The pathophysiology of perinatal hypoxic-ischemic insults has been investigated exhaustively to identify the components that must be blocked to reduce neurologic injury in the newborn. Among potential therapeutic strategies for neuroprotection, administration of magnesium has been the object of experimental studies and, recently, clinical trials. This interest is related to the compound's potential effect of blocking glutamate-controlled N-methyl-D-aspartate (NMDA) receptors and the voltage-dependent calcium channels, preventing the influx of extracellular calcium into the neurons, as well as its action as a membrane stabilizer. To date, results have been variable and are not sufficient to recommend this therapy in newborns who have perinatal asphyxia.