White matter injury after neonatal encephalopathy is associated with thalamic metabolite perturbations.


Journal

EBioMedicine
ISSN: 2352-3964
Titre abrégé: EBioMedicine
Pays: Netherlands
ID NLM: 101647039

Informations de publication

Date de publication:
Feb 2020
Historique:
received: 29 10 2019
revised: 20 01 2020
accepted: 22 01 2020
pubmed: 18 2 2020
medline: 9 10 2020
entrez: 17 2 2020
Statut: ppublish

Résumé

Although thalamic magnetic resonance (MR) spectroscopy (MRS) accurately predicts adverse outcomes after neonatal encephalopathy, its utility in infants without MR visible deep brain nuclei injury is not known. We examined thalamic MRS metabolite perturbations in encephalopathic infants with white matter (WM) injury with or without cortical injury and its associations with adverse outcomes. We performed a subgroup analysis of all infants recruited to the MARBLE study with isolated WM or mixed WM/cortical injury, but no visible injury to the basal ganglia/thalamus (BGT) or posterior limb of the internal capsule (PLIC). We used binary logistic regression to examine the association of MRS biomarkers with three outcomes (i) WM injury score (1 vs. 2/3); (ii) cortical injury scores (0/1 vs. 2/3); and (iii) adverse outcomes (defined as death, moderate/severe disability) at two years (yes/no). We also assessed the accuracy of MRS for predicting adverse outcome. Of the 107 infants included in the analysis, five had adverse outcome. Reduced thalamic N-acetylaspartate concentration [NAA] (odds ratio 0.4 (95% CI 0.18-0.93)) and elevated thalamic Lactate/NAA peak area ratio (odds ratio 3.37 (95% CI 1.45-7.82)) were significantly associated with higher WM injury scores, but not with cortical injury. Thalamic [NAA] (≤5.6 mmol/kg/wet weight) had the best accuracy for predicting adverse outcomes (sensitivity 1.00 (95% CI 0.16-1.00); specificity 0.95 (95% CI 0.84-0.99)). Thalamic NAA is reduced in encephalopathic infants without MR visible deep brain nuclei injury and may be a useful predictor of adverse outcomes. The National Institute for Health Research (NIHR).

Sections du résumé

BACKGROUND BACKGROUND
Although thalamic magnetic resonance (MR) spectroscopy (MRS) accurately predicts adverse outcomes after neonatal encephalopathy, its utility in infants without MR visible deep brain nuclei injury is not known. We examined thalamic MRS metabolite perturbations in encephalopathic infants with white matter (WM) injury with or without cortical injury and its associations with adverse outcomes.
METHODS METHODS
We performed a subgroup analysis of all infants recruited to the MARBLE study with isolated WM or mixed WM/cortical injury, but no visible injury to the basal ganglia/thalamus (BGT) or posterior limb of the internal capsule (PLIC). We used binary logistic regression to examine the association of MRS biomarkers with three outcomes (i) WM injury score (1 vs. 2/3); (ii) cortical injury scores (0/1 vs. 2/3); and (iii) adverse outcomes (defined as death, moderate/severe disability) at two years (yes/no). We also assessed the accuracy of MRS for predicting adverse outcome.
FINDINGS RESULTS
Of the 107 infants included in the analysis, five had adverse outcome. Reduced thalamic N-acetylaspartate concentration [NAA] (odds ratio 0.4 (95% CI 0.18-0.93)) and elevated thalamic Lactate/NAA peak area ratio (odds ratio 3.37 (95% CI 1.45-7.82)) were significantly associated with higher WM injury scores, but not with cortical injury. Thalamic [NAA] (≤5.6 mmol/kg/wet weight) had the best accuracy for predicting adverse outcomes (sensitivity 1.00 (95% CI 0.16-1.00); specificity 0.95 (95% CI 0.84-0.99)).
INTERPRETATION CONCLUSIONS
Thalamic NAA is reduced in encephalopathic infants without MR visible deep brain nuclei injury and may be a useful predictor of adverse outcomes.
FUNDING BACKGROUND
The National Institute for Health Research (NIHR).

Identifiants

pubmed: 32062359
pii: S2352-3964(20)30038-4
doi: 10.1016/j.ebiom.2020.102663
pmc: PMC7016374
pii:
doi:

Substances chimiques

Biomarkers 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

102663

Subventions

Organisme : Department of Health
ID : ICA-CDRF-2016-02-071
Pays : United Kingdom
Organisme : Medical Research Council
ID : MR/R001375/1
Pays : United Kingdom

Informations de copyright

Copyright © 2020 The Authors. Published by Elsevier B.V. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of Competing Interest We declare no competing interests.

Références

Cochrane Database Syst Rev. 2013 Jan 31;(1):CD003311
pubmed: 23440789
Lancet Neurol. 2019 Jan;18(1):35-45
pubmed: 30447969
Neuroradiology. 2010 Jun;52(6):555-66
pubmed: 20390260
Arch Dis Child Fetal Neonatal Ed. 2012 Nov;97(6):F398-404
pubmed: 23080477
Eur J Paediatr Neurol. 2013 Sep;17(5):492-7
pubmed: 23603010
Ann Neurol. 1992 Jan;31(1):14-21
pubmed: 1543346
J Pediatr. 2012 Nov;161(5):799-807
pubmed: 22682614
Pediatrics. 2010 Feb;125(2):e382-95
pubmed: 20083516
Am J Perinatol. 2000;17(3):113-20
pubmed: 11012134
Dev Med Child Neurol. 2009 Jan;51(1):46-52
pubmed: 19018834
J Perinatol. 2014 Aug;34(8):629-33
pubmed: 24743133
J Pediatr. 2015 Nov;167(5):987-93.e3
pubmed: 26387012
Brain Res. 2003 Dec 12;993(1-2):101-10
pubmed: 14642835
Pediatrics. 2008 May;121(5):906-14
pubmed: 18450893
Trials. 2017 Sep 18;18(1):432
pubmed: 28923118
Lancet Neurol. 2010 Jan;9(1):39-45
pubmed: 19896902
EBioMedicine. 2019 Sep;47:484-491
pubmed: 31451436
Brain Dev. 2013 Jan;35(1):26-31
pubmed: 22082686
Dev Med Child Neurol. 2009 Aug;51(8):622-8
pubmed: 19416329
J Pediatr. 2005 Apr;146(4):453-60
pubmed: 15812446
J Pediatr. 2019 Mar;206:66-71.e1
pubmed: 30414629
Pediatr Radiol. 2018 Jun;48(6):865-874
pubmed: 29417166
Neural Plast. 2016;2016:4901014
pubmed: 27047695
BMJ Open. 2015 Sep 30;5(9):e008912
pubmed: 26423856
Pediatr Res. 2017 Sep;82(3):518-526
pubmed: 28561815
Arch Dis Child Fetal Neonatal Ed. 2019 Jul;104(4):F424-F432
pubmed: 30322975

Auteurs

Paolo Montaldo (P)

Centre for Perinatal Neuroscience, Department of Brain Sciences, Imperial College London, London, UK; Department of Neonatal Intensive Care, Università degli Studi della Campania Luigi Vanvitelli, Naples, Italy. Electronic address: p.montaldo@imperial.ac.uk.

Phoebe Ivain (P)

Centre for Perinatal Neuroscience, Department of Brain Sciences, Imperial College London, London, UK.

Pete Lally (P)

Centre for Perinatal Neuroscience, Department of Brain Sciences, Imperial College London, London, UK.

Paul Bassett (P)

Statsconsultancy Ltd., Amersham, UK.

Stuti Pant (S)

Centre for Perinatal Neuroscience, Department of Brain Sciences, Imperial College London, London, UK.

Vania Oliveira (V)

Centre for Perinatal Neuroscience, Department of Brain Sciences, Imperial College London, London, UK.

Josephine Mendoza (J)

Centre for Perinatal Neuroscience, Department of Brain Sciences, Imperial College London, London, UK.

Maria Morales (M)

Centre for Perinatal Neuroscience, Department of Brain Sciences, Imperial College London, London, UK.

Ravi Swamy (R)

Centre for Perinatal Neuroscience, Department of Brain Sciences, Imperial College London, London, UK.

Seetha Shankaran (S)

Neonatal-Perinatal Medicine, Wayne State University, USA.

Sudhin Thayyil (S)

Centre for Perinatal Neuroscience, Department of Brain Sciences, Imperial College London, London, UK.

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Classifications MeSH