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Subacute Changes in N-Acetylaspartate (NAA) Following Ischemic Stroke: A Serial MR Spectroscopy Pilot Study
Preservation of neuronal tissue is crucial for recovery after stroke, but studies suggest that prolonged neuronal loss occurs following acute ischaemia. This study assessed the temporal pattern of neuronal loss in subacute ischemic stroke patients using (1)H magnetic resonance spectroscopy, in paral...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7399797/ https://www.ncbi.nlm.nih.gov/pubmed/32708540 http://dx.doi.org/10.3390/diagnostics10070482 |
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author | Mazibuko, Ndaba Tuura, Ruth O’Gorman Sztriha, Laszlo O’Daly, Owen Barker, Gareth J. Williams, Steven C. R. O’Sullivan, Michael Kalra, Lalit |
author_facet | Mazibuko, Ndaba Tuura, Ruth O’Gorman Sztriha, Laszlo O’Daly, Owen Barker, Gareth J. Williams, Steven C. R. O’Sullivan, Michael Kalra, Lalit |
author_sort | Mazibuko, Ndaba |
collection | PubMed |
description | Preservation of neuronal tissue is crucial for recovery after stroke, but studies suggest that prolonged neuronal loss occurs following acute ischaemia. This study assessed the temporal pattern of neuronal loss in subacute ischemic stroke patients using (1)H magnetic resonance spectroscopy, in parallel with functional recovery at 2, 6 and 12 weeks after stroke. Specifically, we measured N-acetylaspartate (NAA), choline, myoinositol, creatine and lactate concentrations in the ipsilesional and contralesional thalamus of 15 first-ever acute ischaemic stroke patients and 15 control participants and correlated MRS concentrations with motor recovery, measured at 12 weeks using the Fugl–Meyer scale. NAA in the ipsilesional thalamus fell significantly between 2 and 12 weeks (10.0 to 7.97 mmol/L, p = 0.003), while choline, myoinositol and lactate concentrations increased (p = 0.025, p = 0.031, p = 0.001, respectively). Higher NAA concentrations in the ipsilesional thalamus at 2 and 12 weeks correlated with higher Fugl Meyer scores at 12 weeks (p = 0.004 and p = 0.006, respectively). While these results should be considered preliminary given the modest sample size, the progressive fall in NAA and late increases in choline, myoinositol and lactate may indicate progressive non-ischaemic neuronal loss, metabolically depressed neurons and/or diaschisis effects, which have a detrimental effect on motor recovery. Interventions that can potentially limit this ongoing subacute tissue damage may improve stroke recovery. |
format | Online Article Text |
id | pubmed-7399797 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-73997972020-08-17 Subacute Changes in N-Acetylaspartate (NAA) Following Ischemic Stroke: A Serial MR Spectroscopy Pilot Study Mazibuko, Ndaba Tuura, Ruth O’Gorman Sztriha, Laszlo O’Daly, Owen Barker, Gareth J. Williams, Steven C. R. O’Sullivan, Michael Kalra, Lalit Diagnostics (Basel) Article Preservation of neuronal tissue is crucial for recovery after stroke, but studies suggest that prolonged neuronal loss occurs following acute ischaemia. This study assessed the temporal pattern of neuronal loss in subacute ischemic stroke patients using (1)H magnetic resonance spectroscopy, in parallel with functional recovery at 2, 6 and 12 weeks after stroke. Specifically, we measured N-acetylaspartate (NAA), choline, myoinositol, creatine and lactate concentrations in the ipsilesional and contralesional thalamus of 15 first-ever acute ischaemic stroke patients and 15 control participants and correlated MRS concentrations with motor recovery, measured at 12 weeks using the Fugl–Meyer scale. NAA in the ipsilesional thalamus fell significantly between 2 and 12 weeks (10.0 to 7.97 mmol/L, p = 0.003), while choline, myoinositol and lactate concentrations increased (p = 0.025, p = 0.031, p = 0.001, respectively). Higher NAA concentrations in the ipsilesional thalamus at 2 and 12 weeks correlated with higher Fugl Meyer scores at 12 weeks (p = 0.004 and p = 0.006, respectively). While these results should be considered preliminary given the modest sample size, the progressive fall in NAA and late increases in choline, myoinositol and lactate may indicate progressive non-ischaemic neuronal loss, metabolically depressed neurons and/or diaschisis effects, which have a detrimental effect on motor recovery. Interventions that can potentially limit this ongoing subacute tissue damage may improve stroke recovery. MDPI 2020-07-16 /pmc/articles/PMC7399797/ /pubmed/32708540 http://dx.doi.org/10.3390/diagnostics10070482 Text en © 2020 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Article Mazibuko, Ndaba Tuura, Ruth O’Gorman Sztriha, Laszlo O’Daly, Owen Barker, Gareth J. Williams, Steven C. R. O’Sullivan, Michael Kalra, Lalit Subacute Changes in N-Acetylaspartate (NAA) Following Ischemic Stroke: A Serial MR Spectroscopy Pilot Study |
title | Subacute Changes in N-Acetylaspartate (NAA) Following Ischemic Stroke: A Serial MR Spectroscopy Pilot Study |
title_full | Subacute Changes in N-Acetylaspartate (NAA) Following Ischemic Stroke: A Serial MR Spectroscopy Pilot Study |
title_fullStr | Subacute Changes in N-Acetylaspartate (NAA) Following Ischemic Stroke: A Serial MR Spectroscopy Pilot Study |
title_full_unstemmed | Subacute Changes in N-Acetylaspartate (NAA) Following Ischemic Stroke: A Serial MR Spectroscopy Pilot Study |
title_short | Subacute Changes in N-Acetylaspartate (NAA) Following Ischemic Stroke: A Serial MR Spectroscopy Pilot Study |
title_sort | subacute changes in n-acetylaspartate (naa) following ischemic stroke: a serial mr spectroscopy pilot study |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7399797/ https://www.ncbi.nlm.nih.gov/pubmed/32708540 http://dx.doi.org/10.3390/diagnostics10070482 |
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