Delayed Sleep-Phase Syndrome (780.55-0)
Synonyms and Key Words: Phase lag, phase delay, sleep-onset insomnia, morning
sleepiness, stable asynchrony relative to typical environmental pattern.
Delayed sleep-phase syndrome is a disorder in which the major sleep episode is delayed in
relation to the desired clock time, resulting in symptoms of sleep-onset insomnia or
difficulty in awakening at the desired time.
Delayed sleep-phase syndrome (DSPS) is marked by: (1) sleep-onset and wake times that are
intractably later than desired, (2) actual sleep-onset times at nearly the same daily clock hour,
(3) little or no reported difficulty in maintaining sleep once sleep has begun, (4) extreme
difficulty awakening at the desired time in the morning, and (5) a relatively severe to absolute
inability to advance the sleep phase to earlier hours by enforcing conventional sleep and wake
times. Typically, the patients complain primarily of chronic difficulty in falling asleep until
between 2 a.m. and 6 a.m. or difficulty awakening at the desired or necessary time in the
morning to fulfill social or occupational obligations. Daytime sleepiness, especially in the
morning hours, occurs variably, depending largely on the degree of sleep loss that ensues due to
the patient’s attempts to meet his or her social obligations by getting up “on time.” When not
obliged to maintain a strict schedule (e.g., on weekends or during vacations), the patient sleeps
normally but at a delayed phase relative to local time.
Associated Features: Patients with DSPS are usually perplexed that they cannot find a way to
fall asleep more quickly. Their efforts to advance the timing of sleep onset (early bedtime, help
from family or friends in getting up in the morning, relaxation techniques, or the ingestion of
hypnotic medications) yield little permanent success. Hypnotics in normal doses are often
described as having little or no effect at all in aiding sleep onset and may only aggravate the
daytime symptoms of difficulty awakening and sleepiness. Chronic dependence on hypnotics or
alcohol for sleep is unusual but, when present, complicates the clinical situation. More
commonly, patients give a history of having tried multiple sedating agents, which were
abandoned because of only transient efficacy.
Patients with DSPS typically score high as “night people” on the owl-lark questionnaire and
state that they feel and function best and are most alert during the late evening and night
hours. In pure cases of DSPS, a carefully kept sleep-wake log documents a consistent pattern of
sleep onsets, usually later than 2 a.m.; few to no awakenings once sleep is achieved; curtailed
sleep during the work or school week (if the patient has not given up on getting up); and lengthy
(9- to 12-hour) sleeps, with late morning to midafternoon arising times on weekends. In cases
where the clinical situation is complicated by chronic alcohol or hypnotic use or abuse, or in the
context of major mental difficulties, sleep-wake logs may also show frequent awakenings during
the delayed sleep period. Sleep-wake logs obtained during periods when morning social
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obligations are lessened or absent (vacations, long weekends, unemployment, school
suspension) show fairly consistent, but also consistently “late,” sleep and arising times.
Course: The duration of DSPS symptomatology varies from months to decades in cases
reported in the literature. Adolescence appears to be a particularly vulnerable life stage for
the development of the syndrome. However, the histories of some adult patients extend back
to early childhood, and pediatric sleep clinicians have described prepubertal children with the
Predisposing Factors: Many DSPS patients report that their difficulties began after a period of
late-night studying or partying, or after employment on the evening or night shift, following which
they found it impossible to resume sleeping on a conventional schedule despite the resumption
of conventional work or school hours. DSPS may be induced by alterations in the photoperiod,
such as is seen in individuals living at latitudes above the Arctic Circle. In such cases, the onset of
the disorder is precipitated by the dark period of the seasonal light-dark cycle.
Prevalence: The exact prevalence is unknown, but the disorder is probably uncommon,
representing a small proportion (5% to 10%) of patients presenting to sleep disorders centers
with the complaint of insomnia. The prevalence in the general population is unknown. One survey
study of adolescents found evidence suggesting a 7% prevalence in this age group. There may be
individuals who adapt to the pattern by taking evening or night jobs.
Age of Onset: Adolescence appears to be the most common period of life for the onset of
DSPS, but childhood cases have been reported. Onset after age 30 is rare.
Sex Ratio: Case series in the literature have varied between a 10:1 male:female ratio in
adolescents to 1:1 in a mixed series of adults and adolescents.
Familial Pattern: None known.
Pathology: The current understanding of the pathophysiology of DSPS rests on the application
of the principles of phase-response curves, largely derived from experiments in lower animals, to
the human sleep-wake cycle. Patients with DSPS are thought to have a relatively weak ability to
phase advance their circadian systems in response to normal environmental time cues
(zeitgebers). Transient sources of sleep-onset delay (late-night studying, night-shift work, certain
mental illnesses), which are ordinarily dealt with within a few days by individuals with normal
phase-response capability, unmask this weakness in phase resetting in the patient with DSPS.
That some ability to phase reset is present in DSPS is demonstrated by the regular, albeit late-to-
bed-late-to-arise, sleep schedule the patients adopt during vacations.
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Complications: Occupational, school, and social dysfunctions of varying degrees are a typical
accompaniment of DSPS and are often the major complaint that brings the patient to clinical
attention. Absenteeism and chronic tardiness are poorly tolerated in the school and day-shift
work settings, and many patients with DSPS come to be regarded as lazy, unmotivated, or
mentally ill by their families, peers, and superiors in the business or school environment, even in
the context of otherwise good social and mental functioning. Whether DSPS results directly in
clinical depression, or vice versa, is unknown, but many patients express consid- erable despair
and hopelessness over sleeping normally again. Chronic sedative or alcohol use or abuse
accompanies some cases as a complicating feature.
Polysomnographic Features: The most consistent abnormality in the polysomnographic
recordings of patients with DSPS is a prolonged (usually greater than 30 minutes) sleep latency
when the recordings occur during the patients’ habitual sleeping hours (e.g., 4 a.m. to noon).
Sleep efficiencies tend to be somewhat low for age (75% to 85%), but most of the inefficiency is
due to the prolonged sleep latency. Some patients have modest shortening of the REM latency
(e.g., to 50 to 70 minutes). Sleep is largely free of arousals once the patient is asleep. Sleep
architecture and amount are also within normal limits for age in cases that are not
complicated by concurrent drug or alcohol use or a major mental disorder. No pathologies of
sleep (e.g., sleep apnea syndrome or periodic limb movement disorder) that could account for
the complaints of insomnia and day- time sleepiness are present.
When patients are recorded at the socially acceptable or preferred time, that is earlier than
their habitual sleep time (e.g., 11 p.m. to 7 a.m.), the sleep latency is prolonged and the
patients experience difficulty in awakening. A multiple sleep latency test (MSLT) performed
after such a sleep period can show shorter sleep latencies on the morning naps compared to
the afternoon naps.
Other Laboratory Test Features: Continuous core body temperature monitoring in a small
group of DSPS patients who were sleeping on their habitual schedules showed that their
average absolute low temperature values occurred at or after the mid-low phase (midpoint of
that portion of the rhythm below the mean) of the temperature rhythm. By contrast, in normal
age- and sex-matched subjects, the absolute low temperature occurred before the mid-low
Differential Diagnosis: A pattern of delayed sleep onset occurs in some previously unaffected
individuals with the start of major mental disturbances, in particular in the excited phase of
bipolar affective disorder and during schizophrenic decompensations. In bipolar mania,
however, sleep is also typically shortened, and such patients have no difficulty arising at a
conventional hour. In addition, the delayed sleep pattern is usually transient in major mental
disorders and covaries with the mental symptoms in severity over time. Persistence of phase-
delayed sleep after remission of the mental symptoms suggests that the patient has DSPS that
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was unmasked by the initial mental disturbance.
Patients with DSPS should also be differentiated from individuals who habitually go to sleep
and awaken late for social reasons but then complain of sleep- onset insomnia and difficult
morning awakening on the sporadic days that they must go to bed and get up early. Such
individuals suffer instead from a transient sleep-wake-cycle disturbance, compounded by sleep
loss, which usually accompanies an acute-phase shift. Such cases are better categorized as
inadequate sleep hygiene. Reestablishment of a regular, more conventional sleep schedule
achieves rapid and appreciable success in the transient case, whereas it is ineffective in DSPS.
Diagnostic Criteria: Delayed Sleep-Phase syndrome (780.55-0)
A. The patient has a complaint of an inability to fall asleep at the desired clock time, an
inability to awaken spontaneously at the desired time of awakening, or excessive
B. There is a phase delay of the major sleep episode in relation to the desired time for
C. The symptoms are present for at least 1 month.
D. When not required to maintain a strict schedule (e.g., vacation time), patients will
exhibit all of the following:
1. Have a habitual sleep period that is sound and of normal quality and duration
2. Awaken spontaneously
3. Maintain stable entrainment to a 24-hour sleep-wake pattern at a delayed phase
E. Sleep-wake logs that are maintained daily for a period of at least two weeks must
demonstrate evidence of a delay in the timing of the habitual sleep period.
F. One of the following laboratory methods must demonstrate a delay in the timing of the
habitual sleep period:
1. Twenty-four-hour polysomnographic monitoring (or by means of two consecutive
nights of polysomnography and an intervening multiple sleep latency test)
2. Continuous temperature monitoring showing that the time of the absolute
temperature nadir is delayed into the second half of the habitual (delayed) sleep
G. The symptoms do not meet the criteria for any other sleep disorder causing inability to
initiate sleep or excessive sleepiness.
Note: If the sleep disorder is believed to be socially or environmentally induced, state and
code as delayed sleep-phase syndrome (extrinsic type). If there is evidence that the sleep
disorder is due to an abnormal circadian pace- maker or its entrainment mechanism, state
and code as delayed sleep-phase syndrome (intrinsic type).
Minimal Criteria: A plus B plus C plus D plus E.
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Mild: The patient has a habitual inability to fall asleep within a mean of two hours of the
desired sleep time, over at least a one-month period, and the dis- order is associated with
little or mild impairment of social or occupational functioning.
Moderate: The patient has a habitual inability to fall asleep within a mean of three hours of
the desired sleep time, over at least a one-month period, and the disorder is associated
with moderate impairment of social or occupational functioning.
Severe: The patient has a habitual inability to fall asleep within a mean of four hours of the
desired sleep time, over at least a one-month period, and the dis- order is associated with
severe impairment of social or occupational functioning.
Acute: 3 months or less.
Subacute: More than 3 months but less than 1 year.
Chronic: 1 year or longer.
Czeisler CA, Richardson GS, Coleman RM, et al. Chronotherapy: resetting the circadian clock of patients with delayed sleep
phase insomnia. Sleep 1981; 4: 1–21.
Lingjaerde O, Bratlid T, Hansen T. Insomnia during the “dark period” in northern Norway. An explorative, controlled trial with
light treatment. Acta Psychiatr Scand 1985; 71: 506–512.
Thorpy MJ, Korman E, Spielman AJ, Glovinsky PB. Delayed sleep-phase syndrome in adolescents. J Adolesc Health Care
1988; 9: 22–27.
Weitzman ED, Czeisler CA, Coleman RM, et al. Delayed sleep-phase syndrome. A chronobiological dis- order with sleep-
onset insomnia. Arch Gen Psychiatry 1981; 38: 737–746.
Adapted from: www.aasmnet.org
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