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Nocturnal Sleep and Daytime Sleepiness in Normal Subjects with HLA-DQB1*0602
Author(s) -
Emmanuel Mignot,
Terry Young,
Lin Liu,
L Finn
Publication year - 1999
Publication title -
sleep
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.222
H-Index - 207
eISSN - 1550-9109
pISSN - 0161-8105
DOI - 10.1093/sleep/22.3.347
Subject(s) - multiple sleep latency test , polysomnography , narcolepsy , excessive daytime sleepiness , epworth sleepiness scale , psychology , population , sleep debt , sleep (system call) , subclinical infection , medicine , audiology , sleep disorder , insomnia , psychiatry , neurology , electroencephalography , operating system , environmental health , computer science
Narcolepsy, a neurological disorder characterized by excessive daytime sleepiness and abnormal REM sleep, is known to be tightly associated with the Human Leukocyte Antigen (HLA) DQ allele DQB1*0602. In this study, we have explored the possibility that normal subjects carrying this HLA allele (25% of the general population) could display subclinical REM sleep abnormalities and increased daytime sleepiness. Data from 525 middle-aged adults enrolled in the Wisconsin Sleep Cohort study were used for this analysis. Nocturnal polysomnography, sleep latency during the multiple sleep latency test (MSLT), and questionnaire items pertaining to excessive daytime sleepiness were compared between DQB1*0602 positive (n = 132) and negative (n = 393) participants. Results indicate shorter REM latency whether or not the latency was adjusted for wake after sleep onset (p = 0.003) and p = 0.02 respectively), increased sleep efficiency (p = 0.06) and decreased percent time spent in stage I sleep (p = 0.02) during nocturnal polysomnography in DQB1*0602 subjects. Data gathered using the Multiple Sleep Latency Test or the Epworth and Stanford sleepiness scales did not differentiate between DQB1*0602 positive and negative subjects. These results support the hypothesis that polymorphisms at the level of HLA DQ modulates sleep tendencies in humans.

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