Does Obstructive Sleep Apnea Increase Cognitive Deficits in Pediatric Sickle Cell Disease?

Abstract

Objective: Although pediatric obstructive sleep apnea (OSA) is estimated to affect 2–3% of the general population, its prevalence in sickle cell disease (SCD) is much higher, with research suggesting a prevalence rate of upwards of 40%. Despite the similar underlying pathophysiological mechanisms of neurocognitive effects in pediatric OSA and SCD, there is a scarcity of information on how these two conditions interact. The aim of the present study was to better understand the contribution of sleep apnea to neurocognitive deficits in children diagnosed with SCD. Method: The present study assessed cognitive function in 26 children with comorbid SCD and OSA, 39 matched comparisons with SCD only, and 59 matched comparison children without a chronic health condition. Results: There were significant differences on measures of processing speed and reading decoding, with children without a chronic health condition scoring better than both chronic health condition groups. Additionally, the no chronic health condition group performed better on a test of quantitative knowledge and reasoning and a test of visual-spatial construction than the SCD only group. Contrary to our hypotheses, there were no between group differences suggesting an additive impact of OSA on cognition. Exploratory analyses revealed associations within the group that had OSA showing that more severe OSA correlated with lower performance on measures of processing speed and quantitative knowledge/reasoning. Conclusion: Children with comorbid OSA and SCD do not present with greater deficits in cognitive functioning than children with SCD alone. However, severe OSA may confer additional risk for neurocognitive impairments.

The burden of sleep disordered breathing in children with sickle cell disease

“…However, subgroup analysis of children with mild and severe OSA showed significant difference for the Test of Language Development‐oral vocabulary 59 (TOLD‐OV) (9.9 vs. 7.7, p < .05) and for the Woodcock‐Johnson Tests of Cognitive Abilities, 3rd edition—applied problems (WJIII‐AP) (101.2 vs. 86.7, p < .05) 60 . Similar results were shown by Bills, whereby increased OSA severity, rather than a diagnosis of mild OSA, was associated with deficits in cognitive functioning 56 …”

“…Scores of IQ were correlated with percentage of TST with SpO 2 < 95%, indicating that nocturnal oxygen desaturation may be a contributing factor to executive dysfunction in children with SCD 12 . However, an increased OSA severity, rather than a diagnosis of OSA, appeared to be associated with deficits in cognitive functioning 56 . This suggests the importance of avoiding nocturnal severe and/or frequent oxygen desaturation and sleep fragmentation to preserve neurocognitive function in children with SCD.…”

“…12 However, an increased OSA severity, rather than a diagnosis of OSA, appeared to be associated with deficits in cognitive functioning. 56 This suggests the importance of avoiding nocturnal severe and/or frequent oxygen desaturation and sleep fragmentation to preserve neurocognitive function in children with SCD.…”

Developmental Profile of Sleep and Its Potential Impact on Daytime Functioning from Childhood to Adulthood in Sickle Cell Anaemia

“…The high occurrence of SDB and night waking in our sample further contributes to nocturnal sleep disturbances. Children with SCA and sleep-disordered breathing (SDB) may experience processing speed difficulties [ 6 ], a cognitive domain important to responding quickly and processing information in one’s environment. Additionally, nocturnal oxygen desaturation, experienced during episodes of SDB, are associated with worse executive function in children with SCA [ 41 ].…”

“…Polymerised haemoglobin also carries less oxygen and the sickled cell may stick to and block blood vessels [ 1 ]. Chronic hypoxia on exposure to sleep-disordered breathing (SDB), e.g., obstructive sleep apnoea (OSA), might increase the risk for structural and functional brain abnormalities leading to poor cognitive function [ 2 , 3 , 4 , 5 , 6 ]. The prevalence of SDB diagnosed with polysomnography (PSG) in SCA is high, ranging from 36% to 69% [ 7 , 8 , 9 ], due mainly to hyperplasia of adenoids and tonsils causing upper-airway obstruction [ 10 ], particularly in young children, although the anatomy of bony structures may also play a part [ 11 ].…”