Abstract

Daytime EEG-polygraph recordings were obtained weekly from birth to 12–13 weeks, and at 26 and 52 weeks of age in 7 Trisomy-21 infants. The babies remain alive and are relatively well at ages 20–53 months. All 81 EEGs obtained were within normal limits for age. Derived data were compared with similar data from 17 normal full term infants. The tracé alternant pattern disappeared later in the Trisomy-21 than in the control group (mean ages 55.6 days vs. 33.4 days post term; P < 0.001). Rolandic sleep spindles appeared later in the Trisomy-21 group (mean ages 62.0 days vs. 43.8 days; P < 0.01). The shift from active sleep onset to quiet sleep onset also occurred later in the Trisomy-21 group (mean ages 46.4 days vs. 37.1 days; not significant), while the overall incidence of quiet sleep onset during the first 3 months of life was significantly lower for the Trisomy-21 group than for the control group ( P < 0.02). Attainment of ‘infantile’ EEG-sleep patterns occurred at 55–82 days post term (mean 66.2) for the Trisomy-21 group and at 27–66 days (mean 46.4) for the control group ( P < 0.01). Sleep spindle bursts during slow wave sleep were less abundant in the Trisomy-21 group than in the control group throughout the first year (2.96 vs. 4.08 bursts/min; P <0.01), and their interhemispheric synchrony did not improve significantly by 12 months of age. Indeterminate sleep as a percetage of total sleep time was higher for the Trisomy-21 group than for the control group during the first 12 weeks of life (18.1% vs. 10.6%; P < 0.001), primarily at the expense of quiet sleep (51.4% for the Trisomy-21 group and 60.6% for the control group; P < 0.05). Finally, frontal sharp waves disappeared later in the Trisomy-21 group than in the control group (64.6 days vs. 39.1 days; P < 0.001). Developmental quotients at 8 months of age were significantly negatively correlated with age at disappearance of tracé alternant, age at appearance of rolandic sleep spindles, and age at disappearance of frontal sharp waves. The present results demonstrate significant retardation in the maturation of brain electrical activity in Trisomy-21 infants, which is correlated with delayed early behavioral development, but not with the presence of conventional signs of EEG abnormality.

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