1 Delayed Sleep Phase Syndrome Table of Contents Introduction 1 Causes 2 Symptoms 2 Testing 3 Sleep diary 3 Actigraphy 3 Treatment 3 Bright light therapy 3 Chronotherapy 4 Sleep hygiene 5 Melatonin 5 Vitamin b12 5 Depression 5 Non-24-hour persistent disturbance 6 Introduction Delayed sleep phase syndrome (DSPS), sometimes called phase lag syndrome, is a sleep disorder of circadian rhythm. However, unlike jet lag, and the effects of shift work, delayed sleep phase syndrome is a persistent disorder. In fact, in clinical settings, it is, perhaps, the most commonly seen complication of sleep-wake patterns. Delayed sleep phase syndrome results from a disturbance between the patient s internal biological clock and the external environment. Again, unlike jet lag, this desynchronization is not activated by travel or change in external environment. Rather, the patient s propensity to fall asleep is simply delayed in relation to that of the general public. Subsequently, a patient who is experiencing DSPS is out of phase with the routine that governs most of his or her life. A person with this disorder is typically unable to fall asleep before 2 a.m. and has great difficulty waking early, say by 7 a.m. These people are sometimes called night owls or described as not being morning people. If allowed to sleep a full seven to eight hours, i.e. until 10 a.m., they feel rested and function normally. Unfortunately, this is not usually the case. The main difficulty for a person with DSPS is meeting the expectations of society, i.e. functioning early for school or work. A person with DSPS may lose jobs or fail courses in school. So, this syndrome affects individuals on a social level at the same time that it compromises their health and hygiene. Patients with DSPS may initially refer to their symptoms as insomnia. Again, the significance that society places on traditional sleep-wake patterns usually dictates what is normal. And as soon as people deviate from a normal sleep pattern, they tend to assume they are not capable of sleep at all. But this is not true. Patients who suffer from DSPS are able to get plentiful sleep; it s just postponed. If they can sleep until they are ready to wake, patients with DSPS can experience rewarding sleep. The reality is that DSPS usually makes it hard to wake up, as the patient simultaneously indulges his or her late night sleep routine and yields to the wake routine of society. Diagnosis is based on sleep history, and treatment ranges from learning to respond differently to external indicators of sleep-wake time to practicing new and proper sleep habits.
2 Incidence The exact incidence of delayed sleep phase syndrome is unknown. In one recent study, DSPS accounted for 40 percent of disorders involving sleep-wake schedules among 5,000 participants. It is estimated to affect 7 percent of teenagers and to be the cause in 10 percent of chronic insomnia cases. Although DSPS usually surfaces in childhood, it is seen most frequently in young adults, especially men, which suggests a concurrence with lifestyle. The precise medical cause of DSPS is unknown. Circadian rhythms, which regulate the internal biological clock and influence such functions as sleep-wake patterns, are usually described as being out-of-phase in DSPS. If we think of sleep as happening on a continuum, then it is possible to imagine that the circadian rhythms of patients with DSPS signal sleep at delayed intervals. DSPS is often seen in patients who experience head trauma or serious illness. Perhaps the body s natural healing processes subsume normal circadian rhythm during these times and render the biological clock unable to reset or resynchronize itself. Causes DSPS is often thought to be sustained by lifestyle rather than to shape it. Many physicians observe people in careers that allow alternative sleep-wake patterns, like work-athome jobs, computer programming, or artistic careers. The lifestyle associated with these types of jobs may feed the disorder. However, DSPS seems counterproductive to other, more predictable work schedules. Symptoms Delayed sleep phase syndrome is characterized predominantly by the inability to fall asleep before early morning (i.e., 12 midnight to 3 a.m.). Subsequently, people with DSPS have great difficulty waking in the morning, leading to the principal social complication. Unlike insomnia, DSPS does not repeatedly keep a person from sleeping. Insomniacs wish to sleep, but cannot do so, whether at a desired time or not. Someone with DSPS can fall asleep whenever the body signals it is time and sleepiness does not usually occur before this delayed period. Instead of interfering with daily activities, as insomnia would, DSPS may actually suit their lifestyle. However, in cases where DSPS severely imposes upon a person s schedule, subsequent stress and anxiety may lead to sleep onset insomnia. That is, if a person realizes it is important to sleep at a certain time, he or she may attempt to sleep before the body s sleep phase occurs. Thus, patients who do not receive treatment may experience advanced symptoms, like excessive daytime sleepiness, fatigue, disturbed eating habits, and general maladjustment to mainstream schedules. Patients with DSPS sometimes have difficulty keeping jobs that require them to perform early in the morning. Driving or operating equipment in the early morning can be dangerous. A person with delayed sleep phase syndrome may select a night job or a second shift job. And, unfortunately, some people with DSPS become dependent on alcohol or sedatives in an attempt to induce sleep. But substance abuse only complicates the disorder and the body s efforts to reconcile sleep-wake habits. Studies of high school students have also shown correlations between poor performance (lower GPAs) and less sleep. Students who get more sleep have been known to get better grades, to feel more rested during the school day, and to require less naptime. The onset of high-school-related stress and rapidly changing social habits may ignite a disturbance in sleep, resulting in DSPS. In other cases, people with DSPS are alert, ready, responsive, creative, productive, quick, athletic, etc., just at different times of the day and night. If sleep phase is accommodated by lifestyle, symptoms will not occur.
3 Testing There is no diagnostic test for DSPS. Its diagnosis is based on the patient s history of sleep, i.e. inability to fall asleep until the middle of the night and difficulty waking up in the morning. Although DSPS is a physiological disturbance, there is no physical evidence to confirm it. Physicians often seek to exclude behavioral or lifestyle preferences as causes for DSPS. In fact, DSPS can be an involuntary condition. One needs to also exclude other causes of sleep onset insomnia and related disorders, such as inadequate sleep hygiene or psychophysiologic insomnia. Other sleep disorders that cause excessive daytime sleepiness, such as obstructive sleep apnea or periodic limb movement disorder, may superficially resemble delayed sleep phase syndrome, with a difficult wake period. Generally, if a person does not experience delayed sleep phase more than a few times a week for a month, DSPS is not present. There are several diagnostic measures that can be used at home to assess sleep condition. Sleep Diary Patients sometimes maintain a sleep diary, which can be very beneficial to the diagnosis of delayed sleep phase syndrome. A sleep diary allows one to document a late sleep onset time and a delayed wake up time. The typical diary includes bedtime, estimated sleep latency (how long it takes to fall asleep), the number of awakenings during the night, the length of these awakenings, the number of times one gets out of bed, total sleep time, how one feels upon waking in the morning, and the number and quality of daytime naps. The diary is normally kept for a minimum of two weeks. It allows the patient and the physician to review sleep patterns, which may be consistent or inconsistent with DSPS. Actigraphy Actigraphy is another activity that is used in the diagnosis of DSPS. An inconspicuous monitoring device, resembling a wristwatch, is usually worn on the wrist. In addition to monitoring circadian rhythm, pain response, and response to medication, these devices measure motion that is consistent with sleep and wake and record it throughout the night. The data can then be retrieved from the device and analyzed for sleep-wake time relationships or indications of DSPS. Treatment All forms of treating DSPS are aimed at rephasing the patient s circadian rhythm and sleep pattern. The ultimate goal is to synchronize the patient with societal routine and the subsequent demands that lifestyle, employment, or school place on him or her. The patient wants to wake up at a given time feeling refreshed and functional. Since the ability to wake up and function normally is dependent on an adequate amount of sleep, the patient adjusts to an earlier bedtime. Sleep therapy of this kind usually combines proper sleep hygiene practice and external stimulus therapy. Benzodiazepines are sometimes used to modify sleep-wake patterns, but their efficacy is not proven for DSPS. The two main external therapeutic methods used to advance the patient s sleep phase are bright light therapy and chronotherapy. When combined, these therapies are known to produce significant results. Bright Light Therapy Early morning exposure to bright light tends to advance sleep onset at night and, ostensibly, to lead to an early wake time. Delayed sleep phase syndrome patients are, therefore, consistently exposed to bright light early in the morning. Because it can be difficult to get bright sunlight exposure early in the morning, especially in winter, artificial light is often used.
4 Patients often receive bright light therapy at home, with the use of a light box. A light box emits a standard dosage of 5,000 to 10,000 lux (a measure of illumination) of white light. The patient sits in front of the light at a specified distance for approximately 30 minutes to one hour after waking in the morning. The dosage and timing of the light varies among patients. For instance, light given at 8 a.m. may have no effect on a certain patient, but exposing this patient to light at 7 a.m. may advance sleep onset by one to three hours. Furthermore, one hour of bright light exposure may actually cause insomnia for a patient with DSPS, while only 15 minutes may satisfactorily advance sleep onset. Generally, the earlier in the day that bright light therapy can be administered, the better. Most physicians recommend the window between 6 a.m. and 8 a.m. Therapy that is administered during these times will probably be more effective in influencing circadian rhythm and advancing sleep phase. The farther one sits from the light source, the greater its effects are diminished- by as much as 75 percent at twice a distance. Again, the safe, effective environment for therapy differs from patient to patient. An alternative to the light box is a light visor, which is sold commercially by medical specialists. Patients may feel confined by sitting with the light box every morning. In cases where early morning sunlight is plentiful, a patient may find that he or she feels better walking outside while wearing the visor. During exposure to light therapy, it is important to take the same precautions that one would take with exposure to normal sun and bright light. A therapeutic light source should have a UV (ultraviolet) filter. Also, because bright light therapy can adversely affect vision in certain cases, a physician should assess conditions and diseases of the eye prior to treatment. Some patients feel hyperactive after routine bright light therapy and others experience headache. These factors define individual exposure levels and frequencies. Finally, patients with DSPS should avoid bright light exposure in the early evening because early evening light exposure tends to delay sleep onset. Chronotherapy Chronotherapy was the original treatment for DSPS, first suggested by C.A. Czeisler in Chronotherapy is used to manipulate the sleep-wake cycle in an attempt to change the patient s underlying circadian rhythm. Specifically, the patient progressively goes to bed and wakes three hours later than the night before, until he or she moves around the clock and can consistently sleep earlier. A hypothetical sleep schedule may look like this: Night Bedtime Wake Time 1st night 4 a.m. 12 p.m. 2nd night 7 a.m. 3 p.m. 3rd night 10 a.m. 6 p.m. 4th light 1 p.m. 9 p.m. 5th night 4 p.m. 12 p.m. 6th night 7 p.m. 3 a.m. 7th night 10 p.m. 6 a.m. Once consistent sleep-wake habits are established, they may be adjusted slightly. Patients typically strive for a sleep time between 10 p.m. and 11 p.m. and a wake time of 7 a.m. It is usually easier to stay up longer than it is to go to sleep earlier. Likewise, delayed chronotherapy of this type takes advantage of the natural progressive shift in circadian rhythm. It is highly effective for delayed sleep phase syndrome, but does not repair 100 percent of DSPS cases. Some patients cannot reset their phase cycles with this technique, and a few experience insomnia. It is very important to maintain a regular, scheduled wake-up time following therapy. In fact, some clinicians believe that straying at all from a schedule will nullify the effects of chronotherapy.
5 Also, chronotherapy can interfere with prescriptions and indications associated with other disorders. For example, chronotherapy is not advised for patients who take insulin or who have immune system disorders. Patients should consult a physician experienced in treating sleep disorders, who will know how DSPS treatment combines with other treatments. Sleep Hygiene Although both bright light therapy and chronotherapy are optional treatments that may or may not influence DSPS, beneficial sleep hygiene is essential to recovery from DSPS. Important sleep hygiene habits include exercising in the early part of the day as opposed to the evening, making slight variations in sleep and wake times, practicing stress reduction techniques, and avoiding caffeine, alcohol, and tobacco. Different strategies work for different patients; some adopt or discard a habit cold turkey, while others change their behavior slowly. Because sleep is a delicate environment for all DSPS patients, patient and physician must custom tailor sleep therapy techniques during treatment. Actually, people often outgrow DSPS naturally, though this may take a few months to a few years. Again, this suggests that DSPS is brought on by lifestyle as often as it may cause it. Melatonin Melatonin is a controversial treatment whose recommendation is currently limited. Like all new treatments, there is simply not enough evidence to speak for or against the success rate for melatonin treatment. It does, however, reduce the severity of jet lag for some travelers, which suggests that it assists in the manipulation of circadian rhythm. Melatonin, which is also associated with diet, is a hormone secreted by the pineal gland in the brain. This secretion occurs only during dark, especially when the body prepares for sleep; it is suppressed by exposure to light. Again, it seems to be involved in the onset of sleep and the maintenance of the biological clock. It has been synthesized for medicinal and therapeutic use, and is usually taken 30 minutes before bedtime. Indeed, some studies have shown melatonin to advance sleep phase in patients with DSPS. There is much concern among the sleep medicine community that the melatonin currently available for purchase is not standardized. The exact dosage of melatonin required to treat DSPS, its efficacy, and its adverse effects have not been studied in any great detail and currently cannot be recommended for therapy. Some people feel sluggish or achy after taking melatonin. Furthermore, it may complicate pregnancy, nursing, cardiovascular conditions, and depression. Sleeping pills are often misclassified with melatonin, because both are taken orally. Sleeping pills, however, are not very effective in inducing sleep in people with DSPS and are not indicated for continual use. At best, generalized synthetic sleep aids provide only temporary relief from sleep difficulty. They do not address the underlying causes of sleep disorder. Vitamin B12 Currently, vitamin B12 is treated like a wonder worker for all types of conditions and disorders, from sleep disorders to depression. And, certainly, it is a necessary component of proper nutrition and overall bodily function. People deficient in B12 usually compensate by swallowing it in pill form, although it is often prescribed as an injection in cases of severe deficiency. It has improved sleep for some DSPS patients by quickening sleep onset and seemingly regulating bedtime. However, its precise function in sleep regulation is not fully understood. Therefore, it is not considered a particularly influential treatment and is not prescribed widely. Depression Delayed sleep phase syndrome has been linked to psychiatric disorders, specifically recurrent mood disorders and certain types of time- or event-specific depression, like seasonal
6 affective disorder (SAD). Like other complications peripheral to DSPS, depression is thought to cause, as well as be caused by, the disorder. Sleep disturbance is commonly assumed to be present in most cases of depression. It is estimated that 90 percent of depressed patients experience some form of sleep disorder. And improved sleep among patients with psychiatric disorder indicates to both patients and physicians that recovery is imminent. Rapid eye movement (REM) sleep quality and duration is thought to affect psychiatric depression. And, at the least, REM sleep onset and REM-related wakefulness patterns in cases of delayed-advanced sleep phase resemble those associated with depression. This basic premise among researchers has led them to more carefully observe the role that circadian rhythms play in depression, which, in turn, has given way to the REM Phase Advance Hypothesis (Wever 1979). In summary, researchers hypothesize that there are two major circadian processes at work in sleep-mood function that regulate (1) REM sleep and temperature and (2) sleep-wake patterns. The REM process is phase-advanced relative to the process governing sleep onset. A desynchronized shift might cause REM abnormalities characteristic of depression and sleep disorders. However, this assumption is qualified by the fact that DSPS and other circadian disorders are treated successfully by the purposeful shift of sleep-wake patterns and, ultimately, by circadian rhythm change. It stands to reason that methodical change in sleep-wake routine affects, at least temporarily, rhythmic patterns. So, it seems that the delicate balance between normal rhythm and proper function is as adaptable to change as it is vulnerable. Rapid eye movement sleep manipulation produces effects similar to those caused by antidepressant medications, like tricyclics. These treatments allow patients to function better in daily routine for longer periods of time. Unfortunately, the research results are still inconclusive. Non-24-Hour Persistent Disturbance Although, its exact incidence and prevalence are not known, non-24-hour sleep-wake syndrome is a related non-transient sleep disorder that affects fewer people than does DSPS. This condition results from a person inadvertently delaying bedtime and then, subsequently, attempting sleep at a conventional time. The underlying cause of the syndrome is, again, circadian rhythm disruption. The patient repetitively delays sleep, influences rhythm, and then surprises circadian patterns with a sudden re-adherence to conventional sleep indicators. Disruption stems from the inability to phase-compensate for each day that bedtime has been delayed. In the case of DSPS, patients typically train themselves, gradually, to respond to external indicators of sleep-wake time. With non-24-hour sleep-wake syndrome, the patient essentially hosts a free-for-all of stimuli and dependent circadian rhythm, in which the once predictable coupling of these two sleep agents becomes erratic and disruptive. Often, phase advance techniques are used to treat non-24-hour sleep-wake syndrome, until conventional bedtime is consistent.