Children with severe obstructive sleep apnea demonstrate decreased IQ and other neuropsychological deficits, and have metabolic brain abnormalities that can be seen on imaging, indicating possible neuronal injury, according to a new study.
“We speculate that untreated [obstructive sleep apnea] could permanently alter the trajectory of a developing child's ultimate cognitive potential, resulting in a lifetime of health and economic impacts,” wrote Dr. Ann C. Halbower of Johns Hopkins University, Baltimore, and her colleagues in the August 22 issue of the global online journal Public Library of Science Medicine.
The findings do not necessarily indicate a causal relationship between obstructive sleep apnea (OSA) and neuronal abnormalities, they noted. “It remains to be determined if early identification and treatment can reverse the neuronal and performance deficits,” the authors wrote. However, the findings show altered neuronal metabolites in both the hippocampus and right frontal cortex of children with OSA.
“This is truly concerning because we saw changes that suggest brain injury in areas of the brain that house critical cognitive functions, such as attention, learning, and working memory,” Dr. Halbower said in a written statement. The cross-sectional study included 19 children with moderate-severe OSA (defined as an apnea-hypopnea index of 8 or higher as measured by polysomnography) and 12 healthy, nonsnoring children as controls. The groups were matched for age, ethnicity, gender, and socioeconomic status.
Neuropsychological evaluations performed on all subjects revealed that children with OSA had significantly lower scores, compared with controls, on full-scale IQ, and lower performance on measures of executive function, including verbal working memory and word fluency. There were no significant differences between the groups on any other neuropsychological variables, although a trend toward decreased visual-spatial memory and verbal memory in children with OSA might have gained statistical significance with larger numbers, the authors noted. (See box.)
A subset of 26 out of 31 subjects underwent one or two proton magnetic resonance spectroscopy (MRS) studies to detect both steady-state levels and ratios of three brain metabolites: N-acetylaspartate (NAA), choline (Cho), and creatine (Cr).
Single-voxel MRS comparisons of the left hippocampus in six children with OSA and six controls showed that the OSA group had a significant decrease in hippocampal NAA:Cho ratios, and a significant increase in Cho:Cr, “indicating abnormal neuronal metabolism in the static state,” the authors noted. MRS imaging of cortical structures showed a significant decrease in the NAA:Cho ratio in the right frontal cortex of seven children with OSA, compared with six controls.
There were no significant differences in cerebellar Cho:Cr or NAA:Cho ratios in five controls and seven children with OSA–although with larger numbers the latter ratio might have reached significance, the authors suggested.
The OSA subjects were significantly more overweight or obese than controls. “If obesity and [sleep-disordered breathing] interact, these combined problems, as well as lifestyle factors linked with obesity (such as television time), may play an important role in exacerbating neuropsychological impairments associated with sleep apnea,” they wrote.
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