The possible causes of<unk>  are 2-fold: (1), extrinsic: isolation from daily light cycles (such as working in an environment completely devoid of natural lighting); and (2), intrinsic: where some condition, such as blindness or malfunctioning biochemical response to light in the subject, prevent normal levels of light-activated melatonin release. Melatonin is responsible for<unk>  regulation, and its release is controlled by the amount of light entering the eyes. Sighted Sighted people with<unk> -24 appear to be more rare than blind people with the<unk> , and the etiology of their circadian<unk>  is less well understood. At least one case of a sighted person developing<unk> -24 was preceded by head injury; another patient diagnosed with the<unk>  was later found to have a "large pituitary adenoma that involved the optic chiasma". Thus the problem appears to be neurological. Specifically, it is thought to involve abnormal functioning of the suprachiasmatic nucleus (SCN) in the hypothalamus.See also subsequent: Several other cases have been preceded by chronotherapy, a prescribed treatment for delayed<unk>  phase<unk> . "Studies in animals suggest that a hypernyctohemeral syndrome could occur as a physiologic aftereffect of lengthening the<unk><unk> wake cycle with chronotherapy". According to the American Academy of<unk>  Medicine (AASM), "patients with free-running (FRD) rhythms are thought to reflect a failure of entrainment". There have been several experimental studies of sighted people with the<unk> . McArthur et al. reported treating a sighted patient who "appeared to be subsensitive to bright light". In other words, the brain (or the retina) does not react normally to light (people with the<unk>  may or may not, however, be unusually subjectively sensitive to light; one study found that they were more sensitive than the control group). In 2002 Uchiyama et al. examined five sighted<unk> -24 patients who showed, during the study, a<unk><unk> wake cycle averaging 25.12<unk> s. That is appreciably longer than the<unk> .02-hour average shown by the control subjects in that study, which was near the average innate cycle for healthy adults of all ages: the<unk> .18<unk> s found by Charles Czeisler. The literature usually refers to a "one- to two-hour" delay per<unk> -hour day (i.e. a 25- to 26-hour cycle). Uchiyama et al. had earlier determined that sighted<unk> -24 patients' minimum core body temperature occurs much earlier in the<unk>  episode than the normal two<unk> s before awakening. They suggest that the long interval between the temperature trough and awakening makes illumination upon awakening virtually ineffective, as per the phase response curve (PRC) for light. In their clinical review in 2007, Okawa and Uchiyama reported that people with<unk> -24 have a mean habitual<unk>  duration of nine to ten<unk> s and that their circadian periods average<unk> .8<unk> s. Blind As stated above, the majority of patients with<unk> -24 are totally blind. The failure of entrainment is explained by the loss of photic input to the circadian clock.<unk> -24 is rare among visually impaired patients who retain at least some light perception; even minimal light exposure can synchronize the body clock. A few cases have been described in which patients are subjectively blind, but are normally entrained and have an intact response to the suppressing effects of light on melatonin secretion, indicating preserved neural pathways between the retina and hypothalamus.
Non-24-hour sleep–wake disorder
Circadian rhythm sleep disorder
Delayed sleep phase disorder
Irregular sleep–wake rhythm
Advanced sleep phase disorder
Shift work sleep disorder
Excessive daytime sleepiness
Sleep state misperception