Underlying Etiology
There are several hypotheses regarding the mechanisms that underlie cognitive difficulties in children with SDB. Studies have suggested that cognitive sequalae are a product of episodic decreases in oxyhemoglobin saturation,11,17 disrupted sleep continuity,11,17 and disrupted sleep architecture17 that occur in children with SDB. These changes are thought to affect children across the spectrum of SDB severity, including children with PS.11 Some studies suggest that the stress of intermittent hypoxia and sleep disruption may elicit inflammatory markers.5,28 A high-sensitivity C-reactive protein (hs-CRP), which measures general levels of inflammation in the body, is elevated in children with OSA compared to children without OSA.28 Hs-CRP is also elevated in children with OSA who have cognitive deficits compared to children with OSA who do not have cognitive deficits.28 Therefore, systemic inflammation may increase neurocognitive impairment in children with SDB. An additional study that investigated the role of increased adiposity on cognitive abilities in children with SDB reported that increased central adiposity influences cognition through mechanisms of low grade, chronic inflammation.5 Therefore, obesity and SDB can both contribute to chronic inflammatory responses, which are associated with decreased cognitive abilities in some children with SDB.5,28
Since increased inflammation is not associated with decreased cognition in all children with SDB, there is likely a combination of genetic and environmental factors that interact to elicit neurocognitive risk. Polymorphisms in the NOX gene or its subunits56 as well as apoliprotein E allelic variants57 have been implicated in underlying gene-related susceptibility for neurocognitive deficits in children with SDB. Therefore, some children may have a unique and complex SDB phenotype that predisposes them to cognitive challenges.