<unk>  is a disorder of the body's timing system—the biological clock. Individuals with<unk>  might have an unusually long circadian cycle, might have a reduced response to the resetting effect of daylight on the body clock, and/or may respond overly to the delaying effects of evening light and too little to the advancing effect of light earlier in the day. In support of the increased sensitivity to evening light hypothesis, "the percentage of melatonin suppression by a bright light stimulus of 1,000 lux administered 2 hours prior to the melatonin peak has been reported to be greater in 15<unk>  patients than in 15 controls." The altered phase relationship between the timing of sleep and the circadian rhythm of body core temperature has been reported previously in<unk>  patients studied in entrained conditions. That such an alteration has also been observed in temporal isolation (free-running clock) supports the notion that the etiology of<unk>  goes beyond simply a reduced capacity to achieve and maintain the appropriate phase relationship between sleep timing and the 24-hour day. Rather, the disorder may also reflect a fundamental inability of the endogenous circadian timing system to maintain normal internal phase relationships among physiological systems, and to properly adjust those internal relationships within the confines of the 24-hour day. In normal subjects, the phase relationship between sleep and temperature changes in temporal isolation relative to that observed under entrained conditions: in isolation, tmin tends to occur toward the beginning of sleep, whereas under entrained conditions, tmin occurs toward the end of the sleep period—a change in phase angle of several hours;<unk>  patients may have a reduced capacity to achieve such a change in phase angle in response to entrainment. Possibly as a consequence of these altered internal phase relationships, that the quality of sleep in<unk>  may be substantially poorer than that of normal subjects, even when bedtimes and wake times are self-selected. A<unk>  subject exhibited an average sleep onset latency twice that of the 3 control subjects and almost twice the amount of wakefulness after sleep onset (WASO) as control subjects, resulting in significantly poorer sleep efficiency. Also, the temporal distribution of slow wave sleep was significantly altered in the<unk>  subject. This finding may suggest that, in addition to abnormal circadian clock function,<unk>  may be characterized by alteration(s) in the homeostatic regulation of sleep, as well. Specifically, the rate with which Process S is depleted during sleep may be slowed. This could, conceivably, contribute to the excessive sleep inertia upon awakening that is often reported by<unk>  sufferers. It has also been hypothesized that, due to the altered phase angle between sleep and temperature observed in<unk> , and the tendency for longer sleep periods, these individuals may simply sleep through the phase-advance portion of the light PRC. Though quite limited in terms of the total number of<unk>  patients studied, such data seem to contradict the notion that<unk>  is merely a disorder of sleep timing, rather than a disorder of the sleep system itself. People with normal circadian systems can generally fall asleep quickly at night if they slept too little the night before. Falling asleep earlier will in turn automatically help to advance their circadian clocks due to decreased light exposure in the evening. In contrast, people with<unk>  have difficulty falling asleep before their usual sleep time, even if they are sleep-deprived. Sleep deprivation does not reset the circadian clock of<unk>  patients, as it does with normal people. People with the disorder who try to live on a normal schedule cannot fall asleep at a "reasonable" hour and have extreme difficulty waking because their biological clocks are not in phase with that schedule. Non-DSPD people who do not adjust well to working a night shift have similar symptoms (diagnosed as shift-work sleep disorder). In most cases, it is not known what causes the abnormality in the biological clocks of<unk>  patients.<unk>  tends to run in families, and a growing body of evidence suggests that the problem is associated with the hPer3 (human period 3) gene and CRY1 gene. There have been several documented cases of<unk>  and non-24-hour sleep–wake disorder developing after traumatic head injury. There have been cases of<unk>  developing into non-24-hour sleep–wake disorder, a severe and debilitating disorder in which the individual sleeps later each day.
Delayed sleep phase disorder
Insomnia
Circadian rhythm sleep disorder
Non-24-hour sleep–wake disorder
Advanced sleep phase disorder
Shift work sleep disorder
Nightmare disorder
Rapid eye movement sleep behavior disorder