Prolonged interval from body temperature nadir to sleep offset in patients with delayed sleep phase syndrome
Department of Psychophysiology, National Institute of Mental Health, National Center for Neurology and Psychiatry, Ichikawa, Japan. Sleep
(Impact Factor: 4.59).
In order to clarify the relationship between sleep-wake and core body temperature rhythms in the delayed sleep phase syndrome (DSPS), we conducted simultaneous monitoring of these rhythms in seven patients with DSPS and nine healthy control subjects for 6-10 days during their conventional sleep-wake schedules. The sleep onset and offset times were determined visually from sleep logs, and the temperature data were fitted to 24-hour cosinor curves by the least squares method. The sleep onset and offset times and temperature nadir were delayed significantly in patients with DSPS compared with the control subjects (p = 0.01, 0.003 and 0.02, respectively). We also found that sleep length and the temperature nadir to sleep offset interval were significantly longer in the DSPS than the control group (p = 0.03 and 0.02, respectively). The latter finding suggests that 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.
Available from: Kelly Glazer Baron
- "Mis - alignment between the biological timing and sleep / wake timing has been proposed as one of the mech - anisms that causes the sleep / wake dysfunction in DSPD . Many studies have documented that sleep / wake timing and circadian markers are delayed in this population relative to healthy controls ( Chang et al . , 2009 ; Ozaki et al . , 1996 ; Shibui et al . , 1999 ; Uchiyama et al . , 2000a"
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ABSTRACT: Circadian rhythms are near 24-h patterns of physiology and behaviour that are present independent of external cues including hormones, body temperature, mood, and sleep propensity. The term ‘circadian misalignment’ describes a variety of circumstances, such as inappropriately timed sleep and wake, misalignment of sleep/wake with feeding rhythms, or misaligned central and peripheral rhythms. The predominance of early research focused on misalignment of sleep to the biological night. However, discovery of clock genes and the presence of peripheral circadian oscillators have expanded the definitions of misalignment. Experimental studies conducted in animal models and humans have provided evidence of potential mechanisms that link misalignment to negative outcomes. These include dysregulation of feeding behaviours, changes in appetite stimulating hormones, glucose metabolism and mood. This review has two foci: (1) to describe how circadian misalignment has been defined and evaluated in laboratory and field experiments, and (2) to describe evidence linking different types of circadian misalignment to increased risk for physical (cardiovascular disease, diabetes, obesity, cancer) and psychiatric (depression, bipolar, schizophrenia, attention deficit) disorders. This review will describe the role of circadian misalignment as a risk factor for disease in the general population and in clinical populations, including circadian rhythm sleep disorders and psychiatric disorders.
- "Many studies have shown delayed markers of circadian rhythm, such as dim light melatonin onset (DLMO) (Chang et al., 2009;Shibui et al., 1999;Wyatt et al., 2006) and core body temperature nadir (Chang et al., 2009;Watanabe et al., 2003) in patients with DSPD. The endogenous phase delay may be caused by abnormally long spontaneous circadian periods (Regestein and Monk, 1995) or by a reduced ability to adequately phase advance (Czeisler et al., 1981;Ozaki et al., 1996). However, endogenous circadian rhythm disturbances may not be the sole cause underlying the disorder. "
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ABSTRACT: Delayed sleep phase disorder is characterized by a delay in the timing of the major sleep period relative to conventional norms. The sleep period itself has traditionally been described as normal. Nevertheless, it is possible that sleep regulatory mechanism disturbances associated with the disorder may affect sleep duration and/or architecture. Polysomnographic data that may shed light on the issue are scarce. Hence, the aim of this study was to examine polysomnographic measures of sleep in adolescents and young adults with delayed sleep phase disorder, and to compare findings to that of healthy controls. A second aim was to estimate dim light melatonin onset as a marker of circadian rhythm and to investigate the phase angle relationship (time interval) between dim light melatonin onset and the sleep period. Data from 54 adolescents and young adults were analysed, 35 diagnosed with delayed sleep phase disorder and 19 healthy controls. Results show delayed timing of sleep in participants with delayed sleep phase disorder, but once sleep was initiated no group differences in sleep parameters were observed. Dim light melatonin onset was delayed in participants with delayed sleep phase disorder, but no difference in phase angle was observed between the groups. In conclusion, both sleep and dim light melatonin onset were delayed in participants with delayed sleep phase disorder. The sleep period appeared to occur at the same circadian phase in both groups, and once sleep was initiated no differences in sleep parameters were observed.
Available from: ncbi.nlm.nih.gov
- "Some believe that the condition represents an extreme manifestation of the delayed circadian preference observed in concert with pubertal development (Carskadon et al., 1997; Carskadon et al., 1993; Jenni et al., 2005). Longer intervals from the core body temperature minimum to sleep offset have been reported among DSPD subjects in comparison to controls, suggesting a contribution from decreased exposure to the phase advance portion of the light phase response curve (PRC) as an etiological factor (Ozaki et al., 1996; Uchiyama et al., 2000; Watanabe et al., 2003). More recent studies (one of which included adolescents (Chang et al., 2009) have not replicated these findings, however (Chang et al., 2009; Mundey et al., 2005; Wyatt et al., 2006). "
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ABSTRACT: The objective of this study was to compare light exposure and sleep parameters between adolescents with delayed sleep phase disorder (DSPD; n=16, 15.3±1.8 yrs) and unaffected controls (n=22, 13.7±2.4 yrs) using a prospective cohort design. Participants wore wrist actigraphs with photosensors for 14 days. Mean hourly lux levels from 20:00 to 05:00 h and 05:00 to 14:00 h were examined, in addition to the 9-h intervals prior to sleep onset and after sleep offset. Sleep parameters were compared separately, and were also included as covariates within models that analyzed associations with specified light intervals. Additional covariates included group and school night status. Adolescent delayed sleep phase subjects received more evening (p< .02, 22:00-02:00 h) and less morning (p .05, 08:00-09:00 h and 10:00-12:00 h) light than controls, but had less pre-sleep exposure with adjustments for the time of sleep onset (p< .03, 5-7 h prior to onset hour). No differences were identified with respect to the sleep offset interval. Increased total sleep time and later sleep offset times were associated with decreased evening (p< .001 and p= .02, respectively) and morning (p= .01 and p< .001, respectively) light exposure, and later sleep onset times were associated with increased evening exposure (p< .001). Increased total sleep time also correlated with increased exposure during the 9 h before sleep onset (p= .01), and a later sleep onset time corresponded with decreased light exposure during the same interval (p< .001). Outcomes persisted regardless of school night status. In conclusion, light exposure interpretation requires adjustments for sleep timing among adolescents with DSPD. Pre- and post-sleep light exposures do not appear to contribute directly to phase delays. Sensitivity to morning light may be reduced among adolescents with DSPD.
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