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.