Update on mechanisms of the pathophysiology of neonatal encephalopathy.

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dc.contributor.author Davidson, Joanne O
dc.contributor.author Gonzalez, Fernando
dc.contributor.author Gressens, Pierre
dc.contributor.author Gunn, Alistair J
dc.contributor.author Newborn Brain Society Guidelines and Publications Committee
dc.coverage.spatial Netherlands
dc.date.accessioned 2021-08-02T03:28:16Z
dc.date.available 2021-08-02T03:28:16Z
dc.date.issued 2021-7-8
dc.identifier.issn 1744-165X
dc.identifier.uri https://hdl.handle.net/2292/55753
dc.description.abstract Therapeutic hypothermia is now well established to significantly improve survival without disability after neonatal encephalopathy (NE). To further improve outcomes, we need to better understand the mechanisms of brain injury. The central finding, which offers the potential for neuroprotective and neurorestorative interventions, is that brain damage after perinatal hypoxia-ischemia evolves slowly over time. Although brain cells may die during profound hypoxia-ischemia, even after surprisingly severe insults many cells show transient recovery of oxidative metabolism during a "latent" phase characterized by actively suppressed neural metabolism and activity. Critically, after moderate to severe hypoxia-ischemia, this transient recovery is followed after ~6 h by a phase of secondary deterioration, with delayed seizures, failure of mitochondrial function, cytotoxic edema, and cell death over ~72 h. This is followed by a tertiary phase of remodeling and recovery. This review discusses the mechanisms of injury that occur during the primary, latent, secondary and tertiary phases of injury and potential treatments that target one or more of these phases. By analogy with therapeutic hypothermia, treatment as early as possible in the latent phase is likely to have the greatest potential to prevent injury ("neuroprotection"). In the secondary phase of injury, anticonvulsants can attenuate seizures, but show limited neuroprotection. Encouragingly, there is now increasing preclinical evidence that late, neurorestorative interventions have potential to improve long-term outcomes.
dc.format.medium Print-Electronic
dc.language eng
dc.publisher Elsevier BV
dc.relation.ispartofseries Seminars in fetal & neonatal medicine
dc.rights Items in ResearchSpace are protected by copyright, with all rights reserved, unless otherwise indicated. Previously published items are made available in accordance with the copyright policy of the publisher.
dc.rights.uri https://researchspace.auckland.ac.nz/docs/uoa-docs/rights.htm
dc.subject Newborn Brain Society Guidelines and Publications Committee
dc.subject Anoxic depolarization
dc.subject Connexin Hemichannels
dc.subject Neonatal enceophalopathy
dc.subject Neurorestoration
dc.subject Seizures
dc.subject Tertiary cell loss
dc.subject Therapeutic hypothermia
dc.subject 1103 Clinical Sciences
dc.subject 1114 Paediatrics and Reproductive Medicine
dc.title Update on mechanisms of the pathophysiology of neonatal encephalopathy.
dc.type Journal Article
dc.identifier.doi 10.1016/j.siny.2021.101267
pubs.begin-page 101267
dc.date.updated 2021-07-24T03:00:45Z
dc.rights.holder Copyright: The author en
pubs.author-url https://www.ncbi.nlm.nih.gov/pubmed/34274259
pubs.publication-status Published
dc.rights.accessrights http://purl.org/eprint/accessRights/RestrictedAccess en
pubs.subtype Review
pubs.subtype Journal Article
pubs.elements-id 860273
dc.identifier.eissn 1878-0946
dc.identifier.pii S1744-165X(21)00075-5
pubs.number 101267

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