The etiology of delayed sleep phase disorder

Micic, Gorica; Lovato, Nicole; Gradisar, Michael; Ferguson, Sally A.; Burgess, Helen J.; Lack, Leon

doi:10.1016/j.smrv.2015.06.004

Cited by 68 publications

(46 citation statements)

References 92 publications

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“…A delayed sleep schedule is a frequent complaint in adolescents and young adults (Micic et al., ), and is often associated with a late circadian phase (Micic et al., ; Saxvig et al., ). We found in young adults complaining of a late sleep schedule that a later circadian phase was associated with higher non‐visual sensitivity to light.…”

Section: Introductionmentioning

confidence: 99%

Home versus laboratory assessments of melatonin production and melatonin onset in young adults complaining of a delayed sleep schedule

Moderie

Maren

Paquet

et al. 2019

Journal of Sleep Research

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Recent evidence points toward an association between higher non‐visual sensitivity to light and a later circadian phase in young adults complaining of a delayed sleep schedule. Light exposure in the evening may therefore induce a larger suppression of melatonin production in these individuals, which might: (a) bias home estimates of melatonin onset; and (b) decrease sleep propensity at bedtime. In this study, we compared home and laboratory melatonin onsets and production in sleep‐delayed and control participants, using saliva samples collected in the 3 hr preceding habitual bedtime. The mean light intensity measured during saliva sampling at home was ~10 lux in both groups. Melatonin suppression at home was significant, averaging 31% and 24% in sleep‐delayed and control individuals, respectively. Group difference in melatonin suppression was not significant. Estimates of melatonin onset were on average 27 min later at home than in laboratory conditions, with no group difference. Looking specifically at sleep‐delayed participants, there was no correlation between non‐visual sensitivity to light and home–laboratory differences in melatonin onsets. However, higher light sensitivity was associated with greater melatonin suppression in the hour before habitual bedtime. Greater melatonin suppression before bedtime was also associated with a later circadian phase. These results indicate that the validity of home estimates of melatonin onset is similar in sleep‐delayed and in control individuals. Results also suggest that increased non‐visual sensitivity to light could impact melatonin secretion in sleep‐delayed individuals and contribute to a late bedtime by delaying circadian phase and decreasing sleep propensity.

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Section: Introductionmentioning

confidence: 99%

Home versus laboratory assessments of melatonin production and melatonin onset in young adults complaining of a delayed sleep schedule

Moderie

Maren

Paquet

et al. 2019

Journal of Sleep Research

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“…Another biologic predisposing factor could be a susceptibility of the sleep and circadian system for phase delay owing to a long circadian period, heightened responsiveness to the melatonin-suppressing effect of light in the evening, or slow accumulation and dissipation of homeostatic sleep drive. 40 If the social demand to wake up early in the morning lessens during the postinjury recovery period, the sleep phase follows the circadian signals and shifts to later hours in people with a predisposition for phase delay. This could lead to a vicious cycle in which longer light exposure in the evening and lack of light exposure in the morning further delay the circadian cycle.…”

Section: Openmentioning

confidence: 99%

Circadian rhythm in the assessment of postconcussion insomnia: a cross-sectional observational study

Zalai

Girard

Cusimano

et al. 2020

cmajo

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raumatic brain injury (TBI) is the leading cause of disability among young adults, and the incidence is increasing in Canada. 1,2 Mild TBI (mTBI), including concussion, accounts for the majority (70%-90%) of treated TBI cases and has the largest contribution to injuryrelated disability. 3 Early detection and effective management of medical conditions that hinder recovery could prevent disability and substantially reduce societal costs. In this regard, sleep disruptions are key modifiable targets that magnify the sequelae of mTBI. 4 Insomnia-difficulties falling or staying asleep, or early-morning final awakening-is the most common persistent sleep symptom after mTBI 5,6 and is particularly prevalent following mTBI compared to more severe forms. 4 Moreover, insomnia after concussion worsens fatigue, pain, cognition and mood, and predicts poor overall prognosis for recovery, greater disability and mental disorders. 7-11 Given that disorders of sleep and wakefulness can be treated effectively, treatment holds the promise of improving the management of persistent postconcussive symptoms and hastening recovery from mTBI. Recent reports 4,12,13 emphasize the need for multimodal sleep and circadian assessments; however, these are not common practice, and research remains limited. Standard assessment of insomnia relies on patients' subjective report, and the recommended first-line treatment is cog-nitive behavioural therapy. 14,15 Importantly, however, circadian rhythm sleep-wake disorders (CRSWDs) that may underlie symptoms of insomnia require fundamentally different assessment and treatment (Appendix 1, available at www. cmajopen.ca/content/8/1/E142/suppl/DC1). These disorders arise if there is a disruption of the endogenous circadian system or a misalignment between the internal circadian rhythm and the external environment. The best biologic marker of CRSWDs is abnormal dim-light onset of melatonin production, and the behavioural diagnostic feature is that the sleep phase is markedly delayed, advanced or irregular relative to environmental time and social norms 16 (Appendix 1). Rates and mechanisms of CRSWDs in mTBI are not well characterized, but evidence indicates that brain trauma can disrupt systems that regulate circadian rhythms, such as suprachiasmatic nucleus function, gene expression, neural plasticity,

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“…DSWPD is likely due to a multitude of co-occurring factors, including: (1) a longer endogenous circadian period [3], (2) increased sensitivity or exposure to evening light [4], (3) decreased sensitivity or exposure to morning light [1], (4) reduced homeostatic sleep pressure in the evening [5], (5) comorbid features of an insomnia disorder [6], (6) light exposure associated with forced early awakenings causing phase delays [1], (7) a slower rise in evening melatonin levels [7], and (8) partial sleep deprivation which can reduce phase advances to morning light [8]. All these factors can drive the circadian promotion of sleep to later clock times, thus perpetuating and promoting DSWPD [9]. …”

Section: 0 Introductionmentioning

confidence: 99%

Sleep and circadian variability in people with delayed sleep–wake phase disorder versus healthy controls

et al. 2017

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Objective/Background To compare sleep and circadian variability in adults with delayed sleep-wake phase disorder (DSWPD) to healthy controls. Patients/Methods Forty participants (22 DSWPD, 18 healthy controls) completed a 10-day protocol, consisting of DLMO assessments on two consecutive nights, a five-day study break, followed by two more DLMO assessments. All participants were instructed to sleep within one hour of their self-reported average sleep schedule for the last four days of the study break. We analyzed the participants’ wrist actigraphy data during these four days to examine intraindividual variability in sleep timing, duration and efficiency. We also examined shifts in the DLMO from before and after the study break. Results and Conclusions Under the same conditions, people with DSWPD had significantly more variable wake times and total sleep time than healthy controls (p≤0.015). Intraindividual variability in sleep onset time and sleep efficiency was similar between the two groups (p≥0.30). The DLMO was relatively stable across the study break, with only 11% of controls but 27% of DSWPDs showed more than a one hour shift in the DLMO. Only in the DSWPD sample was greater sleep variability associated with a larger shift in the DLMO (r=0.46, p=0.03). These results suggest that intraindividual variability in sleep can be higher in DSWPD versus healthy controls, and this may impact variability in the DLMO. DSWPD patients with higher intraindividual variability in sleep are more likely to have a shifting DLMO, which could impact sleep symptoms and the optimal timing of light and/or melatonin treatment for DSWPD.

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The etiology of delayed sleep phase disorder

Cited by 68 publications

References 92 publications

Home versus laboratory assessments of melatonin production and melatonin onset in young adults complaining of a delayed sleep schedule

Home versus laboratory assessments of melatonin production and melatonin onset in young adults complaining of a delayed sleep schedule

Circadian rhythm in the assessment of postconcussion insomnia: a cross-sectional observational study

Sleep and circadian variability in people with delayed sleep–wake phase disorder versus healthy controls

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