Contribution of acute infarcts to cerebral small vessel disease progression.


Journal

Annals of neurology
ISSN: 1531-8249
Titre abrégé: Ann Neurol
Pays: United States
ID NLM: 7707449

Informations de publication

Date de publication:
10 2019
Historique:
received: 17 04 2019
revised: 18 07 2019
accepted: 18 07 2019
pubmed: 25 7 2019
medline: 21 4 2020
entrez: 25 7 2019
Statut: ppublish

Résumé

To determine the contribution of acute infarcts, evidenced by diffusion-weighted imaging positive (DWI+) lesions, to progression of white matter hyperintensities (WMH) and other cerebral small vessel disease (SVD) markers. We performed monthly 3T magnetic resonance imaging (MRI) for 10 consecutive months in 54 elderly individuals with SVD. MRI included high-resolution multishell DWI, and 3-dimensional fluid-attenuated inversion recovery, T1, and susceptibility-weighted imaging. We determined DWI+ lesion evolution, WMH progression rate (ml/mo), and number of incident lacunes and microbleeds, and calculated for each marker the proportion of progression explained by DWI+ lesions. We identified 39 DWI+ lesions on 21 of 472 DWI scans in 9 of 54 subjects. Of the 36 DWI+ lesions with follow-up MRI, 2 evolved into WMH, 4 evolved into a lacune (3 with cavity <3mm), 3 evolved into a microbleed, and 27 were not detectable on follow-up. WMH volume increased at a median rate of 0.027 ml/mo (interquartile range = 0.005-0.073), but was not significantly higher in subjects with DWI+ lesions compared to those without (p = 0.195). Of the 2 DWI+ lesions evolving into WMH on follow-up, one explained 23% of the total WMH volume increase in one subject, whereas the WMH regressed in the other subject. DWI+ lesions preceded 4 of 5 incident lacunes and 3 of 10 incident microbleeds. DWI+ lesions explain only a small proportion of the total WMH progression. Hence, WMH progression seems to be mostly driven by factors other than acute infarcts. DWI+ lesions explain the majority of incident lacunes and small cavities, and almost one-third of incident microbleeds, confirming that WMH, lacunes, and microbleeds, although heterogeneous on MRI, can have a common initial appearance on MRI. ANN NEUROL 2019;86:582-592.

Identifiants

pubmed: 31340067
doi: 10.1002/ana.25556
pmc: PMC6771732
doi:

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

582-592

Subventions

Organisme : European Union
ID : 666881
Pays : International
Organisme : Dutch Heart Foundation
ID : 2012T077
Pays : International
Organisme : Dutch Heart Foundation
ID : 2014 T060
Pays : International
Organisme : Dutch Heart Foundation
ID : 2016T044
Pays : International
Organisme : Netherlands Organization for Health Research and Development, ZonMw
ID : 016126351
Pays : International
Organisme : Netherlands Organization for Health Research and Development, ZonMw
ID : 015008048
Pays : International
Organisme : German Research Foundation
ID : DU1626/1-1
Pays : International

Commentaires et corrections

Type : ErratumIn

Informations de copyright

© 2019 The Authors. Annals of Neurology published by Wiley Periodicals, Inc. on behalf of American Neurological Association.

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Auteurs

Annemieke Ter Telgte (A)

Department of Neurology, Donders Institute for Brain, Cognition and Behaviour, Radboud University Medical Center, Nijmegen, the Netherlands.

Kim Wiegertjes (K)

Department of Neurology, Donders Institute for Brain, Cognition and Behaviour, Radboud University Medical Center, Nijmegen, the Netherlands.

Benno Gesierich (B)

Institute for Stroke and Dementia Research (ISD), University Hospital, LMU Munich, Munich, Germany.

José P Marques (JP)

Donders Institute for Brain, Cognition and Behaviour, Centre for Cognitive Neuroimaging, Radboud University, Nijmegen, the Netherlands.

Mathias Huebner (M)

Institute for Stroke and Dementia Research (ISD), University Hospital, LMU Munich, Munich, Germany.

Jabke J de Klerk (JJ)

Department of Neurology, Donders Institute for Brain, Cognition and Behaviour, Radboud University Medical Center, Nijmegen, the Netherlands.

Floris H B M Schreuder (FHBM)

Department of Neurology, Donders Institute for Brain, Cognition and Behaviour, Radboud University Medical Center, Nijmegen, the Netherlands.

Miguel A Araque Caballero (MA)

Institute for Stroke and Dementia Research (ISD), University Hospital, LMU Munich, Munich, Germany.
German Center for Neurodegenerative Diseases (DZNE Munich), Munich, Germany.

Hugo J Kuijf (HJ)

Image Sciences Institute, University Medical Center Utrecht, Utrecht, the Netherlands.

David G Norris (DG)

Donders Institute for Brain, Cognition and Behaviour, Centre for Cognitive Neuroimaging, Radboud University, Nijmegen, the Netherlands.

Catharina J M Klijn (CJM)

Department of Neurology, Donders Institute for Brain, Cognition and Behaviour, Radboud University Medical Center, Nijmegen, the Netherlands.

Martin Dichgans (M)

Institute for Stroke and Dementia Research (ISD), University Hospital, LMU Munich, Munich, Germany.
German Center for Neurodegenerative Diseases (DZNE Munich), Munich, Germany.
Munich Cluster for Systems Neurology (SyNergy), Munich, Germany.

Anil M Tuladhar (AM)

Department of Neurology, Donders Institute for Brain, Cognition and Behaviour, Radboud University Medical Center, Nijmegen, the Netherlands.

Marco Duering (M)

Institute for Stroke and Dementia Research (ISD), University Hospital, LMU Munich, Munich, Germany.
Munich Cluster for Systems Neurology (SyNergy), Munich, Germany.

Frank-Erik de Leeuw (FE)

Department of Neurology, Donders Institute for Brain, Cognition and Behaviour, Radboud University Medical Center, Nijmegen, the Netherlands.

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