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      Perinatal Hypoxic-Ischemic Encephalopathy

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      Author(s): 1 , 2, 3, 4, 5 , *
      Publication date (Electronic):
      Journal: Journal of Biomedicine and Biotechnology
      Publisher: Hindawi Publishing Corporation

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          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.

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          Most cited references55

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          Neonatal brain injury.

          Donna Ferriero (2004)
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            Glutamate-induced neuronal death: a succession of necrosis or apoptosis depending on mitochondrial function.

            Maria Ankarcrona, Jeannette M. Dypbukt, Emanuela Bonfoco … (1995)
            During ischemic brain injury, glutamate accumulation leads to overstimulation of postsynaptic glutamate receptors with intracellular Ca2+ overload and neuronal cell death. Here we show that glutamate can induce either early necrosis or delayed apoptosis in cultures of cerebellar granule cells. During and shortly after exposure to glutamate, a subpopulation of neurons died by necrosis. In these cells, mitochondrial membrane potential collapsed, nuclei swelled, and intracellular debris were scattered in the incubation medium. Neurons surviving the early necrotic phase recovered mitochondrial potential and energy levels. Later, they underwent apoptosis, as shown by the formation of apoptotic nuclei and by chromatin degradation into high and low molecular weight fragments. These results suggest that mitochondrial function is a critical factor that determines the mode of neuronal death in excitotoxicity.
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              A systematic review of the role of intrapartum hypoxia-ischemia in the causation of neonatal encephalopathy.

              Ernest M. Graham, Kristy Ruis, Adam Hartman … (2008)
              The object of this review was to determine the incidence, morbidity, and mortality of an umbilical arterial pH < 7.0; the incidence of hypoxic-ischemic encephalopathy; and the proportion of cerebral palsy associated with intrapartum hypoxia-ischemia in nonanomalous term infants. A systematic review of the English language literature on the association between intrapartum hypoxia-ischemia and neonatal encephalopathy was conducted by using Pubmed and Embase. For nonanomalous term infants, the incidence of an umbilical arterial pH < 7.0 at birth is 3.7 of 1000, of which 51 of 297 (17.2%) survived with neonatal neurologic morbidity, 45 of 276 (16.3%) had seizures, and 24 of 407 (5.9%) died during the neonatal period. The incidence of neonatal neurologic morbidity and mortality for term infants born with cord pH < 7.0 was 23.1%. The incidence of hypoxic-ischemic encephalopathy is 2.5 of 1000 live births. The proportion of cerebral palsy associated with intrapartum hypoxia-ischemia is 14.5%. The vast majority of cases of cerebral palsy in nonanomalous term infants are not associated with intrapartum hypoxia-ischemia.
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                Author and article information

                Journal
                Journal ID (nlm-ta): J Biomed Biotechnol
                Journal ID (publisher-id): JBB
                Title: Journal of Biomedicine and Biotechnology
                Publisher: Hindawi Publishing Corporation
                ISSN (Print): 1110-7243
                ISSN (Electronic): 1110-7251
                Publication date (Print): 2011
                Publication date (Electronic): 13 December 2010
                Volume: 2011
                Electronic Location Identifier: 609813
                Affiliations
                1Department of Pediatrics, Chi Mei Medical Center, Tainan, Taiwan
                2Graduate Institute of Medicine, Kaohsiung Medical University, No. 100, Zihyou 1st Road, Sanmin District Kaohsiung City 807, Taiwan
                3Center of Excellence for Environmental Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan
                4Department of Pediatrics, Kaohsiung Medical University Hospital, Kaohsiung, Taiwan
                5Department of Marine Biotechnology and Resources, National Sun Yat-sen University, Kaohsiung, Taiwan
                Author notes

                Academic Editor: Oreste Gualillo

                Article
                DOI: 10.1155/2011/609813
                PMC ID: 3010686
                PubMed ID: 21197402
                SO-VID: 4db81903-39fe-4250-94ea-1bc97daf03b4
                Copyright © Copyright © 2011 M.-C. Lai and S.-N. Yang.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 15 September 2010
                Date accepted : 8 November 2010
                Categories
                Subject: Review Article

                ScienceOpen disciplines: Molecular medicine
                Data availability:
                ScienceOpen disciplines: Molecular medicine

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