Location Of Cerebral Microbleeds Research Articles

Intracranial hemorrhage risk in patients with cerebral microbleeds after mechanical thrombectomy for acute ischemic stroke: asystematic review andmeta-analysis.

Background and purpose intracranial hemorrhage risk in patients with cerebral microbleeds (CMBs) after mechanical thrombectomy for acute ischemic stroke (AIS) was investigated. We searched PubMed and Embase from inception to 29 August 2023 for relevant studies, calculated pooled odds ratio (ORs) of intracerebral hemorrhage (ICH) subtypes in AIS patients with CMB presence, 1-4 or ≥ 5 CMBs versus CMB absence, and with different CMB locations after mechanical thrombectomy. ICH subtypes included any ICH, symptomatic and asymptomatic ICH, hemorrhage outside infarct (including subarachnoid hemorrhage), hemorrhagic infarction, and parenchymal hemorrhage after mechanical thrombectomy. Five eligible studies enrolling 2051 patients were included. No significant association was shown between CMB locations (lobar, deep, infratentorial or mixed) and ICH risk. CMB presence or 1-4 CMBs did not significantly increase the risk of any ICH, symptomatic or asymptomatic ICH, ICH outside infarct, subarachnoid hemorrhage, hemorrhagic infarction, or parenchymal hemorrhage. CMBs ≥ 5 increased the risk of any ICH (OR 2.58, 95% CI 1.16-5.72), parenchymal hemorrhage (OR 3.38, 95% CI 1.43-7.97) and parenchymal hemorrhage-2 (OR 5.33, 2.05-13.86), without increasing hemorrhagic infarction or parenchymal haemorrhage-1 risk. After adjusted for possible confounding factors, increases in CMB burden were associated with hemorrhagic complications but not with symptomatic ICH. In AIS patients who received mechanical thrombectomy, no association was shown between CMB location and ICH risk. ICH risk was not significantly increased by CMB presence or 1-4 CMBs. ICH risk in patients with ≥ 5 CMBs requires further study.

Abstract WP170: Patients With Cerebral Microbleeds Are More Likely to Have Poor Collaterals at the Time of Mechanical Thrombectomy

Introduction: Collateral cerebrovasculature is important for the survival of penumbral tissue in patients with large vessel occlusive (LVO) stroke, and adequate collateralization is associated with favorable outcomes. The presence of cerebral microbleeds (CMB) have been implicated in vessel wall remodeling and impaired vasoreactivity. We investigated whether the presence of deep and/or lobar CMB predicts poor collateral recruitment in patients with LVO stroke who underwent thrombectomy (MT). Methods: We performed a retrospective, single-center study of adults who presented with LVO stroke and had MT between January 2012-June 2020. CT angiography of head prior to MT was used to assess collateral status with poor status defined as ≤50% filling and good status as >50% filling. CMBs were assessed using T2*-weighted gradient echo or susceptibility weighted magnetic resonance images. Location of CMB was further characterized as deep vs. lobar using consensus definitions. Poor stroke outcome was defined as modified Rankin Scale (mRS) ≥3 at 90 days. Multivariable logistic regressions were performed to evaluate the associations between CMB, CMB types (lobar, deep, lobar+deep) and poor collaterals after adjusting for vascular risk factors. Results: Consecutive 151 subjects were included (mean age 68±15 years, 47% women), with a median NIHSS of 18. CMB were identified in 57 subjects (37.4%). Of these, 20.5% had lobar CMB, 5.3% had deep CMB and 11.9% had combined lobar & deep CMB. Patients with CMB had higher odds of having poor collaterals compared to those without CMB (OR 1.56, 95% CI 1.09-2.23, P=0.015). The association of CMB with poor collaterals was strongest in patients with combined lobar & deep CMB (OR 4.78, 95% CI 1.43-15.93, P=0.011), compared with those with exclusively deep CMB (OR 2.78, 95% CI 0.44-17.62, P=0.278) or lobar CMB (OR 0.52, 95% CI 0.19-1.38, P=0.188). Patients with poor collaterals were more likely to have poor outcome compared with those with good collaterals (48.4% vs. 31.0%, P=0.03). Conclusion: Cerebral microbleeds are independently associated with poor collateral recruitment when adjusted for traditional vascular risk factors. Further study is warranted to elucidate the differential effects of CMB types on collateral recruitment.

Correlation between Cerebral Microbleeds and White Matter Changes on MRI using Microbleed Anatomical Rating and Fazekas Scales: A Cross-sectional Study

Introduction: Cerebral Microbleeds (CMBs) are small perivascular haemosiderin deposits in the brain that indicate bleeding events. The location of CMBs can provide insights into their underlying causes. CMBs found in peripheral lobar locations are often associated with cerebral amyloid angiopathy, while those occurring in deeper brain regions are more likely linked to hypertensive arteriopathy. White matter changes, known as Leukoaraiosis, have been linked to adverse cognitive functions, share risk factors with hypertension and microbleeds, and are associated with the severity of CMBs. Aim: To determine the correlation between CMBs and white matter changes on Magnetic Resonance Imagning (MRI) using the Microbleed Anatomical Rating Scale (MARS) and Fazekas scales. Materials and Methods: An analytical cross-sectional study was conducted in the Department of Radiodiagnosis, MS Ramaiah Hospitals, Bengaluru, Karnataka, India between November 2019 and June 2021, involving 65 subjects who underwent MRI brain scans at a tertiary care institute and were found to have microbleeds. Brain MRIs were performed using a 1.5 Tesla MRI Scanning Unit. Microbleeds were graded using the MARS, while white matter changes were graded using the Fazekas scale. The Chi-square test was employed to assess the significance of categorical data, and Spearman’s correlation was used to determine the correlation between MARS and Fazekas scale variables. Results: The subjects had a mean age range of 61 to 70 years, with a male-to-female ratio of 2:1. There was a significant correlation between MARS grade and Fazekas scale (p<0.001) with a correlation coefficient (r-value) of 1. The most commonly associated stroke subtype was lacunar infarct. Conclusion: There is a significant correlation between Leukoaraiosis (LA) and CMBs, indicating the end results of small vessel ischaemia and bleeding.

Deep-Learning-Based MRI Microbleeds Detection for Cerebral Small Vessel Disease on Quantitative Susceptibility Mapping.

Cerebral microbleeds (CMB) are indicators of severe cerebral small vessel disease (CSVD) that can be identified through hemosiderin-sensitive sequences in MRI. Specifically, quantitative susceptibility mapping (QSM) and deep learning were applied to detect CMBs in MRI. To automatically detect CMB on QSM, we proposed a two-stage deep learning pipeline. Retrospective. A total number of 1843 CMBs from 393 patients (69 ± 12) with cerebral small vessel disease were included in this study. Seventy-eight subjects (70 ± 13) were used as external testing. 3 T/QSM. The proposed pipeline consisted of two stages. In stage I, 2.5D fast radial symmetry transform (FRST) algorithm along with a one-layer convolutional network was used to identify CMB candidate regions in QSM images. In stage II, the V-Net was utilized to reduce false positives. The V-Net was trained using CMB and non CMB labels, which allowed for high-level feature extraction and differentiation between CMBs and CMB mimics like vessels. The location of CMB was assessed according to the microbleeds anatomical rating scale (MARS) system. The sensitivity and positive predicative value (PPV) were reported to evaluate the performance of the model. The number of false positive per subject was presented. Our pipeline demonstrated high sensitivities of up to 94.9% at stage I and 93.5% at stage II. The overall sensitivity was 88.9%, and the false positive rate per subject was 2.87. With respect to MARS, sensitivities of above 85% were observed for nine different brain regions. We have presented a deep learning pipeline for detecting CMB in the CSVD cohort, along with a semi-automated MARS scoring system using the proposed method. Our results demonstrated the successful application of deep learning for CMB detection on QSM and outperformed previous handcrafted methods. 2 TECHNICAL EFFICACY: Stage 2.

Correlation between lipid-lowering therapy and cerebral microbleeds.

To investigate if there is a correlation between lipid-lowering treatment with statins and the occurrence, number, and location of cerebral microbleeds (CMBs) among patients with ischemic cerebrovascular disease (ICVD), and also to compare treatment with atorvastatin and rosuvastatin in terms of the occurrence of CMBs and their differences. In this retrospective study, we included patients who were diagnosed with ICVD and underwent susceptibility weighted imaging (SWI) in a grade A tertiary hospital from October 1, 2014 to October 1, 2022. We collected information on previous statin use, past medical history, clinical test indicators, and imaging data. We found that out of 522 patients, 310 patients (59.4%) had no CMB and 212 patients (40.6%) had CMBs. There was no statistically significant correlation between prior statin use, the occurrence, and number of CMBs in patients diagnosed with ICVD (P < 0.05). As for the location of CMB, there was a statistically significant correlation between prior statin use and lobar CMBs (P < 0.048). However, there was no statistically significant correlation between the use of atorvastatin and rosuvastatin and the occurrence of CMBs (P > 0.05). There was no independent correlation between previous statin use, and the occurrence, and number of CMBs in patients with ICVD. As for CMBs in different locations, there was a correlation between previous use of statin and lobar CMBs. There was no significant difference between atorvastatin and rosuvastatin in the occurrence of CMBs in patients with ICVD.

Impact of Cerebral Microbleeds on Gait, Balance, and Upper Extremities Function in Cerebral Small Vessel Disease.

White matter hyperintensites (WMHs) , lacunes and brain atrophy have been demonstrated to be positively related to gait disorder. However, cerebral microbleeds (CMBs) as a manifestation of cerebral small vessel disease (CSVD) is still under-investigated. Therefore, correlations between CMBs and upper extremity, gait and balance performance were investigated in this study. A cross-sectional study of middle-aged to older adults was conducted. CSVD burden was measured with magnetic resonance imaging (MRI) and the location and number of CMBs were analysed. Gait and balance functions were evaluated using a four meter walkway, Tinetti, Timed-Up-and-Go (TUG) and Short Physical Performance Battery (SPPB) tests. Upper extremity function was measured by 10 repeated pronation-supination time, 10 repeated finger tapping time, and 10 repeated opening and closings of the hands. A total of 224 participants were included in this study, with a mean age of 60.6 ± 10.5 years. The prevalence of CMB was 34.8% and most was lobar. Multiple linear regression analysis showed that CMB was associated with lower gait velocity, wider stride width, longer TUG test time, and poor performance on Tinetti and SPPB tests independently of other coexisting CSVD markers and risk factors. These relationships appeared to be explained by CMBs in the frontal, temporal, basal ganglia and infratentorial regions. The motor function of upper extremity also had independent correlations with CMBs especially in frontal, parietal, and temporal areas, and in the basal ganglia. CMBs were found to be associated with both gait, balance and upper extremity disturbances. The presence of CMB seems to be another major driving force for CSVD on lower and upper extremity impairment in healthy elderly subjects.

Impaired Kidney Function Small Vessel Disease Markers and Its Association with Periventricular White Matter Hyperintensities (P3-5.016)

<h3>Objective:</h3> We hypothesize that impaired kidney function is differentially associated with brain markers of SVD, and the association is greater with SVD markers restricted to deep, penetrating arteries. <h3>Background:</h3> Small vessel disease (SVD) is a condition associated with aging and vascular risk factors to which the brain and kidney are susceptible. However, whether kidney dysfunction may directly contribute to brain SVD as opposed to both organs being affected as an epiphenomenon of aging is less clear. <h3>Design/Methods:</h3> We leveraged existing data from our institution stroke registry. Odds ratio (OR), estimate, confidence intervals (CI), and p values were calculated. We rated visually the presence an anatomical location of cerebral microbleeds and chronic lacunar infarcts and used the Fazekas scale to semi-quantitate white matter hyperintensities. We created linear regression models adjusted for age, sex, race/ethnicity and vascular risk factors to evaluate the relationship between kidney function (defined as self-reported chronic kidney disease or creatinine on admission). <h3>Results:</h3> We included 973 patients (mean age 65±16 years, 51 % female). The prevalence of self-reported CKD/ESRD was 14% and the mean creatinine on admission was 1.61±2.04 mg/dl. The prevalence of chronic brain infarct was 40%, cerebral microbleeds 24%, and all had some degree of white matter hyperintensity. Calculated OR for deep location CMB in CKD/ESRD patients was 1.83 (p= 0.076). Beta estimate for periventricular WMH was 0.40 (p= 0.031) in CKD/ESRD patients and 0.51 (p= ≤0.01) in relation to the creatinine levels on admission. <h3>Conclusions:</h3> There is association between previous history of CKD-ESRD and creatinine levels on admission with periventricular WMH. These data also hint a possible association between CMB of deep location with history of CKD-ESRD, but a bigger sample is required for significance. <b>Disclosure:</b> Dr. Murguia Fuentes has nothing to disclose. Dr. Khasiyev has nothing to disclose. Dr. Gurel has nothing to disclose. Dr. Spagnolo-Allende has nothing to disclose. Dr. Rahman has nothing to disclose. Dr. Bueno has nothing to disclose. Mr. Murguia Fuentes has nothing to disclose. The institution of Dr. Marshall has received research support from NIH. Dr. Marshall has received publishing royalties from a publication relating to health care. Dr. Elkind has received personal compensation for serving as an employee of American Heart Association. Dr. Elkind has received personal compensation in the range of $10,000-$49,999 for serving as a Consultant for Atria Academy. The institution of Dr. Elkind has received research support from BMS-Pfizer Alliance for Eliquis. The institution of Dr. Elkind has received research support from Roche. Dr. Elkind has received publishing royalties from a publication relating to health care. Dr. Elkind has a non-compensated relationship as a Officer with American Heart Association that is relevant to AAN interests or activities. Dr. Gutierrez has received personal compensation in the range of $500-$4,999 for serving as an Expert Witness for Roetzel &amp; Andress, JOHN ASTUNO, JR. L.L.C.. The institution of Dr. Gutierrez has received research support from NIH. Dr. Gutierrez has received publishing royalties from a publication relating to health care. Dr. Gutierrez has received publishing royalties from a publication relating to health care.

Abstract TP100: Transfer Learning Based Cerebral Microbleed Detection As An Mri Biomarker For Cerebral Amyloid Angiopathy Spectrum Diseases

Objectives: Quantifying cerebral microbleeds (CMBs) in cerebral amyloid angiopathy (CAA) is important, however manual counting of CMBs on brain MRI is laborious. This work aims to develop a novel automatic deep learning segmentation algorithm for fast and accurate quantification of CMBs on brain MRIs. Method: We used (a) internal dataset (susceptibility-weighted imaging [SWI] clinical scans from 83 patients with CAA) with heterogeneous protocols on 1.5T and 3T scanners and manual CMB segmentation by 2 readers, and (b) public dataset (57 SWI scans from 30 patients with Alzheimer’s and CMB locations). The data was split into training, validation, and testing subsets (internal: 50/20/13; Public: 38/9/10). Preprocessing included N3 bias field correction, brain extraction, and up-sampling to a fixed in-plane resolution (0.2mm). Model used multi-channel 2D input (Fig1.b) and mimicked manual CMB segmentation. We trained base-model initially using the public dataset and then applied transfer learning using the internal dataset to segment CMBs in clinical scans. We evaluated model’s performance by sensitivity (S), precision (P), number of false positives per scan (FPC) and F1-score (F1). Results: On 10 public test scans, base model performed well (S 0.81, P 0.74, FPC 0.60, F1 0.77) but had high FPC for 13 internal test scans (S 1.00, P 0.15, FPC 4.31, F1 0.26). After transfer learning, the precision, FPC and F1-score were improved for internal scans (S 0.80, P 0.80, FPC 0.15, F1 0.80). Conclusion: Refined deep-learning based CMB counting algorithms could quantify CMBs for heterogeneous clinical MRI dataset with good sensitivity, precision, and false positivity. This method may accelerate further CAA clinical diagnosis and research.

Abstract TP183: Impaired Kidney Function Small Vessel Disease Markers And Its Association With Periventricular White Matter Hyperintensities

Introduction: Small vessel disease (SVD) is a condition associated with aging and vascular risk factors to which the brain and kidney are susceptible. However, whether kidney dysfunction may directly contribute to brain SVD as opposed to both organs being affected as an epiphenomenon of aging is less clear. We hypothesize that impaired kidney function is differentially associated with brain markers of SVD, and the association is greater with SVD markers restricted to deep, penetrating arteries. Methods: We leveraged existing data from the Columbia University Irving Medical Center/ New York Presbyterian Hospital Stroke Registry. Odds ratio (OR), estimate, confidence intervals (CI), and p values were calculated. We rated visually the presence an anatomical location of cerebral microbleeds and chronic lacunar infarcts and used the Fazekas scale to semi-quantitate white matter hyperintensities. We created linear regression models adjusted for age, sex, race/ethnicity and vascular risk factors to evaluate the relationship between kidney function (defined as self-reported chronic kidney disease or creatinine on admission). Results: We included 973 patients (mean age 65±16 years, 51 % female). The prevalence of self-reported CKD/ESRD was 14% and the mean creatinine on admission was 1.61±2.04 mg/dl. The prevalence of chronic brain infarct was 40%, cerebral microbleeds 24%, and all had some degree of white matter hyperintensity. Conclusion: There is association between previous history of CKD-ESRD and creatinine levels on admission with periventricular WMH. These data also hint a possible association between CMB of deep location with history of CKD-ESRD, but a bigger sample is required for significance.

Do Children with Immune Thrombocytopenia Have Cerebral Microbleeds?

Background Children with immune thrombocytopenia (ITP) have a low platelet count due to autoimmune destruction and reduced platelet production. ITP increases bleeding risk, with potentially devastating consequences. However, most children have mild disease that resolves spontaneously (Cooper 2014). For this reason, international guidelines recommend observation unless there is overt bleeding (Neunert et al. 2019; Provan et al. 2019). This has resulted in fewer patients exposed to treatment, but there are few data evaluating the safety and impact of this approach. Patients with ITP often have petechiae associated with thrombocytopenia. We hypothesised that a similar process may be occurring in the brain parenchyma. Using susceptibility weighted magnetic resonance imaging (SW-MRI-a technique that is particularly sensitive to haemosiderin deposition), we have previously identified occult cerebral microbleeds (CMBs) in 43% of thrombocytopenic adults with ITP (Cooper et al. 2020). Studies in other disorders have associated CMBs with impaired cognitive function (Morrison et al. 2017). This method has not previously been used to evaluate thrombocytopenic children. Methods 38 children aged 8-17 years old with a diagnosis of ITP and a platelet count under 30 x109/L at any time during their disease course, underwent SW-MRI. Recruitment was from the paediatric immune haematology clinic at Imperial College Healthcare NHS Trust specialist ITP centre. SW-MRI were assessed by two neuroradiologists blinded to clinical details. Number, size and location of CMBs were correlated with clinical metadata including paediatric bleeding questionnaire (PBQ) score, validated cognitive testing (Cogstate), health-related quality of life (HRQoL) scores and fatigue scores. We compared imaging data to 20 age-matched healthy controls (siblings from another SW-MRI Imperial College study using the same imaging protocol). Results The study cohort was 55% male with median age of 12.4 years (range 8-18 years). 66% had chronic ITP (lasting over 12 months) and 76% had active disease (platelet count below 100 x109/L or were on treatment) at the time of MRI. Median disease duration was 33 months (range 1-129 months). Of the cohort, 73% had received treatment including: tranexamic acid, steroids, thrombopoietin-receptor agonists-TPO-RA, intravenous immunoglobulins (IVIg), rituximab and others, with a median treatment episodes of 3 and 68% are currently on TPO-RA treatment. Of 38 patients, 5 (13%) had a detectable CMB (median 3 CMBs, range 1-10); no CMBs were detected in controls. All patients with CMBs had chronic ITP. The patient with the highest CMB burden had 10 CMBs in total (Figure 1). He had multi-refractory disease, 3002 days with a platelet count under 10 x 109/L, a paediatric bleeding score of 14 and minimal responses to IVIg, prednisone, dexamethasone, rituximab, eltrombopag, romiplostim, sirolimus and mycophenolate mofetil. There was a statistically significant correlation with higher PBQ score and the presence of CMBs (p=0.047 using the Mann-Whitney U test); no participants with a bleeding score under 4 had a CMB (PBQ median score 5, range 1-19); conversely many patients with a higher bleeding score did not have a CMB either (Figure 2). There was no correlation with disease duration and CMBs. Cognitive impairment, fatigue and reduced HRQoL were not associated with CMBs. Discussion Although there is heterogeneity in this cohort, the high proportion of chronic ITP and treated patients reflects referrals to an ITP specialist centre. The proportion of children with a CMB is lower than in adults, however disease duration is shorter in this cohort. As none of the children with acute ITP or a bleeding score less than 4 had CMBs, this may support the practice of observing asymptomatic patients whilst awaiting spontaneous remission, although confirmation from a larger cohort is needed. SW-MRI may also be valuable in stratifying patients with intermediate bleeding scores for therapy. In this study, CMBs were not associated with poor HRQoL, fatigue or cognitive impairment. A national study with differing centres is required to better understand the significance of this novel finding of CMBs in childhood ITP. Figure 1View largeDownload PPTFigure 1View largeDownload PPT Close modal

Urinary Immunoglobulin G Is Associated with Deep and Infratentorial Cerebral Microbleeds in Stroke Patients

Background: Cerebral microbleeds (CMBs) detected on susceptibility-weighted imaging (SWI) are associated with cerebral small vessel disease. Chronic kidney disease and microalbuminuria have been associated with the presence of CMBs in stroke patients. Urinary immunoglobulin G (IgG) is measured to document glomerular injury; however, the relationship between urinary IgG and CMBs is unknown. Methods: We retrospectively enrolled consecutive patients who had been admitted with transient ischemic attack (TIA) or ischemic stroke and identified those who had undergone SWI and a spot urine test. The location of CMBs was classified on magnetic resonance imaging as strictly lobar, deep/infratentorial (D/I), or mixed areas. We analyzed the association between urinary IgG and the presence and location of CMBs. Results: We included 298 patients (86 female, median age 70 years, median eGFR 65.8 mL/min/1.73 m²). Positive urinary IgG and CMB results were found in 58 (19%) and 160 patients (54%), respectively. Urinary IgG positivity was significantly associated with CMBs compared with non-CMBs (28% vs. 9%, p < 0.001), and with D/I or mixed CMBs compared with non-D/I or mixed CMBs (34% vs. 10%, p < 0.001). Multivariate analysis revealed that urinary IgG and hypertension positivity were strongly associated with D/I or mixed CMBs (OR 3.479, 95% CI: 1.776–6.818, p < 0.001; OR 3.415, 95% CI: 1.863–6.258, p < 0.001). Conclusions: Urinary IgG was associated with the prevalence of D/I or mixed location CMBs in TIA or ischemic stroke patients. Our findings provide new insights into the association between urinary IgG and the distribution of CMBs.

Analysis of Risk Factors for Cerebral Microbleeds and the Relationship between Cerebral Microbleeds and Cognitive Impairment.

(1) Background: Cerebral microbleeds (CMBs) are attracting increasing attention. Nevertheless, the risk factors for CMBs remain poorly identified, and the relationship between CMBs and cognitive impairment is still up for debate; (2) Objective: The present study analyzed the risk factors for CMBs and probed into the potential correlations between the presence, number, and location of CMBs and cognition; (3) Methods: This study enrolled 406 subjects who underwent both brain 3.0-T magnetic resonance imaging scans and cognitive testing. Spearman correlation was used to assess the relationship between the number of CMBs and cognition. Multiple linear regression was utilized to analyze the relationship between the regions of CMBs and each cognitive domain; (4) Results: Multivariate logistic regression analysis results showed that age (odds ratio (OR) = 1.045, 95% confidence interval (95%CI; 1.009, 1.082)), smoking (OR = 3.604, 95%CI (1.995, 6.509)), hypertension (OR = 3.607, 95%CI (2.204, 5.901)), total cholesterol (OR = 0.611, 95%CI (0.467, 0.799)), and Amyloid-β1-42 (Aβ1-42) (OR = 1.028, 95%CI (1.018, 1.037)) were the influencing factors of CMBs. Education years (OR = 0.959, 95%CI (0.930, 0.988)), white matter lesions (OR = 2.687, 95%CI (1.782, 4.051)), and CMBs (OR = 21.246, 95%CI (5.728, 21.576)) were the risk factors for cognitive impairment. Hypertension increased the probability of deep CMBs (OR = 12.54, 95%CI (2.21, 71.28)), while Aβ1-42 elevated the probability of lobar CMBs (OR = 1.02, 95%CI (1.00, 1.03)). There was a linear correlation between the number of CMBs and Montreal Cognitive Assessment scores (r = -0.756, p &lt; 0.001). However, CMBs in each region were not related to specific cognitive domains (p &gt; 0.05), except CMBs in the mixed group that were negatively correlated with attention (OR = -0.669, 95%CI (-0.034, -5.270)); (5) Conclusions: Taken together, serum Aβ1-42 levels are related to the presence of CMBs. Cognitive impairment is correlated with the number of CMBs rather than their region. These findings suggest that CMBs play a role in cognitive impairment and that CMBs mark the presence of diffuse vascular injury and neurodegenerative brain damage.

White matter degradation near cerebral microbleeds is associated with cognitive change after mild traumatic brain injury

To explore how cerebral microbleeds (CMBs) accompanying mild traumatic brain injury (mTBI) reflect white matter (WM) degradation and cognitive decline, magnetic resonance images were acquired from 62 mTBI adults (imaged ∼7 days and ∼6 months post-injury) and 203 matched healthy controls. On average, mTBI participants had a count of 2.7 ± 2.6 traumatic CMBs in WM, located 6.1 ± 4.4 mm from cortex. At ∼6-month follow-up, 97% of CMBs were associated with significant reductions (34% ± 11%, q < 0.05) in the fractional anisotropy of WM streamlines within ∼1 cm of CMB locations. Male sex and older age were significant risk factors for larger reductions (q < 0.05). For CMBs in the corpus callosum, cingulum bundle, inferior and middle longitudinal fasciculi, fractional anisotropy changes were significantly and positively associated with changes in cognitive functions mediated by these structures (q < 0.05). Our findings distinguish traumatic from non-traumatic CMBs by virtue of surrounding WM alterations and challenge the assumption that traumatic CMBs are neurocognitively silent. Thus, mTBI with CMB findings can be described as a clinical endophenotype warranting longitudinal cognitive assessment.

Association between antiplatelet medication and cerebral microbleeds in stroke-free population.

BACKGROUNDCerebral microbleeds (CMBs) may increase the risk of future intracerebral hemorrhage and ischemic stroke. However, It is unclear whether antiplatelet medication is associated with CMBs. This study aimed to investigate the association between antiplatelet medication and CMBs in a community-based stroke-free population.METHODSIn this cross-sectional study, stroke-free participants aged 18–85 years were recruited from a community in Beijing, China. Demographic, clinical, and antiplatelet medication data were collected through a questionnaire, and all participants underwent blood tests and brain magnetic resonance imaging at 3.0T. The presence, count, and location of CMBs were evaluated using susceptibility-weighted imaging. The association between antiplatelet medication and the presence of CMBs was analyzed using multivariable logistic regression. The associations between antiplatelet medication and CMBs by location (lobar, deep brain or infratentorial, and mixed regions) were also analyzed using multinomial logistic regression. A linear regression analysis was conducted to determine the association between antiplatelet medication and the log-transformed number of CMBs.RESULTSOf the 544 participants (mean age: 58.65 ± 13.66 years, 217 males), 119 participants (21.88%) had CMBs, and 64 participants (11.76%) used antiplatelet medication. Antiplatelet medication was found to be associated with CMBs at any location [odds ratio (OR) = 2.39, 95% CI: 1.24–4.58] and lobar region (OR = 2.83, 95% CI: 1.36–5.86), but not with the number of CMBs (β = 0.14, 95% CI: -0.21–0.48). Among antiplatelet medications, aspirin use was found to be associated with any CMB (OR = 3.17, 95% CI: 1.49–6.72) and lobar CMBs (OR = 3.61, 95% CI: 1.57–8.26).CONCLUSIONSAntiplatelet medication was associated with CMBs in stroke-free participants, particularly lobar CMBs. Among antiplatelet medications, aspirin use was associated with any CMB and lobar CMBs. Our findings suggest that it might be essential to optimize the management of antiplatelet medication in the stroke-free population with a higher burden of vascular risk factors to reduce the potential risk of CMBs.

The Association Between Standard Electrocardiography and Cerebral Small Vessel Disease in a Memory Clinic Study.

P-wave terminal force in lead V1 (PTFV1) on electrocardiography has been associated with atrial fibrillation and ischemic stroke. To investigate whether PTFV1 is associated with cerebral small vessel disease (CSVD) markers and etiological subtypes of cognitive impairment and dementia. Participants were recruited from ongoing memory clinic study between August 2010 to January 2019. All participants underwent physical and medical evaluation along with an electrocardiography and 3 T brain magnetic resonance imaging. Participants were classified as no cognitive impairment, cognitive impairment no dementia, vascular cognitive impairment no dementia, and dementia subtypes (Alzheimer's disease and vascular dementia). Elevated PTFV1 was defined as > 4,000μV×ms and measured manually on ECG. Of 408 participants, 78 (19.1%) had elevated PTFV1 (37 women [47%]; mean [SD] age, 73.8 [7.2] years). The participants with elevated PTFV1 had higher burden of lacunes, cerebral microbleeds (CMB), and cortical microinfarcts. As for the CMB location, persons with strictly deep CMB and mixed CMB had significantly higher PTFV1 than those with no CMB (p = 0.005, p = 0.007). Regardless of adjustment for cardiovascular risk factors and/or heart diseases, elevated PTFV1 was significantly associated with presence of CMB (odds ratio, 2.26; 95% CI,1.33-3.91). Elevated PTFV1 was associated with CSVD, especially deep CMB. PTFV1 in vascular dementia was also higher compared to Alzheimer's disease. Thus, PTFV1 might be a potential surrogate marker of brain-heart connection and vascular brain damage.

Lobar Cerebral Microbleeds Are Associated With Cognitive Decline in Patients With Type 2 Diabetes Mellitus

PurposeCombined the number, volume, and location of cerebral microbleeds (CMBs), this study aimed to explore the different features of CMBs and their correlation with cognitive ability in patients with type 2 diabetes mellitus (T2DM).MethodsThis study recruited 95 patients with T2DM and 80 healthy control (HC) individuals. AccuBrain®, an automated tool, was used to obtain the number and volume of CMBs. The scores on global cognition and five cognitive domains were derived from a battery of cognitive tests. The logistic regression and multivariate linear regression were conducted to determine the relationship between the CMBs (number, volume, and location) and cognitive ability in patients with T2DM.ResultsAfter adjusting for several variables, the total volume of CMBs (OR = 0.332, 95%CI: 0.133–0.825, and p = 0.018) was independent risk factor for cognitive impairment, whereas the total number of CMBs was not (OR = 0933, 95%CI: 0.794–1.097, and p = 0.400). Furthermore, the volume of CMBs in lobar regions was independently associated with working memory (β = −0.239, 95%CI: −0.565 to −0.035, and p = 0.027). However, no significant correlation between the number of CMBs (both lobar and deep/infratentorium) and any cognitive domains was observed.ConclusionsLobar CMBs was related with cognitive impairment in patients with T2DM and might be a potential early warning signal. Compared with the counting analysis, the quantitative method offered a more sensitive and objective measurement for studying imaging features of CMBs.

Abstract 70: Racial Differences In Small Vessel Disease Measured In MRI Of Stroke/ TIA Patients

Introduction: White matter hyperintensities (WMH) and cerebral microbleeds (CMB) are manifestations of small vessel disease (SVD), a surrogate for vascular cognitive impairment. Few studies have systematically investigated the racial differences in SVD among African American (AA) and white stroke/TIA patients. Methods: MRI scans of consecutive ischemic stroke and TIA patients admitted to our tertiary stroke center were assessed as a part of a stroke study. Deep and periventricular WMHs (DWMHs and PVWMHs, respectively) were rated visually on axial FLAIR images using the 4-point Fazekas scale and categorized into none/mild (grades 0 and 1) or moderate/severe (grades 2 and 3). Subsequently T2*-weighted MRI scans for the number, location, and topography of CMBs, as well as patients’ demographic, clinical information, and periodontal disease (PD) were evaluated. Student t-tests were performed to test continuous variables. X 2 tests were used to compare categorical variables. Multivariable analysis using multiple logistic regression was used to test the association between AA and SVD. Results: Among a total of 861 consecutive patients (741 stroke, 120 TIA), 469 AA patients were compared with 360 white for moderate/severe PVWMH (38%), DWMH (32%) and CMB≥5 (3%). Those with moderate/severe PVWMH were older (age 68±11 vs. 61±12, p&lt;0.001), more likely to be male (42% vs. 35%, p=0.02), hypertensive (40% vs. 26%, p=0.02), diabetic (43% vs. 34%, p=0.007), and have severe PD (41% vs. 35%, p=0.07). AA race was associated with PVWMH (Adj. OR 1.9, 95% 1.4-2.7) when adjusted for age, gender, hypertension, diabetes, and PD. Those with moderate/severe DWMH were older (age 68±10 vs. 62±13, p&lt;0.001), and more likely to be hypertensive (33% vs. 24%, p=0.09), diabetic (37% vs. 27%, p=0.003), and have severe PD (36% vs. 28%, p=0.01). AA race was associated with DWMH (Adj. OR 1.5, 95% 1.1-2.2) when adjusted for age, hypertension, diabetes, and PD. Those with CMB≥5 were more likely to be hypertensive (5% vs. 1%, p=0.008). AA race was associated with CMB≥5 (Adj. OR 4.1, 95% 1.3-12.6) when adjusted for age and hypertension. Conclusion: We report significant independent association between AA race and various manifestations of SVD including moderate/severe DWMH, PVWMH, and CMB≥5.

Neuropathologic and clinical correlates of cerebral microbleeds in community‐based older adults

Cerebral microbleeds (CMBs) are common in older adults and have been linked to hypertension, cognitive decline, and CAA. However, it remains unclear what the neuropathologic correlates of CMBs are in community-based older adults. The aim of this study was to determine the neuropathologic and clinical correlates of CMBs in community-based older adults when controlling for demographic factors, and also to investigate the relationship between neuropathologies and the location of CMBs in the brain. A total of 289 participants from two longitudinal cohort studies of aging, the Rush Memory and Aging Project and Religious Orders Study, were included in this work. Participants received annual clinical evaluation and cognitive assessment, ex-vivo MRI, and neuropathologic examination by a board-certified neuropathologist (blinded to clinical and imaging findings) on one brain hemisphere (Fig. 1). A total of 8 pathologies were assessed (Fig. 2). Manual identification of CMBs on ex-vivo T2*-weighted gradient echo images was done by an experienced rater blinded to all clinical and pathological information. The total number of CMBs as well as the number of CMBs per lobe were recorded for each participant. Poisson regression was used to investigate the associations of the total and regional number of CMBs with neuropathologies and clinical factors, controlling for demographics and postmortem interval. A significance threshold of p<0.01 was used after applying Bonferroni correction. The total number of CMBs in the whole brain was associated with CAA (beta=0.0517, p<0.0001), diabetes (beta=0.0997, p<0.0001), and arteriosclerosis (beta=0.0535, p=0.0007). The number of CMBs in the frontal lobe was also associated with CAA (beta=0.0796, p<0.0001), diabetes (beta=0.1531, p<0.0001), and arteriosclerosis (beta=0.0792, p<0.0001). The number of CMBs in the occipital and temporal lobes were correlated with diabetes (beta=0.2208, p=0.0006). In the basal ganglia, there was a slight association between number of microbleeds and microinfarcts (beta=0.1774, p=0.0075). The present study on the neuropathologic and clinical correlates of cerebral microbleeds combined detailed neuropathologic examination and ex-vivo MRI in a large number of community-based older adults. CMBs were shown to be associated with CAA, arteriosclerosis, and diabetes in the whole brain and in the frontal lobe.

Abstract 10971: Prevalence and Risk Factors of Silent Brain Microbleeds in Patients with Severe Valvular Heart Disease

Introduction: The presence of cerebral microbleeds (CMBs) has been described using MRI in patients with cardiovascular risk factors or prior stroke and could predict future cognitive dysfunction or cardiovascular mortality. CMBs are highly frequent (&gt; 50%) in patients with infective endocarditis (IE). However, the association of CMBs and clinical factors in patients' valvular disease without IE remains unclear. Hypothesis: Valvular heart disease without IE confers a risk factor for microbleeds. Methods: We retrospectively examined data from the consecutive 96 patients ( 72 ± 9 years, 49 men) with severe valvular disease who underwent T2*-weighted brain MRI before cardiac surgery. The patients with neurological abnormalities or IE were excluded. Conventional echocardiography was performed to evaluate the left ventricular volume and valvular abnormalities. CMBs were coded by researchers blind to clinical details, who independently assessed the presence and location of CMBs using a standardized form. The study population consisted of 59 patients with severe aortic stenosis (AS) (group A) and 40 patients with severe aortic or mitral regurgitation (group B). Results: CMBs were found in 26 patients (27%), 14 (15%) had multiple CMBs. CMBs were most frequently seen in the lobar locations (69%), followed by deep or infratentorial locations (62%). No significant relationship was found between CMBs in dyslipidemia, diabetes mellitus, smoking status, anticoagulant, and antiplatelet therapy in both groups. In group A, the HAS-BLED score was higher in patients with CMBs, and the presence of CMBs was associated with hypertension (P&lt;0.05); however, no significant differences were observed in the left ventricular mass index (LVMI), LV end-diastolic volume (LVEDV), any aortic valve severity parameters. In group B, there were significant differences in LVMI and LVEDV between patients with CMBs and those without (154 ± 40 g/m 2 vs 125 ± 32 g/m 2 , P &lt; 0.01 ; 150 ± 39 ml vs 111 ± 38 ml, P&lt;0.01). Conclusion: CMBs were frequently observed in severe valvular heart disease without IE. The presence of CMBs was independent of antiplatelet or anticoagulant therapy. In aortic or mitral regurgitation patients, LV remodeling may contribute to the development of CMBs.

Cerebral microbleeds following thoracic endovascular aortic repair.

Stroke and neurological injury are a complication of thoracic endovascular aortic repair (TEVAR). Cerebral microbleeds (CMBs) are common in patients with white matter damage to the brain secondary to chronic vasculopathy. The aim of this study was to examine the occurrence of CMBs after TEVAR, and to evaluate their association with patient and procedural factors. Patients who underwent TEVAR between September 2018 and January 2020 in two specialist European aortic centres were analysed. All patients underwent postoperative susceptibility-weighted MRI. The location and number of CMBs were identified, and analysed with regard to procedural aspects, clinical outcome, and Fazekas score as an indicator of pre-existing vascular leucoencephalopathy. Some 91 patients were included in the study. A total of 1531 CMBs were detected in 58 of 91 patients (64 per cent). In the majority of affected patients, CMBs were found bilaterally (79 per cent). Unilateral CMBs in the right or left hemisphere occurred in 16 and 5 per cent of patients respectively (P < 0.001). More CMBs were found in the middle cerebral than in the vertebrobasilar/posterior and anterior cerebral artery territories (mean(s.d.) 3.35(5.56) versus 2.26(4.05) versus 0.97(2.87); P = 0.045). Multivariable analysis showed an increased probability of CMBs after placement of TEVAR stent-grafts with a proximal diameter of at least 40 mm (odds ratio (OR) 6.85, 95 per cent c.i. 1.65 to 41.59; P = 0.007) and in patients with a higher Fazekas score on postoperative T2-weighted MRI (OR 2.62, 1.06 to 7.92; P = 0.037). CMBs on postoperative MRI are common after endovascular repair in the aortic arch. Their occurrence appears to be associated with key aspects of the procedure and pre-existing vascular leucoencephalopathy.