Delayed sleep-wake phase disorder

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 highest in adolescents and young adults, with rates estimated between 3.3 and 4.6 percent [1-8]. Comparisons of individual studies are complicated by the use of inconsistent diagnostic criteria and the use of evening chronotype as a proxy for actual DSWPD. 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.

The prevalence of DSWPD in adults is lower, with estimates between 0.2 to 1.7 percent [1-7]. Although the prevalence of familial DSWPD has not been established, a family history is often present among afflicted individuals [9]. 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 [3,24-29].

●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.

●Intrinsic differences in sleep homeostasis – Analyses of sleep electroencephalography suggests that slow wave activity (a proxy of the sleep homeostatic mechanism) decreases in magnitude in the first sleep cycle among those with evening chronotypes compared with those with normal or intermediate chronotypes, despite similar baseline sleep among groups [9].

●Genetic factors – Genetic factors may play a role in the pathogenesis of DSWPD. A study of unrelated families showing strong heritability of the disorder described a gain of function mutation in the CRY1 clock gene, which creates a transcriptional inhibitor with enhanced affinity for circadian activator proteins CLOCK and BMAL1 [9].

●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 (figure 1) on a school or work night [24].

Patients with DSWPD may endorse social consequences of delayed sleep phase, such as chronic tardiness, repeated school absences, and family discord [50]. Morning awakenings may require intensive parent, caregiver, 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 [51], 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 [12-20,22,52]. 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) [53]. 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 [26,54-57]. 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 [56]. 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 [36,58,59]. 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 [25,26,30,60-63]. 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 [63]. In another cohort of predominantly adult patients with DSWPD, 64 percent of patients endorsed depressive symptoms of at least moderate severity [64]. Other studies have found an approximately threefold higher prevalence of seasonal affective disorder in patients with DSWPD than in controls [65].

Limited data suggest that higher degrees of circadian misalignment correlate with depression severity as well as poor responsiveness to antidepressant therapy [64,66-68]. A delayed circadian preference has been described in adults with bipolar I disorder, in some cases correlating with higher illness recurrence rates [69,70]; similar associations have been reported in children with bipolar I disorder [71] and adults with obsessive compulsive disorder [72-74], although the data are not entirely consistent [75].

DSWPD has been occasionally reported in children with comorbid attention deficit hyperactivity disorder (ADHD) and sleep-onset complaints [76,77]. 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 [78]. (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 (table 1). 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 11:00 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 2 and table 3) 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 [79,80]. 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. (See "Actigraphy in the evaluation of sleep disorders".)

Longitudinal monitoring among patients with DSWPD should demonstrate a persistently delayed sleep-wake schedule on both weekdays and weekends (figure 2), 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 [81]. 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 [82].

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 [83-85]. Normative values have not been established, however, and significant overlap may exist between affected and unaffected populations [86-88]. 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 (table 1) [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 2). 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 (table 4). 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 "Evaluation and diagnosis of insomnia in adults", section on 'Clinical features'.)

Among other circadian rhythm sleep-wake disorders, non-24-hour sleep-wake rhythm disorder (N24SWD) can have overlapping clinical features with DSWPD. N24SWD is primarily encountered in individuals with complete light perception blindness but has also been described in sighted individuals. In fact, sighted individuals may display evening circadian preference or DSWPD before development of N24SWD. The key distinguishing feature of N24SWD is that sleep-wake patterns are not fixed. As an example, an individual with N24SWD may fall asleep in the early morning hours (eg, 2:00 AM) similar to someone with DSWPD; however, sleep tendency moves progressively later each day, and symptoms depend on the degree of alignment between the drifting sleep period and the desired sleep bout. N24SWD is reviewed in more detail separately. (See "Non-24-hour sleep-wake rhythm disorder".)

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 [38,89,90]. 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 6 hours centered 12 hours from the midpoint of the unrestricted weekend sleep bout have no counter-effects on circadian rhythms [91].

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 [39,77,92]. 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 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 increase total sleep time and mitigate associated impairments [14,93-101], although benefits may be modest and transient in some cases [99]. 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 [102].

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 [92].

Patients with a concomitant chronic insomnia disorder may respond to adjunctive behavioral therapy [103]. 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 "Cognitive behavioral therapy for insomnia in adults".)

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 [92].

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

●In a randomized trial of 116 patients with DSWPD (mean age 29 years), patients were treated with melatonin 0.5 mg or placebo one hour before the desired bedtime; both groups received behavioral sleep-wake scheduling at the desired bedtime [104]. After four weeks, melatonin advanced sleep onset by 34 minutes relative to baseline compared with placebo, as measured by actigraphy. Patient-reported sleep quality, insomnia severity, and functional disability also improved with melatonin, and adverse effects were similar between groups.

●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 [105]. 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 [92].

●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) [76,106]. Dosing varied slightly between trials; melatonin was taken at 6:00 PM or 7:00 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 [92]. Actigraphically-assessed sleep onset time also advanced. Total sleep time improved by approximately 30 to 40 minutes [76,106].

●In a combined analysis of two trials in adults with DSWPD and comorbid depression (n = 28), melatonin (5 mg, timed between 7:00 PM and 9:00 PM) was associated with improved objective total sleep time (mean difference 41 minutes) and initial sleep latency (mean difference -44 minutes) compared with placebo [92]. 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 [107].

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 [108-113], 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.

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 [114]. 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 [115]. 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 [108].

Although theoretical concerns exist in children and adolescents about effects of melatonin on growth hormone regulation (10 mg dose) [116], and on reproductive function and development (3 mg dose) [117], 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/caregivers, and 65 percent of the participants continued to use the medication daily [118].

●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 [119,120].

●Tanner stages were assessed serially in a questionnaire-based study involving Dutch children and adolescents using melatonin during prepuberty [121]. 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 [122-124]. 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 [122].

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 [122]. 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 AM and 7:30 AM was advised.

●Concomitant multicomponent behavioral education with parent/caregiver 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 [123]. Other novel modalities such as dawn simulators are of interest but have not yet been studied in patients with DSWPD [125].

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 [126]. 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 [55,127], other reports describe resistance to the effects of traditional hypnotics in patients with DSWPD [128,129].

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Parasomnias, hypersomnias, and circadian rhythm disorders".)

SUMMARY AND RECOMMENDATIONS

●Epidemiology – Delayed sleep-wake phase disorder (DSWPD) is the most common circadian rhythm disturbance in adolescents and young adults, reported in approximately 5 percent of teenagers. (See 'Epidemiology' above.)

●Clinical features – DSWPD is akin to a pronounced "night owl" circadian preference. 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. This results in chronic sleep restriction, impaired daytime function, and an increased risk of depression and other psychiatric disorders. (See 'Clinical features' above.)

●Diagnosis – DSWPD is a clinical diagnosis that should be suspected in patients who have difficulty falling asleep at times necessary to obtain sufficient nightly sleep, difficulty waking up in the morning, and complaints of distress or impaired daytime functioning (table 1). (See 'Clinical history' above and 'Diagnostic criteria' above.)

The diagnosis is confirmed by the presence of a consistent circadian phase delay on sleep logs, actigraphy (figure 2), or both, recorded over at least seven days. Polysomnography is only indicated if there is clinical suspicion for a comorbid sleep disorder such as obstructive sleep apnea. (See 'Sleep logs and actigraphy' above and 'Morningness-eveningness questionnaire' above.)

●Differential diagnosis – DSWPD is often confused with chronic insomnia (table 4). Unlike patients with insomnia, those with DSWPD have no difficulties sleeping or obtaining an adequate amount of sleep when they can go to sleep and wake up at times that are matched with their circadian phase. (See 'Differential diagnosis' above.)

●Initial management – Initial management of all patients with DSWPD should address external factors that may exacerbate or contribute to the phase delay. Specifically, we advise patients to:

•Minimize or eliminate caffeine, nicotine, and alcohol

•Avoid daytime naps

•Refrain from stimulating activities before the desired bedtime

•Avoid sleeping in on weekends more than 30 minutes past the weekday wake up time

In addition, we advise patients to gradually advance evening bedtimes and morning wake times toward a targeted goal and then strictly adhere to this fixed sleep-wake schedule. For mildly affected patients, these behavioral interventions may be sufficient to relieve symptoms. (See 'Behavioral modifications' above.)

●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 (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 therapy – 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.)

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