Delayed Sleep Phase Syndrome Research Articles

Poor recovery sleep after sleep deprivation in delayed sleep phase syndrome.

To clarify disturbances in sleep regulation in patients with delayed sleep phase syndrome (DSPS), we studied three patients with DSPS and seven healthy controls. Sleep propensity and melatonin rhythms after 24-h sleep deprivation were investigated under dim light condition by using the ultra-short sleep-wake schedule. The sleep propensity curves displayed clear differences between DSPS patients and the controls. During the subjective day when melatonin was not produced, recovery sleep after the sleep deprivation did not occur in DSPS patients, while recovery sleep occurred during the subjective day in controls. This suggests that DSPS may involve problems related to the homeostatic regulation of sleep after sleep deprivation.

Effects of phototherapy in patients with delayed sleep phase syndrome.

Phototherapy was given to six patients with delayed sleep phase syndrome (DSPS). Polysomnography (PSG) and core body temperature were examined before and after phototherapy. Phototherapy was administered to each patient for 5 days, and this treatment not only advanced the delayed sleep phase but also delayed the time of minimum body temperature in all patients. On the PSG, decreases in total sleep time and amounts of stages 2 and REM were observed after phototherapy. These results suggest that phototherapy is effective even in the short term in advancing delays in sleep phase and time of minimum body temperature in DSPS patients.

Classification of the sleeping pattern of normal adults.

A questionnaire concerning their sleep-related lifestyle and mental health was mailed to people aged in their twenties to fifties living in the Fukushima (North East), Tokyo (Central, Metropolitan) and Okayama (West) areas of Japan. We classified the sleeping pattern of 3642 people (1702 men, 1940 women; mean age 41.3+/-10.67) by multivariational analyses (factor analysis and cluster analysis). They were classified into six groups and defined as 'poor sleeper group' (30.0%), 'good sleeper group' (28.3%), 'long sleeper group' (8.2%), 'short sleeper group' (18.5%), 'irregular sleeper group' (11.3%), and 'Delayed Sleep Phase Syndrome group' (3.7%) based on their characteristics of the factor pattern.

Demography of sleep disturbances associated with circadian rhythm disorders in Japan.

To clarify the demography of delayed sleep phase syndrome (DSPS), non-24-h sleep-wake syndrome, and irregular sleep-wake pattern in Japan, a cross-sectional nationwide epidemiological survey was conducted. 1525 adults (age: 15-59 years) were randomly sampled from telephone directories, and they received screening questions over the phone. Persons who were suspected of having the disorders were requested to fill out the second questionnaire, and asked to keep a sleep log for 4 weeks. Diagnoses were made according to the International Classification of Sleep Disorders criteria. As a result, the prevalence of DSPS was estimated to be 0.13%.

Prevalence of Delayed Sleep Phase Syndrome in Adolescents: A School-Based Survey

Prevalence of Delayed Sleep Phase Syndrome in Adolescents: A School-Based Survey

Melatonin rhythms in delayed sleep phase syndrome.

The aim of this study was to compare circadian and sleep characteristics between patients with delayed sleep phase syndrome (DSPS) and healthy controls. The authors studied 8 DSPS patients and 15 normal controls. Serum melatonin concentration was assessed every hour for 24 h under dim light conditions. The sleep phase and the melatonin rhythm in DSPS patients were significantly delayed compared to those in normal controls. Sleep length was significantly greater in DSPS patients compared to that in controls, but the duration of melatonin secretion did not differ between the two groups. The final awakening, relative to melatonin onset, melatonin midpoint, and melatonin offset, was significantly longer in DSPS patients than in controls. By contrast, the timing of sleep onset relative to melatonin rhythm did not differ between the two groups. The authors found a significant positive correlation between sleep phase markers and melatonin phase markers in DSPS. They postulate that a delayed circadian pacemaker may be responsible for delayed sleep phase syndrome. The alteration of phase angle between melatonin rhythm and sleep phase suggested that not only the delay of the circadian clock but also a functional disturbance of the sleep-wake mechanism underlies DSPS.

Use of melatonin in the treatment of phase shift and sleep disorders.

When administered to humans the pineal hormone melatonin can phase shift a number of circadian rhythms. This property has prompted the investigation of exogenous melatonin in sleep disorders known to have an underlying chronophysiological basis (i.e. circadian rhythm sleep disorders). Both in field and simulated studies of jet lag and shift work suitably timed melatonin improved sleep and, in some cases, hastened readaptation of the circadian rhythms following the phase shift. Melatonin treatment has also been evaluated in the circadian sleep disorders: delayed sleep phase syndrome (DSPS) and non-24-hour sleep wake disorder. Compared with placebo, melatonin advanced the sleep period in subjects with DSPS. Melatonin also improved a number of sleep parameters in blind subjects suffering from non-24-hour sleep wake disorder.

The Use of Melatonin for the Treatment of Insomnia

The pineal product melatonin is involved in the regulation of the sleep/wake cycle in humans. In blind individuals and in people travelling through time zones, melatonin rhythms are sometimes unsynchronized with the diel cycle, and nocturnal sleep may be disturbed. Low or distorted melatonin rhythms have repeatedly been reported in middle aged and elderly insomniacs. Melatonin administration effectively synchronized the sleep wake cycle in blind individuals and in subjects suffering from jet lag and advanced sleep onset in subjects suffering from delayed sleep phase syndrome. In elderly insomniacs, melatonin replacement therapy significantly decreased sleep latency, and/or increased sleep efficiency and decreased wake time after sleep onset. In addition, melatonin substitution facilitated benzodiazepine discontinuation in chronic users. These data show an association between melatonin rhythm disturbances and difficulties to promote or maintain sleep at night. Specific melatonin formulations may be useful to treat circadian-rhythm-related sleep disorders and age-related insomnia.

Orcadian Rhythm Sleep Disorders: Toward a More Precise Definition and Diagnosis

The present article presents a survey of the characteristics of our case series of 322 patients suffering from circadian rhythm sleep disorders (CRSDs), a case-control study comparing a group of 50 CRSD patients and 56 age- and gender-matched normal subjects, and a proposal for new guidelines for improving the diagnosis of CRSD. The major findings were that 83.5% of our CRSD patients who seek medical help are of the delayed sleep phase syndrome (DSPS) type; 89.6% report that the onset of CRSD occurred in early childhood or adolescence; CRSD exhibits no gender differences; a familial trait exists in 44% of patients; and learning disorders (19.3%) and personality disorders (22.4%) in the DSPS-type patients are of high prevalence. The findings of this study point to the importance of clinician awareness of the clinical picture of patients presenting with CRSD so that early diagnosis and effective treatment can be achieved to prevent harmful consequences.

Light mask 500 lux treatment for delayed sleep phase syndrome

1. 1. Bright light exposure has been demonstrated as an effective treatment for circadian rhythm sleep disorders. Recent studies suggest that more moderate intensities of light might affect endogenous rhythms. A light mask treatment, using light applied through eyelids during sleep, was tested for Delayed Sleep Phase Syndrome. 2. 2. The active light group ( n = 5) received 500 lux light for 3 hours prior to awakening for 12 days. The placebo light group ( n = 5) received 0. 1 lux light with the same timing. Circadian rhythm phase was assessed from core body temperature and urinary 6-sulfatoxymelatonin measurements. The SIGH-SAD-SR mood scale was administered to assess mood. 3. 3. There were slight trends toward a phase advance of the body temperature rhythm and a phase delay of the melatonin rhythm, and both groups reported anti-depressant benefits. However, no statistically significant effects of 500 lux light mask treatment were demonstrated compared with the placebo-light treatment. 4. 4. More extensive studies will be required to clarify the factors of dose-response and phase-response.

Frequency of delayed sleep phase syndrome among hospitalized adolescent psychiatric patients

Previous research seems to indicate that a substantial percentage of patients with delayed sleep phase syndrome (DSPS) also suffer from personality disorders. In the present study, we attempted to ascertain whether, in a population of hospitalized psychiatric patients, we would find a greater frequency of DSPS among patients suffering from personality disorders than among patients suffering from any of the other psychiatric disorders. Sixty-three hospitalized adolescents took part in the study. None of them had any diagnosed medical disorders, and all were being treated with psychiatric drugs. Ten subjects were diagnosed as suffering from DSPS according to a sleep–wake schedule structured interview. As hypothesized, subjects diagnosed as suffering from personality disorders had a significantly higher probability of also suffering from DSPS. Additional findings were that patients with DSPS were more likely to have received an Axis II diagnosis only, and were more likely to be diagnosed as suffering from a distinct group of disorders characterized by affective lability. The latter finding may be due to the sleepiness that accompanies DSPS. The findings of the present study suggest that there may be an interrelationship between DSPS and personality disorders, and may lend some support to the hypothesis that inborn peculiarities in the sleep–wake rhythm lead to the social and functional difficulties characteristic of personality disorders.

Clinical features of circadian rhythm sleep disorders in outpatients

The clinical data of 86 cases of primary circadian rhythm sleep disorder (primary CRSD) were retrospectively examined and compared to 40 cases of secondary circadian rhythm sleep disorder (secondary CRSD), who had presented with some kind of psychiatric or medical disorder, and had exhibited sleep-wake rhythm disorders that were judged to be secondary CRSD based on sleep logs. The comparison of cases found that: (i) the mean age at first presentation to the clinic was significantly younger for primary CRSD compared to secondary CRSD; (ii) more secondary CRSD cases were unemployed than were Primary CRSD cases; (iii) more cases in the secondary CRSD group had a clear trigger for sleep-wake rhythm disorder onset than cases in the primary CRSD group; and (iv) the types of sleep-wake rhythm disorders in the primary CRSD group consisted of delayed sleep phase syndrome (DSPS), 72 (83.7%), non-24 pattern, 11 (12.8%), and irregular, 3 (3.5%). In the secondary CRSD group there were 25 (62.5%) cases of DSPS pattern, 1 (2.5%) of non-24 pattern and 14 (35.0%) with irregular pattern. The 56 (65.1%) cases with primary CRSD showed good response to vitamin B12 and bright light therapy; however, 28 (70.0%) cases with secondary CRSD did not respond to such therapies.

Clinical characteristics of circadian rhythm sleep disorders.

From our practice at the sleep disorders clinic in Kohnodai Hospital, National Center of Neurology and Psychiatry (NCNP), we report the clinical characteristics of circadian sleep-wake rhythm disorders. Nearly 90% of circadian rhythm sleep disorders were diagnosed as delayed sleep phase syndrome (DSPS) or as non-24 sleep-wake syndrome (non-24). While DSPS was equally common in males and females, non-24 was more frequently seen in men. It was of psychiatric interest that a considerable number of patients had depressive states in the course of their circadian rhythm sleep disorders. Difficulty in adapting to social life was more severe in patients with non-24 than in those with DSPS.

Melatonin treatment for circadian rhythm sleep disorders.

We administered 1-3 mg melatonin to 11 patients (eight men, three women, aged 16-46 years) with circadian rhythm sleep disorders; nine with delayed sleep phase syndrome and two with non-24-hour sleep-wake syndrome. Sleep logs were recorded throughout the study periods and actigraph and rectal temperature were monitored during treatment periods. Melatonin was administered 1-2 h before the desirable bedtime for expected phase-shifting, or 0.5-1 h before habitual bedtime for gradual advance expecting an hypnotic effect of the melatonin. Melatonin treatments were successful in 6/11 patients. Timing and dose of melatonin administration, together with its pharmacological properties for circadian rhythm sleep disorders, should be further studied.

Evaluating the Role of Melatonin in the Long-Term Treatment of Delayed Sleep Phase Syndrome (DSPS)

Delayed sleep phase syndrome (DSPS) involves a mismatch between the usual daily schedule required by the individual's environment and his or her circadian sleep-wake pattern. Patients suffering from DSPS are treated with chronotherapy, light therapy, or melatonin administration. While chro-notherapy and light therapy are demanding and difficult treatments that usually lead to compliance problems, melatonin administration is a relatively simple and easy treatment option. Previous studies carried out on relatively small samples of DSPS patients have shown that melatonin has a sleep-promoting and entraining action when taken in the evening. The present study, which accompanied routine treatment in our sleep clinic, examined the efficiency of melatonin treatment in a relatively large population of DSPS subjects by means of subjective reports. The 61 subjects, 37 males and 24 females, were diagnosed with DSPS by means of clinical assessment and actigraphy at our sleep clinic. Their mean pretreatment falling asleep and waking times were 03: 09 (SD = 86.22 minutes) and 11: 31 (SD = 98.58 minutes), respectively. They were treated with a 6-week course of 5 mg of oral melatonin taken daily at 22: 00. A survey questionnaire was sent to the home of each subject 12–18 months after the end of the treatment; the survey investigated the efficiency of the melatonin treatment and its possible side effects. Of the patients, 96.7% reported that the melatonin treatment was helpful, with almost no side effects. Of these, 91.5% reported a relapse to their pretreatment sleeping patterns within 1 year of the end of treatment. Only 28.8% reported that the relapse occurred within 1 week. The pretreatment falling asleep and waking times of patients in whom the changes were retained for a relatively long period of time were significantly earlier than those of patients whose relapse was immediate (t = 2.18, p <. 05; t = 2.39, p <. 05, respectively), with no difference in sleep duration. The implications of these findings, as well as further research possibilities, are discussed.

Melationin

Currently available as a dietary supplement, the pineal hormone melatonin is portrayed by the media as a formidable weapon against disease and aging. Accordingly, primary health care providers should be cognizant of which of its proposed uses are supported by biomedical research and which are, as yet, unproven. Melatonin entrains circadian rhythms and, thus, can treat jet lag, delayed sleep phase syndrome, and sleep disorders in the blind and in some neurologically impaired children. By virtue of its hypnotic effect, melatonin can mitigate insomnia in the elderly. Reductions in melatonin secretion have been associated with many disorders, including cardiovascular disease, Alzheimer's, diabetes, SIDS, and aging; however, melatonin's role in their etiology and/or pathophysiology is unproven. Preliminary studies suggest a possible adjuvant therapeutic role for melatonin in cancer therapy. Melatonin secretion is reduced by alcohol, caffeine, and some commonly prescribed drugs. Since tolerance, fatigue, and other side effects have been reported, melatonin use on consecutive nights should be avoided and only the lowest effective hypnotic dose should be taken.

Effects of light and chronotherapy on human circadian rhythms in delayed sleep phase syndrome: Cytokines, cortisol, growth hormone, and the sleep-wake cycle

Delayed sleep phase syndrome (DSPS) is a chronobiological disorder with a normal sleep pattern but with chronic sleep-onset insomnia, which develops due to a delayed action of circadian pacemakers resulting in a chronic tendency of endogenous rhythms to drift (Weitzman et al 1981). Therapies that have been tried to adjust the sleepwake cycle include chronotherapy, light treatment, triazolam, melatonin, and vitamin B lz administration (Rosenthal et al 1990, Regestein and Monk 1995). As bright light has been shown to be an effective manipulator of circadian pacemakers, it is widely used as a treatment of chronobiological rhythm disorders. The best way to evaluate treatment success is to investigate the sleep pattern or circadian rhythms. The objective of our study was to look at the phase-shifting effect of morning light treatment and the alteration of the sleep-wake cycle on human cortisol,

DISORDERS OF THE CIRCADIAN SLEEP–WAKE CYCLE

This article reviews several disorders of the circadian sleep-wake cycle, including delayed sleep phase syndrome, advanced sleep phase syndrome, non-24-hour sleep-wake syndrome, irregular sleep-wake pattern, time zone change (jet lag) syndrome, and shift work sleep disorder. For each disorder, the cause, diagnostic work-up, and management are outlined.

Vitamin B 12 affects non-photic entrainment of circadian locomotor activity rhythms in mice

Administration of vitamin B 12 (VB12) has been reported to normalize human sleep-wake rhythm disorders such as non-24-h sleep-wake syndrome (HNS), delayed sleep phase syndrome (DSPS) or insomnia. However, the mechanisms of the action of VB 12 on the rhythm disorders are unknown. In the present study, therefore, effects of VB 12 on circadian rhythms of locomotor activity were examined in mice. In the first experiment, CBA/J mice were maintained under continuous light condition (LL) or blinded, and after free-running rhythms became stable, the mice were intraperitoneally injected with either VB12 or saline at a fixed time every day. In all the mice with τ > 24 h, saline injections resulted in entrainment of circadian rhythms, whereas not all the mice with τ < 24 h entrained to the injection. In contrast to saline injections, VB12 injections did not always induce entrainment and about half of the mice with τ > 24 h free-ran during the injection. In the second experiment, the amount of phase advances of circadian rhythms induced by a single injection of saline at circadian time (CT) 11 under LL was compared between the mice with and without VB 12 silastic tubes. The results showed that the amplitude of phase advances was smaller in the mice with VB 12 than those without V1312. In the third experiment, daily injections of saline were given to the mice with VB12 silastic tubes maintained under LL. In this chronic treatment of VB12 as well, attenuating effects of VB 12 on saline-induced entrainment were observed. These results suggest that VB 12 affects the mechanisms implicated in non-photic entrainment of circadian rhythms in mice.

Inhibition of melatonin secretion onset by low levels of illumination.

Melatonin is a hormone released during darkness under the control of the hypothalamic circadian pacemaker. It has been shown that melatonin is suppressed by light as a function of intensity, with low levels of illumination producing small effects and more intense light greater, but not complete inhibition. The studies which lead to these conclusions administered light subsequent to the secretion pattern being well established. Light as low as 250 lux administered during the normal onset of secretion can reduce melatonin to below detectable levels. The onset of melatonin secretion was delayed for at least an hour during 250 lux exposure and did not rise until termination of light exposure (two hours after control melatonin onset) with higher illumination (500, 1000 and 2500 lux). This tentatively indicates that duration of the inhibition is intensity dependent. It is suggested that the experimental paradigm used in the present study may be a more realistic representation of the effect of normal light exposure (both natural and artificial) on the circadian system, and that findings may be pertinent to the aetiology of certain sleep onset insomnias, which would include delayed sleep phase syndrome (DSPS) and adaptation to shift work.