Secondary thalamic atrophy related to brain infarction may contribute to post-stroke cognitive impairment.


Journal

Journal of stroke and cerebrovascular diseases : the official journal of National Stroke Association
ISSN: 1532-8511
Titre abrégé: J Stroke Cerebrovasc Dis
Pays: United States
ID NLM: 9111633

Informations de publication

Date de publication:
Feb 2023
Historique:
received: 27 07 2022
revised: 24 10 2022
accepted: 10 11 2022
pubmed: 11 12 2022
medline: 11 1 2023
entrez: 10 12 2022
Statut: ppublish

Résumé

The thalamus is a key brain hub that is globally connected to many cortical regions. Previous work highlights thalamic contributions to multiple cognitive functions, but few studies have measured thalamic volume changes or cognitive correlates. This study investigates associations between thalamic volumes and post-stroke cognitive function. Participants with non-thalamic brain infarcts (3-42 months) underwent MRI and cognitive testing. Focal infarcts and thalami were traced manually. In cases with bilateral infarcts, the side of the primary infarct volume defined the hemisphere involved. Brain parcellation and volumetrics were extracted using a standardized and previously validated neuroimaging pipeline. Age and gender-matched healthy controls provided normal comparative thalamic volumes. Thalamic atrophy was considered when the volume exceeded 2 standard deviations greater than the controls. Thalamic volumes ipsilateral to the infarct in stroke patients (n=55) were smaller than left (4.4 ± 1.4 vs. 5.4 ± 0.5 cc, p < 0.001) and right (4.4 ± 1.4 vs. 5.5 ± 0.6 cc, p < 0.001) thalamic volumes in the controls. After controlling for head-size and global brain atrophy, infarct volume independently correlated with ipsilateral thalamic volume (β= -0.069, p=0.024). Left thalamic atrophy correlated significantly with poorer cognitive performance (β = 4.177, p = 0.008), after controlling for demographics and infarct volumes. Our results suggest that the remote effect of infarction on ipsilateral thalamic volume is associated with global post-stroke cognitive impairment.

Sections du résumé

BACKGROUND AND PURPOSE OBJECTIVE
The thalamus is a key brain hub that is globally connected to many cortical regions. Previous work highlights thalamic contributions to multiple cognitive functions, but few studies have measured thalamic volume changes or cognitive correlates. This study investigates associations between thalamic volumes and post-stroke cognitive function.
METHODS METHODS
Participants with non-thalamic brain infarcts (3-42 months) underwent MRI and cognitive testing. Focal infarcts and thalami were traced manually. In cases with bilateral infarcts, the side of the primary infarct volume defined the hemisphere involved. Brain parcellation and volumetrics were extracted using a standardized and previously validated neuroimaging pipeline. Age and gender-matched healthy controls provided normal comparative thalamic volumes. Thalamic atrophy was considered when the volume exceeded 2 standard deviations greater than the controls.
RESULTS RESULTS
Thalamic volumes ipsilateral to the infarct in stroke patients (n=55) were smaller than left (4.4 ± 1.4 vs. 5.4 ± 0.5 cc, p < 0.001) and right (4.4 ± 1.4 vs. 5.5 ± 0.6 cc, p < 0.001) thalamic volumes in the controls. After controlling for head-size and global brain atrophy, infarct volume independently correlated with ipsilateral thalamic volume (β= -0.069, p=0.024). Left thalamic atrophy correlated significantly with poorer cognitive performance (β = 4.177, p = 0.008), after controlling for demographics and infarct volumes.
CONCLUSIONS CONCLUSIONS
Our results suggest that the remote effect of infarction on ipsilateral thalamic volume is associated with global post-stroke cognitive impairment.

Identifiants

pubmed: 36495644
pii: S1052-3057(22)00587-0
doi: 10.1016/j.jstrokecerebrovasdis.2022.106895
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

106895

Informations de copyright

Copyright © 2022 Elsevier Inc. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of Competing Interest All authors declare that there are no conflicts of interest

Auteurs

Jieli Geng (J)

Department of Neurology, Renji Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, China.

Fuqiang Gao (F)

LC Campbell Cognitive Neurology, Dr. Sandra Black Centre for Brain Resilience & Recovery, Hurvitz Brain Sciences Research Program, Sunnybrook Research Institute, University of Toronto, Ontario, Canada.

Joel Ramirez (J)

LC Campbell Cognitive Neurology, Dr. Sandra Black Centre for Brain Resilience & Recovery, Hurvitz Brain Sciences Research Program, Sunnybrook Research Institute, University of Toronto, Ontario, Canada; Heart and Stroke Foundation Canadian Partnership for Stroke Recovery (Sunnybrook site), Toronto, Ontario, Canada.

Kie Honjo (K)

LC Campbell Cognitive Neurology, Dr. Sandra Black Centre for Brain Resilience & Recovery, Hurvitz Brain Sciences Research Program, Sunnybrook Research Institute, University of Toronto, Ontario, Canada; Heart and Stroke Foundation Canadian Partnership for Stroke Recovery (Sunnybrook site), Toronto, Ontario, Canada.

Melissa F Holmes (MF)

LC Campbell Cognitive Neurology, Dr. Sandra Black Centre for Brain Resilience & Recovery, Hurvitz Brain Sciences Research Program, Sunnybrook Research Institute, University of Toronto, Ontario, Canada.

Sabrina Adamo (S)

LC Campbell Cognitive Neurology, Dr. Sandra Black Centre for Brain Resilience & Recovery, Hurvitz Brain Sciences Research Program, Sunnybrook Research Institute, University of Toronto, Ontario, Canada.

Miracle Ozzoude (M)

LC Campbell Cognitive Neurology, Dr. Sandra Black Centre for Brain Resilience & Recovery, Hurvitz Brain Sciences Research Program, Sunnybrook Research Institute, University of Toronto, Ontario, Canada.

Gregory M Szilagyi (GM)

LC Campbell Cognitive Neurology, Dr. Sandra Black Centre for Brain Resilience & Recovery, Hurvitz Brain Sciences Research Program, Sunnybrook Research Institute, University of Toronto, Ontario, Canada.

Christopher J M Scott (CJM)

LC Campbell Cognitive Neurology, Dr. Sandra Black Centre for Brain Resilience & Recovery, Hurvitz Brain Sciences Research Program, Sunnybrook Research Institute, University of Toronto, Ontario, Canada.

Glen T Stebbins (GT)

Department of Neurological Sciences, Rush University Medical Center, Chicago, IL, USA.

David L Nyenhuis (DL)

Hauenstein Neuroscience Center, Saint Mary's Health Care, Grand Rapids, MI, USA; LCC International University.

Maged Goubran (M)

LC Campbell Cognitive Neurology, Dr. Sandra Black Centre for Brain Resilience & Recovery, Hurvitz Brain Sciences Research Program, Sunnybrook Research Institute, University of Toronto, Ontario, Canada; Heart and Stroke Foundation Canadian Partnership for Stroke Recovery (Sunnybrook site), Toronto, Ontario, Canada; Department of Medical Biophysics, University of Toronto, Ontario, Canada.

Sandra E Black (SE)

LC Campbell Cognitive Neurology, Dr. Sandra Black Centre for Brain Resilience & Recovery, Hurvitz Brain Sciences Research Program, Sunnybrook Research Institute, University of Toronto, Ontario, Canada; Heart and Stroke Foundation Canadian Partnership for Stroke Recovery (Sunnybrook site), Toronto, Ontario, Canada; Department of Medicine (Neurology), Sunnybrook Health Sciences Centre and University of Toronto, Ontario, Canada. Electronic address: sandra.black@sunnybrook.ca.

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Classifications MeSH