AT leads to significant improvements in indices of sleep-disordered breathing in children. However, residual disease is present in a large proportion of children after AT, particularly among older (>7 yr) or obese children. In addition, the presence of severe OSAS in nonobese children or of chronic asthma warrants post-AT nocturnal polysomnography, in view of the higher risk for residual OSAS.

Obstructive sleep apnea (OSA) in children has emerged not only as a relatively prevalent condition but also as a disease that imposes a large array of morbidities, some of which may have long-term implications, well into adulthood. The major consequences of pediatric OSA involve neurobehavioral, cardiovascular, and endocrine and metabolic systems. The underlying pathophysiological mechanisms of OSA-induced end-organ injury are now being unraveled, and clearly involve oxidative and inflammatory pathways. However, the roles of individual susceptibility (as dictated by single-nucleotide polymorphisms), and of environmental and lifestyle conditions (such as diet, physical, and intellectual activity), may account for a substantial component of the variance in phenotype. Moreover, the clinical prototypic pediatric patient of the early 1990s has been insidiously replaced by a different phenotypic presentation that strikingly resembles that of adults afflicted by the disease. As such, analogous to diabetes, the terms type I and type II pediatric OSA have been proposed. The different manifestations of these two entities and their clinical course and approaches to management are reviewed.

OSA does not appear to induce insulin resistance in nonobese pediatric patients but seems to play a significant role in obese patients. The significant improvements in lipid profiles, C-reactive protein, and apolipoprotein B after adenotonsillectomy in the two groups suggest a pathogenic role for OSA in lipid homeostasis and systemic inflammation independent of the degree of adiposity.

Rationale: Sleep-disordered breathing (SDB) in children is associated with cognitive challenges. However, potential associations between SDB severity and neurocognitive function, as well as the presence of an SDB cutoff, have not been fully explored.Objectives: To determine whether SDB-associated adverse changes in neurocognitive functioning are severity dependent.Methods: A total of 1,010 snoring and nonsnoring children ages 5-7 years were prospectively recruited from public schools and underwent polysomnography and neurocognitive assessments of intellectual, attention, memory, language, and executive function development. The children were subdivided into four severity groups on the basis of apnea-hypopnea index (AHI), followed by comparisons of cognitive function, with a particular focus on standardized subtests of intellectual, language, attention, memory, and executive function.Measurement and Main Results: Differential Ability Scales Verbal (P , 0.001) and Nonverbal (P = 0.002) performance, as well as global conceptual ability (IQ) (P , 0.001) scores, differed significantly across the groups, with individuals with higher AHI showing worse performance. Additionally, specific NEPSY (a Developmental Neuropsychological Assessment) subscores focused on attention and executive skills differed across the groups, indicating differences in levels of engagement and problem solving. Children with higher AHI (.5 per hour of total sleep time) were significantly more impaired than all three lower AHI groups, indicating a dose-response impact of SDB.Conclusions: This large community-based sample of children highlights the significant deleterious impact of SDB, particularly in children with moderate to severe obstructive sleep apnea, and also that even snoring alone affects neurocognitive function. By affecting developing capabilities, as illustrated by cognitive measures in a severity-graded manner, SDB could adversely impact children's capacity to attain academic and adaptive goals, ultimately hampering their ability to reach independence. Our findings support the need for increased awareness of SDB, with particular emphasis on children with more severe obstructive sleep apnea.

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Neural network-based automated analyses of nSp recordings provide accurate identification of OSA severity among habitually snoring children with a high pretest probability of OSA. Thus, nocturnal oximetry may enable a simple and effective diagnostic alternative to nocturnal polysomnography, leading to more timely interventions and potentially improved outcomes.

Rationale: Obstructive sleep apnea (OSA) in children is associated with substantial neurobehavioral and cognitive dysfunction. However, not all children with OSA exhibit altered cognitive performance. Objectives: To assess the magnitude of the systemic inflammatory response, as measured by high-sensitivity C-reactive protein (hsCRP) serum levels which may identify children with OSA at higher susceptibility for cognitive morbidity. Methods: Habitually snoring children and nonsnoring children (total, 278; age range, 5-7 yr) were recruited from the community, and underwent overnight polysomnography and neurocognitive testing and a blood draw the next morning. Snoring children were divided into OSA and no-OSA groups, and children with OSA were further subdivided into those with two or more abnormal cognitive subtests and into those with normal cognitive scores. Serum levels of hsCRP were also measured. Measurements and Main

A 6-week treatment with intranasal budesonide effectively reduced the severity of mild obstructive sleep apnea syndrome and the magnitude of the underlying adenoidal hypertrophy, and this effect persisted for at least 8 weeks after cessation of therapy. These findings justify the use of topical steroids as the initial therapeutic option in otherwise healthy children with mild obstructive sleep apnea.