4.6 Article

Developmental Changes in the Human Sleep EEG During Early Adolescence

Journal

SLEEP
Volume 33, Issue 6, Pages 801-809

Publisher

OXFORD UNIV PRESS INC
DOI: 10.1093/sleep/33.6.801

Keywords

Sleep EEG; development; adolescence; time-frequency analysis

Funding

  1. National Institute on Alcohol Abuse and Alcoholism [AA13252, AA07459-21]
  2. NATIONAL INSTITUTE ON ALCOHOL ABUSE AND ALCOHOLISM [T32AA007459, R01AA013252] Funding Source: NIH RePORTER

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Study Objectives: To use time-frequency analysis to characterize developmental changes in the human sleep electroencephalogram (EEG) across early adolescence. Design: Sleep EEG was recorded when children were 9/10 years old and 1 to 3 years later after sleeping at home on a fixed schedule for at least one week. Setting: A 4-bed sleep laboratory. Participants: Fourteen (5 girls) healthy children ages 9/10 (mean = 10.13, SD = +/- 0.51) years at initial and 11 to 13 (mean = 12.28, SD = +/- 0.62) years at follow-up. Interventions: N/A. Measurements and Results: All-night polysomnography was performed at each assessment and sleep stages were scored with Rechtschaffen and Kales criteria. Slow wave sleep minutes decreased from the initial to the follow-up session by 29%, while minutes of stage 2 increased by 17%. NREM and REM sleep EEG spectra from two central and two occipital leads were examined for developmental changes. All-night analyses showed a significant decrease of EEG power from the initial to follow-up session across a range of frequencies during NREM and REM sleep. This decline occurred across leads and states in the delta/theta bands (3.8 - 7 Hz). Time-frequency analyses indicated that this effect was consistent across the night. The decline in power with age was most pronounced in the left central and right occipital leads. The frequency of greatest power in the sigma band (11 - 16 Hz) was significantly higher at follow-up. Conclusions: This longitudinal analysis highlights asymmetrical frequency-specific declines in sleep EEG spectral power with early adolescent maturation, which may reflect early signs of the cortical synaptic pruning in the healthy adolescent.

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