title: Childhood obstructive sleep apnea associates with neuropsychological deficits and neuronal brain injury.
abstract: BACKGROUND
  Childhood obstructive sleep apnea (OSA) is associated with neuropsychological deficits of memory, learning, and executive function. There is no evidence of neuronal brain injury in children with OSA. We hypothesized that childhood OSA is associated with neuropsychological performance dysfunction, and with neuronal metabolite alterations in the brain, indicative of neuronal injury in areas corresponding to neuropsychological function.
  
  
  RESULTS
  We conducted a cross-sectional study of 31 children (19 with OSA and 12 healthy controls, aged 6-16 y) group-matched by age, ethnicity, gender, and socioeconomic status. Participants underwent polysomnography and neuropsychological assessments. Proton magnetic resonance spectroscopic imaging was performed on a subset of children with OSA and on matched controls. Neuropsychological test scores and mean neuronal metabolite ratios of target brain areas were compared. Relative to controls, children with severe OSA had significant deficits in IQ and executive functions (verbal working memory and verbal fluency). Children with OSA demonstrated decreases of the mean neuronal metabolite ratio N-acetyl aspartate/choline in the left hippocampus (controls: 1.29, standard deviation [SD] 0.21; OSA: 0.91, SD 0.05; p = 0.001) and right frontal cortex (controls: 2.2, SD 0.4; OSA: 1.6, SD 0.4; p = 0.03).
  
  
  CONCLUSIONS
  Childhood OSA is associated with deficits of IQ and executive function and also with possible neuronal injury in the hippocampus and frontal cortex. We speculate that untreated childhood OSA could permanently alter a developing child's cognitive potential.
authors.affiliation: Department of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. ahalbowe@jhmi.edu
authors.forename: Ann C
authors.initials: AC
authors.lastname: Halbower
authors.forename: Mahaveer
authors.initials: M
authors.lastname: Degaonkar
authors.forename: Peter B
authors.initials: PB
authors.lastname: Barker
authors.forename: Christopher J
authors.initials: CJ
authors.lastname: Earley
authors.forename: Carole L
authors.initials: CL
authors.lastname: Marcus
authors.forename: Philip L
authors.initials: PL
authors.lastname: Smith
authors.forename: M Cristine
authors.initials: MC
authors.lastname: Prahme
authors.forename: E Mark
authors.initials: EM
authors.lastname: Mahone
mesh_terms: D000293:Adolescent; D001224:Aspartic Acid / Q000378:metabolism; D001930:Brain Injuries / Q000150:complications*; D016022:Case-Control Studies; D002540:Cerebral Cortex / Q000000981:diagnostic imaging; D002648:Child; D002794:Choline / Q000378:metabolism; D003430:Cross-Sectional Studies; D003710:Demography; D005260:Female; D006624:Hippocampus / Q000000981:diagnostic imaging / Q000378:metabolism / Q000473:pathology; D006801:Humans; D008279:Magnetic Resonance Imaging; D008297:Male; D009474:Neurons / Q000473:pathology*; D009483:Neuropsychological Tests; D017286:Polysomnography; D011859:Radiography; D012129:Respiratory Function Tests; D020181:Sleep Apnea, Obstructive / Q000150:complications*
chemical_list: D001224:Aspartic Acid; D002794:Choline