Biological and Behavioural Basis of Delayed Sleep-Wake Phase Disorder

Author: Gorica Micic

Micic, Gorica, 2016 Biological and Behavioural Basis of Delayed Sleep-Wake Phase Disorder, Flinders University, School of Psychology

This electronic version is made publicly available by Flinders University in accordance with its open access policy for student theses. Copyright in this thesis remains with the author. This thesis may incorporate third party material which has been used by the author pursuant to Fair Dealing exceptions. If you are the owner of any included third party copyright material and/or you believe that any material has been made available without permission of the copyright owner please contact with the details.


Delayed Sleep-Wake Phase Disorder (DSWPD) is a debilitating sleep disturbance, associated with significant morbidity and reduction in patients’ quality of life. It is the most common circadian rhythm sleep disorder and particularly prevalent in adolescents and insomnia patients with prevalence ranges of 7-16% (American Academy Of Sleep Medicine; AASM, 2014, Gradisar et al., 2011; Lack et al., 2009). DSWPD arises when patients’ sleep-wake behaviour is timed significantly later relative to their necessary or conventional sleep times. Due to recurrent complaints of difficulty falling asleep and waking up at appropriate times, currently assumed aetiology for DSWPD suggests a chronic delay of the circadian system (AASM, 2014). The use of morning bright light therapy and evening exogenous melatonin administration have been shown to advance circadian rhythms and have the potential to treat the disorder (Cajochen et al., 2005; Dawson, Lack, & Morris, 1993; Lack et al., 2009). However, limited empirical literature is available regarding their efficacy in treatment of DSWPD (Barlett, Biggs & Armstrong, 2013; Auger et al., 2015) with patient relapse reportedly common in clinical settings (Alvarez, Dahlitz, Vignau, & Parkes, 1992; Saxvig et al., 2014; Wilhlemsen-Langeland et al., 2013a). Poor treatment outcomes have stimulated speculation that the disorder may be caused by other hypothesized aetiologies, such as abnormally longer circadian period oscillations or tau (i.e., the time taken to complete one circadian cycle). Using an 80-hour “forced-desynchrony” protocol, the main aim of the present study was to investigate the proposed explanation that DSWPD is driven by a longer tau. This protocol involves a series of 1-hour long ‘days’ whereby participants are given 20-minute sleep opportunities alternating with 40-minutes of enforced wakefulness. Twenty-six patients with DSWPD (N = 17 male, mean age = 21.9 ± 5.0 years) according to diagnostic criteria (AASM, 2014) and 18 healthy, control sleepers (N = 10 male, mean age = 23.7 ± 5.1 years) were selected from a community-based sample. An opportune sample of 4 patients did not meet DSWPD criteria, rather met Non-24-Hour Sleep-Wake Rhythm Disorder (N24SWD) diagnosis and were also included in the study (N = 3 male, mean age = 25.75 ± 4.99 years). Dim Light Melatonin Onset (DLMO) and core body temperature were measured across the 80-hour protocol to identify the timing of biological circadian rhythms and the circadian period length. Furthermore, behavioural rhythms were monitored via subjective sleepiness ratings, sleep latency measures and the psychomotor vigilance task. As a secondary aim, relationships between personality profiles using the Big Five Factors (NEO-Personality Inventory-Revised), circadian rhythms and sleep disturbances were examined to further understand if personality types as associated with circadian misalignment. Consistent with hypotheses, circadian rhythms were generally longer for DSWPD patients relative to controls. Specifically, measures of melatonin and core temperature depicted significantly longer taus in DSWPD patients relative to controls. Melatonin and core temperature circadian rhythm period lengths were longer still in N24SWD patients compared to DSWPD and controls. Further scrutiny of biological (i.e., melatonin, core body temperature) and behavioural rhythms (i.e., subjective/objective sleepiness, vigilance) indicated significantly greater phase angle differences between DSWPD patients’ sleep propensity and core temperature circadian rhythms compared to controls. Additionally, DSWPD patients had reduced rates of melatonin secretion during the first half of their nocturnal period implying that there may be a deficiency of early melatonin production in the melatoin profile of DSWPD patients. Personality profiles were also different between groups largely consistent with recent reports (Wilhlemsen-Langeland et al., 2013b). Particularly, patients who indicated lower scores on the Conscientiousness dimension were of greater DSWPD severity. These findings help explain the persistent tendency of DSWPD to delay, along with their frequent failure to respond to treatment and high relapse rate. They suggest that the disorder is not homogenous and that various approaches to therapy are necessary to target different causes of sleep delays.

Keywords: delayed sleep phase; aetiology; treatment; circadian rhythm sleep disorders; phase markers; homeostatic sleep drive; circadian rhythm period; tau; light; diagnosis; adolescence; ultradian constant routine; free-running; sleepiness; personality
Subject: Psychology thesis

Thesis type: Doctor of Philosophy
Completed: 2016
School: School of Psychology
Supervisor: Prof Leon Lack