Children with Down syndrome have many predisposing factors for the obstructive sleep apnea syndrome (OSAS), yet the type and severity of OSAS in this population has not been characterized. Fifty-three subjects with Down syndrome (mean age 7.4 ± 1.2 [SE] years; range 2 weeks to 51 years) were studied. Chest wall movement, heart rate, electrooculogram, end-tidal Po2 and Pco2, transcutaneous Po2 and Pco2, and arterial oxygen saturation were measured during a daytime nap polysomnogram. Sixteen of these children also underwent overnight polysomnography. Nap polysomnograms were abnormal in 77% of children; 45% had obstructive sleep apnea (OSA), 4% had central apnea, and 6% had mixed apneas; 66% had hypoventilation (end-tidal Pco2, >45 mm Hg) and 32% desaturation (arterial oxygen saturation <90%). Overnight studies were abnormal in 100% of children, with OSA in 63%, hypoventilation in 81%, and desaturation in 56%. Nap studies significantly underestimated the presence of abnormalities when compared to overnight polysomnograms. Seventeen (32%) of the children were referred for testing because OSAS was clinically suspected, but there was no clinical suspicion of OSAS in 36 (68%) children. Neither age, obesity, nor the presence of congenital heart disease affected the incidence of OSA, desaturation, or hypoventilation. Polysomnograms improved in all 8 children who underwent tonsilletomy and adenoidectomy, but they normalized in only 3. It is concluded that children with Down syndrome frequently have OSAS, with OSA, hypoxemia, and hypoventilation. Obstructive sleep apnea syndrome is seen frequently in those children in whom it is not clinically suspected. It is speculated that OSAS may contribute to the unexplained pulmonary hypertension seen in children with Down syndrome.
Ventilatory responses to peripheral chemoreceptor stimuli are absent in patients with Prader-Willi syndrome (PWS) during wakefulness. Because arousal from sleep after rapidly developing hypoxia may require intact peripheral chemoreceptor function, we hypothesized that blunted hypoxic arousal responses during sleep Stage 3/4 would be present in PWS. Thirteen patients with PWS (mean age, 23.4 +/- 3.7 +/- SEM yr; 46% male; body mass index [BMI], 28.9 +/- 1.6 kg/m2) and 11 matched control subjects (mean age 28.0 +/- 5.4 yr; 54% male; BMI, 28.8 +/- 3.1 kg/m2) were studied. An abrupt decrease in inspired O2 tension to 80 mm Hg was introduced until arousal occurred or for a maximum of 3 min. One of the 13 patients with PWS and seven of the 11 control subjects were aroused by the hypoxic challenge (p < 0.02). During hypoxia, heart rate increased by 9 +/- 2% in the PWS group versus 22 +/- 4% in the control group (p < 0.005). Respiratory rate did not change in the PWS group (4 +/- 2%; p = NS), but it increased by 13 +/- 2% in the control group (p < 0.02). We conclude that abnormal arousal and cardiorespiratory responses to hypoxia are frequent in PWS. We postulate that intact peripheral chemoreceptor function is an important component underlying arousal mechanisms to rapidly developing hypoxia during sleep.
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