Delayed sleep phase type is the most common of the CRSDs (7). It was first characterized by Weitzman et al. in 1981 Patients with DSPT report a chronic inability to fall asleep and wake up at a desired clock time to meet their work schedules, but do describe undisturbed late sleep on vacations (8). In addition to delayed sleep, wake times the circadian phase of these patients, as measured by melatonin and core body temperature, is also delayed (48, 49 and 50). In a study of 66 subjects, dim light melatonin onset occurred 2 hours later and core body temperature nadir 2.5 hours later than controls (50). Furthermore, circadian phase appears stable in DSPT subjects across multiple measurements despite an ad libitum sleep schedule (49). The exact pathophysiology of DSPT is unknown. However, several factors may be implicated in the persistent delayed sleep phase relative to the 24-hour environment, including circadian period, light sensitivity, phase angle, and the homeostatic sleep drive.

One proposed explanation is that patients with DSPT have a longer endogenous circadian period or tau that regulates the sleep-wake cycle (9). In one patient with DSPT placed in temporal isolation, circadian period measured 25.38 hours as compared to 24.44 hours in aged matched controls subsisting in the same environment (51). Although the usual human circadian period is slightly longer than 24 hours, this further lengthening may result in difficulty entraining to the 24-hour day. Evidence also suggests that some patients with DSPT may be hypersensitive to evening light, which can serve as a delay signal to the circadian clock (10). Alternatively, DSPT patients may have decreased sensitivity to morning light such that its phase advancing effects are reduced. However, other studies demonstrate that the advance portion of the phase response curve to light is actually masked due to sleep offset occurring relatively later with respect to the core body temperature nadir than normal controls (52). Th is alteration of the relationship between sleep timing with respect to phase markers (or phase angle) is another possible mechanism to explain DSPT, with studies demonstrating a significantly longer interval of time elapsing between the time of highest circadian propensity for sleep and wake time in these patients as compared to controls (52,53). Th is finding, in addition to increased slow wave sleep in the latter part of the sleep period, may suggest an abnormality in the dissipation of the homeostatic sleep drive (51). The accumulation of homeostatic drive is likely altered as well since DSPT patients often demonstrate increased sleep onset latency (despite attempting sleep at the preferred times) and inability to sufficiently recover sleep after sleep deprivation (51,53,54). Therefore, although DSPT is often regarded solely as a disorder of circadian timing, impairment of homeostatic regulation may play a significant role (8,11,12). However, other evidence is not supportive of these findings with a study of 66 DSPT patients demonstrating no difference in sleep onset latency, total sleep duration, or phase angle as compared to controls (50). Additionally, while evaluating the therapeutic response to a light mask in a group of DSPT subjects, two subgroups were delineated: those with melatonin acrophases prior to 0600 and longer sleep offset phase angles, and those with melatonin acrophases after 0600 and shorter sleep offset phase angles (55). These findings could indicate the possibility of heterogeneity within DSPT patients. Finally, genetic factors are likely to play a role in the pathogenesis of DSPT. For example, there are familial forms of DSPT, and polymorphisms in circadian genes such as Per3, arylalkylamine N-acetyltransferase, HLA, and Clock have been reported in “evening types” and DSPT (13, 14, 15 and 16).