Neurocognitive function in children with obstructive sleep apnoea syndrome due to adenotonsillar hypertrophy

OBJECTIVE: It is clear from epidemiological studies that there are increased rates of behavioural cognitive and educational disturbance amongst sleep disturbed children in general. However these problems are particularly common in the context of upper airways obstruction due to adenotonsillar hypertrophy. In the worst cases this may result in obstructive sleep apnoea syndrome (OSAS) characterised by prolonged partial upper airways obstruction (hypopnea) and/or intermittent complete obstruction (apnoea) that disrupts both gas exchange (hypercarbia and hypoxia) and normal sleep (arousals). The causal pathway for neurocognitive deficits is unclear. Beebe and Gozal proposed that frontal lobe function may be adversely affected by the hypoxia and sleep arousals characteristic of OSAS. Animal models have also suggested that hypoxia leads to long-term changes in frontal dopaminergic pathways . However without evidence of functional brain abnormality the implications for a similar pathophysiology in children with OSAS remain implied but not confirmed.METHOD: In order to address this limitation of the literature we used a combination of neuropsychological non-invasive transcranial Doppler and event-related potential techniques. Here we present preliminary analyses obtained from 17 children (3-7 years) with OSAS (apnoea-hypopnoea index > 1) confirmed by attended polysomonography and 14 healthy controls of similar age.RESULTS: These data reveal significantly increased levels of abnormal behaviour assessed by the Behaviour Rating Inventory of Executive Function (BRIEF(P)) in OSAS children (p<.05) but mean IQ scores (WPPSI-III) are in the average range in both groups. Importantly velocity of blood flow in the middle cerebral artery was significantly increased in OSAS children (p<.001) and correlated positively with BRIEF(P) scores.CONCLUSION: The finding of significant group differences on behavioural measures supports previous studies. We now extend the literature by providing novel evidence of abnormal brain function