Abstract

Delayed Sleep Phase Disorder (DSPD) is characterized as an abnormally delayed sleep period. The currently assumed aetiology is simply a phase-delay in individuals’ biological body clocks. However, DSPD cases treated to produce a corrective phase advance are very prone to relapse. It has been suggested that this may be due to an abnormally long period length (time taken to complete one cycle of the rhythm). Circadian period lengths of endogenous core body temperature and salivary melatonin were measured to investigate this premise. Following rigorous screening procedures, nine healthy controls and nine persons with DSPD were selected for a 80-h protocol consisting of an ultradian modified constant routine in order to measure the endogenous circadian rhythms. Participants resided in a dimly lit (<15 lux), time-free environment in semi-supine position. They followed “1-h days” which involved 20-min sleep opportunities alternating with 40-min of enforced wakefulness. Core body temperature and salivary melatonin were recorded hourly and best fit temperature curves and dim light melatonin onsets were determined to derive circadian period length measures from the 80-h of data. Although core temperature period lengths showed a trend in DSPD to be longer than controls, this trend was not statistically significant in this study. However, the melatonin period length was on average 23.4 min longer ( p = .010) in the DSPD group ( M = 24.64 h, SD = 0.35) than the healthy control sleepers ( M = 24.25 h, SD = 0.21). Together these findings suggest that abnormally long biological circadian rhythms contribute to delayed sleeping patterns of individuals with DSPD. These outcomes may explain patients’ persistent tendency to delay and relapse post-treatment. Therefore, continuing treatment with morning bright light stimulation and early evening low dose melatonin administration are recommended to treat DSPD and prevent relapse. Australian Research Council grant # DP120101401.

Full Text
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