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

Objective: Delayed sleep phase syndrome (DSPS) is a condition in which the patient is unable to reset or phase-advance his/her sleep timing properly a fter transient sleep delay and consequently shows persistent sleep phase de lay. Prior studies suggested that DSPS is associated with a phase delay in the circadian pacemaker, but there was no evidence to explain the patient's inability to reset sleep phase. Subjects and Methods: We used an ultra-short sleep-wake schedule together w ith simultaneous measurement of dim light melatonin rhythm after 24-hour sl eep deprivation to allow the differential observation of diurnal sleep prop ensity fluctuation both from circadian and homeostatic aspects in 11 patien ts with DSPS (17-37 years; 8 men, 3 women) and 15 healthy controls (19-32 y ears; 8 men,7 women). Setting: NA Patients or Participants: NA Interventions: NA Results: DSPS patients showed less ability to compensate for previous sleep loss during their circadian day and first hours of their circadian nightti me determined by dim light melatonin onset compared with controls, while co ntrols compensated for previous sleep loss at most circadian times. Though shapes of dim light melatonin rhythm did not differ between the groups, pha se angle between melatonin and sleep propensity rhythms was wider in DSPS p atients than in controls. Conclusions: These findings suggest that poor compensatory function for sle ep loss predisposes DSPS patients to failure to reset their sleep phase. Ou r results provide implications for understanding not only the pathophysiolo gy of DSPS but also the biological basis for why some people can change the ir sleep schedule easily according to personal or social demands while othe rs cannot.