Altered phase relation between sleep timing and core body temperature rhythm in delayed sleep phase syndrome and non-24-hour sleep–wake syndrome in humans

  title={Altered phase relation between sleep timing and core body temperature rhythm in delayed sleep phase syndrome and non-24-hour sleep–wake syndrome in humans},
  author={Makoto Uchiyama and Masako Okawa and Kayo Shibui and Keiko Kim and Hirokuni Tagaya and Yoshihisa Kudo and Yuichi Kamei and Tatsuro Hayakawa and Jujiro Urata and Kiyohisa Takahashi},
  journal={Neuroscience Letters},

Sleep Timing and Circadian Phase in Delayed Sleep Phase Syndrome

The results suggest that the symptoms of insomnia and excessive daytime sleepiness in DSPS patients living under entrained real-life conditions cannot be explained by an alteration in the phase relationship between sleep-wake patterns and other physiological circadian rhythms.

Circadian Melatonin and Temperature Taus in Delayed Sleep-wake Phase Disorder and Non-24-hour Sleep-wake Rhythm Disorder Patients

Investigating the period lengths of the endogenous core body temperature rhythm and melatonin rhythm in delayed sleep-wake phase disorder patients (DSWPD) and N24SWD patients compared with normally entrained individuals indicated that longer taus of circadian rhythms may contribute to the DSWPD patients’ persistent tendency to delay, their frequent failure to respond to treatment, and their relapse following treatment.

Circadian tau differences and rhythm associations in Delayed Sleep-Wake Phase Disorder and sighted Non-24-Hour Sleep-Wake Rhythm Disorder.

People with DSWPD and N24SWD exhibit significantly longer biological circadian rhythm period lengths compared to controls suggesting abnormal phase relationship between biological rhythms and behavioral sleep period or potentially conditioned sleep onset insomnia.

Larger phase angle between sleep propensity and melatonin rhythms in sighted humans with non-24-hour sleep-wake syndrome.

It was postulated that Non-24 sufferers' delayed SP onset relative to the circadian pacemaker may accelerate the light-induced phase-delay, leading to sleep-wake cycle that is longer than 24 hours.

Melatonin, cortisol and thyroid-stimulating hormone rhythms are delayed in patients with delayed sleep phase syndrome

It is postulate that sleep-phase delay in patients with DSPS is a consequence of the phase delay of the circadian pacemaker, therefore, suggesting that phase delay in the circadian clock is responsible for this disorder.

Integration of human sleep-wake regulation and circadian rhythmicity.

Findings on the physiological and molecular-genetic correlates of circadian sleep disorders suggest that the timing of the sleep-wake cycle and circadian rhythms is closely integrated but is, in part, regulated differentially.

Sleep-wake profiles and circadian rhythms of core temperature and melatonin in young people with affective disorders.

Can the circadian phase be estimated from self-reported sleep timing in patients with Delayed Sleep Wake Phase Disorder to guide timing of chronobiologic treatment?

It is suggested that self-reported sleep timing may be useful clinically to predict a therapeutically relevant circadian phase in DSWPD.



Prolonged interval from body temperature nadir to sleep offset in patients with delayed sleep phase syndrome.

The inability of the patients with DSPS to normally phase-advance their circadian rhythm may be a consequence of masking of the advance portion of their phase-response curve by the last hours of their prolonged sleep episodes.

Melatonin Rhythms in 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 delayed sleep phase syndrome.

Poor compensatory function for sleep loss as a pathogenic factor in patients with delayed sleep phase syndrome.

It is suggested that poor compensatory function for sleep loss predisposes DSPS patients to failure to reset their sleep phase and provides implications for understanding not only the pathophysiology of DSPS but also the biological basis for why some people can change their sleep schedule easily according to personal or social demands while others cannot.

Delayed phase jumps of sleep onset in a patient with non-24-hour sleep-wake syndrome.

Results suggest that DP jumps in the patient may occur due to illumination of the delay portion of the phase-response curve.

Chronotherapy: resetting the circadian clocks of patients with delayed sleep phase insomnia.

A brief drug-free rescheduling treatment for Delayed Sleep Phase insomnia, a syndrome characterized by sleep-onset insomnia with difficulty in morning awakening, which was designed to reset patients' biological clocks by the phase delay route.

The delayed sleep phase syndrome: clinical and investigative findings in 14 subjects.

The syndrome causes severe disruption to education, work and family life, and different patterns of sleep phase delay seen in the syndrome include stable, progressive, irregular and non-24 hour sleep-wake cycles.

Long-term ambulatory temperature monitoring in a subject with a hypernychthemeral sleep--wake cycle disturbance.

It is raised the possibility that 24 hr was beyond the range of entrainment of the subject's circadian temperature cycle during the study, and it is postulate that his hypernychthemeral cycles were the result of either a primary defect in the mechanism of entraining or "weakened" social zeitgebers due to a personality disorder.

Successful treatment of human non-24-hour sleep-wake syndrome.

A case in which a non-24-h sleep-wake cycle appeared as a late complication of a more fundamental disturbance in the quality of sleep (difficulty falling asleep, frequent awakenings, nonrefreshing sleep) and was treated with thyroxine for borderline hypothyroidism, flurazepam and vitamin B12.

Sleep propensity free-runs with the temperature, melatonin and cortisol rhythms in a totally blind person.

The sleep propensity rhythm (as defined by an ultrashort sleep-wake schedule) free-ran with the melatonin, temperature and cortisol rhythms in a 44-year-old totally blind man even though he maintained a conventional sleep schedule and did not complain of clinically significant insomnia or excessive daytime sleepiness.