پیری و خواب در سندرم ویلیامز: زوال تسریع شده خواب و موج آهسته تنزل یافته کاهش خواب
|کد مقاله||سال انتشار||مقاله انگلیسی||ترجمه فارسی||تعداد کلمات|
|40123||2014||10 صفحه PDF||سفارش دهید||محاسبه نشده|
Publisher : Elsevier - Science Direct (الزویر - ساینس دایرکت)
Journal : Research in Developmental Disabilities, Volume 35, Issue 12, December 2014, Pages 3226–3235
Specific developmental and aging trajectories characterize sleep electroencephalogram (EEG) of typically developing (TD) subjects. Williams syndrome (WS) is marked by sleep alterations and accelerated aging of several anatomo-functional and cognitive measures. Here we test the hypothesis of a premature aging of sleep in WS. Age-related changes of home recorded sleep EEG of 42 subjects (21 WS, 21 age- and gender matched TD subjects, age: 6–29 years) were tested by Pearson correlations and homogeneity-of-slopes analysis. Typical developmental/aging effects of sleep EEGs were observed in TD subjects. Accelerated aging in WS was confirmed by overall sleep/wake measures. Specifically, premature aging was evident in accelerated age-dependent declines in WS subjects’ sleep efficiency, as well as in steeper age-related rises in wakefulness and wake after sleep onset (WASO) of the WS group. In contrast, NREM sleep-related measures indicated atypical decelerations of the developmental trends of WS subjects, characterized by the slowing down of the age-related slow wave sleep (SWS) declines mirrored by the lack of age-dependent increase in Stage 2 (S2) sleep. Age-effects in sleep EEG power spectra were not different among the groups. Objectively measured sleep disruption of subjects with WS is age-dependent and increasing with age. Moreover, these data suggest atypical pre- and postpubertal neural development in WS, with sleep/wake balance and REM sleep time indicating accelerated aging while NREM sleep composition revealing signs of an as yet unidentified, perhaps compensatory developmental delay.