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The future risks of childhood sleep-disordered breathing.

THE PAST DECADE HAS SEEN INCREASING AWARENESS OF THE IMPORTANCE OF SLEEP-DISORDERED BREATHING (SDB) IN CHILDREN. AS THE EPIDEMIC OF OBESITY extends to ever younger ages, the obesity-related SDB typical of adults will become increasingly prevalent in childhood. Its management will likely be similar to that of obesity-related SDB in adults, albeit with greater urgency due to possible effects on growth and development and with likely greater difficulty in achieving adherence to therapy. In young children, however, adenotonsillar hypertrophy remains a more important cause of SDB and its management presents a different set of issues. Adenotonsillectomy may be curative in a majority of cases but is not without significant morbidity. When polysomnography reveals overt obstructive sleep apnea in a symptomatic child with adenotonsillar hypertrophy, the decision to perform adenoidectomy or tonsillectomy is not difficult. There is increasing evidence, however, that SDB symptoms in children are associated with problem behaviors, sleepiness, and poorer cognitive function even in the absence of obstructive sleep apnea.1,2 If mild SDB, characterized by snoring and increased airway resistance in the absence of gas exchange abnormalities, is indeed a cause of behavioral and cognitive impairment, then its public health impact may be quite large. Important questions about the behavioral and cognitive consequences of mild SDB in children remain to be answered, however, before embarking on major public health or medical treatment initiatives. First, the causal nature of the association remains uncertain. Several small studies have demonstrated improvements in behavior, cognitive function, and academic performance following adenotonsillectomy in children with obstructive sleep apnea.3-7 These studies indicate that overt obstructive sleep apnea does cause behavioral and cognitive impairment that is at least partially reversible, but provide limited evidence regarding children with “primary” snoring. Cognitive impairment in SDB is commonly attributed to the effects of hypoxemia. An important effect of hypoxemia is supported by recent experiments demonstrating increased cortical and hippocampal neuron apoptosis and impaired spatial learning in rats exposed to intermittent hypoxia, effects which are greatest at an age corresponding to early childhood in humans.8,9 However, experimental sleep fragmentation and sleep deprivation studies, mostly conducted in adults, provide unequivocal evidence that sleep disruption has behavioral and cognitive consequences that are not dependent on gas exchange abnormalities (recently reviewed in reference 10). Neither the numerous observational studies of the correlates of SDB in humans, nor the interventional studies conducted to date, are able to distinguish the relative contributions of sleep disruption and gas exchange abnormalities to the behavioral and cognitive consequences of SDB. Second, even if the association is causal, what are its long-term consequences? Unfortunately, little is known about the natural history of SDB or its consequences in young children. One large survey study suggests spontaneous resolution of snoring in 50% of habitually snoring 4to 5-year-old children over a two-year period.11 If the cognitive and behavioral effects of SDB are similarly reversible, specific therapeutic interventions such as adenotonsillectomy may not be warranted in large numbers of children simply to hasten their natural resolution. Conversely, early childhood is a period of rapid development of executive brain function. It is plausible that sleep disturbance during this critical period might lead to permanent impairment of executive function, as suggested by one retrospective study that found a stronger association of poor academic performance at age 13 to 14 years with early childhood snoring than with current snoring.12 If impairment of executive function is persistent, then identification and treatment of children at risk for such impairment would be of major public health importance. The study by Chervin et al in this issue of SLEEP begins to address this question.13 Although based on a fairly small number of observations, this study provides prospective evidence that the presence of SDB symptoms in children age 2-13 years is associated with an approximately 3-fold increase in the prevalence of hyperactive behaviors 4 years later. Although baseline and follow-up SDB symptoms were highly correlated, fewer than 1⁄2 of children with habitual snoring at baseline were habitual snorers 4 years later. When both baseline and follow-up SDB symptoms are included in logistic regression models, the association with hyperactive behaviors is stronger for baseline symptoms and is little affected by adjustment for symptoms at follow-up. While the authors considered 5 separate measures of SDB symptoms, the concordance of findings across these measures should allay concerns regarding multiple comparisons. The sole outcome measure is the Hyperactivity Index of the Conners’ Parent Rating Scale, a wellvalidated and widely used measure of childhood behavior problems. The definition of hyperactive behavior used in this study, a score of 60 or more on the Hyperactivity Index, is only 1 standard deviation above the normal mean for this measure and would not be considered a diagnostic clinical abnormality. Given the high prevalence of SDB symptoms in young children, however, even modest decrements in executive function may have impacts on learning and performance that are quite important at the population level. The Future Risks of Childhood Sleep-Disordered Breathing