Contrast leakage distant from the hematoma in patients with spontaneous ICH: A 7 T MRI study

Disruption of the blood–brain barrier (BBB) might play a role in the pathophysiology of cerebral small vessel disease-related ICH. The aim of this study was to assess presence and extent of contrast agent leakage distant from the hematoma as a marker of BBB disruption in patients with spontaneous ICH. We prospectively performed 7 tesla MRI in adult patients with spontaneous ICH and assessed contrast leakage distant from the hematoma on 3D FLAIR images. Thirty-one patients were included (mean age 60 years, 29% women). Median time between ICH and MRI was 20 days (IQR 9–67 days). Seventeen patients (54%; seven lobar, nine deep, one infratentorial ICH) had contrast leakage, located cortical in 16 and cortical and deep in one patient. Patients with contrast leakage more often had lobar cerebral microbleeds (CMBs; 77%) than those without (36%; RR 2.5, 95% CI 1.1–5.7) and a higher number of lobar CMBs (patients with contrast leakage: median 2, IQR 1–8 versus those without: median 0, IQR 0–2; p = 0.02). This study shows that contrast leakage distant from the hematoma is common in days to weeks after spontaneous ICH. It is located predominantly cortical and related to lobar CMBs and therefore possibly to cerebral amyloid angiopathy.

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P4-078: REPRESENTATION OF BLOOD FLOW IN PERFORATING BASAL GANGLIA ARTERIES OF PATIENTS WITH CEREBRAL SMALL VESSEL DISEASE (CSVD) AT 7 TESLA MRI

Alzheimer s & Dementia ◽

10.1016/j.jalz.2019.06.3738 ◽

2019 ◽

Vol 15 ◽

pp. P1304-P1304

Author(s):

Valentina Perosa ◽

Emrah Düzel ◽

Tine Arts ◽

Stefanie Schreiber ◽

Anne Assmann ◽

...

Keyword(s):

Blood Flow ◽

Basal Ganglia ◽

Small Vessel Disease ◽

Cerebral Small Vessel Disease ◽

Small Vessel ◽

7 Tesla ◽

Vessel Disease ◽

7 Tesla Mri

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Abstract 3208: Sensitivity and Reliability of SWI Compared to T2* GRE MRI for Detection of Microbleeds in Cerebral Amyloid Angiopathy

Stroke ◽

10.1161/str.43.suppl_1.a3208 ◽

2012 ◽

Vol 43 (suppl_1) ◽

Author(s):

Ah-Ling Cheng ◽

Cheryl R McCreary ◽

M. L Lauzon ◽

Richard Frayne ◽

Mayank Goyal ◽

...

Keyword(s):

Cerebral Amyloid Angiopathy ◽

Small Vessel Disease ◽

Intraclass Correlation ◽

Case Series ◽

Cerebral Small Vessel Disease ◽

Small Vessel ◽

Amyloid Angiopathy ◽

Healthy Controls ◽

Vessel Disease ◽

Cerebral Amyloid

Introduction: Case examples and small case series suggest that MRI susceptibility weighted imaging (SWI) may be more sensitive for cerebral microbleed (CMB) detection compared to MRI T2* gradient-recalled echo (GRE). However, there are few data on CMB counts measured by SWI vs. GRE, or inter-rater reliability, in groups of patients with cerebral small vessel disease. We used data from a prospective cohort study of cerebral amyloid angiopathy (CAA), a cerebral small-vessel disease marked by high numbers of CMBs, to quantify the sensitivity and reliability of SWI vs. GRE for CMB detection. Methods: Nine patients with symptomatic CAA (mean age 71±8.3; 7 males and 2 females) and 21 healthy non-CAA controls (mean age 68±6.3; 10 M/11 F) underwent T2* GRE and SWI on a 3.0T MR scanner. Probable CAA was diagnosed according to the Boston criteria prior to study entry using information from clinical MRI with GRE sequences. Two raters (labeled 1 and 2) independently interpreted the GRE and SWI scans blinded to clinical information. The phase-filtered magnitude image was used for SWI interpretation. Agreement reliability was assessed using the kappa coefficient (where a kappa of ≥0.60 indicates good agreement) or the intraclass correlation coefficient (ICC). Results: Overall, the raters identified 1,432 CMBs in the 9 CAA cases (range 1-434 per patient) and 8 CMBs in the healthy controls (range 0-3). Rater 1 identified CMBs in 5/21 healthy controls on SWI and 5/21 on GRE, while rater 2 identified CMBs in 4/21 on SWI and 3/21 on GRE (kappa 0.70 for GRE and 0.57 for SWI). In CAA cases more CMBs were seen on SWI compared to the GRE sequence but the difference was significant only for rater 1 (rater 1: on average 85% more per patient on SWI than on GRE, p=0.008; rater 2: 19% more, p=0.25). Among CAA cases the reliability between raters was poor for GRE (ICC 0.36) but excellent for SWI (0.94, p<0.05 for comparison with GRE). Review suggested that the differing reliability was because rater 1 was less likely than rater 2 to identify faint lesions on GRE as CMB, whereas these lesions were more conspicuous on SWI. If SWI rather than GRE were used to determine CAA status according to the Boston criteria, all 9 CAA cases would remain classified as probable CAA but 2/21 controls would be reclassified as either possible (n=1) or probable (n=1) asymptomatic CAA based on the detection of one or more lobar microbleeds on SWI. Conclusions: SWI confers greater reliability as well as greater sensitivity for CMB detection compared to GRE, and should be the preferred sequence for quantifying CMBs. SWI may more frequently identify lobar microbleeds that could represent asymptomatic CAA. Further research is needed to determine whether the Boston criteria require revision to take into account the greater sensitivity of SWI for CMB detection.

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Prevention of Cerebral Small Vessel Disease

Seminars in Neurology ◽

10.1055/s-0037-1603468 ◽

2017 ◽

Vol 37 (03) ◽

pp. 316-325 ◽

Cited By ~ 1

Author(s):

Eric Smith

Keyword(s):

Ischemic Stroke ◽

Intracerebral Hemorrhage ◽

Cerebral Amyloid Angiopathy ◽

Small Vessel Disease ◽

Unmet Need ◽

Cerebral Small Vessel Disease ◽

Small Vessel ◽

Amyloid Angiopathy ◽

Vessel Disease ◽

Cerebral Amyloid

AbstractCerebral small vessel disease can cause either ischemic stroke or intracerebral hemorrhage. Accounting for up to 25% of all strokes, it is also the second biggest contributor to the risk of dementia, and is the most common incidentally discovered finding on brain imaging. There are two main causes of cerebral small vessel disease: arteriolosclerotic small vessel disease (with hypertension as the main modifiable risk factor) and cerebral amyloid angiopathy (predominantly caused by β-amyloid deposits limited to the cerebral small arteries, arterioles, and capillaries). Prevention should include the treatment of hypertension and diabetes, if present, and the modification of lifestyle factors such as obesity and poor nutrition. Patients with small subcortical ischemic strokes should be treated with antithrombotics; dual antiplatelet therapy may be more effective than aspirin for the first 3 weeks following acute stroke, but is not more effective than aspirin for long-term prevention. Unresolved questions include the effectiveness of nonaspirin prevention strategies to prevent early recurrence or stroke extension in small subcortical ischemic stroke, and whether symptomatic or silent small vessel disease should influence decisions regarding selection for carotid revascularization or anticoagulation for atrial fibrillation. There is an unmet need for disease-modifying preventive therapies for cerebral amyloid angiopathy, the second most-common cause of spontaneous intracerebral hemorrhage.

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Association of Memory Impairment With Concomitant Tau Pathology in Patients With Cerebral Amyloid Angiopathy

Neurology ◽

10.1212/wnl.0000000000011745 ◽

2021 ◽

Vol 96 (15) ◽

pp. e1975-e1986

Author(s):

Dorothee Schoemaker ◽

Andreas Charidimou ◽

Maria Clara Zanon Zotin ◽

Nicolas Raposo ◽

Keith A. Johnson ◽

...

Keyword(s):

Cerebral Amyloid Angiopathy ◽

Memory Impairment ◽

Small Vessel Disease ◽

Hippocampal Volume ◽

Cerebral Small Vessel Disease ◽

Amyloid Angiopathy ◽

Tau Pathology ◽

Vessel Disease ◽

Tau Pet ◽

Cerebral Amyloid

ObjectiveRelying on tau-PET imaging, this cross-sectional study explored whether memory impairment is linked to the presence of concomitant tau pathology in individuals with cerebral amyloid angiopathy (CAA).MethodsForty-six patients with probable CAA underwent a neuropsychological examination and an MRI for quantification of structural markers of cerebral small vessel disease. A subset of these participants also completed a [11C]-Pittsburgh compound B (n = 39) and [18F]-flortaucipir (n = 40) PET for in vivo estimation of amyloid and tau burden, respectively. Participants were classified as amnestic or nonamnestic on the basis of neuropsychological performance. Statistical analyses were performed to examine differences in cognition, structural markers of cerebral small vessel disease, and amyloid- and tau-PET retention between participants with amnestic and those with nonamnestic CAA.ResultsPatients with probable CAA with an amnestic presentation displayed a globally more severe profile of cognitive impairment, smaller hippocampal volume (p < 0.001), and increased tau-PET binding in regions susceptible to Alzheimer disease neurodegeneration (p = 0.003) compared to their nonamnestic counterparts. Amnestic and nonamnestic patients with CAA did not differ on any other MRI markers or on amyloid-PET binding. In a generalized linear model including all evaluated neuroimaging markers, tau-PET retention (β = −0.85, p = 0.001) and hippocampal volume (β = 0.64 p = 0.01) were the only significant predictors of memory performance. The cognitive profile of patients with CAA with an elevated tau-PET retention was distinctly characterized by a significantly lower performance on the memory domain (p = 0.004).ConclusionsThese results suggest that the presence of objective memory impairment in patients with probable CAA could serve as a marker for underlying tau pathology.Classification of EvidenceThis study provides Class II evidence that tau-PET retention is related to the presence of objective memory impairment in patients with CAA.

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Cerebral Small Vessel Disease and Cerebral Amyloid Angiopathy

10.36253/978-88-6453-779-5 ◽

2019 ◽

Author(s):

Raffaella Valenti

Keyword(s):

Cognitive Rehabilitation ◽

Small Vessel Disease ◽

Prognostic Significance ◽

Cerebral Small Vessel Disease ◽

Small Vessel ◽

Elderly Subjects ◽

Amyloid Angiopathy ◽

Vessel Disease ◽

Cerebral Amyloid ◽

The Brain

Sporadic cerebral small vessel disease (SVD) is considered to be among the most commonly known neuropathological processes in the brain, hosting a crucial role in stroke, cognitive impairment, and functional loss in elderly subjects. We investigated clinical (neuroimaging and cognitive) biomarkers in the SVD, through a series of analyses from our five studies. Sporadic cerebral SVD is a complex ‘micro-world’ to be globally considered. All the relevant lesion types and SVD neuroimaging burden should be taken into account. The cumulative effects of microangiopathy burden in the brain of patients affected by SVD are crucial. Cognitive rehabilitation could represent a promising approach to prevent vascular dementia or to improve cognitive performances in patients with cerebral SVD. Longitudinal studies may provide more robust information about the progression and prognostic significance of our findings.

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7 Tesla MRI in Cerebral Small Vessel Disease

International Journal of Stroke ◽

10.1111/ijs.12490 ◽

2015 ◽

Vol 10 (5) ◽

pp. 659-664 ◽

Cited By ~ 12

Author(s):

Philip Benjamin ◽

Olivia Viessmann ◽

Andrew D. MacKinnon ◽

Peter Jezzard ◽

Hugh S. Markus

Keyword(s):

Small Vessel Disease ◽

Cerebral Small Vessel Disease ◽

Small Vessel ◽

7 Tesla ◽

Vessel Disease ◽

7 Tesla Mri

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Significance of Cortical Micro-Infarcts in the Human Brain

10.53902/sojnn.2021.01.000503 ◽

2021 ◽

Vol 1 (1) ◽

Author(s):

Jacques L De Reuck

Keyword(s):

Vascular Dementia ◽

Cerebral Amyloid Angiopathy ◽

Small Vessel Disease ◽

Cerebral Small Vessel Disease ◽

Small Vessel ◽

Amyloid Angiopathy ◽

White Matter Changes ◽

Vessel Disease ◽

Neurodegenerative Dementia ◽

Cerebral Amyloid

Cortical micro-infarcts are due to cerebral small vessel disease. In contrast to the arteriosclerotic type of cerebral small vessel disease, cortical micro-infarcts are mainly related and due to cerebral amyloid angiopathy. Alzheimer’s disease is the most frequent neurodegenerative dementia disease associated to cerebral amyloid angiopathy and cortical micro-infarcts. Vascular dementia cannot only be due to lacunar infarcts and ischemic white matter changes, but can also be caused by cortical micro-infarcts. The latter are a frequent cause of vascular dementia and decrease globally the cerebral blood flow.

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Cerebral microbleeds: Spatial distribution implications

Translational Neuroscience ◽

10.2478/s13380-014-0217-7 ◽

2014 ◽

Vol 5 (2) ◽

Cited By ~ 3

Author(s):

Elizabeth Loehrer ◽

Meike Vernooij ◽

M. Ikram

Keyword(s):

Spatial Distribution ◽

Genetic Risk ◽

Clinical Course ◽

Small Vessel Disease ◽

Cerebral Small Vessel Disease ◽

Cerebral Microbleeds ◽

Amyloid Angiopathy ◽

Vessel Disease ◽

Cerebral Amyloid ◽

Underlying Pathology

AbstractCerebral microbleeds are considered an imaging marker of cerebral small vessel disease. The location of microbleeds is thought to reflect the underlying pathology. Microbleeds in the deep and infratentorial region are thought to reflect hypertensive arteriopathy whereas lobar microbleeds are associated clinically with cerebral amyloid angiopathy (CAA). Aside from patient populations, microbleeds are frequently observed in seemingly asymptomatic populations. Moreover, many elderly, both in clinical and preclinical populations, have multiple coexisting pathologies in their brains, which complicates the interpretation of cerebral microbleeds, especially early in the clinical course. In this commentary, we discuss the influence of the strongest genetic risk factor for CAA, Apolipoprotein E (APOE), in the spatial distribution of microbleeds, and we additionally address issues in interpretation and implication of the location of microbleeds in clinical and asymptomatic populations.

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Distribution of lacunes in cerebral amyloid angiopathy and hypertensive small vessel disease

Neurology ◽

10.1212/wnl.0000000000004007 ◽

2017 ◽

Vol 88 (23) ◽

pp. 2162-2168 ◽

Cited By ~ 43

Author(s):

Marco Pasi ◽

Gregoire Boulouis ◽

Panagiotis Fotiadis ◽

Eitan Auriel ◽

Andreas Charidimou ◽

...

Keyword(s):

Cerebral Amyloid Angiopathy ◽

Small Vessel Disease ◽

Small Vessel ◽

White Matter Hyperintensity ◽

Amyloid Angiopathy ◽

Vessel Disease ◽

Close Relationship ◽

Cerebral Amyloid ◽

Highly Correlated ◽

The Relationship

Objective:To evaluate whether the burden of deep and lobar lacunes differs between patients with intracerebral hemorrhage (ICH) with definite/probable cerebral amyloid angiopathy (CAA) per the Boston criteria and hypertensive small vessel disease (HTN-SVD; ICH in basal ganglia, thalami, brainstem).Methods:We defined lobar and deep lacunes similar to the topographic distribution used for ICH and cerebral microbleeds (CMBs). We then compared their distribution between patients with CAA-ICH and those with strictly deep CMB and ICH (HTN-ICH). The independent associations of lacune location with the diagnosis of CAA-ICH and HTN-ICH were evaluated with multivariable models. The relationship between lobar lacunes and white matter hyperintensity (WMH) volume was evaluated by means of partial correlation analyses adjusted for age and a validated visual scale.Results:In our final cohort of 316 patients with ICH, lacunes were frequent (24.7%), with similar rates in 191 patients with CAA and 125 with HTN-ICH (23% vs 27.2%, p = 0.4). Lobar lacunes were more commonly present in CAA (20.4% vs 5.7%, p < 0.001), while deep lacunes were more frequent in HTN-ICH (15.2% vs 2.1%, p < 0.001). After correction for demographics and clinical and neuroimaging markers of SVD, lobar lacunes were associated with CAA (p = 0.003) and deep lacunes with HTN-ICH (p < 0.001). Lobar lacunes in 80% of the cases were at least in contact with WMH, and after adjustment for age, they were highly correlated to WMH volume (r = 0.42, p < 0.001).Conclusions:Lobar lacunes are associated with CAA, whereas deep lacunes are more frequent in HTN-SVD. Lobar lacunes seem to have a close relationship with WMH, suggesting a possible common origin.

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