Aging and sleep in Williams syndrome: accelerated sleep deterioration and decelerated slow wave sleep decrement.
Sleep in Williams syndrome deteriorates faster with age—track it closely in adolescence and adulthood.
01Research in Context
What this study did
Bódizs et al. (2014) tracked sleep changes across age in people with Williams syndrome.
They used overnight sleep recordings to compare how sleep depth and quality shift from childhood to adulthood.
What they found
Overall sleep got worse faster in Williams syndrome than in typical peers.
Surprisingly, the deepest sleep stage—slow-wave sleep—faded more slowly in Williams syndrome than expected.
How this fits with other research
Masi et al. (2022) saw sleep troubles grow with age in autistic youth, matching the worsening trend here.
Hanson et al. (2013) found three out of four older adults with intellectual disability have at least one sleep problem, showing sleep issues are common across neurodevelopmental groups.
Miezah et al. (2020) showed wide cognitive scatter in Williams syndrome; together these papers flag that both day and night functioning vary greatly, so always assess individually.
Why it matters
If you serve teens or adults with Williams syndrome, add simple sleep questions to your intake. Poor sleep can boost problem behavior and dull learning. A quick parent or staff log can spot trouble early and guide referrals for sleep studies or bedtime interventions.
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02At a glance
03Original abstract
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.
Research in developmental disabilities, 2014 · doi:10.1016/j.ridd.2014.07.056