Fig. 2.1
Sample sleep logs. Sleep logs showing sleep-wake routines for Hannah. Note the feeling of daytime tiredness on school days ceases during winter break when a liberal sleep schedule is allowed
The International Classification of Sleep Disorders, Third Edition (ICSD-3), lists DSWPD (formerly known as Delayed Sleep Phase Syndrome) under the broad category of Circadian Rhythm Sleep-Wake Disorders (CRSWD) [1]. In DSWPD, the problem lies with an inability to initiate sleep at a socially acceptable time at night. In affected individuals, the habitual sleep-wake timing is usually delayed by more than 2 h as compared to the conventional timing, even when an opportunity to sleep is available. This may present very commonly as insomnia of sleep onset, given the appearance of difficulty initiating sleep. Once asleep, an individual with DSWPD usually does not experience difficulty maintaining sleep. As a second component, the individual will report problems waking up at an acceptable time the following day. Typically, this results in delays getting out of bed and trouble coming to full functional alertness upon awakening. This “sleep inertia” is common if the affected individuals have to curtail their sleep to meet social obligations such as going to school on time. However, a key feature of this disorder, assuming no other medical, psychiatric, or sleep-related comorbidities, is that the sleep duration, quality, and subsequent wakeful behavior and function is usually normal if the person does not have any obligations to wake up at a certain time the next day. Taken together, if left to select their own sleep and rise times, the affected person prefers to go to bed and get up significantly later than would be expected for the age and societal norms and report no other sleep-related problems if allowed to keep their favored schedules. Finally, since it is not uncommon for similar changes in sleep-wake behaviors to occur from time to time in normal individuals due to transient social or medical reasons, a firm diagnosis requires that the problem be present for 3 months or longer and that it be substantiated by sleep logs or actigraphy typically spanning a period of a fortnight or more (Fig. 2.2).
Fig. 2.2
Sample actigraphy chart. An actigraphy is a wrist watch-like device with an embedded accelerometer which can graph rest-activity cycles as a surrogate for sleep-wake. In the graphic, the clock hours are on the top (00:00 denotes midnight) and days of the week are on the vertical axis. Dark vertical lines in each row denote wrist activity implying wakefulness. This data is from another patient seen by the authors who exhibited late bedtime (red line) and rise times (blue line) except on 3 days when the teen did make it to school on time!
DSWPD affects 7 to 16 % of adolescents and young adults [1]. Genetic factors such as polymorphisms in the circadian clock gene hPer3, arylalkylamine N-acetyltransferase, human leukocyte antigen, and Clock have been reported to be associated with DSWPD [2–5]. Some familial aggregation has also been described [6]. Environmental, social, and behavioral factors also play an important role in the development and perpetuation of this disorder. DSWPD is a chronic disorder which may last into the middle and geriatric ages although the prevalence appears to decrease with increasing age [7, 8].
Pitfalls
DSWPD is a relatively common disorder that is frequently missed in the primary care setting.
DSWPD can be difficult to diagnose during the academic school year given societal obligations to rise early.
Learning Points
If excessive daytime sleepiness is a chief compliant, sleep logs are a important diagnostic tool (actigraphy is useful if available).
An adolescent with DSWPD will not experience difficulties initiating sleep or excessive daytime sleepiness if allowed to sleep and wake based on their personal circadian rhythm .
Once asleep, adolescents with DSWPD generally do not experience difficulties maintaining sleep.
Case Presentation 2
Andrew is a laconic 15-year-old male who presents with his mother for an initial sleep clinic visit with complaints of decreasing academic performance, increased moodiness, behavioral concerns, and an inability to initiate sleep. He denies symptoms of snoring, restless legs, cataplexy, hypnagogic hallucinations, or sleep paralysis.
Past psychiatric evaluation found a lack of motivation and follow-through on recommended therapy. He was also prescribed trazodone to assist with sleep initiation, but Andrew’s mother states it has not been beneficial. His pediatrician also prescribed methylphenidate on a hunch that he was experiencing EDS. This drug caused him to lose weight and feel restless, and the medication was stopped.
When interviewed without his mother, Andrew admits feeling tired in the morning and experiencing difficulty waking for school. He also voices fear that his parents think he is “crazy” or on drugs. Andrew confesses he felt awkward at the psychiatrist’s office when he heard trazodone can cause his penis “to become painful” and he chose to not take the medication. His mother is unaware of this. He denies being sexually active, consuming alcohol or recreational drugs. Andrew states he does drink some caffeine , usually Mountain Dew, in the morning to help him concentrate at school and clear his foggy brain. He does not doze in class but occasionally naps on the bus.
When asked about his sleep habits during school breaks, Andrew confesses that twice a year his family vacations in Hawaii and that he feels fine. While in Hawaii, he is in bed by 10:00 pm, he initiates sleep quickly, and is up before his family and ready to hit the beach. He often teases his family who appear to be experiencing jetlag for the whole week they are on vacation.
His physical examination is unremarkable and a urine drug screen is negative.
A diagnosis of DSWPD is made. The circadian rhythm is explained to Andrew and his mother. Andrew’s interest in biology and science, and validation that he is not “crazy” evoke a flurry of questions. He is eager to try phase advancement with the help of low-dose melatonin and morning exposure to sunlight. His mother describes his sister’s bedroom as facing East, and it is agreed to have him switch rooms with his sister to allow morning sunlight exposure and use room-darkening shades at night.
Discussion
While several case reports have documented the effectiveness of phase shifting, there have been no controlled trials in adolescents [9]. Phase advancement is best used when a targeted sleep onset time and the current sleep onset time are less than 3 h apart. Bedtimes and wake-times are gradually moved earlier (by 15 to 30 min a day) until the targeted sleep and wake-times are reached. The starting bedtime is set at a time that the adolescent is consistently able to initiate sleep quickly. The pace (shifting times earlier every 1 day, 2 days, 3 days) and time increments (shifting by 5 min, 15 min, 30 min) is case specific and dependent on patient response to treatment and how quickly the shift in bedtime and wake-times must be accomplished. The longer the delayed sleep phase has been sustained, the more gradual the process might need to be (Table 2.1).
Table 2.1
Sample phase advancement schedule
Bedtime | Waketime | |||||||
|---|---|---|---|---|---|---|---|---|
Current | 12:00 AM | 9:00 AM | ||||||
Night 1 | 11:45 PM | 8:45 AM | ||||||
Night 2 | 11:30 PM | 8:30 AM | ||||||
Night 3 | 11:15 PM | 8:15 AM | ||||||
Night 4 | 11:00 PM | 8:00 AM | ||||||
Use of over-the-counter melatonin is also a treatment option in DSWPD. Melatonin is a hormone secreted by the human pineal gland in a well-defined 24-h cycle. During the daytime, levels of melatonin are nearly absent and will rise into the evening as one nears their usual bedtime. During the nighttime, levels of melatonin remain relatively constant and will decline as one nears a typical waketime [10]. The American Academy of Sleep Medicine (AASM) has recently released an updated clinical practice guideline for the treatment of intrinsic CRSWDs, which suggests that there is some evidence to support the use of strategically timed melatonin to treat DSWPD in children and adolescents [11]. Several studies have found physiologic doses of oral melatonin (0.3–0.5 mg) administered in afternoon or early evening hours (i.e., 5–7 h before typical sleep onset) seem to be most effective in advancing the sleep phase [9]. However, inappropriately timed melatonin could worsen a phase delay. Melatonin can also have hypnotic effects when given in larger doses just before bedtime. Unfortunately, at this time there is no consensus on the ideal time to take melatonin to achieve a phase advance [9] but research suggests a predictable physiological response [12] (Fig. 2.3a).
Fig. 2.3
(a) Melatonin phase response curve. The three pulse phase response curve (PRC) to 3 mg of exogenous melatonin generated from subjects free-running during an ultradian LD cycle. Phase shifts of the DLMO are plotted against the time of administration of the melatonin pill relative to the baseline DLMO (top x-axis). The average baseline DLMO is represented by the upward arrow, the average DLMOff by the downward arrow, and the average assigned baseline sleep times from before the laboratory sessions are enclosed by the vertical lines. Each dot represents the phase shift of an individual subject, calculated by subtracting the phase shift during the placebo session (free-run) from the phase shift during the melatonin session. The curved line illustrates the dual harmonic curve fit. The average clock time axis (bottom x-axis) corresponds to the average baseline sleep times. This PRC can be applied to people with different sleep schedules by moving the average clock time axis until the vertical lines align with the individual’s sleep schedule. Figure and legend reprinted with permission from [12].Fig. 2.3 (continued) (b) Light phase response curve The PRC to the bright light stimulus using melatonin midpoints as the circadian phase marker. Phase advances (positive values) and delays (negative values) are plotted against the time of the center of the light exposure relative to the melatonin midpoint on the pre-stimulus CR (defined to be 22 h), with the core body temperature minimum assumed to occur 2 h later at 0 h. Data points from circadian phases 6–18 are double plotted. The filled circles represent data from salivary melatonin in subject 1 8K8 from whom blood samples were not acquired. The solid curve is a dual harmonic function fitted through all of the data points. The horizontal dashed line represents the anticipated 0.54 h average delay drift of the pacemaker between the pre- and post-stimulus phase assessments. Figure and legend reprinted with permission from [13]
Another treatment modality for phase advancement that should be considered is bright light therapy which shows a similar phase response physiology [13] (Fig. 2.3b). By exposing an adolescent to bright light at an appropriate time, the circadian rhythm may be shifted earlier, allowing an adolescent to initiate sleep earlier. However, much like melatonin dosages, there are no currently established guidelines regarding intensity, duration, and time of light exposure. It should be noted that light exposure at the wrong time could exacerbate a phase delay. In simple cases and sunny places, light exposure may be as easy as eating breakfast in a sunny area or early morning sun exposure. In more complicated cases or cloudy areas, regimented exposure for 20–30 min to bright light (2500 to 10,000 lux) from specially designed light boxes in the early morning (e.g., 6:00 to 8:00 am) may be beneficial [9]. There are a number of commercially available bright light therapy models that can be purchased online.
As with melatonin , knowledge of phase response to light therapy is essential since wrongly timed light can worsen DSWPD. Thus, bright light should also be avoided in the evening or late in the day through the use of dark glasses or dimming of lights. The concept behind strategic avoidance of light is based on the known melatonin-suppressing effect of light. Exposure to light in the evening and before the core body temperature minimum (CBTmin) leads to phase delays [14]. The greater the intensity and duration of light exposure, the greater the effects on the circadian rhythm [15, 16]. Thus, a combination of melatonin and bright light therapy is frequently used for phase advancement (Fig. 2.4).
Fig. 2.4
Phase advancement using melatonin and bright light therapy. Normal sleep time is dependent on the circadian clock. In normal persons, endogenous melatonin rises in the evening a little before natural sleep onset and falls to low levels before natural awakening in phase with external time cues such as sunlight (blue curve). In delayed sleep-wake phase disorder this rhythm is shifted to a later clock time such that the person goes to sleep and rises later relative to acceptable social norms (red curve). Therapy with low-dose exogenous melatonin early in the evening (blue arrow) and/or bright light in the morning (red arrow) has been used to shift the circadian phase towards normal (phase advancement)
An alternative treatment option to phase advancement is phase delay (chronotherapy) which is typically used in more severe cases of DSWPD, when the shift needed is greater than 3 h (Table 2.2). Chronotherapy involves delaying bedtime and waketime by 2–3 h every 1–2 days based on the fact that for most people it is often easier to go to bed and initiate sleep later than it is to initiate sleep earlier, allowing for larger shifts to occur. Because shifts in bedtime are larger during chronotherapy, the circadian rhythm can be reset quickly. As a corollary, this is best done during school breaks [17]. Research has found that chronotherapy is highly effective particularly when used in conjunction with bright light therapy [18, 19].
Table 2.2
Sample phase delay schedule (chronotherapy)
Related posts:
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
