Pre-existing brain damage and association between severity and prior cognitive impairment in ischemic stroke patients.


Journal

Journal of neuroradiology = Journal de neuroradiologie
ISSN: 0150-9861
Titre abrégé: J Neuroradiol
Pays: France
ID NLM: 7705086

Informations de publication

Date de publication:
Feb 2023
Historique:
received: 18 11 2021
revised: 10 02 2022
accepted: 03 03 2022
pubmed: 16 3 2022
medline: 31 1 2023
entrez: 15 3 2022
Statut: ppublish

Résumé

We evaluated whether pre-existing brain damage may explain greater severity in cognitively-impaired patients with ischemic stroke (IS). IS patients were retrieved from the population-based registry of Dijon, France. Pre-existing damage (leukoaraiosis, old vascular brain lesions, cortical and central brain atrophy) was assessed on initial CT-scan. Association between prestroke cognitive status defined as no impairment, mild cognitive impairment (MCI), or dementia, and clinical severity at IS onset assessed with the NIHSS score was evaluated using ordinal regression analysis. Mediation analysis was performed to assess pre-existing brain lesions as mediators of the relationship between cognitive status and severity. Among the 916 included patients (mean age 76.8 ± 15.0 years, 54.3% women), those with pre-existing MCI (n = 115, median NIHSS [IQR]: 6 [2-15]) or dementia (n = 147, median NIHSS: 6 [3-15]) had a greater severity than patients without (n = 654, median NIHSS: 3 [1-9]) in univariate analysis (OR=1.69; 95% CI: 1.18-2.42, p = 0.004, and OR=2.06; 95% CI: 1.49-2.84, p < 0.001, respectively). Old cortical lesion (OR=1.53, p = 0.002), central atrophy (OR=1.41, p = 0.005), cortical atrophy (OR=1.90, p < 0.001) and moderate (OR=1.41, p = 0.005) or severe (OR=1.84, p = 0.002) leukoaraiosis were also associated with greater severity. After adjustments, pre-existing MCI (OR=1.52; 95% CI: 1.03-2.26, p = 0.037) or dementia (OR=1.94; 95% CI: 1.32-2.86, p = 0.001) remained associated with higher severity at IS onset, independently of confounding factors including imaging variables. Association between cognitive impairment and severity was not mediated by pre-existing visible brain damages. Impaired brain ischemic tolerance in IS patients with prior cognitive impairment could involve other mechanisms than pre-existing visible brain damage.

Sections du résumé

BACKGROUND BACKGROUND
We evaluated whether pre-existing brain damage may explain greater severity in cognitively-impaired patients with ischemic stroke (IS).
METHODS METHODS
IS patients were retrieved from the population-based registry of Dijon, France. Pre-existing damage (leukoaraiosis, old vascular brain lesions, cortical and central brain atrophy) was assessed on initial CT-scan. Association between prestroke cognitive status defined as no impairment, mild cognitive impairment (MCI), or dementia, and clinical severity at IS onset assessed with the NIHSS score was evaluated using ordinal regression analysis. Mediation analysis was performed to assess pre-existing brain lesions as mediators of the relationship between cognitive status and severity.
RESULTS RESULTS
Among the 916 included patients (mean age 76.8 ± 15.0 years, 54.3% women), those with pre-existing MCI (n = 115, median NIHSS [IQR]: 6 [2-15]) or dementia (n = 147, median NIHSS: 6 [3-15]) had a greater severity than patients without (n = 654, median NIHSS: 3 [1-9]) in univariate analysis (OR=1.69; 95% CI: 1.18-2.42, p = 0.004, and OR=2.06; 95% CI: 1.49-2.84, p < 0.001, respectively). Old cortical lesion (OR=1.53, p = 0.002), central atrophy (OR=1.41, p = 0.005), cortical atrophy (OR=1.90, p < 0.001) and moderate (OR=1.41, p = 0.005) or severe (OR=1.84, p = 0.002) leukoaraiosis were also associated with greater severity. After adjustments, pre-existing MCI (OR=1.52; 95% CI: 1.03-2.26, p = 0.037) or dementia (OR=1.94; 95% CI: 1.32-2.86, p = 0.001) remained associated with higher severity at IS onset, independently of confounding factors including imaging variables. Association between cognitive impairment and severity was not mediated by pre-existing visible brain damages.
CONCLUSION CONCLUSIONS
Impaired brain ischemic tolerance in IS patients with prior cognitive impairment could involve other mechanisms than pre-existing visible brain damage.

Identifiants

pubmed: 35289302
pii: S0150-9861(22)00097-9
doi: 10.1016/j.neurad.2022.03.001
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

16-21

Informations de copyright

Copyright © 2022 Elsevier Masson SAS. All rights reserved.

Auteurs

Valentin Pinguet (V)

Dijon Stroke Registry, EA7460, Pathophysiology and Epidemiology of Cardio-cerebrovascular disease (PEC2), University of Burgundy, 14 rue Paul Gaffarel, Dijon 21079, France; Department of Neuroimaging, University Hospital of Dijon, France.

Gauthier Duloquin (G)

Dijon Stroke Registry, EA7460, Pathophysiology and Epidemiology of Cardio-cerebrovascular disease (PEC2), University of Burgundy, 14 rue Paul Gaffarel, Dijon 21079, France; Department of Neurology, University Hospital of Dijon, France.

Thomas Thibault (T)

INSERM CIC-1432 Clinical Investigation Center, Clinical Epidemiology, University Hospital of Dijon, France; Internal Medicine and Systemic Diseases unit, University Hospital of Dijon, France.

Hervé Devilliers (H)

INSERM CIC-1432 Clinical Investigation Center, Clinical Epidemiology, University Hospital of Dijon, France; Internal Medicine and Systemic Diseases unit, University Hospital of Dijon, France.

Pierre-Olivier Comby (PO)

Dijon Stroke Registry, EA7460, Pathophysiology and Epidemiology of Cardio-cerebrovascular disease (PEC2), University of Burgundy, 14 rue Paul Gaffarel, Dijon 21079, France; Department of Neuroimaging, University Hospital of Dijon, France.

Valentin Crespy (V)

Dijon Stroke Registry, EA7460, Pathophysiology and Epidemiology of Cardio-cerebrovascular disease (PEC2), University of Burgundy, 14 rue Paul Gaffarel, Dijon 21079, France; Department of Vascular Surgery, University Hospital of Dijon, France.

Frédéric Ricolfi (F)

Department of Neuroimaging, University Hospital of Dijon, France.

Catherine Vergely (C)

Dijon Stroke Registry, EA7460, Pathophysiology and Epidemiology of Cardio-cerebrovascular disease (PEC2), University of Burgundy, 14 rue Paul Gaffarel, Dijon 21079, France.

Maurice Giroud (M)

Dijon Stroke Registry, EA7460, Pathophysiology and Epidemiology of Cardio-cerebrovascular disease (PEC2), University of Burgundy, 14 rue Paul Gaffarel, Dijon 21079, France; Department of Neurology, University Hospital of Dijon, France.

Yannick Béjot (Y)

Dijon Stroke Registry, EA7460, Pathophysiology and Epidemiology of Cardio-cerebrovascular disease (PEC2), University of Burgundy, 14 rue Paul Gaffarel, Dijon 21079, France; Department of Neurology, University Hospital of Dijon, France. Electronic address: yannick.bejot@chu-dijon.fr.

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