Background
birth injury, hypothermia, brain injury, HIE, brain damage, Ischemia
HYPOXIC ISCHEMIC ENCEPHALOPATHY, ISCHEMIA, HYPOXIC-ISCHEMIC ENCEPHALOPATHY (HIE)
Hypoxic-ischemic encephalopathy (HIE) is a type of birth injury that leads to neonatal brain damage [Infants who experience moderate HIE have a 10% risk of fatality, and those who live have a 30% risk of disabilities. Infants with severe HIE have a 60% risk of fatality, and nearly all of the survivors experience disabilities [Ischemia in the brain triggers a series of metabolic reactions that result in an influx of sodium (Na +) and calcium (Ca2 +) into cells resulting in the release of neurotransmitters like glutamate, causing cell excitotoxicity and the formation of free radicals that stimulate synthesis of nitric oxide (NO) which can react with superoxide causing subsequent brain injury [There are several treatment options used now for HIE as xenon, erythropoietin, melatonin, and stem cell therapy. The clinical use of these neuroprotective drugs in HIE is suboptimal due to inefficiency and /or treatment-induced undesirable side effects [Potential therapies of hypoxic ischemic encephalopathy and their mechanism of actionsHowever, the only available effective neuroprotector so far is therapeutic hypothermia which can’t be used in several situations such as gestational age less than 36 weeks, birth weight less than 2000 g, and more than 6 h of age at the time of initiating therapeutic hypothermia [Citicoline, refers to the exogenously supplied form of cytidine 5-diphosphocholine (CDP-choline), is a product of the rate-limiting step in the synthesis of phosphatidylcholine from choline. Citicoline is rapidly absorbed when taken orally because it is digested in the gut into cytidine and choline [Citicoline could be a promising new neuroprotector in HIE as its mechanism of action helps in the regeneration of neuronal cells by several actions. As HIE induces cell apoptosis, citicoline provides neurorepair by inhibiting different steps of the ischemic cascade protecting the injured tissue against early and delayed mechanisms responsible for ischemic brain injury such as inhibition of glutamate accumulation, regeneration of the injured cell membrane, increasing brain plasticity and repair, increasing useful neurotransmitters such as dopamine and acetylcholine, and preventing free radicle formation [In this study, we assessed the effect of citicoline as a neuroprotector in neonates with moderate and severe HIE.