Please use this identifier to cite or link to this item: https://doi.org/10.1136/archdischild-2014-306284
Title: New horizons for newborn brain protection: Enhancing endogenous neuroprotection
Authors: Hassell, K.J
Ezzati, M
Alonso-Alconada, D
Hausenloy, D.J 
Robertson, N.J
Keywords: cannabinoid
erythropoietin
melatonin
cannabinoid
erythropoietin
melatonin
neuroprotective agent
brain injury
brain protection
human
hypothermia
induced hypothermia
ischemic postconditioning
meta analysis (topic)
neuroprotection
newborn
pathogenesis
patient safety
phase 1 clinical trial (topic)
phase 2 clinical trial (topic)
phase 3 clinical trial (topic)
priority journal
randomized controlled trial (topic)
reperfusion
Review
adverse effects
Asphyxia Neonatorum
brain
drug effects
Hypoxia-Ischemia, Brain
neuroprotection
pathophysiology
procedures
Asphyxia Neonatorum
Brain
Cannabinoids
Erythropoietin
Humans
Hypothermia, Induced
Hypoxia-Ischemia, Brain
Infant, Newborn
Melatonin
Neuroprotection
Neuroprotective Agents
Issue Date: 2015
Publisher: BMJ Publishing Group
Citation: Hassell, K.J, Ezzati, M, Alonso-Alconada, D, Hausenloy, D.J, Robertson, N.J (2015). New horizons for newborn brain protection: Enhancing endogenous neuroprotection. Archives of Disease in Childhood: Fetal and Neonatal Edition 100 (6) : F541-F551. ScholarBank@NUS Repository. https://doi.org/10.1136/archdischild-2014-306284
Rights: Attribution 4.0 International
Abstract: Intrapartum-related events are the third leading cause of childhood mortality worldwide and result in one million neurodisabled survivors each year. Infants exposed to a perinatal insult typically present with neonatal encephalopathy (NE). The contribution of pure hypoxiaischaemia (HI) to NE has been debated; over the last decade, the sensitising effect of inflammation in the aetiology of NE and neurodisability is recognised. Therapeutic hypothermia is standard care for NE in high-income countries; however, its benefit in encephalopathic babies with sepsis or in those born following chorioamnionitis is unclear. It is now recognised that the phases of brain injury extend into a tertiary phase, which lasts for weeks to years after the initial insult and opens up new possibilities for therapy. There has been a recent focus on understanding endogenous neuroprotection and how to boost it or to supplement its effectors therapeutically once damage to the brain has occurred as in NE. In this review, we focus on strategies that can augment the body's own endogenous neuroprotection. We discuss in particular remote ischaemic postconditioning whereby endogenous brain tolerance can be activated through hypoxia/reperfusion stimuli started immediately after the index hypoxic-ischaemic insult. Therapeutic hypothermia, melatonin, erythropoietin and cannabinoids are examples of ways we can supplement the endogenous response to HI to obtain its full neuroprotective potential. Achieving the correct balance of interventions at the correct time in relation to the nature and stage of injury will be a significant challenge in the next decade.
Source Title: Archives of Disease in Childhood: Fetal and Neonatal Edition
URI: https://scholarbank.nus.edu.sg/handle/10635/179641
ISSN: 1359-2998
DOI: 10.1136/archdischild-2014-306284
Rights: Attribution 4.0 International
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