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Published ahead of print on March 30, 2007, doi:10.1164/rccm.200610-1519OC

Am. J. Respir. Crit. Care Med., Volume 176, Number 2, July 2007, 188-193

A more recent version of this article appeared on July 15, 2007
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Submitted on October 21, 2006
Accepted on March 29, 2007

C Reactive Protein, Obstructive Sleep Apnea, and Cognitive Dysfunction in School-Aged Children

David Gozal1*, Valerie McLaughlin Crabtree1, Oscar Sans Capdevila1, Lisa A Witcher1, and Leila Kheirandish-Gozal1

1 Department of Pediatrics, Kosair Children's Hospital Research Institute, and Division of Pediatric Sleep Medicine, University of Louisville, Louisville, KY, USA

* To whom correspondence should be addressed. E-mail: david.gozal{at}louisville.edu.

Background: Obstructive sleep apnea (OSA) in children is associated with substantial neurobehavioral and cognitive dysfunction. However, not all children with OSA exhibit altered cognitive performance. Thus, we hypothesized that the magnitude of the systemic inflammatory response, as measured by high sensitivity C reactive protein serum levels may identify children at higher susceptibility for cognitive morbidity in children with OSA. Methods and Results: 278 habitually-snoring and non-snoring children ages 5-7 years were recruited from the community, and underwent overnight polysomnography, and neurocognitive testing and a blood draw the next morning. Snoring children were divided into OSA or no OSA, and OSA children were further subdivided into those with ≥2 abnormal cognitive subtests and into those with normal cognitive scores. Serum levels of hsCRP were also measured. Among snoring children without OSA, mean hsCRP was 0.19±0.07 mg/dL compared with 0.36±0.11 mg/dL in those with OSA (p<0.01). Furthermore, hsCRP was 0.48±0.12 mg/dL in children with OSA and cognitive deficits, compared to 0.21±0.08 mg/dL in children with OSA and normal cognitive scores (p<0.002). Conclusions: hsCRP levels are higher in children with OSA, and particularly in those who develop neurocognitive deficits, suggesting that the magnitude of the inflammatory responses elicited by OSA is a major determinant of increased risk for neurocognitive dysfunction.
Key words: inflammation; sleep disordered breathing; intermittent hypoxia; sleep fragmentation




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