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.