Two new UCLA studies have identified brain irregularities in children who suffer from congenital central hypoventilation syndrome (CCHS), a disease in which children stop breathing during sleep, often resulting in their suffocation and death. The scientists tested how CCHS children's brains react to carbon dioxide and low oxygen levels in comparison to the brains of healthy children.
Several unexpected regions in the healthy children's brains responded to the gases — particularly in sites that perceive and react to the sensation of breathlessness during suffocation. The same regions in CCHS children's brains responded poorly or not at all. This may explain why the children do not struggle to breathe when their lungs shut down — even after turning blue from lack of air.
The findings suggest that the irregular brain mechanisms provoking CCHS may also underlie sudden infant death syndrome (SIDS). Children afflicted by the two conditions share many of the same symptoms and health problems.
Authors of the studies are: Ronald Harper, professor of neurobiology, and Paul Macey, neurobiology postdoctoral researcher, at the David Geffen School of Medicine at UCLA.
· Journal of Neurophysiology, Nov. 3
"Hypoventilation reveals central nervous system respiratory control mechanisms"
· Journal of Applied Physiology, Nov. 5
"Hypoxia reveals posterior thalamic, cerebellar, midbrain and limbic deficits in congenital central hypoventilation syndrome"
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