Abstract
Perinatal brain injury at term is common and often manifests with neonatal encephalopathy including seizures. The most common aetiologies are hypoxic–ischaemic encephalopathy, intracranial haemorrhage and neonatal stroke. Besides clinical and biochemical assessment the diagnostic evaluation rely mostly on EEG and neuroimaging including cranial ultrasound and magnetic resonance imaging. The mechanisms underlying hypoxic–ischaemic brain injury are only partly understood but include excitotoxicity, mitochondrial perturbation, necrosis/apoptosis and inflammation. Neuroprotective treatment of newborns suffering from hypoxic–ischaemic encephalopathy with hypothermia has proven effective and has been introduced as a clinical routine. Ongoing studies are exploring various add-on therapies including erythropoietin, xenon, topiramate, melatonin and stem cells.
Highlights
Perinatal brain injury in the term infant is common in both developed and underprivileged countries
Neonatal encephalopathy occurs in 1–3 per 1000 infants born at term and is most commonly due to hypoxia–ischaemia (Glass et al, 2009; Ronen et al, 1999; Vasudevan and Levene, 2013)
Risk factors for hypoxic–ischaemic encephalopathy include a gestational age above 41 weeks, prolonged membrane rupture, abnormal cardiotocography, thick meconium, sentinel event, shoulder dystocia, tight nuchal cord, failed vacuum (Martinez-Biarge et al, 2013), and white matter injury, which was associated with hypoglycaemia and mutations in the MTHFR gene resulting in elevated levels of plasma homocysteine (Harteman et al, 2013a)
Summary
Perinatal brain injury in the term infant is common in both developed and underprivileged countries. Mechanisms of secondary brain injury The specific mechanisms of secondary damage are only partly understood, but excitotoxicity, mitochondrial impairment, intracellular regulation of Ca2+, oxygen and nitrosative stress, deficiency of trophic factors and inflammation are all implicated in the process (Hagberg et al, 2014, 2015; Thornton et al, 2012). Both accidental and regulated (e.g. apoptosis, necroptosis) cell death appears critical in the execution phase of cellular demise (Thornton and Hagberg, 2015; Johnston, 2005).
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