> Table of Contents > Delayed Sleep-Wake Phase Disorder (DSWPD)
Delayed Sleep-Wake Phase Disorder (DSWPD)
Adam J. Sorscher, MD
image BASICS
DESCRIPTION
  • Circadian rhythm sleep disorders (CRSDs) are a family of conditions that occur when an individual's preferred timing of sleep is not synchronized to commitments to job, school, family, or social engagements. In CRSDs, intrinsic sleep is normal (i.e., there is no sleep fragmenting condition such as obstructive sleep apnea or periodic limb movement disorder). However, when forced by obligations to attempt sleep at nonpreferred times, individuals with CRSDs may complain of both sleep-initiation insomnia and excessive sleepiness in their wake time. These symptoms resolve entirely if the individual is allowed to sleep at his or her preferred time.
  • Delayed sleep-wake phase disorder (DSWPD) is marked by a stable but persistent inability to initiate sleep at a desired time. Individuals are typically unable to initiate sleep until 2 to 6 hours later than societal norms (typically after 2 AM), and this frequently results in insufficient sleep/sleepiness in the day that follows.
EPIDEMIOLOGY
DSWPD is the most common circadian rhythm disorder seen by referral in sleep medicine clinics.
Prevalence
DSWPD has an estimated prevalence of 0.1-0.2% in the general population. It is most common in adolescents, with a prevalence of 7-16%.
ETIOLOGY AND PATHOPHYSIOLOGY
In all mammals, an oscillating signal from the suprachiasmatic nucleus (SCN) in the anterior hypothalamus establishes circadian rhythms, including the propensity to be awake or asleep. The average period of this signal in humans is 24.2 hours, slightly longer than the environmental day. Certain factors, most significantly morning light, shift the timing of the circadian rhythm and thereby synchronize it to the shorter environmental cycle day by day. DSWPD occurs when the circadian rhythm is not adequately synchronized to the shorter 24-hour environmental cycle, creating a mismatch between them. Some theories to account for inadequate synchronization are that it occurs in individuals who have an abnormally long circadian period (>25 hours) or whose circadian clock does not properly respond to synchronizing agents such as light (1).
  • Release of melatonin from the pineal gland in the evening initiates a cascade of events that usually triggers sleep behavior several hours later. Studies suggest that the timing of melatonin release within the circadian cycle is delayed by 40 to 120 minutes in late adolescence compared with prepuberty. This suggests that the tendency for teenagers to delay sleep onset is largely a genetically programmed developmental phenomenon.
  • DSWPD is the result of biologic, behavioral, and psychosocial factors. The relative contributions of genetically predetermined endogenous factors (the shifting of the circadian phase just described) versus voluntary behaviors that delay bedtime are not fully delineated.
Genetics
Emerging evidence indicates a genetic component to DSWPD—a positive family history is reported in approximately 40% of individuals. In one familial case report, DSWPD was shown to occur in an autosomal dominant inheritance pattern. Polymorphisms in circadian rhythm genes such as hPer3 and clock among individuals with DSWPD constitute evidence of a genetic component to the disorder (2).
RISK FACTORS
DSWPD primarily affects adolescents and young adults—a cohort who have a biologic tendency to delay the onset of sleep yet often need to be up early for school/work responsibilities. Children with autism spectrum disorders also frequently have disturbed circadian rhythm cycles.
GENERAL PREVENTION
In DSWPD (and all CRSDs), careful attention to sleep hygiene is necessary to establish and maintain a desired sleep schedule. The most important behavioral practices needed to prevent an undesirably late fall-asleep time are as follows:
  • Maintain a regular sleep/wake schedule 7 days/week.
  • Avoid daytime napping.
  • Minimize caffeine and stimulants.
  • Avoid stimulating activities in the late evening, such as computer, TV, and social interactions. A 30-minute “wind-down” time prior to bedtime in which homework, socializing, and electronic devices are off-limits is helpful.
  • If computer screens are to be used in the evening, consider “apps” that filter out blue and green wavelengths because these frequencies are especially potent at further delaying the onset of sleep.
  • Attempt to arise at a similar time on weekends as on school/work mornings—adolescents who sleep ad lib on the weekends (sometimes into the afternoon) often find that they have especially great difficulty initiating sleep on Sunday night and, thus, get the week off to a bad start.
image DIAGNOSIS
PHYSICAL EXAM
Explore for features of sleep apnea, a competing cause of hypersomnolence: obesity/large neck circumference; hypertension; crowded oropharynx
DIFFERENTIAL DIAGNOSIS
DSWPD and other CRSDs are unique in that they are often marked by the twin complaints of insomnia when attempting to sleep and hypersomnolence in the wake period. Other sleep disorders usually cause either insomnia or hypersomnolence but not both. DSWPD and other CRSDs resolve entirely if the individual is allowed to sleep at his or her preferred time.
DIAGNOSTIC TESTS & INTERPRETATION
  • Diagnosis of DSWPD is made primarily by thorough history taking.
  • Sleep logs completed over 3 weeks time graphically reveal fall-asleep times that are consistently 2 to 6 hours later than societal norms and much later wake-up times (not infrequently in the afternoon) on days off from school/work (3)[B].
  • Wrist actigraphy (using a wristwatch-like device with an accelerometer), undertaken for 3 weeks, also provides an accurate display of sleep and wake timing but is usually not reimbursable by insurance and is not needed if the individual can complete sleep logs (3)[B].
  • Testing in the sleep lab is not indicated unless a suspicion exists of comorbid intrinsic disorders of sleep, such as sleep apnea, narcolepsy, or parasomnias (unusual behaviors arising out of sleep) (3)[A].
image TREATMENT
  • The goal of treatment in DSWPD is to help the individual consistently initiate sleep at an earlier time. The principal therapies that advance sleep onset are light and melatonin (factors that shift the circadian rhythm are called zeitgebers). Comparatively, light is much more potent than melatonin in its phase-shifting ability. The phase-shifting effects of light and melatonin depend on the timing at which they are provided as depicted in the phase-response
    P.261

    curve (see online version). Key points: Light will advance sleep onset to an earlier time if provided after the body's temperature nadir that occurs ˜2/3 through the habitual sleep phase and for several hours thereafter. Proper timing is critical because exposure to light in the evening or before the temperature nadir (i.e., in the initial 2/3 of the sleep period) will have the opposite effect—it will further delay sleep onset. For melatonin, the most potent phase-advancing effect occurs if it is provided in the evening, 4 to 6 hours before an individual's usual sleep onset time.
  • Use the following rules to guide prescribing of light in order to advance sleep phase (3)[B]:
    • No single rule exists for intensity, duration, or wavelength for light therapy. Most protocols employ a 2,500 to 10,000 lux full-spectrum light box, set 2 to 3 feet from the individual for 30 to 120 minutes. A common prescription is 10,000 lux box for 30 minutes upon awakening in the morning. Retailers of full-spectrum light boxes abound on the Internet. Sunlight, when present in the morning in warm-weather seasons, is equally effective.
    • Prescribe exposure to full-spectrum light immediately upon awakening. (Note: Although the phase-advancing effect of light is actually greatest if it is provided immediately after the body temperature nadir that occurs ˜2/3 through the sleep period, the strategy of waiting until the habitual waking time is preferred for these reasons: [i] it acknowledges that it is onerous for the individual to wake up artificially early for light therapy and [ii] it minimizes the risk of unintentionally providing light before the temperature nadir, which further delays the sleep phase.)
    • Light exposure in the evening has the effect of delaying sleep phase and worsening DSWPD. Instruct individuals to limit light exposure in the evening (consider using sunglasses or curtailing outdoor activities in warm-weather months).
    • Contraindications to phototherapy include retinopathy, photosensitivity, and bipolar disorder.
MEDICATION
  • Prescribe melatonin to be taken 4 to 6 hours before the habitual (usual) fall-asleep time, not at bedtime. Melatonin in minute doses is as effective as higher doses in producing phase-shift; therefore, use the lowest dose available—usually 1 or 3 mg (3)[B].
  • Once earlier sleep onset and wake-up occurs, adjust the timing of therapies every 3 to 5 days— continue to use light directly upon awakening; provide melatonin earlier and earlier in the evening corresponding to 4 to 6 hours before the newly observed fall-asleep time.
ISSUES FOR REFERRAL
  • Referral for evaluation and testing at a sleep clinic is not necessary in most cases of DSWPD. The chief indications for referral are suspicion of the following comorbid disorders:
    • Obstructive sleep apnea: indicated by loud snoring, obesity/large neck, witnessed apneas, and history of hypertension
    • Narcolepsy: indicated by severe levels of daytime sleepiness, despite adequate sleep quantity, and sometimes accompanied by cataplexy (bouts of sudden muscular weakness triggered by strong emotions)
    • Parasomnias: undesirable experiential/behavioral phenomena that arise out of sleep, such as dangerous sleepwalking or dream-enactment behavior
  • In addition, many individuals with the complaint of insomnia/sleepiness have comorbid mental health disorders, primarily depression and possibly substance abuse. Referral for mental health disorders/substance abuse treatment is indicated if these are present.
ADDITIONAL THERAPIES
  • Chronotherapy is an older strategy in which the individual is instructed to delay sleep and wake times by 2 to 3 hours every 2 to 3 days, shifting the sleep cycle across the 24-hour day, until the individual reaches a desired bedtime. Carried out over several weeks, this protocol is extremely disruptive to daytime schedules and also has not been demonstrated to be effective. It is seldom used (4).
  • Some early reports suggest that vitamin B12 has circadian phase-shifting properties. This finding has not been confirmed in subsequent investigations, and presently, no evidence seen of benefit to the use of this supplement in CRSDs (3)[B].
  • Use of sedative-hypnotic medications to treat the insomnia component and stimulant medications to treat daytime sleepiness has not been shown to be effective in the context of DSWPD (3)[C].
image ONGOING CARE
Remind patients to practice healthy sleep behaviors (see “General Prevention”) if they wish to maintain an earlier sleep/wake pattern.
PATIENT EDUCATION
http://www.aafp.org/afp/1999/0401/p1918.html
REFERENCES
1. Wyatt JK, Stepanski EJ, Kirkby J. Circadian phase in delayed sleep phase syndrome: predictors and temporal stability across multiple assessments. Sleep. 2006;29(8):1075-1080.
2. Ebisawa T, Uchiyama M, Kajimura N, et al. Association of structural polymorphisms in the human period3 gene with delayed sleep phase syndrome. EMBO Rep. 2001;2(4):342-346.
3. Morgenthaler TI, Lee-Chiong T, Alessi C, et al. Practice parameters for the clinical evaluation and treatment of circadian rhythm sleep disorders. An American Academy of Sleep Medicine report. Sleep. 2007;30(11):1445-1459.
4. 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(11):1484-1501.
Additional Reading
&NA;
  • Barion A, Zee PC. A clinical approach to circadian rhythm sleep disorders. Sleep Med. 2007;8(6): 566-577.
  • Kanathur N, Harrington J, Lee-Chiong T Jr. Circadian rhythm sleep disorders. Clin Chest Med. 2010;31(2):319-325.
  • Kripke DF, Rex KM, Ancoli-Israel S, et al. Delayed sleep phase cases and controls. J Circadian Rhythms. 2008;6:6.
  • Wilson SJ, Nutt DJ, Alford C, et al. British Association for Psychopharmacology consensus statement on evidence-based treatment of insomnia, parasomnias and circadian rhythm disorders. J Psychopharmacol. 2010;24(11):1577-1601.
Codes
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ICD10
G47.21 Circadian rhythm sleep disorder, delayed sleep phase type
Clinical Pearls
&NA;
  • The tendency to become “night-owlish” with adolescence is, to a large extent, a biologically programmed phenomenon, not strictly a behavioral choice. Enlightened public policy would recognize this and allow for later start times for high schools.
  • DSWPD can be diagnosed with careful history taking and sleep logs; referral for formal sleep studies is usually not indicated.
  • Use of light and melatonin can shift habitual sleep onset and offset time by their action on the human circadian rhythm.
  • To maintain a desirable sleep phase, individuals with DSWPD usually need to maintain meticulous attention to sleep hygiene, including a regular sleep/wake schedule 7 days/week, to avoid lapsing into a delayed phase pattern.