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Oxidative Metabolism, Apoptosis and Perinatal Brain Injury

Perinatal hypoxic‐ischaemic injury (HII) is a significant cause of neurodevelopmental impairment and disability. Studies employing 31P magnetic resonance spectroscopy to measure phosphorus metabolites in situ in the brains of newborn infants and animals have demonstrated that transient hypoxia‐ischaemia leads to a delayed disruption in cerebral energy metabolism, the magnitude of which correlates with the subsequent neurodevelopmental impairment.