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F1000Prime Rep. 2014 Jan 2;6:6. doi: 10.12703/P6-6. eCollection 2014.

Perinatal neuroprotection.

Author information

1
513 Parnassus Avenue, Room HSE-1634, Box 0556, San Francisco, CA 94143-0556 USA.
2
106 Irving Street, NW, Room POB 108, Washington, DC 20010 USA.
3
505 Parnassus Avenue, Moffitt 1478, Box 0132, San Francisco, CA 94143-0132 USA.

Abstract

Fetal or neonatal brain injury can result in lifelong neurologic disability. The most significant risk factor for perinatal brain injury is prematurity; however, in absolute numbers, full-term infants represent the majority of affected children. Research on strategies to prevent or mitigate the impact of perinatal brain injury ("perinatal neuroprotection") has established the mitigating roles of magnesium sulfate administration for preterm infants and therapeutic hypothermia for term infants with suspected perinatal brain injury. Banked umbilical cord blood, erythropoietin, and a number of other agents that may improve neuronal repair show promise for improving outcomes following perinatal brain injury in animal models. Other preventative strategies include delayed umbilical cord clamping in preterm infants and progesterone in women with prior preterm birth or short cervix and avoidance of infections. Despite these advances, we have not successfully decreased the rate of preterm birth, nor are we able to predict term infants at risk of hypoxic brain injury in order to intervene prior to the hypoxic event. Further, we lack the ability to modulate the sequelae of neuronal cell insults or the ability to repair brain injury after it has been sustained. As a consequence, despite exciting advances in the field of perinatal neuroprotection, perinatal brain injury still impacts thousands of newborns each year with significant long-term morbidity and mortality.

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