In 1888–1890, August Knoblauch produced a cognitive model for music processing and termed it amusia. This model for music processing was the earliest produced.While the possibility that certain individuals may be born with musical deficits is not a new notion, the first documented case of congenital amusia was published only in 2002. The study was conducted with a female volunteer, referred to as Monica, who declared herself to be musically impaired in response to an advertisement in the newspaper. Monica had no psychiatric or neurological history, nor did she have any hearing loss. MRI scans showed no abnormalities. Monica also scored above average on a standard intelligence test, and her working memory was evaluated and found to be normal. However, Monica had a lifelong inability to recognize or perceive music, which had persisted even after involvement with music through church choir and band during her childhood and teenage years. Monica said that she does not enjoy listening to music because, to her, it sounded like noise and evoked a stressful response. In order to determine if Monicas disorder was amusia, she was subjected to the MBEA series of tests. One of the tests dealt with Monicas difficulties in discriminating pitch variations in sequential notes. In this test, a pair of melodies was played, and Monica was asked if the second melody in the pair contained a wrong note. Monicas score on this test was well below the average score generated by the control group.
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.