الفهرس 
introduction and aim of the workOnly 14 pages are availabe for public view
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Abstract
Bi11h asphyxia is a relatively common clinical event. There is over¬’helming evidence that an excessive concentration of extracellular lutamate and other excitatory amino acids has a crucial role in the athogenesis of neuronal death following brain ischaemia. Magnesium sulphate has been shown to reduce the severity of hypoxic-ischaemicr’1; Ibrain damage in immature rats since the divalent Mg acts as a glutamate receptor antagonist to the extent that it blocks the neuronal influx of Ca within the ion channel. Pro inflammatory cytokines contribute to the progression of perinatal brain injury, and these mediators are important targets for neuroprotective interventions in the acute post-injury period. Interventions designed to modify the concentration of cytokines are being currently evaluated in experimental models. The NMDA receptor antagonists have been shown to decrease the additional of cytokines; IL-6 IL-lf3 and TNF-a which is caused by hypoxia. The present study was conducted to assess the effect of magnesium sulphate on the clinical outcome of neonatal asphyxia including: HIE, convulsions, state of reflexes and state at discharge. As well as to study the effect of magnesium sulphate on the levels of certain proinflammatory cytokines; IL-6, IL-I f3 & TNF -u and neuroexcitatory amino acids; aspartate and glutamate in the cerebrospinal fluid of full-term asphyxiated newborns.