Perinatal hypoxic-ischemic encephalopathy.

Ming-Chi Lai,San-Nan Yang

doi:10.1155/2011/609813

Abstract

Perinatal hypoxic-ischemic encephalopathy (HIE) is an important cause of brain injury in the newborn and can result in long-term devastating consequences. Perinatal hypoxia is a vital cause of long-term neurologic complications varying from mild behavioural deficits to severe seizure, mental retardation, and/or cerebral palsy in the newborn. In the mammalian developing brain, ongoing research into pathophysiological mechanism of neuronal injury and therapeutic strategy after perinatal hypoxia is still limited. With the advent of promising therapy of hypothermia in HIE, this paper reviews the pathophysiology of HIE and the future potential neuroprotective strategies for clinical potential for hypoxia sufferers.

Highlights

Perinatal hypoxic-ischemic encephalopathy (HIE) occurs in one to three per 1000 live full-term births [1]
Initial decrease in high-energy phosphates will result in impairment of ATP-dependent Na+-K+ pump, which in the severe insult causes an acute influx of Na+, Cl−, and water with consequent cell swelling, cell lysis, and early cell death by necrosis whereas in less severe insult causes membrane depolarization followed by a cascade of excitotoxicity and oxidative stress leading to a delayed cell death, principally apoptosis
The principal form of hypoxia-ischemic brain injury in the immature brain involves cerebral white matter, causing periventricular leukomalacia (PVL), and the data indicate an implication of a particular maturation-dependent intrinsic vulnerability of premyelinating oligodendrocytes to both endogenous and exogenous reactive oxygen species [35,36,37]

Summary

Introduction

Perinatal hypoxic-ischemic encephalopathy (HIE) occurs in one to three per 1000 live full-term births [1]. The outcomes of HIE are devastating and permanent, making it a major burden for the patient, the family, and society. It is critical to identify and develop therapeutic strategies to reduce brain injury in newborns with HIE. The underlying pathophysiology of perinatal HIE is difficult to study in the human, the neonatal rat model for HI brain injury has been developed to model this human condition. Much of what we know is derived from studies conducted in animal models. Rodents were the most frequently used animals in HIE research, followed by piglets and sheep [3]

Gestational and Chronological Age

Potential Therapies for Neonatal Hypoxic-Ischemic Encephalopathy

Conclusion