No abstract

No abstract

SUMMARY We studied the effect of alcohol ingestion on sleep-induced breathing abnormalities and arterial oxyhaemoglobin saturation in seven patients with a range of sleep-induced upper airway occlusion. The characteristics of each patient's sleep-induced breathing abnormality was established on one or more control all-night studies, and then a further all-night study was done immediately following alcohol ingestion. Alcohol increased the duration and frequency of the occlusive episodes in five patients with obstructive sleep apnoea, and resulted in a marked increase in the degree of hypoxaemia in the first hour of sleep. In two patients with benign chronic snoring, alcohol induced frank obstructive sleep apnoea during the first hour of sleep. We suggest that the increased tendency to develop obstructive apnoea after alcohol is the result of alcohol-induced oropharyngeal muscle hypotonia, while the increased duration of obstructive apnoeas is the result of alcohol-induced depression of arousal mechanisms.

We analyzed the polysomnographic records of 15 children and 20 infants with obstructive sleep apnea (OSA) to examine the interaction between central and obstructive breathing abnormalities and arousal from sleep. Each patient was matched for age with an infant or child who had no OSA. We found that the majority of respiratory events in infants and children was not terminated with arousal. In children, arousals terminated 39.3 +/- 7.2% of respiratory events during quiet sleep and 37.8 +/- 7.2% of events during active (rapid-eye-movement) sleep. In infants, arousals terminated 7.9 +/- 1.0% of events during quiet sleep and 7.9 +/- 1.2% of events during active sleep. In both infants and children, however, respiratory-related arousals occurred more frequently after obstructive apneas and hypopneas than after central events. Spontaneous arousals occurred in all patients with OSA during quiet and active sleep. The frequency of spontaneous arousals was not different between children with OSA and their matched controls. During active sleep, however, infants with OSA had significantly fewer spontaneous arousals than did control infants. We conclude that arousals is not an important mechanism in the termination of respiratory events in infants and children and that electroencephalographic criteria are not essential to determine the clinical severity of OSA in the pediatric population.