REVIEW ARTICLE
Magnetic Resonance Imaging Findings of Term and Preterm Hypoxic-Ischemic Encephalopathy: A Review of Relevant Animal Models and Correlation to Human Imaging
Kyle A. Jisa, Dillon D. Clarey, Eric S. Peeples*
Article Information
Identifiers and Pagination:
Year: 2018Volume: 12
First Page: 55
Last Page: 65
Publisher ID: TONIJ-12-55
DOI: 10.2174/1874440001812010055
Article History:
Received Date: 19/3/2018Revision Received Date: 7/8/2018
Acceptance Date: 16/9/2018
Electronic publication date: 17/10/2018
Collection year: 2018
open-access license: This is an open access article distributed under the terms of the Creative Commons Attribution 4.0 International Public License (CC-BY 4.0), a copy of which is available at: https://creativecommons.org/licenses/by/4.0/legalcode. This license permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Abstract
Background:
Neonatal hypoxic-ischemic encephalopathy is brain injury caused by decreased perfusion and oxygen delivery that most commonly occurs in the context of delivery complications such as umbilical cord compression or placental abruption. Imaging is a key component for guiding treatment and prediction of prognosis, and the most sensitive clinical imaging modality for the brain injury patterns seen in hypoxic-ischemic encephalopathy is magnetic resonance imaging.
Objective:
The goal of this review is to compare magnetic resonance imaging findings demonstrated in the available animal models of hypoxic-ischemic encephalopathy to those found in preterm (≤ 36 weeks) and term (>36 weeks) human neonates with hypoxic-ischemic encephalopathy, with special attention to the strengths and weaknesses of each model.
Methods:
A structured literature search was performed independently by two authors and the results of the searches were compiled. Animal model, human brain age equivalency, mechanism of injury, and area of brain injury were recorded for comparison to imaging findings in preterm and term human neonates with hypoxic-ischemic encephalopathy.
Conclusion:
Numerous animal models have been developed to better elicit the expected findings that occur after HIE by allowing investigators to control many of the clinical variables that result in injury. Although modeling the same disease process, magnetic resonance imaging findings in the animal models vary with the species and methods used to induce hypoxia and ischemia. The further development of animal models of HIE should include a focus on comparing imaging findings, and not just pathologic findings, to human studies.
