Introduction
Sleep disordered breathing (SDB) represents a wide spectrum of respiratory abnormalities in sleep. These abnormalities range in severity from Primary Snoring (PS) to Obstructive Sleep Apnea (OSA). PS is characterized by vibrations of tissue in the upper airway that occur during sleep without accompanying apnea or hypopnea.1Prevalence rates of PS are estimated at 6% of school aged children.2 OSA is characterized by narrowing or collapse of the airway during sleep, which results in episodic airway obstruction, hypoxia, and subsequent arousal.3Repeated arousals are associated with disrupted sleep architecture, which can result in non-restorative sleep. OSA occurs in approximately 3% of school aged children.4 Currently, the gold standard assessment for the diagnosis of OSA is polysomnography (PSG), which identifies disruptions in sleep stages and cycles.1
There are multiple risk factors associated with pediatric SDB. Commonly cited risk factors in the United States include male gender5 and African American race.5One study reported that African American children were three and a half times more likely to have SDB than white American children.6 Children born before 34 weeks of gestational age and children with asthma6-8 are also at a heightened risk for SDB.9-10 Obesity, as indicated by body mass index (BMI)11-13 or adipose tissue deposits5 is an additional significant risk factor.
There is an extensive body of literature examining the neurocognitive sequalae of SDB in children. This review focuses on literature regarding the cognitive effects of pediatric SDB and the proposed etiology underlying neurocognitive consequences of pediatric SDB. Current discrepancies and limitations of the literature are discussed.