This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Vannucci, S. J. Search for Related Content PubMed Articles by Vannucci, S. J. Related Collections Animal models of human disease Acute Cerebral Infarction Brain Circulation and Metabolism

(Stroke. 2007;38:723.)
© 2007 American Heart Association, Inc.

Cerebral Ischemia and the Developing Brain: Introduction

Cerebral Ischemia and the Developing Brain

Introduction

Susan J. Vannucci, PhD

From the Department of Pediatrics and the Institute of Human Nutrition, Columbia University, New York, New York.

Correspondence to Susan J. Vannucci, Department of Pediatrics and the Institute of Human Nutrition, Columbia University, 3959 Broadway, CHN 10-24, New York, NY, United States 10032. E-mail sv2020@columbia.edu

An extract of the first 250 words of the full text is provided, because this article has no abstract.

The Princeton Conference has focused almost exclusively on cerebrovascular disease in the mature, or adult, brain. This session at the 25th Princeton Conference was quite unique in that the focus was on cerebral ischemia in the developing brain, ie, in both preterm and term infant. Hypoxic-ischemic injury to the developing brain is a major cause of acute mortality and chronic neurological morbidity in infants and children. Statistics suggest an incidence of systemic asphyxia in 2 to 4/1000 full-term births and an incidence approaching 60% in low birth weight, premature newborns.^1,2 Between 20% to 50% of asphyxiated newborns with hypoxic-ischemic encephalopathy die within the newborn period, and up to 25% of the survivors go on to exhibit permanent neuropsychological handicaps, including mental retardation, cerebral palsy, epilepsy or learning disability. Care of the fetus and newborn human infant at risk for developing cerebral hypoxia-ischemia is clearly a high priority in current health care, and an understanding of the pathophysiology of perinatal hypoxic-ischemic brain damage is essential to the design of effective therapeutic interventions.

Much of our current understanding of the pathophysiology of hypoxic-ischemic brain damage derives from the vast body of experimental literature on stroke in the adult brain. From these studies, it is now well established that a cerebral hypoxic-ischemic event severe enough to cause cellular energy depletion initiates a cascade of events including early events of acidosis, glutamate excitotoxicity, and generation of reactive oxygen species, followed by prolonged periods of delayed cell death and inflammation.³ To a certain extent this . . . [Full Text of this Article]