Sleep Apnea in Children May Affect Brain Development

Pam Harrison

March 23, 2017

In children with obstructive sleep apnea (OSA), gray matter volume is significantly reduced in brain regions that control cognition and mood, results from a new imaging study show.

These findings suggest OSA may either induce neuronal loss or delay neuronal growth in this patient population, investigators led by Leila Kheirandish-Gozal, MD, University of Chicago, in Illinois, note.

"We have repeatedly shown that at any level of sleep apnea severity, some children manifest evidence of neurocognitive deficits and others do not," Dr Kheirandish-Gozal told Medscape Medical News.

"And while we would like to believe that cognitive deficits/gray matter losses induced by sleep apnea in children are reversible — particularly when treatment, usually adenotonsillectomy, is instituted early ― this is an important aspect that we will test in future studies," she added.

The study was published online March 17 in Scientific Reports.

"Striking" Differences

Sixteen children with moderate to severe OSA underwent neurocognitive testing along with MRI at the University of Chicago. Findings were then compared with nine healthy children who were matched for age, sex, ethnicity, and weight.

MRI images from the 16 children with OSA were also compared to 191 MRI scans of children who are part of a pediatric MRI database compiled by the National Institutes of Health (NIH).

"The images of gray matter are striking," Dr Kheirandish-Gozal said in a statement. "We do not yet have a precise guide to correlate loss of gray matter with specific cognitive deficits, but there is clear evidence of widespread neuronal damage or loss compared to the general population."

Significant reductions in gray matter volume were observed in MRI scans of the frontal and prefrontal cortices as well as the parietal cortices, the temporal lobe, and the brainstem in children with OSA (P < .05).

"Prefrontal and frontal sites showed volume reductions in all areas, but the bilateral precentral gyrus was not affected," the authors note.

There was no evidence that OSA had an effect on the occipital cortices, but all parietal areas showed reductions in gray matter volume.

The investigators were unable to identify any association between findings on MRI in children with OAS and cognitive performance, as measured by the Differential Ability Scales.

However, higher gray matter volume has been linked to greater intelligence, as measured by IQ tests, but only in older children.

The investigators speculate that any effect that reductions in gray matter volume may have had on the IQ of children in this particular study may be undetectable, owing to their young age.

Animal models of sleep apnea show that neurons are damaged and die because of the way sleep apnea affects the brain. These effects lead to gray matter loss, Dr Kheirandish-Gozal explained.

Alternatively, the maturation and development of the brain may be slowed in children with sleep apnea, resulting in a reduction in gray matter during the period of development when gray matter normally increases.

In a statement, study coinvestigator David Gozal, MD, pointed out that MRI scans cannot determine whether brain cells have shrunk or have been lost completely in children with OSA.

"MRI scans give us a bird's eye view of the apnea-related difference in volume of various parts of the brain, but they don't tell us, at the cellular level, what happened to the affected neurons, or when. So we can't tell exactly when the damage occurred," he added.

However, earlier studies conducted by the same group showed that disease severity correlates with the extent of cognitive deficits when they are detected.

A Step Forward

Commenting on the findings for Medscape Medical News, Raanan Arens, MD, professor of pediatrics, Albert Einstein College of Medicine, and chief of the Division of Respiratory and Sleep Medicine, the Children's Hospital at Montefiore, New York City, said the study was important in that it showed that brain deficits in children with sleep-disordered breathing could correlate with neurocognitive deficits.

Although Dr Arens appreciated the fact that the authors could not detect an increase in neurocognitive deficits in children with OSA in comparision with the control children, "we know that the areas of the brain that were found to be deficient in size control memory, learning, and executive function, which are all very important for the development of the brain."

The failure to detect an effect on cognitive function in this particular study might simply reflect the small sample size and the fact that data on cognitive function were not available for the larger NIH comparator group.

"I think this study is a step forward in the field, first of all because investigators were able to scan the children and analyze brain structures using standardized tools, and they also used an additional database to get a larger number of controls, and that helped strengthen the study as well," Dr Arens said.

The study was supported by the Herbert T. Abelson Chair in Pediatrics. Dr Kheirandish-Gozal, Dr Gozal, and Dr Arens have disclosed no relevant financial relationships.

Sci Rep. Published online March 17, 2017. Full text

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