MRI-visible perivascular spaces in cerebral amyloid angiopathy and hypertensive arteriopathy

Charidimou, Andreas; Boulouis, Grégoire; Pasi, Marco; Auriel, Eitan; Etten, Ellis S. van; Haley, Kellen; Ayres, Alison; Schwab, Kristin; Martínez-Ramírez, Sergi; Goldstein, Joshua N.; Rosand, Jonathan; Viswanathan, Anand; Greenberg, Steven M.; Gurol, M. Edip

doi:10.1212/wnl.0000000000003746

Cited by 238 publications

(280 citation statements)

References 36 publications

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“…On the other hand, in the Alzheimer’s Disease Neuroimaging Initiative (ADNI) study H-EPVS were negatively correlated with the performance in the Mini-Mental State Examination. However, the clinical importance of H-EPVS in cognitive impairment has been poorly studied; in particular, it has been described that in specific conditions as in cerebral amyloid angiopathy, a predominance of EPVS in other locations (ie, CSO) may exist 33. Considering the link between H-EPVS and other markers of cSVD and their potential role in cognition, further studies are needed to assess their clinical implication in diagnosis, prognosis and prevention of dementia.…”

Section: Discussionmentioning

confidence: 99%

Prevalence of hippocampal enlarged perivascular spaces in a sample of patients with hypertension and their relation with vascular risk factors and cognitive function

Jiménez-Baladó

Riba‐Llena

Garde

et al. 2018

J Neurol Neurosurg Psychiatry

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Section: Discussionmentioning

confidence: 99%

Prevalence of hippocampal enlarged perivascular spaces in a sample of patients with hypertension and their relation with vascular risk factors and cognitive function

Jiménez-Baladó

Riba‐Llena

Garde

et al. 2018

J Neurol Neurosurg Psychiatry

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“…Global measures of each SVD type were defined as: (1) total WMH volume normalized for TIV, (2) EPVS-BG, (3) total number of microbleeds, (4) total number of lacunes, and (5) total SVD burden score (Staals et al, 2014). Lacking an established wholebrain measure of EPVS, EPVS-BG were selected to represent "global" EPVS, given its relevance in vascular pathology such as hypertensive arteriopathy and WMH, as opposed to EPVS-CSO which are more commonly linked to cerebral amyloid angiopathy (CAA) (Charidimou et al, 2017). Measures of cognition were MMSE and ACE-R scores.…”

Section: Variables Included In Analysesmentioning

confidence: 99%

Peak Width of Skeletonized Mean Diffusivity as a Marker of Diffuse Cerebrovascular Damage

et al. 2020

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Background: The peak width of skeletonized mean diffusivity (PSMD) has been proposed as a fully automated imaging marker of relevance to cerebral small vessel disease (SVD). We assessed PSMD in relation to conventional SVD markers, global measures of neurodegeneration, and cognition.Methods: 145 participants underwent 3T brain MRI and cognitive assessment. 112 were patients with mild cognitive impairment, Alzheimer's disease, progressive supranuclear palsy, dementia with Lewy bodies, or frontotemporal dementia. PSMD, SVD burden [white matter hyperintensities (WMH), enlarged perivascular spaces (EPVS), microbleeds, lacunes], average mean diffusivity (MD), gray matter (GM), white matter (WM), and total intracranial volume were quantified. Robust linear regression was conducted to examine associations between variables. Dominance analysis assessed the relative importance of markers in predicting various outcomes. Regional analyses examined spatial overlap between PSMD and WMH.Results: PSMD was associated with global and regional SVD measures, especially WMH and microbleeds. Dominance analysis demonstrated that among SVD markers, WMH was the strongest predictor of PSMD. Furthermore, PSMD was more closely associated to WMH than with GM and WM volumes. PSMD was associated with WMH across all regions, and correlations were not significantly stronger in corresponding regions (e.g., frontal PSMD and frontal WMH) compared to non-corresponding regions. PSMD outperformed all four conventional SVD markers and MD in predicting cognition, but was comparable to GM and WM volumes.Discussion: PSMD was robustly associated with established SVD markers. This new measure appears to be a marker of diffuse brain injury, largely due to vascular pathology, and may be a useful and convenient metric of overall cerebrovascular burden.

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“…Pathological studies have shown that CAA with associated hemorrhagic stroke occurs predominantly in lobar and posterior areas [116,117]. Recently, it has been shown that CAA also correlates with perivascular space enlargement, which affects ISF-and CSF-mediated Aβ clearance [99,118]. Vascular amyloid deposition may disrupt perivascular space drainage via a perturbation in normal arteriolar pulsation [14,48].…”

Section: Caa Pathophysiologymentioning

confidence: 99%

“…Aβ deposition may further impair or block perivascular drainage, leading to dilation of perivascular spaces, not only in the cortical grey matter but also in the underlying white matter, which itself is typically not directly affected by CAA. The enlarged perivascular space can reach several millimeters in diameter and may be visible with appropriate brain imaging [100,118,119].…”

Section: Caa Pathophysiologymentioning

confidence: 99%

From Stroke to Dementia: a Comprehensive Review Exposing Tight Interactions Between Stroke and Amyloid-β Formation

Goulay

Romo

Hol

et al. 2019

Transl. Stroke Res.

100

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Stroke and Alzheimer's disease (AD) are cerebral pathologies with high socioeconomic impact that can occur together and mutually interact. Vascular factors predisposing to cerebrovascular disease have also been specifically associated with development of AD, and acute stroke is known to increase the risk to develop dementia. Despite the apparent association, it remains unknown how acute cerebrovascular disease and development of AD are precisely linked and act on each other. It has been suggested that this interaction is strongly related to vascular deposition of amyloid-β (Aβ), i.e., cerebral amyloid angiopathy (CAA). Furthermore, the blood-brain barrier (BBB), perivascular space, and the glymphatic system, the latter proposedly responsible for the drainage of solutes from the brain parenchyma, may represent key pathophysiological pathways linking stroke, Aβ deposition, and dementia. In this review, we propose a hypothetic connection between CAA, stroke, perivascular space integrity, and dementia. Based on relevant pre-clinical research and a few clinical case reports, we speculate that impaired perivascular space integrity, inflammation, hypoxia, and BBB breakdown after stroke can lead to accelerated deposition of Aβ within brain parenchyma and cerebral vessel walls or exacerbation of CAA. The deposition of Aβ in the parenchyma would then be the initiating event leading to synaptic dysfunction, inducing cognitive decline and dementia. Maintaining the clearance of Aβ after stroke could offer a new therapeutic approach to prevent post-stroke cognitive impairment and development into dementia.

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MRI-visible perivascular spaces in cerebral amyloid angiopathy and hypertensive arteriopathy

Abstract: Different patterns of MRI-visible EPVS provide insights into the dominant underlying microangiopathy type in patients with spontaneous ICH.

Cited by 238 publications

References 36 publications

Prevalence of hippocampal enlarged perivascular spaces in a sample of patients with hypertension and their relation with vascular risk factors and cognitive function

Prevalence of hippocampal enlarged perivascular spaces in a sample of patients with hypertension and their relation with vascular risk factors and cognitive function

Peak Width of Skeletonized Mean Diffusivity as a Marker of Diffuse Cerebrovascular Damage

From Stroke to Dementia: a Comprehensive Review Exposing Tight Interactions Between Stroke and Amyloid-β Formation

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