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Grey and white matter atrophy 1 year after stroke aphasia

Dynamic whole-brain changes occur following stroke, and not just in association with recovery. We tested the hypothesis that the presence of a specific behavioural deficit after stroke would be associated with structural decline (atrophy) in the brain regions supporting the affected function, by exa...

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Autores principales: Egorova-Brumley, Natalia, Khlif, Mohamed Salah, Werden, Emilio, Bird, Laura J., Brodtmann, Amy
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Oxford University Press 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8971893/
https://www.ncbi.nlm.nih.gov/pubmed/35368613
http://dx.doi.org/10.1093/braincomms/fcac061
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author Egorova-Brumley, Natalia
Khlif, Mohamed Salah
Werden, Emilio
Bird, Laura J.
Brodtmann, Amy
author_facet Egorova-Brumley, Natalia
Khlif, Mohamed Salah
Werden, Emilio
Bird, Laura J.
Brodtmann, Amy
author_sort Egorova-Brumley, Natalia
collection PubMed
description Dynamic whole-brain changes occur following stroke, and not just in association with recovery. We tested the hypothesis that the presence of a specific behavioural deficit after stroke would be associated with structural decline (atrophy) in the brain regions supporting the affected function, by examining language deficits post-stroke. We quantified whole-brain structural volume changes longitudinally (3–12 months) in stroke participants with (N = 32) and without aphasia (N = 59) as assessed by the Token Test at 3 months post-stroke, compared with a healthy control group (N = 29). While no significant difference in language decline rates (change in Token Test scores from 3 to 12 months) was observed between groups and some participants in the aphasic group improved their scores, stroke participants with aphasia symptoms at 3 months showed significant atrophy (>2%, P = 0.0001) of the left inferior frontal gyrus not observed in either healthy control or non-aphasic groups over the 3–12 months period. We found significant group differences in the inferior frontal gyrus volume, accounting for age, sex, stroke severity at baseline, education and total intracranial volume (Bonferroni-corrected P = 0.0003). In a subset of participants (aphasic N = 14, non-aphasic N = 36, and healthy control N = 25) with available diffusion-weighted imaging data, we found significant atrophy in the corpus callosum and the left superior longitudinal fasciculus in the aphasic compared with the healthy control group. Language deficits at 3 months post-stroke are associated with accelerated structural decline specific to the left inferior frontal gyrus, highlighting that known functional brain reorganization underlying behavioural improvement may occur in parallel with atrophy of brain regions supporting the language function.
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spelling pubmed-89718932022-04-01 Grey and white matter atrophy 1 year after stroke aphasia Egorova-Brumley, Natalia Khlif, Mohamed Salah Werden, Emilio Bird, Laura J. Brodtmann, Amy Brain Commun Original Article Dynamic whole-brain changes occur following stroke, and not just in association with recovery. We tested the hypothesis that the presence of a specific behavioural deficit after stroke would be associated with structural decline (atrophy) in the brain regions supporting the affected function, by examining language deficits post-stroke. We quantified whole-brain structural volume changes longitudinally (3–12 months) in stroke participants with (N = 32) and without aphasia (N = 59) as assessed by the Token Test at 3 months post-stroke, compared with a healthy control group (N = 29). While no significant difference in language decline rates (change in Token Test scores from 3 to 12 months) was observed between groups and some participants in the aphasic group improved their scores, stroke participants with aphasia symptoms at 3 months showed significant atrophy (>2%, P = 0.0001) of the left inferior frontal gyrus not observed in either healthy control or non-aphasic groups over the 3–12 months period. We found significant group differences in the inferior frontal gyrus volume, accounting for age, sex, stroke severity at baseline, education and total intracranial volume (Bonferroni-corrected P = 0.0003). In a subset of participants (aphasic N = 14, non-aphasic N = 36, and healthy control N = 25) with available diffusion-weighted imaging data, we found significant atrophy in the corpus callosum and the left superior longitudinal fasciculus in the aphasic compared with the healthy control group. Language deficits at 3 months post-stroke are associated with accelerated structural decline specific to the left inferior frontal gyrus, highlighting that known functional brain reorganization underlying behavioural improvement may occur in parallel with atrophy of brain regions supporting the language function. Oxford University Press 2022-03-17 /pmc/articles/PMC8971893/ /pubmed/35368613 http://dx.doi.org/10.1093/braincomms/fcac061 Text en © The Author(s) 2022. Published by Oxford University Press on behalf of the Guarantors of Brain. https://creativecommons.org/licenses/by/4.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Article
Egorova-Brumley, Natalia
Khlif, Mohamed Salah
Werden, Emilio
Bird, Laura J.
Brodtmann, Amy
Grey and white matter atrophy 1 year after stroke aphasia
title Grey and white matter atrophy 1 year after stroke aphasia
title_full Grey and white matter atrophy 1 year after stroke aphasia
title_fullStr Grey and white matter atrophy 1 year after stroke aphasia
title_full_unstemmed Grey and white matter atrophy 1 year after stroke aphasia
title_short Grey and white matter atrophy 1 year after stroke aphasia
title_sort grey and white matter atrophy 1 year after stroke aphasia
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8971893/
https://www.ncbi.nlm.nih.gov/pubmed/35368613
http://dx.doi.org/10.1093/braincomms/fcac061
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