemaker (eg, the amplitude of core body temperature changes or melatonin secretion) with increasing age, which may be responsible for decreased sleep consolidation in the elderly. Some studies showed such reduction, whereas others showed none. The elderly may also exhibit changes in the interrelationships between measured circadian outputs (primarily melatonin and core body temperature rhythms) and the sleep-wake cycle, particularly shortening of the time between core body temperature nadir and the habitual waking time, but this is not a universal finding. The changes in sleep consolidation and in sleep timing in the healthy elderly may also be due to reduction in the homeostatic drive for sleep and in the circadian drive that promotes sleep in the early morning. Psychosocial factors (isolation, reduced exposure to light, changes in scheduled activities) may also play a role in the elderly, emphasizing loose coupling between the sleep-wake and the circadian cycles.

At a molecular level, the rhythms of expression of circadian genes Per1, Per2, and Per3 in peripheral blood monocytes in the elderly were as robust as in young subjects, although they were phase advanced. The phase angle between the Per3 (but not Per1 or Per2) expression and the habitual sleep timing was altered in the elderly, suggesting decreased homeostatic sleep drive in the elderly (15). A brief review summarizes the findings and the controversies on the subject of the changes in the circadian system with aging (21).

Interestingly, patients with early-morning insomnia and normal bedtime also exhibited significant advancement of their circadian rhythm; it is possible that, although suffering from a mild advanced sleep phase syndrome, social considerations prevented them from adopting an earlier bedtime. It is difficult to draw clear lines between the normal sleep-wake cycle changes in healthy elderly, early-morning insomnia, and advanced sleep phase syndrome. They may all represent different angles of the same spectrum of age-related changes influenced by psychosocial factors.

The circadian clock consists of a transcription-translation negative feedback loop regulated by activators (CLOCK and BMAL1) and inhibitors (PER and CRY). Several mutations in these genes have been identified in familial cases of advanced sleep-wake phase disorder. In 1999, three large, Caucasian kindreds with familial advanced sleep phase syndrome (FASP) were described. Overall, there were 37 affected individuals (29 affected in one kindred in five generations); the youngest affected patient was eight years old. The disorder segregated as autosomal dominant with high penetrance. They had phase advance of about four hours in the sleep-wake cycle, melatonin, and temperature circadian rhythms. One of the subjects was studied in a time-isolation facility; her circadian period (both sleep-wake and temperature) was 23.3 hours. A missense mutation in one of the circadian genes crucial for resetting the circadian clock in response to light (Per2) in these kindreds was subsequently described. This was the first hereditary circadian rhythm variant described in humans. An additional kindred of eight affected members was described at that time. The disorder also segregated as autosomal dominant. Another two Japanese pedigrees totaling nine individuals with familial advanced sleep phase syndrome were described that had no previously described missense mutation, suggesting a genetic heterogeneity in the familial advanced sleep phase syndrome. A missense mutation in CRY2 (Ala to Thr) is purported to result in familial advanced sleep phase (16). Another missense mutation was described in the CKI-delta circadian gene, which was responsible for familial advanced sleep phase syndrome in another Japanese family. This CKI-delta mutation has also been associated with familial migraine (06). Polymorphisms at another circadian gene (Per1) may be associated with extreme morning preference bordering on advanced sleep phase syndrome. Finally, mutations in the human TIMELESS gene have been shown to impact negative regulators of the circadian clock leading to familial advanced sleep phase (19).

In population-based studies looking at variants in the genes known to cause familial advanced sleep wake phase disorder, the PER3 P415A/H417R variant was associated with earlier sleep timing, although the effect size was only 7.8 minutes compared to four hours in those with familial advanced sleep phase (29). Carriers of pathogenic variants of CRY2 and TIMELESS, however, were not associated with earlier sleep times (29).

Individuals with autism spectrum disorder have been identified as having PER2 variants. Of 5102 individuals with autism spectrum disorder, four were found to have PER2 variants (17). None of them were previously diagnosed with a sleep disorder, but three of them reported sleep difficulties, with one subject having symptoms suggestive of a familial advanced sleep-wake phase disorder. There may be a relationship between circadian dysregulation and autism spectrum disorder, although this area needs further study. It has also been demonstrated that individuals born prematurely with very low birth weight were more likely to have an advanced sleep phase as adults, though the underlying mechanism remains unclear at this point (04).

Management

	• Treatments for advanced sleep-wake phase syndrome use chronobiological principles and include evening exposure to bright light and chronotherapy.
	• Early morning low-dose melatonin has not been systematically studied in advanced sleep-wake disorder.
	• Light therapy is considered a safe therapeutic option with limited side effects.

Treatments for advanced sleep phase syndrome use chronobiological principles to achieve sustained phase shift to the desired sleep-wake schedule. This is performed with intentional changes to amplify environmental time cues using timed light exposure or melatonin. General measures to improve sleep hygiene, exercise, and relaxation may all help to consolidate the new schedule.

Light is the most important zeitgeber to the circadian clock. As described above, bright light exposure has phase-shifting effects with phase advance or delay following early morning or late evening exposure, respectively. Evening exposure to bright light (2500 lux for 2 hours) was found to delay both the sleep-wake and the melatonin rhythm in a patient with advanced sleep phase syndrome, though the AASM Clinical Practice Guidelines published in 2015 do not provide a specific light intensity (03). Various studies have shown varying degrees of efficacy with 2500 lux to 10000 lux. Evening bright light exposure (between 8:00 PM and midnight) delayed circadian phase markers and improved subjective quality of sleep in early-morning insomniacs and in advanced sleep-wake phase disorder. During long-term maintenance treatment, subjective improvement was maintained, but objective changes in sleep parameters were less pronounced. Many commercial light boxes are available, varying in design and light intensity. Longer period of moderate intensity light may be more effective than a shorter exposure period of high intensity light (11), although a more recent paper suggests that 30 minutes of bright light exposure may be sufficient for advancing circadian rhythms (09). It appears that light exposure must be done during the waking hours in order to achieve a phase delay, as a study looking at light delivered through the eyelids of sleeping persons did not show any objective differences between the control and intervention conditions (12).

Melatonin has not been systematically studied in advanced sleep phase syndrome. On theoretical grounds and following its success in other circadian rhythm sleep disorders, early morning low-dose melatonin, either alone or combined with evening bright light exposure, may be beneficial in delaying a patient’s circadian rhythm. Despite the paucity of controlled studies, the original review and practice parameters of the American Academy of Sleep Medicine suggest chronotherapy, timed light exposure, and melatonin administration in the treatment of patients with advanced sleep phase syndrome. However, following criticism about the inclusion of melatonin, the recommendation for use of timed melatonin in this disorder was removed.

Hypnotics to manage early morning insomnia are best avoided.

Outcomes

Light therapy is considered safe if used with recommended intensity and duration (03). Potential side effects include eye irritation, irritability, headache, nausea, sensation of glare, erythema, dryness of eyes and skin, and, rarely, a hypomanic state. This can be managed with adjustment of light intensity, duration of therapy, and humidification. Many patients report initial subjective success; however, relapse is common due to failure to maintain therapy.

References

01: American Academy of Sleep Medicine. ICSD-3, International classification of sleep disorders, 3rd ed. Darien, IL: American Academy of Sleep Medicine, 2014.
02: Aspholm R, Lindbohm ML, Paakkulainen H, Taskinen H, Nurminen T, Tiitinen A. Spontaneous abortions among Finnish flight attendants. J Occup Environ Med 1999;41(6):486-91. PMID 10390700
03: Auger RR, Burgess HJ, Emens JS, Deriy LV, Thomas SM, Sharkey KM. Clinical practice guideline for the treatment of intrinsic circadian rhythm sleep-wake disorders: advanced sleep-wake phase disorder (ASWPD), delayed sleep-wake phase disorder (DSWPD), non-24-hour sleep-wake rhythm disorder (N24SWD), and irregular sleep-wake rhythm disorder (ISWRD). An update for 2015: An American Academy of Sleep Medicine Clinical Practice Guideline. J Clin Sleep Med 2015;11(10):1199-236. PMID 26414986
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05: Bormes G, Love J, Oluwaseun A, et al. Self-directed home-based dim-light melatonin onset collection: the Circadia pilot study. medRxiv 2023. [Epub ahead of print] PMID 37398260
06: Brennan KC, Bates EA, Shapir RE, et al. Casein kinase Idelta mutations in familial migraine and advanced sleep phase. Sci Transl Med 2013;5(183):183ra56. PMID 23636092
07: Coleman MY, McGlashan EM, Vidafar P, Phillips AJK, Cain SW. Advanced melatonin onset relative to sleep in women with unmedicated major depressive disorder. Chronobiol Int 2019;36(10):1373-83. PMID 31368377
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11: Dewan K, Benloucif S, Reid K, Wolfe LF, Zee PC. Light-induced changes of the circadian clock of humans: increasing duration is more effective than increasing light intensity. Sleep 2011;34(5):593-9. PMID 21532952
12: Figueiro MG, Sloane PD, Ward K, et al. Impact of an individually tailored light mask on sleep parameters in older adults with advanced phase sleep disorder. Behav Sleep Med 2020;18(2):226-40. PMID 30588849
13: Frangopoulos F, Nicolaou I, Zannetos S, et al. Setting objective clinical assessment tools for circadian rhythm sleep-wake disorders - a community-based cross-sectional epidemiological study. Nat Sci Sleep 2021;13:791-802. PMID 34163273
14: Gentry NW, Ashbrook LH, Fu YH, Ptáček LJ. Human circadian variations. J Clin Invest 2021;131(16):e148282. PMID 34396981
15: Hida A, Kusanagi H, Satoh K, et al. Expression profiles of PERIOD1, 2, and 3 in peripheral blood mononuclear cells from older subjects. Life Sci 2009;84(1-2):33-7. PMID 19013183
16: Hirano A, Shi G, Jones CR, et al. A Cryptochrome 2 mutation yields advanced sleep phase in humans. ELife 2016b;5. PMID 27529127
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Contributors

All contributors' financial relationships have been reviewed and mitigated to ensure that this and every other article is free from commercial bias.

Author

Tresa Zacharias MD

Dr. Zacharias of Rush University Medical Center has no relevant financial relationships to disclose.
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Editor

Bradley V Vaughn MD

Dr. Vaughn of UNC Hospital Chapel Hill and University of North Carolina School of Medicine has no relevant financial relationships to disclose.
See Profile

Former Authors

Hrayr P Attarian MD
Michael J Howell MD
Daniel Wagner MD (original author), Baruch El-Ad MD, and Annise Wilson MD

Patient Profile

Age range of presentation: 6 to 65+ years
Sex preponderance: male=female
Heredity: heredity may be a factor
Population groups selectively affected: none selectively affected
Occupation groups selectively affected: none selectively affected

ICD & OMIM codes

ICD-9: Disruption of 24 hour sleep wake cycle, unspecified: 780.55
ICD-10: Disorders of the sleep-wake schedule: G47.2

Circadian rhythm sleep disorder, advanced sleep phase type: G47.22

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Advanced sleep-wake phase disorder

Associated Disorders

Affective disorders
Circadian rhythm sleep disorder
Depression
Phase advance

Differential Diagnosis

major depression
chronic sleep deprivation
disrupted nocturnal sleep

Also Relevant

Delayed sleep phase syndrome
Environmental and behavioral sleep disorders
Insufficient sleep syndrome
Irregular sleep-wake rhythm disorder
Sleep disorders
- Sleep and depression
- Sleep and parkinsonism

Clinical Categories

Sleep Disorders

Web References

Clinical Trials

NIH: Sleep Disorders

Advanced sleep-wake phase disorder …

Advanced sleep-wake phase disorder

Introduction

Overview

Key points

Historical note and terminology

Clinical manifestations

Presentation and course

Prognosis and complications

Clinical vignette

Biological basis

Etiology and pathogenesis

Epidemiology

Prevention

Differential diagnosis

Confusing conditions

Diagnostic workup

Management

Outcomes

Special considerations

Pregnancy

Media

References

Contributors

Author

Editor

Former Authors

Patient Profile

ICD & OMIM codes

This is an article preview.
Start a Free Account
to access the full version.

Questions or Comment?

Also in This Category

Telehealth and cognitive behavioral therapy for insomnia (CBT-I)

NonREM parasomnias

Neurologic disorders associated with obesity

Hypersomnolence

Sleep disorders in women

Sleep, stroke, and vascular dementia

Parasomnia overlap disorder and status dissociatus

Stimulant-dependent sleep disorder

	• Sleep logs or actigraphy for 1 to 2 weeks is recommended to confirm the diagnosis of advanced sleep-wake phase disorder.
	• A detailed psychiatry history is needed to rule out mood disorders.
	• Sleep recording at the patient’s usual sleeping hours should show normal sleep-onset latency, staging, and duration for age and should rule out other causes of pathologic sleepiness.

Advanced sleep-wake phase disorder

Introduction

Overview

Key points

Historical note and terminology

Clinical manifestations

Presentation and course

Prognosis and complications

Clinical vignette

Biological basis

Etiology and pathogenesis

Epidemiology

Prevention

Differential diagnosis

Confusing conditions

Diagnostic workup

Management

Outcomes

Special considerations

Pregnancy

Media

References

Contributors

Author

Editor

Former Authors

Patient Profile

ICD & OMIM codes

This is an article preview. Start a Free Account to access the full version.

Questions or Comment?

Also in This Category

Telehealth and cognitive behavioral therapy for insomnia (CBT-I)

NonREM parasomnias

Neurologic disorders associated with obesity

Hypersomnolence

Sleep disorders in women

Sleep, stroke, and vascular dementia

Parasomnia overlap disorder and status dissociatus

Stimulant-dependent sleep disorder

This is an article preview.
Start a Free Account
to access the full version.