Effect of simulated altitude during sleep on moderate-severity OSA.

OBJECTIVE: These studies were conducted to test the hypothesis that isobaric hypoxia would switch OSA to central sleep apnoea (CSA). METHODS: Five adult men (mean age 54.2 +/- 5.5 years, mean BMI 29.9 +/- 6.7 kg/m(2)) with moderate OSA underwent overnight polysomnography at three altitudes. The highest altitude was simulated in a normobaric hypoxic chamber. RESULTS: The obstructive respiratory disturbance index fell from 25.5 +/- 14.4/h at 60 m to 17.3 +/- 9.2/h at 610 m and 0.5 +/- 0.7/h at 2750 m (P = 0.004 compared with 60 m). The central respiratory disturbance index rose from 0.4 +/- 0.5/h at 60 m to 8.1 +/- 5.8/h at 610 m and 78.8 +/- 29.7/h at 2750 m (P < 0.001 compared with 60 m). Mean sleep SaO(2) fell from 94 +/- 1% at 60 m to 93 +/- 1% at 610 m to 85 +/- 4% at 2750 m (P < 0.001 compared with 60 m). CONCLUSION: Moderate severity OSA at sea level (60 m) was completely replaced by severe CSA at a simulated altitude of 2750 m. The authors believe that the OSA resolved because of an increased respiratory drive [corrected] and an increase in upper airway tone, whereas CSA developed because of hypocapnia in non-rapid eye movement sleep.

No evidence of sleep apnea in children with attention deficit hyperactivity disorder.

Children with attention deficit hyperactivity disorder (ADHD) may have a component of sleep apnea causing arousal and contributing to ADHD behavior during the day. Twenty non-ADHD children between 4 and 16 years of age were compared with 18 children with ADHD with use of nocturnal polysomnography (PSG) and psychometric tests. The psychometric testing confirmed that the control group were normal and that the ADHD children fulfilled the diagnostic criteria for ADHD. The PSG showed normal arousal indexes for the ADHD group (9.8 +/- 3.9/hr) and controls (10.2 +/- 3.1/hr), and normal apnea/hypnea indexes for the ADHD group (1.0 +/- 2.4/hr) and controls (0.6 +/- 0.9/hr). The sleep architecture was not significantly different between groups. There were no sleep abnormalities in the ADHD children that could be responsible for, or contributing to, the disorder.