The use of pharmacological approaches to treatment are less successful due to the risks of administering sleep-promoting agents early in the morning. Additional methods of treatment, like timed melatonin administration or hypnotics have been proposed, but determining their safety and efficacy will require further research. Unlike other sleep disorders, ASPD does not necessarily disrupt normal functioning at work during the day and some patients may not complain of excessive daytime sleepiness. Social obligations may cause an individual to stay up later than their circadian rhythm requires, however, they will still wake up very early. If this cycle continues, it can lead to chronic sleep deprivation and other sleep disorders. Epidemiology
ASPD is more common among middle and older adults. The estimated prevalence of ASPD is about 1% in middle-age adults, and is believed to affect men and women equally. The disorder has a strong familial tendency, with 40-50% of affected individuals having relatives with ASPD. A genetic basis has been demonstrated in one form of ASPD, familial advanced sleep phase disorder (FASPS), which implicates missense mutations in genes hPER2 and CKIdelta in producing the advanced sleep phase phenotype. The identification of two different genetic mutations suggests that there is heterogeneity of this disorder. Familial advanced sleep phase syndrome
FASPS symptoms
While advanced sleep and wake times are relatively common, especially among older adults, the extreme phase advance characteristic of familial advanced sleep phase syndrome (also known as familial advanced sleep phase disorder) is rare.
Prognosis
This form of neutropenia disappears in two to three years of a childs life in 95% of cases.The use of prophylactic antibiotics has been successfully demonstrated to reduce infection incidence without causing adverse effects among the 5% of children whose condition does not resolve itself. References


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