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Delayed sleep-wake phase disorder
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Delayed sleep-wake phase disorder
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Nov 2017. | This topic last updated: Aug 31, 2017.

INTRODUCTION — Delayed sleep-wake phase disorder (DSWPD) is the most commonly encountered circadian rhythm sleep-wake phase disorder in adolescents. Like other circadian rhythm disorders, DSWPD results from failure to synchronize internal circadian rhythms to the environmental light/dark cycle.

Individuals with DSWPD have a pronounced "night owl" circadian preference. Affected individuals habitually go to bed and wake up significantly later than conventional or desired times. Unlike unaffected "night owls," patients with DSWPD cannot conform to a sleep schedule that is compatible with personal, professional, or academic obligations.

This topic reviews the clinical features, diagnosis, and management of DSWPD. Behavioral sleep problems and other sleep disorders in children are reviewed separately. (See "Behavioral sleep problems in children" and "Assessment of sleep disorders in children".)

EPIDEMIOLOGY — The prevalence of delayed sleep-wake phase disorder (DSWPD) is not well established, and estimates range widely. Studies using questionnaires, telephone surveys, or mixed subjective and objective measures have identified DSWPD in 0.1 to 3 percent of the general population [1-4].

Studies consistently show a peak prevalence in adolescence, although point estimates in this age group vary by country of origin [2,4-7]. For example, studies of American and Norwegian adolescents have reported a prevalence as high as 7 to 8 percent [7,8], whereas one study involving Japanese young people estimated a prevalence <1 percent, peaking at 1.7 percent among four-year university students [6]. A systematic study involving over 1000 Western European adolescents, aged 15 to 18 years, reported a similarly low rate of circadian disorders of any type (<1 percent) [9]. Differences in school start times (later in Western Europe compared with many high schools in the United States) may explain some of the regional variability.

Males and females seem to be affected in equal proportions.

PATHOPHYSIOLOGY — Delayed sleep-wake phase disorder (DSWPD) is marked by a delay in circadian phase (often measured by melatonin or core body temperature) in addition to delayed sleep-wake times. The pathophysiology of DSWPD is likely heterogeneous, with contributions from a variety of endogenous and exogenous factors. Genetic factors may also play a role, but current evidence is limited [10,11].

Developmental changes in sleep-wake timing – A delay in preferred bedtimes and wake times during the adolescent period has been demonstrated across varying societies worldwide [12-21]. This coincides with a variety of pubertal changes, both physiologic and social [22].

A systematic assessment of circadian preference in >20,000 individuals demonstrated a crescendo pattern of increasing "eveningness" until the age of approximately 20 years, followed by a gradual decline [23]. Adolescent DSWPD may represent an extreme expression of this scheduling preference [5,24-29].

Length of the intrinsic circadian period – Intrinsic circadian periods (tau) longer than 24 hours require greater adjustment to entrain to the 24-hour solar day [30], and there is some evidence that adolescence is associated with a physiologic lengthening of tau [31-33]. Such lengthening may partially explain the propensity for DSWPD. At least one study found a longer median tau in patients with DSWPD compared with healthy controls [34].

Alterations in response to light – Hypersensitivity to nocturnal light exposure has been proposed in DSWPD, although the evidence is mixed. In one study, 2000 lux-hours of nocturnal light exposure was associated with a greater degree of melatonin suppression in adults with DSWPD compared with controls, suggestive of excessive circadian sensitivity to light [35].

Other studies have failed to find similar effects but may not have controlled for differences in daytime light exposure, which can alter the melatonin response [12,22,36]. Alternatively, a blunted phase-advance response to morning light has also been proposed in DSWPD [37-39].

Changes in light exposure – Increased evening light exposure or decreased morning light exposure could theoretically contribute to the DSWPD phenotype, independent of issues regarding sensitivity to light [40,41]. However, a prospective cohort study of light exposure patterns among adolescents found comparatively less pre-sleep light intensity (lux) exposure in those with DSWPD compared with controls, and no differences in the amount of post-sleep light exposure [36].

These results do not preclude the possibility that differences in exposure to certain wavelengths of light play a role in DSWPD. In a pilot study of adults with insomnia, participants who wore "blue-blocker" glasses during the three hours prior to habitual bedtime demonstrated improved subjective sleep quality [42]. Taking into account the circadian sensitivity of the human eye to short wavelength (ie, blue) light [43], these findings are of particular interest in DSWPD.

Other factors – Although not specifically studied in DSWPD, behavioral factors such as increased autonomy with respect to sleep time, employment, and involvement in extracurricular activities all contribute to the general changes in sleep patterns of adolescents [22].

Isolated case reports describe the emergence of DSWPD after traumatic brain injury [44-47]. (See "Sleep-wake disorders in patients with traumatic brain injury", section on 'Symptom spectrum'.)

Psychoactive medications have occasionally been implicated in circadian rhythm disturbances. In a study of seven adults with schizophrenia, receipt of typical antipsychotics (haloperidol and flupenthixol) was associated with circadian dyssynchrony, including delayed and free-running patterns, but no such association was found with clozapine [48]. Cases of DSWPD associated with the initiation of fluvoxamine have also been reported [49].

CLINICAL FEATURES — The core clinical features of delayed sleep-wake phase disorder (DSWPD) are delayed bedtimes and wake times compared with conventional or desired times, resulting in chronic sleep insufficiency and daytime impairment. The disorder most often begins in adolescence and is often accompanied by comorbid depression.

Delayed sleep onset and offset — Delayed sleep-wake phase disorder (DSWPD) can be construed as a pronounced "night owl" circadian preference. Affected individuals habitually go to bed and arise significantly later than conventional or desired times. Bedtimes are usually delayed by two or more hours relative to conventional or socially acceptable times required to obtain sufficient sleep on a school or work night [24].

Patients with DSWPD may endorse social consequences of delayed sleep phase, such as chronic tardiness or repeated school absences. Morning awakenings may require intensive parental or partner involvement and generate significant conflict. Patients may describe excessive sleep inertia (extreme difficulty awakening and confusion) in the morning as a result of curtailed sleep time and awakening during a circadian phase of high sleep propensity [24].

When individuals have the opportunity for unrestricted sleep (eg, on weekends or vacation), sleep duration and sleep quality typically return to normal, although the phase-delay persists (ie, they go to bed late and wake up late).

While some component of "eveningness" is normal during adolescence [50], DSWPD represents a more severe form that interferes significantly with social or occupational functioning. Individuals with DSWPD live at a circadian phase that is incompatible with personal obligations.

Sleep insufficiency — Delayed bedtimes, combined with early school or work start times, contribute to significant reductions in total sleep time per night and chronic sleep restriction [12-20,22,51]. These effects are evident among healthy teenagers and magnified in those with DSWPD.

Data from the Centers for Disease Control and Prevention Youth Risk Behavior Survey indicate that nearly 70 percent of adolescents get insufficient school night sleep (<8 hours nightly), and only 8 percent get optimal sleep (≥9 hours nightly) [52]. In one study that included a variety of objective sleep-wake measurements in 32 adolescent volunteers (25 percent of whom reported <6.5 hours of nightly sleep), objectively measured sleepiness in the early periods of school was equivalent to that of patients with narcolepsy [21].

DSWPD further increases the susceptibility to chronic sleep restriction and associated adverse outcomes [26,53-56]. In a series of 22 adolescents with DSWPD, 59 percent demonstrated poor scholastic performance, and 45 percent had one or more behavioral problems [26]. A cohort of adults with DSWPD scored significantly worse on measures of social functioning and role disability compared with both healthy controls and patients suffering from other chronic disorders such as sleep apnea and depression [55]. Additional consequences of sleep insufficiency are discussed in more detail separately. (See "Insufficient sleep: Definition, epidemiology, and adverse outcomes", section on 'Consequences of chronic sleep insufficiency'.)

Circadian desynchronization also contributes to daytime complaints in patients with DSWPD, independent of chronic sleep restriction or poor sleep quality [36,57]. Circadian desynchronization in DSWPD is akin to jet lag, in that individuals may have low energy and generalized malaise in the daytime because they are attempting to be awake while their circadian alerting signals are low and sleep propensity is high.

Comorbid psychiatric disorders — Comorbid depression is common among patients with DSWPD [25,26,30,58-61]. In a large cohort that included 205 adults with DSWPD, 51 percent of patients reported a lifetime history of depression, and mean depression scale scores were significantly higher in patients with DSWPD compared with controls [61]. In another cohort of predominantly adult patients with DSWPD, 64 percent of patients endorsed depressive symptoms of at least moderate severity [62]. Other studies have found an approximately threefold higher prevalence of seasonal affective disorder in patients with DSWPD than in controls [63].

Limited data suggest that higher degrees of circadian misalignment correlate with depression severity as well as poor responsiveness to antidepressant therapy [62,64-66]. A delayed circadian preference has been described in adults with bipolar I disorder, in some cases correlating with higher illness recurrence rates [67,68]; similar associations have been reported in children with bipolar I disorder [69] and adults with obsessive compulsive disorder [70-72], although the data are not entirely consistent [73].

DSWPD has been occasionally reported in children with comorbid attention deficit hyperactivity disorder (ADHD) and sleep-onset complaints [74,75]. In some of the cases, behavioral symptoms improved with introduction of circadian-based interventions. Dysregulation of melatonin secretion and delayed sleep phase have also been implicated in sleep disturbances among children with autism, among other factors [76]. (See "Autism spectrum disorder in children and adolescents: Pharmacologic interventions", section on 'Sleep disturbance'.)

Clinical course — The natural history of DSWPD is not well known. It typically emerges during adolescence, and without treatment it may be a chronic condition that persists into adulthood [24]. Age-related circadian rhythm changes, including phase advancement, may lessen the propensity for delayed sleep phase in later adulthood. (See "Sleep-wake disturbances and sleep disorders in patients with dementia", section on 'Circadian rhythms'.)

EVALUATION AND DIAGNOSIS — Delayed sleep-wake phase disorder (DSWPD) is a clinical diagnosis that should be suspected among individuals who complain of an inability to fall asleep at conventional or desired times necessary to obtain sufficient nightly sleep, resulting in distress or impaired functioning. Clinical history supplemented by sleep logs and/or actigraphy is sufficient to make the diagnosis in the majority of patients.

Clinical history — Delayed sleep phase should be suspected when individuals endorse a consistent pattern of bedtimes and wake times that are significantly later than conventional or desired clock times. Although normative data on adolescent sleep-wake times are sparse [15], a typical weekday bedtime of midnight or later for those >14 years of age and 11 PM or later for those ≤14 years of age is considered a significant delay.

Wake times on weekdays are less informative than bedtimes, since they are typically mandated by school attendance or work. Both bedtimes and rise times are likely to be later on weekends in patients with delayed sleep phase. Asking about sleep schedules during unrestricted periods (eg, vacation, summer break) can be especially valuable to determine the patient's endogenous circadian rhythm.

The sleep history should include questions about sleep quality and probe for symptoms of other sleep disorders. Most patients with DSWPD describe unimpaired sleep quality when sleeping according to their circadian preference. A history of loud snoring or witnessed pauses in breathing may suggest an alternative or comorbid diagnosis of obstructive sleep apnea (OSA), which would require formal testing to diagnose. (See "Clinical presentation and diagnosis of obstructive sleep apnea in adults", section on 'Diagnostic tests' and "Evaluation of suspected obstructive sleep apnea in children", section on 'Evaluation'.)

Social, emotional, and behavioral factors that may be contributing to delayed sleep phase should also be assessed, including social or occupational commitments that extend late into the evening, use of light-emitting screens (cell phones, tablets, computer screens) before the desired bedtime, and use of caffeine or stimulants in the later part of the day. Depression and anxiety are common comorbidities in patients with DSWPD but may also be associated with alternative diagnoses such as chronic insomnia. (See 'Comorbid psychiatric disorders' above and 'Differential diagnosis' below.)

Sleep logs and actigraphy — Sleep logs or actigraphy supplement the clinical history and provide a more quantitative depiction of delayed sleep phase. All patients should be asked to complete a sleep log for at least seven days (spanning school or work days and free days). Either the 24-hour (form 1) or the consensus sleep diary (table 1 and table 2) can be used. The 24-hour diary visually depicts abnormalities of sleep timing and therefore may be more useful when circadian rhythm sleep-wake disorders are suspected.

Actigraphy is an alternative to a sleep log in patients who have difficulty maintaining a sleep log or when inconsistencies arise between symptom presentation and self-reported sleep. An actigraph is a wrist-worn device, usually placed on the nondominant hand. The device is a compact motion detector; some models also contain photosensors to measure light exposure [77]. (See "Overview of actigraphy".)

Longitudinal monitoring among patients with DSWPD should demonstrate a persistently delayed sleep-wake schedule on both weekdays and weekends (figure 1), with curtailment of total sleep time during periods of enforced awakenings.

Morningness-eveningness questionnaire — "Night owl" tendencies of patients with suspected DSWPD can be further verified with a morningness-eveningness questionnaire [78]. Results of the self-assessment are felt to correspond to an individual's endogenous circadian period or phase. Both print and automated versions of the questionnaire are accessible online.

Although not validated as a diagnostic tool, such questionnaires can be helpful in narrowing the differential diagnosis for sleep-initiation complaints [11]. Scores that do not confirm an "eveningness" circadian preference should prompt a search for alternative explanations for the delayed sleep-wake schedule, such as chronic insomnia disorder.

Other testing — Salivary melatonin immunoassays and other physiologic assessments of circadian phase are primarily research tools, as further validation studies are needed for such testing to be useful clinically [79].

In small studies of mostly adults, DSWPD has been associated with delays in the circadian rhythm of dim light melatonin onset (DLMO), minimum core body temperature (MCBT), and cortisol and thyroid-stimulating hormone secretion [80-82]. Normative values have not been established, however, and significant overlap may exist between affected and unaffected populations [83-85]. Phase assessments may have greater potential to guide the timing of melatonin and light therapy in select patients.

Polysomnography is not indicated in patients with suspected DSWPD unless clinical suspicion arises that a comorbid condition such as obstructive sleep apnea is contributing to sleep-related complaints.

Diagnostic criteria — Diagnostic criteria for DSWPD in the International Classification of Sleep Disorders, third edition (ICSD-3), stipulate that all five of the following conditions must be met [24]:

The phase of the major sleep episode shows a significant delay in relation to the desired or required sleep time and wake-up time, as evidenced by a chronic or recurrent complaint by the patient or a caregiver of inability to fall asleep and difficulty awakening at a desired or required clock time.

The symptoms are present for at least three months.

When patients are allowed to choose their ad libitum schedule, they will exhibit improved sleep quality and duration for age and maintain a delayed phase of the 24-hour sleep-wake pattern.

Sleep log and, whenever possible, actigraphy monitoring for at least seven days (preferably 14 days) demonstrate a delay in the timing of the habitual sleep period (figure 1). Both work or school days and free days must be included within this monitoring.

The sleep disturbance is not better explained by another current sleep disorder, medical or neurologic disorder, mental disorder, medication use, or substance use disorder.

DIFFERENTIAL DIAGNOSIS — The differential diagnosis of delayed sleep-wake phase disorder (DSWPD) includes a variety of alternative causes of difficulty with sleep initiation. Primary considerations include depression and anxiety, which often manifest with sleep-onset complaints, inadequate sleep hygiene (including voluntary sleep restriction), and insomnia. Ultimately many of these conditions co-exist, however, and each may need to be addressed and treated simultaneously.

Chronic insomnia in particular is frequently confused with DSWPD [24]. The two entities can usually be distinguished by asking patients about what happens when they are allowed to sleep according to their desired sleep-wake schedule. Patients with insomnia generally have difficulty initiating sleep regardless of designated sleep time, whereas patients with DSWPD typically can initiate sleep readily when allowed to sleep at desired times. (See "Clinical features and diagnosis of insomnia in adults", section on 'Clinical features'.)

MANAGEMENT — Management of delayed sleep-wake phase disorder (DSWPD) consists primarily of behavioral modifications aimed at gradually advancing bedtimes and rise times to a schedule that aligns with social and occupational constraints, and avoiding poor sleep habits that may exacerbate the problem. Timed melatonin and light therapy, which can help realign the circadian rhythm, are options in refractory patients.

Behavioral modifications — Initial counseling of patients with DSWPD should address external factors that may be exacerbating or contributing to phase delay. This includes review of sleep hygiene practices and the identification of potential substance misuse. In particular, patients should be encouraged to:

Minimize or eliminate caffeine, nicotine, and alcohol

Avoid daytime naps

Refrain from engaging in stimulating activity for at least two hours prior to the desired sleep onset time

We advise patients to avoid sleeping in on weekends by more than 30 minutes compared with the weekday time, as late rise times can themselves cause delays in the circadian phase [38,86,87]. If patients can be convinced to maintain regular rise times, they are better served by taking a midday nap to relieve sleep deprivation. Naps taken during a window of six hours centered 12 hours from the midpoint of the unrestricted weekend sleep bout have no counter-effects on circadian rhythms [88].

For mildly affected patients, gradual advancement of evening bedtimes and morning wake times toward a targeted goal and then strict adherence to this fixed sleep-wake schedule may be sufficient. Evidence to support this approach is limited primarily to young adults with mild symptoms [39,75,89]. In a prospective study of adults aged 18 to 30 years with subthreshold DSWPD (criteria did not require social or occupational impairment), participants advanced their sleep schedules by 1 to 2.5 hours earlier than their average bedtime for one week prior to study entry, and continued this schedule for six days [39]. An average phase advance of 1.4 hours was observed by dim light melatonin onset (DLMO). The majority of patients exhibited decreased sleep time, although this was not unexpected based on the short duration of the intervention.

For adolescents, a later school start time may be sought if practical and available within the district. This intervention alone can significantly increase total sleep time and mitigate associated impairments [14,90-93], although benefits may be modest and transient in some cases [94]. One study reported a 17 percent drop in the average crash rate in adolescents two years subsequent to a one-hour delay in school start times, in conjunction with an increase in mean hours of nightly sleep [95].

In patients who are unable to adhere to earlier bed and rise times, some sleep specialists advise patients to do the opposite of phase advancement, ie, to go to bed and arise later each day until the desired schedule is reached. This is referred to as chronotherapy. While this approach may be considered in refractory patients, there is inadequate evidence to support this as a routine form of treatment [89].

Patients with a concomitant chronic insomnia disorder may respond to adjunctive behavioral therapy [96]. Chronic insomnia comorbid with DSWPD can be identified in part by the persistence of sleep initiation or maintenance difficulties during periods of unrestricted sleep-wake schedules. (See "Treatment of insomnia in adults", section on 'Behavioral therapy'.)

Timed melatonin — For patients who fail to respond to behavioral modifications and sleep-wake scheduling, we suggest a trial of strategically-timed melatonin in the evenings. This is a weak recommendation based on moderate-quality evidence, including several small randomized trials, showing improved sleep onset times and variable changes in physiologic circadian rhythm markers with short-term use of melatonin in both children and adults with DSWPD [89].

Representative studies of melatonin in patients with DSWPD include the following:

In a randomized, double-blinded study, 70 children with DSWPD (age 6 to 12 years, no comorbidities) were randomly assigned to one of three doses of melatonin (0.05, 0.1, or 0.15 mg/kg) or placebo for six nights. The respective mean doses of melatonin were 1.6, 2.9, and 4.4 mg [97]. Melatonin was administered 1.5 to 2.0 hours prior to habitual bedtime. Compared with the placebo group, patients assigned to melatonin had significantly advanced sleep onset (by approximately 60 minutes) and sleep-onset latency (by approximately 30 minutes). Improvement occurred in all three dose levels, and no dose-response relationship was observed. There were no significant differences in DLMO among any of the melatonin groups compared with placebo [89].

Two additional trials by the same group examined the use of melatonin for DSWPD among children 6 to 12 years of age with attention deficit hyperactivity disorder (ADHD) [74,98]. Dosing varied slightly between trials; melatonin was taken at 6 or 7 PM at a dose of 3 or 5 mg. In a combined analysis (n = 132), melatonin advanced DLMO by nearly one hour compared with placebo [89]. Actigraphically-assessed sleep onset time also advanced. Total sleep time improved by approximately 30 to 40 minutes [74,98].

In a combined analysis of two trials in adults with DSWPD and comorbid depression (n = 28), melatonin (5 mg, timed between 7 and 9 PM) was associated with improved objective total sleep time (mean difference 41 minutes) and initial sleep latency (mean difference -44 minutes) compared with placebo [89]. Similar improvements were noted in the subset of patients without comorbid depression (n = 12). One smaller trial of melatonin (0.3 or 3 mg taken 1.5 to 6.5 hours prior to baseline DLMO) in adults with DSWPD failed to show a benefit on any actigraphically-measured sleep outcome [99].

No consensus has emerged on the optimal dosing of melatonin in patients with DSWPD. Based on the evidence reviewed above, we typically advise patients to use a daily dose ranging from 3 to 5 mg. Melatonin should be taken in the early evening, at least 1.5 hours before the desired bedtime. The duration of therapy is individualized based on the observed response; if withdrawal of melatonin after the achievement of advanced sleep-wake phase results in clinical relapse, it can be resumed and continued long term.

Melatonin is well tolerated in most patients and is generally associated with a lack of reported serious adverse effects [100-105], although long-term safety data are limited. Melatonin is considered a dietary supplement in most countries and is therefore not subject to the regulatory standards of over-the-counter or prescription drugs. (See "Physiology and available preparations of melatonin", section on 'Melatonin preparations'.)

A 2005 review by the National Academy of Sciences stated that short-term use of ≤10 mg/day appears to be safe in healthy adults, but recommended caution in children, adolescents, and women of reproductive age, based on sparse reports of various adverse effects in these populations [106]. Adverse effects such as headaches, somnolence, hypotension, hypertension, gastrointestinal upset, and exacerbation of alopecia areata have been reported at higher melatonin doses in healthy adults, and the same effects have been reported with lower doses among those with relevant pre-existing conditions.

Long-term safety data include a randomized trial of 28 days of melatonin (10 mg daily) versus placebo in healthy male adults, which revealed no differences with respect to adverse effects on polysomnographically-recorded sleep, subjective sleepiness, numerous clinical laboratory examinations, and other subjectively-recorded events [107]. Similarly, in a meta-analysis of controlled trials of melatonin used for ≤3 months (10 studies, over 200 subjects), few reports of adverse events were found [100].

Although theoretical concerns exist in children and adolescents about effects of melatonin on growth hormone regulation (10 mg dose) [108], and on reproductive function and development (3 mg dose) [109], the available data from patients are reassuring. As examples:

A long-term follow-up study of pediatric patients with DSWPD and comorbid ADHD who used melatonin doses up to 10 mg over a mean of nearly four years detected no serious adverse effects through serial interviews with parents, and 65 percent of the participants continued to use the medication daily [110].

Another open-label prospective study in patients with neurodevelopmental disabilities and comorbid DSWPD who received controlled-release melatonin for up to 3.8 years (maximum dose 15 mg) also described no adverse events [111,112].

Tanner stages were assessed serially in a questionnaire-based study involving Dutch children and adolescents using melatonin during prepuberty [113]. With a mean follow-up of three years (mean daily dose 2.7 mg), no differences appeared in comparison with age- and sex-matched control statistics in the general Dutch population.

Morning light therapy — Morning light exposure would be expected to shift circadian rhythms earlier and thereby correct a phase delay. Evidence in support of light therapy as an effective intervention in patients with DSWPD is limited, however, and results of small randomized trials have been mixed [114,115]. Nevertheless, given the low-risk nature of the intervention, it is a viable strategy in motivated patients when provided along with behavioral education.

Light boxes are commercially available in various wavelengths and intensities. We generally advise patients to use a broad spectrum white light box. The recommended distance from the source is dependent on the intensity of emitted light, and instructions for distance are typically provided by the manufacturer (eg, 10,000 lux at 5 feet). The light box should be used every morning, with gradually advancing sleep-wake times until the target time is reached, as per the protocol used in the study discussed below [114].

Light therapy can then be continued for maintenance therapy at a consistent time each morning if desired. If a trial off light therapy results in clinical relapse, it can be reintroduced in the same way and then continued long-term once desired sleep-wake times are reached.

Support for a light therapy intervention is based on results of a trial in which 49 adolescents (age 13 to 18 years) with DSWPD were randomly assigned to post-awakening light therapy and behavioral education or a waitlist control group [114]. The intervention consisted of the following components:

Over a period of eight weeks, patients in the intervention group were exposed to either post-awakening natural sunlight (when available) or a broad-spectrum lamp (approximately 1000 lux, proximity to source not specified) for ≥30 minutes daily (two hours maximum).

The timing of light exposure was advanced 30 minutes daily from "natural" wake time, until a target time of 6:00 AM was reached. Light therapy was subsequently discontinued and a regular rise time between 6:30 and 7:30 AM was advised.

Concomitant multicomponent behavioral education with parental involvement, including instructions to reduce evening light, was provided during six 45- to 60-minute sessions.

Compared with controls, patients in the light therapy group had significantly improved subjective total sleep time (mean difference 72 minutes), initial sleep latency (mean difference 43 minutes), and sleep onset and offset times at eight weeks. Improvements from baseline persisted at six months in the intervention group, although the magnitude lessened over time.

A separate trial in adults with DSWPD who were randomly assigned to an active light mask that exposed closed eyelids to 2700 lux of pre-awakening white broad-spectrum light or an inactive control mask found no benefit [115]. Other novel modalities such as dawn simulators are of interest but have not yet been studied in patients with DSWPD [116].

Strategic avoidance of evening light — There may also be benefit to strategic avoidance of evening light, but supporting data are limited.

In an open-label study of 22 adults with DSWPD and comorbid attention deficit hyperactivity disorder, use of amber glasses that blocked wavelengths ≤530 nm from sundown to bedtime plus avoidance of overhead light and caffeine, nicotine, and alcohol resulted in improved total sleep time, initial sleep latency, and sleep quality at two weeks [117]. In a separate study in which adults with insomnia (without stated DSWPD) wore "blue-blocker" (<550 nm) glasses during the three hours prior to habitual bedtime, patients described improved subjective sleep quality compared with the placebo intervention (yellow-tinted glasses that blocked only ultraviolet light) [42].

Importantly, there are no tangible risks associated with these interventions. As to whether these findings can be extrapolated to measures that block light of specific frequencies from media devices (eg, laptops, cell phones) is uncertain. Further, there are stimulating effects independent of light that would not be prevented by the glasses.

Hypnotics — Use of hypnotics to help achieve earlier bedtimes is discouraged in patients with DSWPD. Although there are isolated reports of benefit, typically as an adjunctive treatment with chronotherapy or in selected patients with concomitant conditioned insomnia [54,118], other reports describe resistance to the effects of traditional hypnotics in patients with DSWPD [119,120].


Delayed sleep-wake phase disorder (DSWPD) is the most common circadian rhythm disturbance in adolescents and young adults. A prevalence of up to 7 percent has been reported in American teenagers. (See 'Epidemiology' above.)

A variety of endogenous and exogenous factors likely contribute to the emergence of DSWPD, including a physiologic delay in circadian rhythms corresponding to puberty, possible alterations in sensitivity to the circadian effects of light, changes in light exposure patterns, and social and behavioral factors. (See 'Pathophysiology' above.)

Clinically, DSWPD can be construed as a pronounced "night owl" circadian preference. Affected individuals habitually go to bed and wake up significantly later than conventional or desired times. Bedtimes are usually delayed by two or more hours relative to conventional or socially acceptable times required to obtain sufficient sleep on a school or work night. As a result, individuals have chronic sleep restriction, impaired daytime function or distress, and an increased likelihood of depression and other psychiatric disorders. (See 'Clinical features' above.)

DSWPD should be suspected among individuals who complain of an inability to fall asleep at desired times necessary to obtain sufficient nightly sleep, with resultant distress or impaired functioning. Concomitant difficulty waking up at the targeted time in the morning helps to confirm the diagnosis. A consistent circadian phase delay should be confirmed with sleep logs, actigraphy, or both, recorded over at least seven days. Salivary melatonin sampling is not routinely performed in clinical practice. Polysomnography is only indicated if there is clinical suspicion for a comorbid sleep disorder such as obstructive sleep apnea. (See 'Evaluation and diagnosis' above.)

Initial management of all patients with DSWPD should address external factors that may exacerbate or contribute to the phase delay. We advise patients to avoid sleeping in on weekends more than 30 minutes past the weekday wake up time, as late rise times can themselves cause phase delays. For mildly affected patients, gradual advancement of evening bedtimes and morning wake times toward a targeted goal and then strict adherence to this fixed sleep-wake schedule may be sufficient to relieve symptoms. (See 'Behavioral modifications' above.)

For patients who fail to respond to behavioral modifications and sleep-wake scheduling, we suggest a trial of strategically-timed melatonin in the evenings (Grade 2B). A typical dose of melatonin for DSWPD is 3 to 5 mg daily, taken in the early evening at least 1.5 hours before the desired bedtime. (See 'Timed melatonin' above.)

Morning light exposure combined with behavioral education is a viable strategy in motivated patients. A commercially available broad spectrum white light box can be used for this purpose. The light box should be used every morning, with gradually advancing sleep-wake times until the target time is reached. (See 'Morning light therapy' above.)

Use of hypnotics to help achieve earlier bedtimes is discouraged in patients with DSWPD except in adults with concomitant conditioned insomnia. (See 'Hypnotics' above.)

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  1. Schrader H, Bovim G, Sand T. The prevalence of delayed and advanced sleep phase syndromes. J Sleep Res 1993; 2:51.
  2. Yazaki M, Shirakawa S, Okawa M, Takahashi K. Demography of sleep disturbances associated with circadian rhythm disorders in Japan. Psychiatry Clin Neurosci 1999; 53:267.
  3. Wyatt JK. Delayed sleep phase syndrome: pathophysiology and treatment options. Sleep 2004; 27:1195.
  4. Ando K, Kripke DF, Ancoli-Israel S. Estimated prevalence of delayed and advanced sleep phase syndromes. J Sleep Res 1995; 24:509.
  5. Pelayo R, Thorpy M, Govinski P. Prevalence of delayed sleep phase disorder among adolescents. Sleep Res 1988; 17:392.
  6. Hazama GI, Inoue Y, Kojima K, et al. The prevalence of probable delayed-sleep-phase syndrome in students from junior high school to university in Tottori, Japan. Tohoku J Exp Med 2008; 216:95.
  7. Saxvig IW, Pallesen S, Wilhelmsen-Langeland A, et al. Prevalence and correlates of delayed sleep phase in high school students. Sleep Med 2012; 13:193.
  8. Sivertsen B, Pallesen S, Stormark KM, et al. Delayed sleep phase syndrome in adolescents: prevalence and correlates in a large population based study. BMC Public Health 2013; 13:1163.
  9. Ohayon MM, Roberts RE, Zulley J, et al. Prevalence and patterns of problematic sleep among older adolescents. J Am Acad Child Adolesc Psychiatry 2000; 39:1549.
  10. Ancoli-Israel S, Schnierow B, Kelsoe J, Fink R. A pedigree of one family with delayed sleep phase syndrome. Chronobiol Int 2001; 18:831.
  11. Sack RL, Auckley D, Auger RR, et al. Circadian rhythm sleep disorders: part II, advanced sleep phase disorder, delayed sleep phase disorder, free-running disorder, and irregular sleep-wake rhythm. An American Academy of Sleep Medicine review. Sleep 2007; 30:1484.
  12. Carskadon MA, Acebo C. Regulation of sleepiness in adolescents: update, insights, and speculation. Sleep 2002; 25:606.
  13. Andrade MM, Benedito-Silva AA, Domenice S, et al. Sleep characteristics of adolescents: a longitudinal study. J Adolesc Health 1993; 14:401.
  14. National Sleep Foundation. Adolescent Sleep Needs and Patterns: Research Report and Resource Guide, National Sleep Foundation, Washington, DC 2012.
  15. National Sleep Foundation. 2006 Sleep in America Poll: Summary of Findings. Available at: https://sleepfoundation.org/sites/default/files/2006_summary_of_findings.pdf (Accessed on July 03, 2008).
  16. Laberge L, Petit D, Simard C, et al. Development of sleep patterns in early adolescence. J Sleep Res 2001; 10:59.
  17. Giannotti F, Cortesi F, Sebastiani T, Ottaviano S. Circadian preference, sleep and daytime behaviour in adolescence. J Sleep Res 2002; 11:191.
  18. Gau SF, Soong WT. The transition of sleep-wake patterns in early adolescence. Sleep 2003; 26:449.
  19. Ouyang F, Lu BS, Wang B, et al. Sleep patterns among rural Chinese twin adolescents. Sleep Med 2009; 10:479.
  20. Sadeh A, Dahl RE, Shahar G, Rosenblat-Stein S. Sleep and the transition to adolescence: a longitudinal study. Sleep 2009; 32:1602.
  21. Carskadon MA, Wolfson AR, Acebo C, et al. Adolescent sleep patterns, circadian timing, and sleepiness at a transition to early school days. Sleep 1998; 21:871.
  22. Crowley SJ, Acebo C, Carskadon MA. Sleep, circadian rhythms, and delayed phase in adolescence. Sleep Med 2007; 8:602.
  23. Roenneberg T, Kuehnle T, Pramstaller PP, et al. A marker for the end of adolescence. Curr Biol 2004; 14:R1038.
  24. American Academy of Sleep Medicine. International Classification of Sleep Disorders, 3rd ed, American Academy of Sleep Medicine, Darien, IL 2014.
  25. Dagan Y, Stein D, Steinbock M, et al. Frequency of delayed sleep phase syndrome among hospitalized adolescent psychiatric patients. J Psychosom Res 1998; 45:15.
  26. Thorpy MJ, Korman E, Spielman AJ, Glovinsky PB. Delayed sleep phase syndrome in adolescents. J Adolesc Health Care 1988; 9:22.
  27. Carskadon MA, Vieira C, Acebo C. Association between puberty and delayed phase preference. Sleep 1993; 16:258.
  28. Carskadon MA, Acebo C, Richardson GS, et al. An approach to studying circadian rhythms of adolescent humans. J Biol Rhythms 1997; 12:278.
  29. Jenni OG, Achermann P, Carskadon MA. Homeostatic sleep regulation in adolescents. Sleep 2005; 28:1446.
  30. Weitzman ED, Czeisler CA, Coleman RM, et al. Delayed sleep phase syndrome. A chronobiological disorder with sleep-onset insomnia. Arch Gen Psychiatry 1981; 38:737.
  31. Carskadon MA, Acebo C. Intrinsic circadian period in adolescents versus adults from forced desynchrony. Sleep 2005; 28:A71.
  32. Hummer DL, Jechura TJ, Mahoney MM, Lee TM. Gonadal hormone effects on entrained and free-running circadian activity rhythms in the developing diurnal rodent Octodon degus. Am J Physiol Regul Integr Comp Physiol 2007; 292:R586.
  33. McGinnis MY, Lumia AR, Tetel MJ, et al. Effects of anabolic androgenic steroids on the development and expression of running wheel activity and circadian rhythms in male rats. Physiol Behav 2007; 92:1010.
  34. Micic G, de Bruyn A, Lovato N, et al. The endogenous circadian temperature period length (tau) in delayed sleep phase disorder compared to good sleepers. J Sleep Res 2013; 22:617.
  35. Aoki H, Ozeki Y, Yamada N. Hypersensitivity of melatonin suppression in response to light in patients with delayed sleep phase syndrome. Chronobiol Int 2001; 18:263.
  36. Auger RR, Burgess HJ, Dierkhising RA, et al. Light exposure among adolescents with delayed sleep phase disorder: a prospective cohort study. Chronobiol Int 2011; 28:911.
  37. Hagenauer MH, Perryman JI, Lee TM, Carskadon MA. Adolescent changes in the homeostatic and circadian regulation of sleep. Dev Neurosci 2009; 31:276.
  38. Crowley SJ, Carskadon MA. Modifications to weekend recovery sleep delay circadian phase in older adolescents. Chronobiol Int 2010; 27:1469.
  39. Sharkey KM, Carskadon MA, Figueiro MG, et al. Effects of an advanced sleep schedule and morning short wavelength light exposure on circadian phase in young adults with late sleep schedules. Sleep Med 2011; 12:685.
  40. Figueiro MG, Rea MS. Lack of short-wavelength light during the school day delays dim light melatonin onset (DLMO) in middle school students. Neuro Endocrinol Lett 2010; 31:92.
  41. Harada T, Morisane H, Takeuchi H. Effect of daytime light conditions on sleep habits and morningness-eveningness preference of Japanese students aged 12-15 years. Psychiatry Clin Neurosci 2002; 56:225.
  42. Burkhart K, Phelps JR. Amber lenses to block blue light and improve sleep: a randomized trial. Chronobiol Int 2009; 26:1602.
  43. Brainard GC, Hanifin JP, Greeson JM, et al. Action spectrum for melatonin regulation in humans: evidence for a novel circadian photoreceptor. J Neurosci 2001; 21:6405.
  44. Patten SB, Lauderdale WM. Delayed sleep phase disorder after traumatic brain injury. J Am Acad Child Adolesc Psychiatry 1992; 31:100.
  45. Nagtegaal JE, Kerkhof GA, Smits MG, et al. Traumatic brain injury-associated delayed sleep phase syndrome. Funct Neurol 1997; 12:345.
  46. Quinto C, Gellido C, Chokroverty S, Masdeu J. Posttraumatic delayed sleep phase syndrome. Neurology 2000; 54:250.
  47. Ayalon L, Borodkin K, Dishon L, et al. Circadian rhythm sleep disorders following mild traumatic brain injury. Neurology 2007; 68:1136.
  48. Wirz-Justice A, Haug HJ, Cajochen C. Disturbed circadian rest-activity cycles in schizophrenia patients: an effect of drugs? Schizophr Bull 2001; 27:497.
  49. Hermesh H, Lemberg H, Abadi J, Dagan Y. Circadian rhythm sleep disorders as a possible side effect of fluvoxamine. CNS Spectr 2001; 6:511.
  50. Mercer PW, Merritt SL, Cowell JM. Differences in reported sleep need among adolescents. J Adolesc Health 1998; 23:259.
  51. Wolfson AR, Carskadon MA. Sleep schedules and daytime functioning in adolescents. Child Dev 1998; 69:875.
  52. Eaton DK, McKnight-Eily LR, Lowry R, et al. Prevalence of insufficient, borderline, and optimal hours of sleep among high school students - United States, 2007. J Adolesc Health 2010; 46:399.
  53. Alvarez B, Dahlitz MJ, Vignau J, Parkes JD. The delayed sleep phase syndrome: clinical and investigative findings in 14 subjects. J Neurol Neurosurg Psychiatry 1992; 55:665.
  54. Ohta T, Iwata T, Kayukawa Y, Okada T. Daily activity and persistent sleep-wake schedule disorders. Prog Neuropsychopharmacol Biol Psychiatry 1992; 16:529.
  55. Nagtegaal JE, Laurant MW, Kerkhof GA, et al. Effects of melatonin on the quality of life in patients with delayed sleep phase syndrome. J Psychosom Res 2000; 48:45.
  56. Fernandez-Mendoza J, Iliuodi C, Montes MI, et al. Circadian preference, nighttime sleep and daytime functioning in young adulthood. Sleep Biol Rhythms 2010; 8:52.
  57. Campbell SS, Murphy PJ. Delayed sleep phase disorder in temporal isolation. Sleep 2007; 30:1225.
  58. Regestein QR, Pavlova M. Treatment of delayed sleep phase syndrome. Gen Hosp Psychiatry 1995; 17:335.
  59. Takahashi Y, Hohjoh H, Matsuura K. Predisposing factors in delayed sleep phase syndrome. Psychiatry Clin Neurosci 2000; 54:356.
  60. Shirayama M, Shirayama Y, Iida H, et al. The psychological aspects of patients with delayed sleep phase syndrome (DSPS). Sleep Med 2003; 4:427.
  61. Kripke DF, Rex KM, Ancoli-Israel S, et al. Delayed sleep phase cases and controls. J Circadian Rhythms 2008; 6:6.
  62. Abe T, Inoue Y, Komada Y, et al. Relation between morningness-eveningness score and depressive symptoms among patients with delayed sleep phase syndrome. Sleep Med 2011; 12:680.
  63. Lee HJ, Rex KM, Nievergelt CM, et al. Delayed sleep phase syndrome is related to seasonal affective disorder. J Affect Disord 2011; 133:573.
  64. Rahman SA, Kayumov L, Shapiro CM. Antidepressant action of melatonin in the treatment of Delayed Sleep Phase Syndrome. Sleep Med 2010; 11:131.
  65. Kitamura S, Hida A, Watanabe M, et al. Evening preference is related to the incidence of depressive states independent of sleep-wake conditions. Chronobiol Int 2010; 27:1797.
  66. Okawa M, Uchiyama M. Circadian rhythm sleep disorders: characteristics and entrainment pathology in delayed sleep phase and non-24-h sleep-wake syndrome. Sleep Med Rev 2007; 11:485.
  67. Ahn YM, Chang J, Joo YH, et al. Chronotype distribution in bipolar I disorder and schizophrenia in a Korean sample. Bipolar Disord 2008; 10:271.
  68. Staton D. The impairment of pediatric bipolar sleep: hypotheses regarding a core defect and phenotype-specific sleep disturbances. J Affect Disord 2008; 108:199.
  69. Faedda GL, Teicher MH. Objective measures of activity and attention in the differential diagnosis of psychiatric disorders of childhood. Essent Psychopharmacol 2005; 6:239.
  70. Turner J, Drummond LM, Mukhopadhyay S, et al. A prospective study of delayed sleep phase syndrome in patients with severe resistant obsessive-compulsive disorder. World Psychiatry 2007; 6:108.
  71. Mukhopadhyay S, Fineberg NA, Drummond LM, et al. Delayed sleep phase in severe obsessive-compulsive disorder: a systematic case-report survey. CNS Spectr 2008; 13:406.
  72. Monteleone P, Catapano F, Del Buono G, Maj M. Circadian rhythms of melatonin, cortisol and prolactin in patients with obsessive-compulsive disorder. Acta Psychiatr Scand 1994; 89:411.
  73. Millet B, Touitou Y, Poirier MF, et al. Plasma melatonin and cortisol in patients with obsessive-compulsive disorder: relationship with axillary temperature, physical activity, and clinical symptoms. Biol Psychiatry 1998; 44:874.
  74. Van der Heijden KB, Smits MG, Van Someren EJ, et al. Effect of melatonin on sleep, behavior, and cognition in ADHD and chronic sleep-onset insomnia. J Am Acad Child Adolesc Psychiatry 2007; 46:233.
  75. Dahl RE, Pelham WE, Wierson M. The role of sleep disturbances in attention deficit disorder symptoms: a case study. J Pediatr Psychol 1991; 16:229.
  76. Kotagal S, Broomall E. Sleep in children with autism spectrum disorder. Pediatr Neurol 2012; 47:242.
  77. Morgenthaler T, Alessi C, Friedman L, et al. Practice parameters for the use of actigraphy in the assessment of sleep and sleep disorders: an update for 2007. Sleep 2007; 30:519.
  78. Horne JA, Ostberg O. A self-assessment questionnaire to determine morningness-eveningness in human circadian rhythms. Int J Chronobiol 1976; 4:97.
  79. Sack RL, Auckley D, Auger RR, et al. Circadian rhythm sleep disorders: part I, basic principles, shift work and jet lag disorders. An American Academy of Sleep Medicine review. Sleep 2007; 30:1460.
  80. Shibui K, Uchiyama M, Okawa M. Melatonin rhythms in delayed sleep phase syndrome. J Biol Rhythms 1999; 14:72.
  81. Ozaki S, Uchiyama M, Shirakawa S, Okawa M. Prolonged interval from body temperature nadir to sleep offset in patients with delayed sleep phase syndrome. Sleep 1996; 19:36.
  82. Shibui K, Uchiyama M, Kim K, et al. Melatonin, cortisol and thyroid-stimulating hormone rhythms are delayed in patients with delayed sleep phase syndrome. Sleep Biol Rhythms 2003; 1:209.
  83. Campbell SS, Dawson D, Anderson MW. Alleviation of sleep maintenance insomnia with timed exposure to bright light. J Am Geriatr Soc 1993; 41:829.
  84. Lack L, Wright H. The effect of evening bright light in delaying the circadian rhythms and lengthening the sleep of early morning awakening insomniacs. Sleep 1993; 16:436.
  85. Lack L, Wright H, Kemp K, Gibbon S. The treatment of early-morning awakening insomnia with 2 evenings of bright light. Sleep 2005; 28:616.
  86. Burgess HJ, Eastman CI. A late wake time phase delays the human dim light melatonin rhythm. Neurosci Lett 2006; 395:191.
  87. Taylor A, Wright HR, Lack LC. Sleeping-in on the weekend delays circadian phase and increases sleepiness the following week. Sleep Biol Rhythms 2008; 6:172.
  88. Eastman CI, Gazda CJ, Burgess HJ, et al. Advancing circadian rhythms before eastward flight: a strategy to prevent or reduce jet lag. Sleep 2005; 28:33.
  89. Auger RR, Burgess HJ, Emens JS, et al. 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; 11:1199.
  90. Wahistrom K. Changing times: Findings from the first longitudinal study of later high school start times. NASSP Bulletin 2002; 86:3.
  91. Owens JA, Belon K, Moss P. Impact of delaying school start time on adolescent sleep, mood, and behavior. Arch Pediatr Adolesc Med 2010; 164:608.
  92. Adolescent Sleep Working Group, Committee on Adolescence, Council on School Health. School start times for adolescents. Pediatrics 2014; 134:642.
  93. Watson NF, Martin JL, Wise MS, et al. Delaying Middle School and High School Start Times Promotes Student Health and Performance: An American Academy of Sleep Medicine Position Statement. J Clin Sleep Med 2017; 13:623.
  94. Thacher PV, Onyper SV. Longitudinal Outcomes of Start Time Delay on Sleep, Behavior, and Achievement in High School. Sleep 2016; 39:271.
  95. Danner F, Phillips B. Adolescent sleep, school start times, and teen motor vehicle crashes. J Clin Sleep Med 2008; 4:533.
  96. Morgenthaler T, Kramer M, Alessi C, et al. Practice parameters for the psychological and behavioral treatment of insomnia: an update. An american academy of sleep medicine report. Sleep 2006; 29:1415.
  97. van Geijlswijk IM, van der Heijden KB, Egberts AC, et al. Dose finding of melatonin for chronic idiopathic childhood sleep onset insomnia: an RCT. Psychopharmacology (Berl) 2010; 212:379.
  98. Smits MG, Nagtegaal EE, van der Heijden J, et al. Melatonin for chronic sleep onset insomnia in children: a randomized placebo-controlled trial. J Child Neurol 2001; 16:86.
  99. Mundey K, Benloucif S, Harsanyi K, et al. Phase-dependent treatment of delayed sleep phase syndrome with melatonin. Sleep 2005; 28:1271.
  100. Buscemi N, Vandermeer B, Hooton N, et al. The efficacy and safety of exogenous melatonin for primary sleep disorders. A meta-analysis. J Gen Intern Med 2005; 20:1151.
  101. Ferracioli-Oda E, Qawasmi A, Bloch MH. Meta-analysis: melatonin for the treatment of primary sleep disorders. PLoS One 2013; 8:e63773.
  102. Herxheimer A, Petrie KJ. Melatonin for the prevention and treatment of jet lag. Cochrane Database Syst Rev 2002; :CD001520.
  103. Committee on the Framework for Evaluating the Safety of the Dietary Supplements, Food and Nutrition. Dietary Supplements: A Framework for Evaluating Safety, The National Academies Press, Washington 2005.
  104. Werneke U, Turner T, Priebe S. Complementary medicines in psychiatry: review of effectiveness and safety. Br J Psychiatry 2006; 188:109.
  105. Spadoni G, Bedini A, Rivara S, Mor M. Melatonin receptor agonists: new options for insomnia and depression treatment. CNS Neurosci Ther 2011; 17:733.
  106. National Research Council. Melatonin: Prototype monograph summary. In: Dietary Supplements: A Framework for Evaluating Safety, The National Academies Press, Washington, DC 2005.
  107. Seabra ML, Bignotto M, Pinto LR Jr, Tufik S. Randomized, double-blind clinical trial, controlled with placebo, of the toxicology of chronic melatonin treatment. J Pineal Res 2000; 29:193.
  108. Valcavi R, Zini M, Maestroni GJ, et al. Melatonin stimulates growth hormone secretion through patheways other than the growth hormone-releasing hormone. Clin Endocrinol (Oxf) 1993; 39:193.
  109. Luboshitzky R, Shen-Orr Z, Nave R, et al. Melatonin administration alters semen quality in healthy men. J Androl 2002; 23:572.
  110. Hoebert M, van der Heijden KB, van Geijlswijk IM, Smits MG. Long-term follow-up of melatonin treatment in children with ADHD and chronic sleep onset insomnia. J Pineal Res 2009; 47:1.
  111. Wasdell MB, Jan JE, Bomben MM, et al. A randomized, placebo-controlled trial of controlled release melatonin treatment of delayed sleep phase syndrome and impaired sleep maintenance in children with neurodevelopmental disabilities. J Pineal Res 2008; 44:57.
  112. Carr R, Wasdell MB, Hamilton D, et al. Long-term effectiveness outcome of melatonin therapy in children with treatment-resistant circadian rhythm sleep disorders. J Pineal Res 2007; 43:351.
  113. van Geijlswijk IM, Mol RH, Egberts TC, Smits MG. Evaluation of sleep, puberty and mental health in children with long-term melatonin treatment for chronic idiopathic childhood sleep onset insomnia. Psychopharmacology (Berl) 2011; 216:111.
  114. Gradisar M, Dohnt H, Gardner G, et al. A randomized controlled trial of cognitive-behavior therapy plus bright light therapy for adolescent delayed sleep phase disorder. Sleep 2011; 34:1671.
  115. Cole RJ, Smith JS, Alcalá YC, et al. Bright-light mask treatment of delayed sleep phase syndrome. J Biol Rhythms 2002; 17:89.
  116. Terman M, Jiuan Su Terman . Circadian rhythm phase advance with dawn simulation treatment for winter depression. J Biol Rhythms 2010; 25:297.
  117. Fargason RE, Preston T, Hammond E, et al. Treatment of attention deficit hyperactivity disorder insomnia with blue wavelength light-blocking glasses. Chronophysiol Ther 2013; 3:1.
  118. Ito A, Ando K, Hayakawa T, et al. Long-term course of adult patients with delayed sleep phase syndrome. Jpn J Psychiatry Neurol 1993; 47:563.
  119. Mizuma H, Miyahara Y, Sakamoto T, et al. Two cases of delayed sleep phase syndrome (DSPS). Jpn J Psychiatry Neurol 1991; 45:163.
  120. Yamadera H, Takahashi K, Okawa M. A multicenter study of sleep-wake rhythm disorders: clinical features of sleep-wake rhythm disorders. Psychiatry Clin Neurosci 1996; 50:195.
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