Jason, age 16, has had difficulty with sleep initiation for 2 years. He describes going to bed at 10:30 PM on school nights but falling asleep no sooner than midnight and typically after 1:30 AM. He denies contributions from an “active mind” or environmental disturbances, and his bedroom contains no TV, computer, or other media devices. He does not sleep better with a change in environment. He denies pervasive low mood symptoms and believes his mood hinges predominantly on his ability to achieve sufficient sleep.
Once asleep, Jason generally enjoys good sleep consolidation until he needs to arise at 6:30 AM. His mother awakens him with difficulty, as he often sleeps through his alarm. He sleeps approximately 5 hours nightly during the school week, endorses impaired concentration, and often dozes during his first several classes. When he returns home from school, he finds it very difficult to resist napping.
On weekends he retires at 1 AM or later and typically falls asleep within 30 minutes. He usually awakens at noon but can sleep as late as 4:30 PM. He feels slightly more refreshed on weekends and describes his mood then as improved. During a recent spring break, he felt much better when allowed to sleep as much as he wanted.
Delayed sleep phase disorder (DSPD)—characterized by a pathological “night owl” circadian preference—is seen most commonly in adolescents and is associated with psychiatric morbidity, psychosocial impairment, and poor academic performance. Proper identification of the condition can be enhanced with a variety of assessment tools, and successful treatment requires an awareness of potential endogenous and exogenous contributors.
This article describes what is known about DSPD and uses the case example to illustrate diagnostic assessment and treatment choices. Intriguing data support various pathophysiologic explanations for DSPD (Box 1).1-6 Facilitating the adjustment of patients’ physiologic clocks is the overall goal in managing DSPD.
In individuals normally entrained to the light/dark cycle, circadian rhythms are:
- delayed by evening exposure to bright light (≥ 2,500 lux) prior to the core body temperature minimum (Tmin)
- advanced by morning light exposure after the Tmin.1
These opposing effects attune most people to the light/dark cycle, with sleep and wakefulness occurring on a conventional schedule. Persons with delayed sleep phase disorder (DSPD) live at a delayed phase that resists advancement and is incompatible with their personal and social obligations.
Theories have been proposed, but DSPD’s etiology has not been fully explained. Affected adolescents may exhibit an extreme in circadian preference. Case reports also describe DSPD emerging after traumatic brain injury.2
Intriguing evidence supports various pathophysiologic explanations for DSPD. An abnormally long intrinsic circadian period (>25 hours) was recently demonstrated during temporal isolation in 1 individual with DSPD.3 Both this case report and controlled studies describe deviations from expected relationships between the sleep/wake cycle and physiologic circadian markers. Most consistently described are longer intervals from Tmin4 to sleep offset (final rise time) in DSPD patients compared with controls.
Other research suggests:
Because of their extreme seemingly innate preference to retire and arise at relatively late clock hours (an “eveningness” trait), school-aged patients with DSPD represent a high-risk population for problematic sleepiness. In a survey of 612 high school students, the 63% who felt they needed more sleep on school nights showed a strong eveningness preference (as assessed by questionnaire), compared with students who described getting sufficient sleep.7 Other studies have revealed psychiatric morbidity (including affective and personality disorders), psychosocial impairment, and poor academic performance associated with the condition.8-10
DSPD may affect 7% to 16% of patients presenting with insomnia complaints in sleep medicine clinics.11 The condition appears most common among young cohorts and has been reported to affect up to 7% of adolescents in the United States.12 Its high frequency in this age group may be a pathologic exaggeration of the normal tendency toward delayed timing of sleep and wakefulness linked with pubertal development.13
Sleep and wakefulness regulation
Conceptually, 2 processes govern sleep and wakefulness:
- The homeostatic drive to sleep (process S) is proportional to the duration of sleep restriction and becomes maximal at about 40 hours.
- Circadian regulation (process C) creates a drive for wakefulness that variably opposes process S and depends upon intrinsic rhythms.14
Neurons of the suprachiasmatic nucleus in the hypothalamus exert master coordination of this sleep/wake rhythm, along with other behavioral and physiologic variables.15 Because the typical intrinsic period is slightly longer than 24 hours, synchronization to the 24-hour day (entrainment) is accomplished by environmental inputs (zeitgebers, or “time givers”), the most important of which is exposure to light.16