The Infancy of the Brain and Hyperoxia

Eva Parker

In spite of significant advances in obstetrics and neonatal concentrated care, preterm newborn children often experience the ill effects of neurological impairments in later life. Due to the immaturity of endogenous radical scavenging systems, preterm and full-term infants are typically vulnerable to damage from reactive oxygen species. It is common knowledge that elevated oxygen levels experienced during the crucial stage of maturation have the potential to profoundly influence the processes of development. It is known that supra physiological oxygen concentrations used in the care of critically ill infants or for resuscitation have negative effects on the developing lung and retina, which contributes to the pathophysiology of neonatal diseases like broncho pulmonary dysplasia and prematurity retinopathy. In addition, research conducted in the past ten years suggests that hyperoxia also causes the death of neuronal and glial cells, which contributes to the damage to the white and grey matter found in premature infants. Hyperoxia can alter developmental processes during the crucial stage of brain maturation, disrupting neural plasticity and myelination. Therefore, protective and/or regenerative strategies are highly warranted in situations requiring oxygen supplementation in addition to the development of appropriate monitoring systems. In this section, we provide an overview of the pathophysiology of oxygen exposure on the developing central nervous system and its impact on neonatal brain injury, as well as a summary of the clinical and experimental evidence and potential therapeutic strategies