Microbleeds colocalize with enlarged juxtacortical perivascular spaces in amnestic mild cognitive impairment and early Alzheimer’s disease: A 7 Tesla MRI study

MRI-visible perivascular spaces (PVS) in the semioval centre are associated with cerebral amyloid angiopathy (CAA), but it is unknown if PVS co-localize with MRI markers of CAA. To examine this, we assessed the topographical association between cortical cerebral microbleeds (CMBs) – as an indirect m...

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Published inJournal of cerebral blood flow and metabolism Vol. 40; no. 4; pp. 739 - 746
Main Authors Bouvy, Willem H, van Veluw, Susanne J, Kuijf, Hugo J, Zwanenburg, Jaco JM, Kappelle, Jaap L, Luijten, Peter R, Koek, Huiberdina L, Geerlings, Mirjam I, Biessels, Geert J
Format Journal Article
LanguageEnglish
Published London, England SAGE Publications 01.04.2020
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Summary:MRI-visible perivascular spaces (PVS) in the semioval centre are associated with cerebral amyloid angiopathy (CAA), but it is unknown if PVS co-localize with MRI markers of CAA. To examine this, we assessed the topographical association between cortical cerebral microbleeds (CMBs) – as an indirect marker of CAA – and dilatation of juxtacortical perivascular spaces (jPVS) in 46 patients with amnestic mild cognitive impairment (aMCI) or early Alzheimer’s disease (eAD). The degree of dilatation of jPVS <1 cm around each cortical CMBs was compared with a similar reference site (no CMB) in the contralateral hemisphere, using a 4-point scale. Also, jPVS dilatation was compared between patients with and without cortical CMBs. Eleven patients (24%) had cortical CMBs [total=35, median=1, range=1–14] of whom five had >1 cortical CMBs. The degree of jPVS dilatation was higher around CMBs than at the reference sites [Wilcoxon signed rank test, Z = 2.2, p = 0.03]. Patients with >1 cortical CMBs had a higher degree of jPVS dilation [median=2.2, IQR = 1.8–2.3] than patients without cortical CMBs [median=1.4, IQR = 1.0–1.8], p = 0.02. We found a topographical association between a high degree of jPVS dilatation and cortical CMBs, supporting a common underlying pathophysiology – most likely CAA.
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ISSN:0271-678X
1559-7016
DOI:10.1177/0271678X19838087