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Ogawa Ito, Ai, Akihiro Shindo, Yuichiro Ii, et al. "Microbleeds after Carotid Artery Stenting: Small Embolism May Induce Cerebral Microbleeds." Cerebrovascular Diseases Extra 9, no. 2 (2019): 57–65. http://dx.doi.org/10.1159/000500112.
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Background: Since the advent of magnetic resonance imaging technology, cerebral microbleeds can be diagnosed in vivo. However, the underlying mechanism of cerebral microbleed formation is not fully understood. Objectives: This study aimed to identify the factors associated with cerebral microbleeds after carotid artery stenting (CAS). Method: We retrospectively examined 125 patients who underwent CAS for carotid stenosis. Cerebral microbleeds were investigated using T2*-weighted gradient-echo (GRE) imaging before and after CAS. We analyzed the possible association of new microbleeds with the following risk factors: the number of baseline microbleeds and ischemic cerebral lesions, the occurrence of cerebral hyperperfusion syndrome, and new ischemic cerebral lesions after CAS. Results: Baseline cerebral microbleeds were detected in 53 patients (42.4%). New cerebral microbleeds after CAS were observed in 13 of 125 patients (10.4%) and were exclusively associated with new ischemic lesions but not with other risk factors. No patient showed a merged image of a new cerebral microbleed on GRE imaging or a new ischemic lesion on diffusion-weighted imaging. Lobar and deep microbleeds were noted in 12/13 (92.3%) and 1 patient (7.7%), respectively. Of 12 patients with new microbleeds, 10 (76.9%) and 2 (15.4%) had a new microbleed in the ipsilateral and contralateral hemispheres, respectively. Conclusions: We found that new cerebral microbleeds developed after CAS and that these might be associated with new ischemic lesions, mostly in the territory of the treated carotid artery. We speculate that these microbleeds result from the deoxygenation of hemoglobin in the embolus or, alternatively, small hemorrhagic transformation of ischemic lesions.
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Bianciardi, Marta, Saef Izzy, Bruce R. Rosen, Lawrence L. Wald, and Brian L. Edlow. "Location of Subcortical Microbleeds and Recovery of Consciousness After Severe Traumatic Brain Injury." Neurology 97, no. 2 (2021): e113-e123. http://dx.doi.org/10.1212/wnl.0000000000012192.
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BackgroundIn patients with severe traumatic brain injury (TBI), coma is associated with impaired subcortical arousal mechanisms. However, it is unknown which nuclei involved in arousal (arousal nuclei) are implicated in coma pathogenesis and are compatible with coma recovery.MethodsWe mapped an atlas of arousal nuclei in the brainstem, thalamus, hypothalamus, and basal forebrain onto 3 tesla susceptibility-weighted images (SWI) in 12 patients with acute severe TBI who presented in coma and recovered consciousness within 6 months. We assessed the spatial distribution and volume of SWI microbleeds and evaluated the association of microbleed volume with the duration of unresponsiveness and functional recovery at 6 months.ResultsThere was no single arousal nucleus affected by microbleeds in all patients. Rather, multiple combinations of microbleeds in brainstem, thalamic, and hypothalamic arousal nuclei were associated with coma and were compatible with recovery of consciousness. Microbleeds were frequently detected in the midbrain (100%), thalamus (83%), and pons (75%). Within the brainstem, the microbleed incidence was largest within the mesopontine tegmentum (e.g., pedunculotegmental nucleus, mesencephalic reticular formation) and ventral midbrain (e.g., substantia nigra, ventral tegmental area). Brainstem arousal nuclei were partially affected by microbleeds, with microbleed volume not exceeding 35% of brainstem nucleus volume on average. Compared to microbleed volume within nonarousal brainstem regions, the microbleed volume within arousal brainstem nuclei accounted for a larger proportion of variance in the duration of unresponsiveness and 6-month Glasgow Outcome Scale–Extended scores.ConclusionThese results suggest resilience of arousal mechanisms in the human brain after severe TBI.
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De Sciscio, Michele, Paul De Sciscio, Wilson Vallat, and Timothy Kleinig. "Cerebral microbleed distribution following cardiac surgery can mimic cerebral amyloid angiopathy." BMJ Neurology Open 3, no. 2 (2021): e000166. http://dx.doi.org/10.1136/bmjno-2021-000166.
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Background and aimsHaving anecdotally noted a high frequency of lobar-restricted cerebral microbleeds (CMBs) mimicking cerebral amyloid angiopathy (CAA) in patients with previous cardiac surgery (especially valve replacement) presenting to our transient ischaemic attack (TIA) clinic, we set out to objectively determine the frequency and distribution of microbleeds in this population.MethodsWe performed a retrospective comparative cohort study in consecutive patients presenting to two TIA clinics with either: (1) previous coronary artery bypass grafting (CABG) (n=41); (2) previous valve replacement (n=41) or (3) probable CAA (n=41), as per the Modified Boston Criteria, without prior cardiac surgery. Microbleed number and distribution was determined and compared.ResultsAt least one lobar-restricted microbleed was found in the majority of cardiac surgery patients (65%) and 32/82 (39%) met diagnostic criteria for CAA. Valve replacement patients had a higher microbleed prevalence (90 vs 51%, p<0.01) and lobar-restricted microbleed count (2.6±2.7 vs 1.0±1.4, p<0.01) than post-CABG patients; lobar-restricted microbleed count in both groups was substantially less than in CAA patients (15.5±20.4, p<0.01). In postcardiac surgery patients, subcortical white matter (SWM) microbleeds were proportionally more frequent compared with CAA patients. Receiver operator curve analysis of a ‘location-based’ ratio (calculated as SWM/SWM+strictly-cortical CMBs), revealed an optimal ratio of 0.45 in distinguishing cardiac surgery-associated microbleeds from CAA (sensitivity 0.56, specificity 0.93, area under the curve 0.71).ConclusionLobar-restricted microbleeds are common in patients with past cardiac surgery, however a higher proportion of these CMBs involve the SWM than in patients with CAA.
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Xu, Rui, Chongjie Cheng, Yue Wu, et al. "Microbleeds after Stent-assisted Coil Embolization of Unruptured Intracranial Aneurysms: Incidence, Risk Factors and the Role of Thromboelastography." Current Neurovascular Research 17, no. 4 (2020): 502–9. http://dx.doi.org/10.2174/1567202617999200819161033.
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Objective: To analyze the incidence and risk factors of microbleeds lesions and to use thromboelastography (TEG) to evaluate the relationship between perioperative platelet function and microbleed events in patients with unruptured intracranial aneurysms (UIAs) undergoing Stent-Assisted Coil (SAC) embolization. Methods: We retrospectively enrolled 261 patients with UIAs undergoing SAC embolization between November 2017 and October 2019. All patients received unanimous antiplatelet protocol (aspirin 300 mg and clopidogrel 300 mg). Platelet function was evaluated by TEG, and magnetic resonance susceptibility-weighted imaging (SWI) was performed for microbleeds detection before and after surgery. Univariate and multivariate logistic regression analyses were used to identify potential risk factors for microbleeds following embolization. Results: Microbleed lesions were identified in 122 of 261 patients (46.7%). Most of the microbleeds were asymptomatic, except for 22 patients complaining slight headaches, and 3 patients who developed cerebral hemorrhage after discharge. Among the clinical characters, female, previous intracerebral hemorrhage (ICH) history and TEG parameters variation (higher reaction time (R) and lower maximum amplitude of adenosine diphosphate (MAADP)) were associated with microbleeds occurrence. Subsequent multivariate analysis indicated that gender, hemorrhage history, R, and MAADP were still independent risk factors of microbleeds. The R-value (>7.6 min) and MAADP (<29.2 mm) were predictive values, yielding areas under the receiver operating curve (ROC) of 0.76 (95% CI 0.70 to 0.82) and 0.89 (95% CI 0.86 to 0.93), respectively. Conclusion: The incidence of microbleeds may be high in UIA patients treated with SAC and dual antiplatelet therapy. Lesions occurred more frequently in female patients and patients with ICH history. Among the TEG parameters, the R-value and MAADP were predictors for microbleed events.
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Griffin, Allison D., L. Christine Turtzo, Gunjan Y. Parikh, et al. "Traumatic microbleeds suggest vascular injury and predict disability in traumatic brain injury." Brain 142, no. 11 (2019): 3550–64. http://dx.doi.org/10.1093/brain/awz290.
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Abstract Traumatic microbleeds are small foci of hypointensity seen on T2*-weighted MRI in patients following head trauma that have previously been considered a marker of axonal injury. The linear appearance and location of some traumatic microbleeds suggests a vascular origin. The aims of this study were to: (i) identify and characterize traumatic microbleeds in patients with acute traumatic brain injury; (ii) determine whether appearance of traumatic microbleeds predict clinical outcome; and (iii) describe the pathology underlying traumatic microbleeds in an index patient. Patients presenting to the emergency department following acute head trauma who received a head CT were enrolled within 48 h of injury and received a research MRI. Disability was defined using Glasgow Outcome Scale-Extended ≤6 at follow-up. All magnetic resonance images were interpreted prospectively and were used for subsequent analysis of traumatic microbleeds. Lesions on T2* MRI were stratified based on ‘linear’ streak-like or ‘punctate’ petechial-appearing traumatic microbleeds. The brain of an enrolled subject imaged acutely was procured following death for evaluation of traumatic microbleeds using MRI targeted pathology methods. Of the 439 patients enrolled over 78 months, 31% (134/439) had evidence of punctate and/or linear traumatic microbleeds on MRI. Severity of injury, mechanism of injury, and CT findings were associated with traumatic microbleeds on MRI. The presence of traumatic microbleeds was an independent predictor of disability (P &lt; 0.05; odds ratio = 2.5). No differences were found between patients with punctate versus linear appearing microbleeds. Post-mortem imaging and histology revealed traumatic microbleed co-localization with iron-laden macrophages, predominately seen in perivascular space. Evidence of axonal injury was not observed in co-localized histopathological sections. Traumatic microbleeds were prevalent in the population studied and predictive of worse outcome. The source of traumatic microbleed signal on MRI appeared to be iron-laden macrophages in the perivascular space tracking a network of injured vessels. While axonal injury in association with traumatic microbleeds cannot be excluded, recognizing traumatic microbleeds as a form of traumatic vascular injury may aid in identifying patients who could benefit from new therapies targeting the injured vasculature and secondary injury to parenchyma.
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Shams, Sara, Tobias Granberg, Juha Martola, et al. "Cerebral microbleeds topography and cerebrospinal fluid biomarkers in cognitive impairment." Journal of Cerebral Blood Flow & Metabolism 37, no. 3 (2016): 1006–13. http://dx.doi.org/10.1177/0271678x16649401.
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Cerebral microbleeds, a marker of small vessel disease, are thought to be of importance in cognitive impairment. We aimed to study topographical distribution of cerebral microbleeds, and their involvement in disease pathophysiology, reflected by cerebrospinal fluid biomarkers; 1039 patients undergoing memory investigation underwent lumbar puncture and a brain magnetic resonance imaging scan. Cerebrospinal fluid samples were analyzed for amyloid β(Aβ)42, total tau(T-tau), tau phosphorylated at threonine 18(P-tau) and cerebrospinal fluid/serum albumin ratios. Magnetic resonance imaging sequences were evaluated for small vessel disease markers, including cerebral microbleeds, white matter hyperintensities and lacunes. Low Aβ42 levels were associated with lobar cerebral microbleeds in the whole cohort and Alzheimer’s disease ( P < 0.001). High cerebrospinal fluid/serum albumin ratios were seen with increased number of cerebral microbleeds in the brainstem ( P < 0.001). There were tendencies for increased Aβ42 levels and decreased Tau levels with deep and infratentorial cerebral microbleeds ( P < 0.05). Lobar cerebral microbleeds were associated with white matter hyperintensities and lacunes ( P < 0.001). Probable cerebral amyloid angiopathy-related cerebral microbleeds were associated with low Aβ42 levels and lacunes, whereas probable cerebral amyloid angiopathy-unrelated cerebral microbleeds were associated with white matter hyperintensities ( P < 0.001). Our findings show that cerebral microbleed distribution is associated with different patterns of cerebrospinal fluid biomarkers, supporting different pathogenesis of deep/infratentorial and lobar cerebral microbleeds.
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Ward, Stephanie A., Parnesh Raniga, Nicholas J. Ferris, et al. "ASPREE-NEURO study protocol: A randomized controlled trial to determine the effect of low-dose aspirin on cerebral microbleeds, white matter hyperintensities, cognition, and stroke in the healthy elderly." International Journal of Stroke 12, no. 1 (2016): 108–13. http://dx.doi.org/10.1177/1747493016669848.
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Rationale Cerebral microbleeds seen on brain magnetic resonance imaging are markers of small vessel disease, linked to cognitive dysfunction and increased ischemic and hemorrhagic stroke risk. Observational studies suggest that aspirin use may induce cerebral microbleeds, and associated overt intracranial hemorrhage, but this has not been definitively resolved. Aims ASPREE-NEURO will determine the effect of aspirin on cerebral microbleed development over three years in healthy adults aged 70 years and over, participating in the larger ‘ASPirin in Reducing Events in the Elderly (ASPREE)’ primary prevention study of aspirin. Sample size Five hundred and fifty-nine participants provide 75% power (two-sided p value of 0.05) to determine an average difference of 0.5 cerebral microbleed per person after three years. Methods and design A multi-center, randomized placebo-controlled trial of 100 mg daily aspirin in participants who have brain magnetic resonance imaging at study entry, one and three years after randomization and who undergo cognitive testing at the same time points. Study outcomes The primary outcome is the number of new cerebral microbleeds on magnetic resonance imaging after three years. Secondary outcomes are the number of new cerebral microbleeds after one year, change in volume of white matter hyperintensity, cognitive function, and stroke. Discussion ASPREE-NEURO will resolve whether aspirin affects the presence and number of cerebral microbleeds, their relationship with cognitive performance, and indicate whether consideration of cerebral microbleeds alters the risk-benefit profile of aspirin in primary prevention for older people. Trial registration Australian New Zealand Clinical Trials Registry ACTRN12613001313729.
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Rabelo, Ana GB, Camila VL Teixeira, Thamires NC Magalhães, et al. "Is cerebral microbleed prevalence relevant as a biomarker in amnestic mild cognitive impairment and mild Alzheimer’s disease?" Neuroradiology Journal 30, no. 5 (2017): 477–85. http://dx.doi.org/10.1177/1971400917720465.
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Introduction The search for a reliable neuroimaging biomarker in Alzheimer’s disease is a matter of intense research. The presence of cerebral microbleeds seems to be a potential biomarker. However, it is not clear if the presence of microbleeds has clinical usefulness to differentiate mild Alzheimer’s disease and amnestic mild cognitive impairment from normal aging. We aimed to verify if microbleed prevalence differs among three groups: mild Alzheimer’s disease, amnestic mild cognitive impairment due to Alzheimer’s disease, and normal controls. Moreover, we studied whether microbleeds were associated with apolipoprotein E allele ɛ4 status, cerebrospinal fluid amyloid-beta, total and phosphorylated tau protein levels, vascular factors, and cognition. Methods Twenty-eight mild Alzheimer’s disease patients, 34 with amnestic mild cognitive impairment and 36 cognitively normal elderly subjects underwent: magnetic resonance imaging with a susceptibility-weighted imaging sequence on a 3T scanner, apolipoprotein E genotyping and a full neuropsychological evaluation. Only amnestic mild cognitive impairment and mild Alzheimer’s disease underwent cerebrospinal fluid analysis. We compared the groups and verified if microbleeds were predicted by all other variables. Results Mild Alzheimer’s disease presented a higher prevalence of apolipoprotein E allele ɛ4 in relation to amnestic mild cognitive impairment and control group. No significant differences were found between groups when considering microbleed presence. Logistic regression tests failed to find any relationship between microbleeds and the variables. We performed three different regression models using different independent variables: Model 1 - amyloid-beta, phosphorylated tau protein, total tau, apolipoprotein E allele ɛ4 status, age, and sex; Model 2 - vascular risk factors, age, and sex; Model 3 - cognitive scores sex, age, and education. Conclusion Although microbleeds might be related to the Alzheimer’s disease process, their presence is not a good candidate for a neuroimaging biomarker of the disease, especially in its early phases.
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Jung, Young Hee, Hyemin Jang, Seong Beom Park, et al. "Strictly Lobar Microbleeds Reflect Amyloid Angiopathy Regardless of Cerebral and Cerebellar Compartments." Stroke 51, no. 12 (2020): 3600–3607. http://dx.doi.org/10.1161/strokeaha.119.028487.
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Background and Purpose: We aimed to determine whether lobar cerebellar microbleeds or concomitant lobar cerebellar and deep microbleeds, in the presence of lobar cerebral microbleeds, attribute to underlying advanced cerebral amyloid angiopathy pathology or hypertensive arteriopathy. Methods: We categorized 71 patients with suspected cerebral amyloid angiopathy markers (regardless of the presence of deep and cerebellar microbleeds) into 4 groups according to microbleed distribution: L (strictly lobar cerebral, n=33), L/LCbll (strictly lobar cerebral and strictly lobar cerebellar microbleeds, n=13), L/Cbll/D (lobar, cerebellar, and deep microbleeds, n=17), and L/D (lobar and deep, n=8). We additionally categorized patients with cerebellar microbleeds into 2 groups according to dentate nucleus involvement: strictly lobar cerebellar (n=16) and dentate (n=14). We then compared clinical characteristics, Aβ (amyloid-β) positivity on PET (positron emission tomography), magnetic resonance imaging cerebral amyloid angiopathy markers, and cerebral small vessel disease burden among groups. Results: The frequency of Aβ positivity was higher in the L and L/LCbll groups (81.8% and 84.6%) than in the L/Cbll/D and L/D groups (37.5% and 29.4%; P <0.001), while lacune numbers were lower in the L and L/LCbll groups (1.7±3.3 and 1.7±2.6) than in the L/Cbll/D and L/D groups (8.0±10.3 and 13.4±17.7, P =0.001). The L/LCbll group had more lobar cerebral microbleeds than the L group (93.2±121.8 versus 38.0±40.8, P =0.047). The lobar cerebellar group had a higher Aβ positivity (75% versus 28.6%, P =0.011) and lower lacune number (2.3±3.7 versus 8.6±1.2, P =0.041) than the dentate group. Conclusions: Strictly lobar cerebral and cerebellar microbleeds are related to cerebral amyloid angiopathy, whereas any combination of concurrent lobar and deep microbleeds suggest hypertensive angiopathy regardless of cerebral or cerebellar compartments.
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Sparacia, Gianvincenzo, Francesco Agnello, Giuseppe La Tona, Alberto Iaia, Federico Midiri, and Benedetta Sparacia. "Assessment of cerebral microbleeds by susceptibility-weighted imaging in Alzheimer’s disease patients: A neuroimaging biomarker of the disease." Neuroradiology Journal 30, no. 4 (2017): 330–35. http://dx.doi.org/10.1177/1971400916689483.
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Purpose The objective of this study was to correlate the presence and distribution of cerebral microbleeds in Alzheimer’s disease patients with cerebrospinal fluid biomarkers (amyloid-beta and phosphorylated tau 181 protein levels) and cognitive decline by using susceptibility-weighted imaging magnetic resonance sequences at 1.5 T. Material and methods Fifty-four consecutive Alzheimer’s disease patients underwent brain magnetic resonance imaging at 1.5 T to assess the presence and distribution of cerebral microbleeds on susceptibility-weighted imaging images. The images were analyzed in consensus by two neuroradiologists, each with at least 10 years’ experience. Dementia severity was assessed with the Mini-Mental State Examination score. A multiple regression analysis was performed to assess the associations between the number and location of cerebral microbleed lesions with the age, sex, duration of the disease, cerebrospinal fluid amyloid-beta and phosphorylated tau 181 protein levels, and cognitive functions. Results A total of 296 microbleeds were observed in 54 patients; 38 patients (70.4%) had lobar distribution, 13 patients (24.1%) had non-lobar distribution, and the remaining three patients (5.6%) had mixed distribution, demonstrating that Alzheimer’s disease patients present mainly a lobar distribution of cerebral microbleeds. The age and the duration of the disease were correlated with the number of lobar cerebral microbleeds ( P < 0.001). Cerebrospinal fluid amyloid-beta, phosphorylated tau 181 protein levels, and cognitive decline were correlated with the number of lobar cerebral microbleeds in Alzheimer’s disease patients ( P < 0.001). Conclusion Lobar distribution of cerebral microbleeds is associated with Alzheimer’s disease and the number of lobar cerebral microbleeds directly correlates with cerebrospinal fluid amyloid-beta and phosphorylated tau 181 protein levels and with the cognitive decline of Alzheimer’s disease patients.
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Guidoux, Celine, Jean-Jacques Hauw, Isabelle F. Klein, et al. "Amyloid Angiopathy in Brain Hemorrhage: A Postmortem Neuropathological-Magnetic Resonance Imaging Study." Cerebrovascular Diseases 45, no. 3-4 (2018): 124–31. http://dx.doi.org/10.1159/000486554.
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Background: Risk factors for intracerebral hemorrhage (ICH) include hypertension and cerebral amyloid angiopathy (CAA). The objective of this study was to determine the autopsy prevalence of CAA and the potential overlap with other risk factors among patients who died from ICH and also the correlation of CAA with cerebral microbleeds. Methods: We analyzed 81 consecutive autopsy brains from patients with ICH. Staining for CAA detection was performed. We used an age- and sex-matched control group of routine brain autopsies of nonneurological patients to determine the frequencies of CAA and hypertension. Postmortem 3D T2-weighted gradient-echo magnetic resonance imaging (MRI) with a 1.5-T magnet was performed in 11 brains with ICH (5 with CAA and 6 without) and histological correlation was performed when microbleeds were detected. Results: Hypertension and CAA were found in 69.1 and 24.7% of cases respectively. Among patients with CAA, 65.0% also had hypertension. The prevalence of CAA was similar among non-hypertensive cases and controls (33.3 and 23.1%; p = 0.54), whereas a significant difference was found between hypertensive cases vs. controls (28.9% vs. 0; p = 0.01). MRI documented 48 microbleeds and all 5 brains with CAA had ≥1 microbleed, compared to 3/6 brains without CAA. Among 48 microbleeds on MRI, 45 corresponded histologically to microbleeds surrounding microvessels (23 <200 µm in diameter, 19 between 200 µm and 2 mm, 3 were hemosiderin granules). Conclusions: Both hypertension and CAA frequently coexist in patients with ICH. MRI-detected microbleeds, proven by histological analysis, were twice as common in patients with CAA as in those with hypertensive ICH.
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Heo, Sung Hyuk, Dongwhane Lee, Dokyung Lee, and Dae-Il Chang. "Differentiation of a Symptomatic Cerebral Microbleed from Silent Microbleeds." International Journal of Stroke 9, no. 1 (2013): E2. http://dx.doi.org/10.1111/ijs.12218.
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Caplan, Louis R. "Microbleeds." Circulation 132, no. 6 (2015): 479–80. http://dx.doi.org/10.1161/circulationaha.115.017866.
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Van Belle, Eric, Nicolas Debry, Flavien Vincent, et al. "Cerebral Microbleeds During Transcatheter Aortic Valve Replacement: A Prospective Magnetic Resonance Imaging Cohort." Circulation 146, no. 5 (2022): 383–97. http://dx.doi.org/10.1161/circulationaha.121.057145.
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Background: Cerebral microbleeds (CMBs) have been observed in healthy elderly people undergoing systematic brain magnetic resonance imaging. The potential role of acute triggers on the appearance of CMBs remains unknown. We aimed to describe the incidence of new CMBs after transcatheter aortic valve replacement (TAVR) and to identify clinical and procedural factors associated with new CMBs including hemostatic measures and anticoagulation management. Methods: We evaluated a prospective cohort of patients with symptomatic aortic stenosis referred for TAVR for CMBs (METHYSTROKE [Identification of Epigenetic Risk Factors for Ischemic Complication During the TAVR Procedure in the Elderly]). Standardized neurologic assessment, brain magnetic resonance imaging, and analysis of hemostatic measures including von Willebrand factor were performed before and after TAVR. Numbers and location of microbleeds on preprocedural magnetic resonance imaging and of new microbleeds on postprocedural magnetic resonance imaging were reported by 2 independent neuroradiologists blinded to clinical data. Measures associated with new microbleeds and postprocedural outcome including neurologic functional outcome at 6 months were also examined. Results: A total of 84 patients (47% men, 80.9±5.7 years of age) were included. On preprocedural magnetic resonance imaging, 22 patients (26% [95% CI, 17%–37%]) had at least 1 microbleed. After TAVR, new microbleeds were observed in 19 (23% [95% CI, 14%–33%]) patients. The occurrence of new microbleeds was independent of the presence of microbleeds at baseline and of diffusion-weighted imaging hypersignals. In univariable analysis, a previous history of bleeding ( P =0.01), a higher total dose of heparin ( P =0.02), a prolonged procedure ( P =0.03), absence of protamine reversion ( P =0.04), higher final activated partial thromboplastin time ( P =0.05), lower final von Willebrand factor high-molecular-weight:multimer ratio ( P =0.007), and lower final closure time with adenosine–diphosphate ( P =0.02) were associated with the occurrence of new postprocedural microbleeds. In multivariable analysis, a prolonged procedure (odds ratio, 1.22 [95% CI, 1.03–1.73] for every 5 minutes of fluoroscopy time; P =0.02) and postprocedural acquired von Willebrand factor defect (odds ratio, 1.42 [95% CI, 1.08–1.89] for every lower 0.1 unit of high-molecular-weight:multimer ratio; P =0.004) were independently associated with the occurrence of new postprocedural microbleeds. New CMBs were not associated with changes in neurologic functional outcome or quality of life at 6 months. Conclusions: One out of 4 patients undergoing TAVR has CMBs before the procedure and 1 out of 4 patients develops new CMBs. Procedural or antithrombotic management and persistence of acquired von Willebrand factor defect were associated with the occurrence of new CMBs. Registration: URL: https://www.clinicaltrials.gov ; Unique identifier: NCT02972008.
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Graff-Radford, Jonathan, Timothy Lesnick, Alejandro A. Rabinstein, et al. "Cerebral Microbleeds." Stroke 52, no. 7 (2021): 2347–55. http://dx.doi.org/10.1161/strokeaha.120.031515.
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Background and Purpose: Cerebral microbleeds (CMBs) are represented by small areas of hemosiderin deposition, detected on brain magnetic resonance imaging (MRI), and found in ≈23% of the cognitively normal population over age of 60 years. CMBs predict risk of hemorrhagic and ischemic stroke. They correlate with increased cardiovascular mortality. In this article, we sought to determine in a population-based study whether antithrombotic medications correlate with CMBs and, if present, whether the association was direct or mediated by another variable. Methods: The study consisted of 1253 participants from the population-based Mayo Clinic Study of Aging who underwent T2* gradient-recalled echo magnetic resonance imaging. We tested the relationship between antithrombotic medications and CMB presence and location, using multivariable logistic-regression models. Ordinal logistic models tested the relationship between antithrombotics and CMB frequency. Using structural equation models, we assessed the effect of antithrombotic medications on presence/absence of CMBs and count of CMBs in the CMB-positive group, after considering the effects of age, sex, vascular risk factors, amyloid load by positron emission tomography, and apoE. Results: Two hundred ninety-five participants (26.3%) had CMBs. Among 678 participants taking only antiplatelet medications, 185 (27.3%) had CMBs. Among 95 participants taking only an anticoagulant, 43 (45.3%) had CMBs. Among 44 participants taking an anticoagulant and antiplatelet therapy, 21 (48.8%) had CMBs. Anticoagulants correlated with the presence and frequency of CMBs, whereas antiplatelet agents were not. Structural equation models showed that predictors for presence/absence of CMBs included older age at magnetic resonance imaging, male sex, and anticoagulant use. Predictors of CMB count in the CMB-positive group were male sex and amyloid load. Conclusions: Anticoagulant use correlated with presence of CMBs in the general population. Amyloid positron emission tomography correlated with the count of CMBs in the CMB-positive group.
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Akı, Çağla. "Cerebral Microbleeds." Turkish Journal Of Neurology 25, no. 4 (2020): 263–64. http://dx.doi.org/10.4274/tnd.2019.71135.
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Akı, Çağla. "Cerebral Microbleeds." Turkish Journal Of Neurology 25, no. 4 (2019): 263–64. http://dx.doi.org/10.4274/tnd.galenos.2019.71135.
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Wang, Zhaolu, Yannie O. Y. Soo, and Vincent C. T. Mok. "Cerebral Microbleeds." Stroke 45, no. 9 (2014): 2811–17. http://dx.doi.org/10.1161/strokeaha.114.004286.
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Arkink, Enrico B., Gisela M. Terwindt, Anton J. M. de Craen, et al. "Infratentorial Microbleeds." Stroke 46, no. 7 (2015): 1987–89. http://dx.doi.org/10.1161/strokeaha.115.009604.
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Jeerakathil, Tom, Philip A. Wolf, Alexa Beiser, et al. "Cerebral Microbleeds." Stroke 35, no. 8 (2004): 1831–35. http://dx.doi.org/10.1161/01.str.0000131809.35202.1b.
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Cordonnier, C. "Brain microbleeds." Practical Neurology 10, no. 2 (2010): 94–100. http://dx.doi.org/10.1136/jnnp.2010.206086.
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Goas, Philippe, and Serge Timsit. "Microbleeds cérébraux." La Presse Médicale 39, no. 6 (2010): 632–39. http://dx.doi.org/10.1016/j.lpm.2009.07.026.
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Graff-Radford, Jonathan, Hugo Botha, Alejandro A. Rabinstein, et al. "Cerebral microbleeds." Neurology 92, no. 3 (2018): e253-e262. http://dx.doi.org/10.1212/wnl.0000000000006780.
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ObjectiveTo describe the prevalence of cerebral microbleeds (CMBs) and determine the association between CMBs and β-amyloid burden on PET.MethodsFrom the population-based Mayo Clinic Study of Aging, 1,215 participants (53% male) underwent 3-tesla MRI scans with T2* gradient recalled echo sequences from October 2011 to February 2017. A total of 1,123 participants (92%) underwent 11C-Pittsburgh compound B (PiB)-PET scans. The prevalence of CMBs was derived by adjusting for nonparticipation and standardizing to the Olmsted County, MN, population. The relationship between β-amyloid burden and CMB presence and location was tested using logistic regression models. Ordinal logistic models tested the relationship between CMB frequency and β-amyloid burden.ResultsTwo hundred seventy-four participants (22.6%) had at least one CMB. CMB frequency increased with age by decade (11% aged 60–69 years, 22% 70–79 years, and 39% 80 years and older). After adjusting for age, sex, and hypertension, PiB standardized uptake value ratio (SUVR) was associated with increased odds of a CMB. The association between PiB SUVR and CMBs was location-specific; PiB SUVR was associated with lobar CMBs but not deep CMBs. Age, hypertension, and PiB SUVR were associated with increasing CMB count. CMB density was greatest in parietal and occipital regions; β-amyloid burden correlated with concentration of CMBs in all lobar regions. Among participants with multiple CMBs, greater PiB uptake occurred in the pre- and postcentral gyri superiorly, the superior parietal lobe and precuneus, the angular gyrus, inferior temporal gyrus, and temporal poles.ConclusionsThe prevalence of CMBs increases with age. In this population-based sample, β-amyloid load was associated with lobar but not with deep CMBs.
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Martí-Fàbregas, Joan, Santiago Medrano-Martorell, Elisa Merino, et al. "MRI predicts intracranial hemorrhage in patients who receive long-term oral anticoagulation." Neurology 92, no. 21 (2019): e2432-e2443. http://dx.doi.org/10.1212/wnl.0000000000007532.
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ObjectiveWe tested the hypothesis that the risk of intracranial hemorrhage (ICH) in patients with cardioembolic ischemic stroke who are treated with oral anticoagulants (OAs) can be predicted by evaluating surrogate markers of hemorrhagic-prone cerebral angiopathies using a baseline MRI.MethodsPatients were participants in a multicenter and prospective observational study. They were older than 64 years, had a recent cardioembolic ischemic stroke, and were new users of OAs. They underwent a baseline MRI analysis to evaluate microbleeds, white matter hyperintensities, and cortical superficial siderosis. We collected demographic variables, clinical characteristics, risk scores, and therapeutic data. The primary endpoint was ICH that occurred during follow-up. We performed bivariate and multivariate Cox regression analyses.ResultsWe recruited 937 patients (aged 77.6 ± 6.5 years; 47.9% were men). Microbleeds were detected in 207 patients (22.5%), moderate/severe white matter hyperintensities in 419 (45.1%), and superficial siderosis in 28 patients (3%). After a mean follow-up of 23.1 ± 6.8 months, 18 patients (1.9%) experienced an ICH. In multivariable analysis, microbleeds (hazard ratio 2.7, 95% confidence interval [CI] 1.1–7, p = 0.034) and moderate/severe white matter hyperintensities (hazard ratio 5.7, 95% CI 1.6–20, p = 0.006) were associated with ICH (C index 0.76, 95% CI 0.66–0.85). Rate of ICH was highest in patients with both microbleed and moderate/severe WMH (3.76 per 100 patient-years, 95% CI 1.62–7.4).ConclusionPatients taking OAs who have advanced cerebral small vessel disease, evidenced by microbleeds and moderate to severe white matter hyperintensities, had an increased risk of ICH. Our results should help to determine the risk of prescribing OA for a patient with cardioembolic stroke.ClinicalTrials.gov identifierNCT02238470.
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Wilson, Duncan, and David J. Werring. "Establishing the “meaning” of microbleeds: Clinical context or lobar microbleed burden?" Alzheimer's & Dementia 12, no. 1 (2015): 85–86. http://dx.doi.org/10.1016/j.jalz.2015.09.004.
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Meng, Ningqin, Wei Zhang, Ying Su, Ziming Ye, and Chao Qin. "Antiplatelet therapy may be safe in ischemic stroke patients with cerebral microbleed." Journal of International Medical Research 48, no. 8 (2020): 030006052094939. http://dx.doi.org/10.1177/0300060520949396.
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Objective We examined whether antiplatelet therapy is safe for ischemic stroke patients with cerebral microbleed. Methods We retrospectively analyzed ischemic stroke patients admitted to our hospital from 2015 to 2018. Baseline information was extracted from the computerized database. Adverse events, including symptomatic cerebral hemorrhage, recurrent cerebral infarction, and death, were collected by phone. Results A total of 184 ischemic stroke patients were examined, including 106 with and 78 without cerebral microbleed. No patient experienced symptomatic cerebral hemorrhage after discharge. Patients with cerebral microbleed had a higher prevalence of hypertension (92% vs 74%) and suffered from more serious leukoaraiosis (3.0 ± 1.7 vs 1.3 ± 1.4 points on the Fazekas scale). Leukoaraiosis scores were correlated with the number of cerebral microbleeds (r = 0.42). Conclusions Antiplatelet therapy may be safe for ischemic stroke patients with cerebral microbleed. The risk-benefit ratio should be carefully evaluated before withholding antiplatelet therapy.
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Feng, Chao, Min Fang, Yu Xu, Ting Hua, and Xue-Yuan Liu. "Microbleeds in Late-Life Depression: Comparison of Early- and Late-Onset Depression." BioMed Research International 2014 (2014): 1–7. http://dx.doi.org/10.1155/2014/682092.
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Late-life depression could be classified roughly as early-onset depression (EOD) and late-onset depression (LOD). LOD was proved to be associated with cerebral lesions including white matter hyperintensities (WMH) and silent brain infarctions (SBI), differently from EOD. However, it is unclear whether similar association is present between LOD and microbleeds which are also silent lesions. In this study, 195 patients of late-life depression were evaluated and divided into EOD, presenile-onset depression (POD), and LOD groups; 85 healthy elderly controls were enrolled as controls. Subjects were scanned by MRI including susceptibility weighted images to evaluate white matter hyperintensities (WMH), silent brain infarctions (SBI), and microbleeds. The severity of depression was evaluated with 15-item Geriatric Depression Scale. Psychosocial factors were investigated with Scale of Life Events and Lubben Social Network Scale. Logistic regression and linear regression were performed to identify the independent risk factors for depression. Results showed that LOD patients had higher prevalence of microbleeds than EOD, POD, and control patients. The prevalence of lobar microbleeds and microbleeds in the left hemisphere was the independent risk factor for the occurrence of LOD; a high number of microbleeds were associated with severe state of LOD, whereas life events and lack of social support were more important for EOD and POD. All these results indicated that Microbleeds especially lobar microbleeds and microbleeds in the left hemisphere were associated with LOD but not with EOD.
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Wan, M., A. Ganesh, C. Grassi, and A. Demchuk. "P.077 Mixed autoimmune hemolytic anemia: an unusual cause of ischemic stroke and extensive cerebral microbleeds." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 48, s3 (2021): S41. http://dx.doi.org/10.1017/cjn.2021.356.
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Background: Mixed autoimmune hemolytic anemia (mAIHA) is a rare autoimmune disorder that results in hemolysis with thrombotic complications like ischemic stroke. This is the first case report of cerebral microbleeds secondary to mAIHA. Methods: A literature review of mAIHA and cerebral microbleeds was conducted using the PubMed and Ovid MEDLINE databases from 1980 to 2021. Results: A 76 year old male with congenital deafness and rheumatoid arthritis presented with diffuse livedo reticularis and abdominal pain. He had fulminant hemolysis with new neurologic deficits and altered mental status. CT/CTA of the head and neck were unremarkable. MR brain revealed extensive cerebral microbleeds and multi-territory ischemic strokes. He was diagnosed with mAIHA, started on pulse methylprednisolone, and had no further microbleeds on follow-up MRI. From his clinical picture, common causes of cerebral microbleeds were ruled out such as cerebral amyloid angiopathy and hypertension. The pathogenesis of his microbleeds may be from concomitant severe hypoxia or a prothrombotic state, both previously reported in the literature. Conclusions: This is the first case report of extensive cerebral microbleeds secondary to mAIHA. When a patient develops acute neurologic deficits in the context of mAIHA, extensive cerebral microbleeds may be present possibly due to concomitant severe hypoxia versus a prothrombotic state.
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Kelly, James. "New horizons: managing antithrombotic dilemmas in patients with cerebral amyloid angiopathy." Age and Ageing 50, no. 2 (2021): 347–55. http://dx.doi.org/10.1093/ageing/afaa275.
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Abstract Cerebral amyloid angiopathy (CAA) most commonly presents with lobar intracerebral haemorrhage, though also with transient focal neurological episodes, cognitive impairment, as an incidental finding and rarely acutely or subacutely in patients developing an immune response to amyloid. Convexity subarachnoid haemorrhage, cortical superficial siderosis and lobar cerebral microbleeds are the other signature imaging features. The main implications of a diagnosis are the risk of intracerebral haemorrhage and frequent co-existence of antithrombotic indications. The risk of intracerebral haemorrhage varies by phenotype, being highest in patients with transient focal neurological episodes and lowest in patients with isolated microbleeds. There is only one relevant randomised controlled trial to CAA patients with antithrombotic indications: RESTART showed that in patients presenting with intracerebral haemorrhage while taking antiplatelets, restarting treatment appeared to reduce recurrent intracerebral haemorrhage and improve outcomes. Observational and indirect data are reviewed relevant to other scenarios where there are antithrombotic indications. In patients with a microbleed-only phenotype, the risk of ischaemic stroke exceeds the risk of intracerebral haemorrhage at all cerebral microbleed burdens. In patients with atrial fibrillation (AF), left atrial appendage occlusion, where device closure excludes the left atrial appendage from the circulation, can be considered where the risk of anticoagulation seems prohibitive. Ongoing trials are testing the role of direct oral anticoagulant (DOACs) and left atrial appendage occlusion in patients with intracerebral haemorrhage/AF but in the interim, treatment decisions will need to be individualised and remain difficult.
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Greenberg, Steven M., R. N. Kaveer Nandigam, Pilar Delgado, et al. "Microbleeds Versus Macrobleeds." Stroke 40, no. 7 (2009): 2382–86. http://dx.doi.org/10.1161/strokeaha.109.548974.
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Charidimou, Andreas, and Sara Shams. "Introducing @microbleeds: A pilot Twitter space for cerebral microbleeds research." International Journal of Stroke 11, no. 3 (2016): NP40—NP41. http://dx.doi.org/10.1177/1747493016632251.
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Charidimou, Andreas, Sara Shams, Jose R. Romero, et al. "Clinical significance of cerebral microbleeds on MRI: A comprehensive meta-analysis of risk of intracerebral hemorrhage, ischemic stroke, mortality, and dementia in cohort studies (v1)." International Journal of Stroke 13, no. 5 (2018): 454–68. http://dx.doi.org/10.1177/1747493017751931.
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Background Cerebral microbleeds can confer a high risk of intracerebral hemorrhage, ischemic stroke, death and dementia, but estimated risks remain imprecise and often conflicting. We investigated the association between cerebral microbleeds presence and these outcomes in a large meta-analysis of all published cohorts including: ischemic stroke/TIA, memory clinic, “high risk” elderly populations, and healthy individuals in population-based studies. Methods Cohorts (with > 100 participants) that assessed cerebral microbleeds presence on MRI, with subsequent follow-up (≥3 months) were identified. The association between cerebral microbleeds and each of the outcomes (ischemic stroke, intracerebral hemorrhage, death, and dementia) was quantified using random effects models of (a) unadjusted crude odds ratios and (b) covariate-adjusted hazard rations. Results We identified 31 cohorts ( n = 20,368): 19 ischemic stroke/TIA ( n = 7672), 4 memory clinic ( n = 1957), 3 high risk elderly ( n = 1458) and 5 population-based cohorts ( n = 11,722). Cerebral microbleeds were associated with an increased risk of ischemic stroke (OR: 2.14; 95% CI: 1.58–2.89 and adj-HR: 2.09; 95% CI: 1.71–2.57), but the relative increase in future intracerebral hemorrhage risk was greater (OR: 4.65; 95% CI: 2.68–8.08 and adj-HR: 3.93; 95% CI: 2.71–5.69). Cerebral microbleeds were an independent predictor of all-cause mortality (adj-HR: 1.36; 95% CI: 1.24–1.48). In three population-based studies, cerebral microbleeds were independently associated with incident dementia (adj-HR: 1.35; 95% CI: 1.00–1.82). Results were overall consistent in analyses stratified by different populations, but with different degrees of heterogeneity. Conclusions Our meta-analysis shows that cerebral microbleeds predict an increased risk of stroke, death, and dementia and provides up-to-date effect sizes across different clinical settings. These pooled estimates can inform clinical decisions and trials, further supporting cerebral microbleeds role as biomarkers of underlying subclinical brain pathology in research and clinical settings.
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Reddy, Sujan T., and Sean I. Savitz. "Hypertension-Related Cerebral Microbleeds." Case Reports in Neurology 12, no. 3 (2020): 266–69. http://dx.doi.org/10.1159/000508760.
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Hypertension and cerebral amyloid angiopathy are the most common causes of cerebral microbleeds. The pattern of microbleeds on T2*-weighted gradient echo sequence of magnetic resonance imaging of the brain can be indicative of the etiology of intracerebral hemorrhage. We describe a case of cerebellar hemorrhage with cerebral microbleeds secondary to chronic hypertension.
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Pasi, Marco, Andreas Charidimou, Gregoire Boulouis, et al. "Mixed-location cerebral hemorrhage/microbleeds." Neurology 90, no. 2 (2017): e119-e126. http://dx.doi.org/10.1212/wnl.0000000000004797.
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ObjectiveTo assess the predominant type of cerebral small vessel disease (SVD) and recurrence risk in patients who present with a combination of lobar and deep intracerebral hemorrhage (ICH)/microbleed locations (mixed ICH).MethodsOf 391 consecutive patients with primary ICH enrolled in a prospective registry, 75 (19%) had mixed ICH. Their demographics, clinical/laboratory features, and SVD neuroimaging markers were compared to those of 191 patients with probable cerebral amyloid angiopathy (CAA-ICH) and 125 with hypertensive strictly deep microbleeds and ICH (HTN-ICH). ICH recurrence and case fatality were also analyzed.ResultsPatients with mixed ICH showed a higher burden of vascular risk factors reflected by a higher rate of left ventricular hypertrophy, higher creatinine values, and more lacunes and severe basal ganglia (BG) enlarged perivascular spaces (EPVS) than patients with CAA-ICH (all p < 0.05). In multivariable models mixed ICH diagnosis was associated with higher creatinine levels (odds ratio [OR] 2.5, 95% confidence interval [CI] 1.2–5.0, p = 0.010), more lacunes (OR 3.4, 95% CI 1.7–6.8), and more severe BG EPVS (OR 5.8, 95% CI 1.7–19.7) than patients with CAA-ICH. Conversely, when patients with mixed ICH were compared to patients with HTN-ICH, they were independently associated with older age (OR 1.03, 95% CI 1.02–1.1), more lacunes (OR 2.4, 95% CI 1.1–5.3), and higher microbleed count (OR 1.6, 95% CI 1.3–2.0). Among 90-day survivors, adjusted case fatality rates were similar for all 3 categories. Annual risk of ICH recurrence was 5.1% for mixed ICH, higher than for HTN-ICH but lower than for CAA-ICH (1.6% and 10.4%, respectively).ConclusionsMixed ICH, commonly seen on MRI obtained during etiologic workup, appears to be driven mostly by vascular risk factors similar to HTN-ICH but demonstrates more severe parenchymal damage and higher ICH recurrence risk.
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Duan, Kui, and Yufang Wu. "Meta-Analysis of the Relationship between the Prognosis of Acute Cerebral Infarction Intravenous Lysis and Cerebral Microbleeds Based on Intelligent Medical Care." Contrast Media & Molecular Imaging 2022 (August 29, 2022): 1–11. http://dx.doi.org/10.1155/2022/4329318.
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The accelerated pace of life leads to people’s unhealthy living habits such as irregular diet, irregular work and rest, and fatigued work. The incidence of acute cerebral infarction (ACI) is increasing year by year. Intravenous thrombolysis is the best solution for clinical treatment of ACI, but intravenous thrombolysis increases the risk of cerebral microbleeds and even seriously damages the brain of patients. It is crucial to analyze the relationship between intravenous thrombolysis of ACI and cerebral microbleeds. Using intelligent medical methods such as BP neural network (BPNN), meta-analysis was carried out on the prognosis of ACI intravenous thrombolysis and cerebral microbleeds, and the basic data indicators, living habits indicators, and ACI intravenous thrombolysis indicators of ACI patients were analyzed. The experimental results showed that the odds ratios (OR) of systolic blood pressure before ACI intravenous thrombolysis, blood glucose concentration after ACI intravenous thrombolysis, diastolic blood pressure before ACI intravenous thrombolysis, and diastolic blood pressure after ACI intravenous thrombolysis on cerebral microbleeds after ACI intravenous thrombolysis were 0.97, 0.44, 0.13, and 0.07, respectively. Long-term intravenous thrombolysis with ACI, high systolic blood pressure after NIHSS thrombolysis with high scores, and blood glucose concentration before thrombolysis had OR >1, which were risk factors for cerebral microbleeds after intravenous thrombolysis with ACI. Therefore, paying attention to the risk factors of cerebral microbleeds during ACI intravenous thrombolysis can effectively reduce cerebral microbleeds after ACI intravenous thrombolysis and improve the treatment efficiency of ACI patients.
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Jo, Sungyang, E.-Nae Cheong, Nayoung Kim, et al. "Role of White Matter Abnormalities in the Relationship Between Microbleed Burden and Cognitive Impairment in Cerebral Amyloid Angiopathy." Journal of Alzheimer's Disease 86, no. 2 (2022): 667–78. http://dx.doi.org/10.3233/jad-215094.
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Background: Cerebral amyloid angiopathy (CAA) often presents as cognitive impairment, but the mechanism of cognitive decline is unclear. Recent studies showed that number of microbleeds were associated with cognitive decline. Objective: We aimed to investigate how microbleeds contribute to cognitive impairment in association with white matter tract abnormalities or cortical thickness in CAA. Methods: This retrospective comparative study involved patients with probable CAA according to the Boston criteria (Aβ+ CAA) and patients with Alzheimer’s disease (Aβ+ AD), all of whom showed severe amyloid deposition on amyloid PET. Using mediation analysis, we investigated how FA or cortical thickness mediates the correlation between the number of lobar microbleeds and cognition. Results: We analyzed 30 patients with Aβ+ CAA (age 72.2±7.6, female 53.3%) and 30 patients with Aβ+ AD (age 71.5±7.6, female 53.3%). The two groups showed similar degrees of cortical amyloid deposition in AD-related regions. The Aβ+ CAA group had significantly lower FA values in the clusters of the posterior area than did the Aβ+ AD group (family-wise error-corrected p < 0.05). The correlation between the number of lobar microbleeds and visuospatial function was indirectly mediated by white matter tract abnormality of right posterior thalamic radiation (PTR) and tapetum, while lobar microbleeds and language function was indirectly mediated by the abnormality of left PTR and sagittal stratum. Cortical thickness did not mediate the association between lobar microbleeds and cognition. Conclusion: This result supports the hypothesis that microbleeds burden leads to white matter tract damage and subsequent cognitive decline in CAA.
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Jang, Dong-Kyu, Pil Woo Huh, and Kwan-Sung Lee. "Association of apolipoprotein E gene polymorphism with small-vessel lesions and stroke type in moyamoya disease: a preliminary study." Journal of Neurosurgery 124, no. 6 (2016): 1738–45. http://dx.doi.org/10.3171/2015.5.jns142973.
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OBJECT The present study was conducted to investigate whether microbleeds or microinfarcts are associated with apolipoprotein E (APOE) gene polymorphisms in patients with moyamoya disease (MMD), and if so, whetherAPOE gene polymorphisms are also associated with stroke type in patients with MMD. METHODS This cross-sectional, multicenter study included 86 consecutive patients with MMD who underwent T2*-weighted gradient echo or susceptibility-weighted MR imaging and 83 healthy control volunteers. Baseline clinical and radiological characteristics were recorded at diagnosis, and inter- and intragroup differences in the APOE genotypes were assessed. Multivariate binary logistic regression models were used to determine the association factors for small-vessel lesions (SVLs) and hemorrhagic presentation in patients with MMD. RESULTS There was no difference in APOE gene polymorphism and the incidence of SVLs between patients with MMD and healthy controls (p > 0.05). In the MMD group, 7 (8.1%) patients had microbleeds and 32 (37.2%) patients had microinfarcts. Microbleeds were more frequently identified in patients with hemorrhagic-type than in nonhemorrhagictype MMD (p = 0.003). APOE genotypes differed according to the presence of microbleeds (p = 0.024). APOE ε2 or ε4 carriers also experienced microbleeds more frequently than APOE ε3/ε3 carriers (p = 0.013). In the multivariate regression analysis in patients with MMD, microbleeds were significantly related to APOE ε2 or ε4 carrier status (OR 7.86; 95% CI1.20–51.62; p = 0.032) and cerebral aneurysm (OR 17.31; 95% CI 2.09–143.57; p = 0.008). Microinfarcts were independently associated with hypertension (OR 3.01; 95% CI 1.05–7.86; p = 0.007). Hemorrhagic presentation was markedly associated with microbleeds (OR 10.63; 95% CI 1.11–102.0; p = 0.041). CONCLUSIONS These preliminary results did not show a difference in APOE gene polymorphisms between patients with MMD and healthy persons. However, they imply that APOE gene polymorphisms may play certain roles in the presence of microbleeds but not microinfarcts in patients with MMD. A further confirmatory study is necessary to elucidate the effect of APOE gene polymorphisms and SVLs on the future incidence of stroke in patients with MMD.
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Lesnik Oberstein, S. A. J., R. van den Boom, M. A. van Buchem, et al. "Cerebral microbleeds in CADASIL." Neurology 57, no. 6 (2001): 1066–70. http://dx.doi.org/10.1212/wnl.57.6.1066.
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Fisher, Mark, and Wei Ling Lau. "Of Microbiomes and Microbleeds." Stroke 51, no. 12 (2020): 3489–91. http://dx.doi.org/10.1161/strokeaha.120.032422.
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Wadi, Lara C., Mher Mahoney Grigoryan, Ronald C. Kim, et al. "Mechanisms of Cerebral Microbleeds." Journal of Neuropathology & Experimental Neurology 79, no. 10 (2020): 1093–99. http://dx.doi.org/10.1093/jnen/nlaa082.
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Abstract Cerebral microbleeds (CMB) are a common MRI finding, representing underlying cerebral microhemorrhages (CMH). The etiology of CMB and microhemorrhages is obscure. We conducted a pathological investigation of CMH, combining standard and immunohistological analyses of postmortem human brains. We analyzed 5 brain regions (middle frontal gyrus, occipital pole, rostral cingulate cortex, caudal cingulate cortex, and basal ganglia) of 76 brain bank subjects (mean age ± SE 90 ± 1.4 years). Prussian blue positivity, used as an index of CMH, was subjected to quantitative analysis for all 5 brain regions. Brains from the top and bottom quartiles (n = 19 each) were compared for quantitative immunohistological findings of smooth muscle actin, claudin-5, and fibrinogen, and for Sclerosis Index (SI) (a measure of arteriolar remodeling). Brains in the top quartile (i.e. with most extensive CMH) had significantly higher SI in the 5 brain regions combined (0.379 ± 0.007 vs 0.355 ± 0.008; p &lt; 0.05). These findings indicate significant coexistence of arteriolar remodeling with CMH. While these findings provide clues to mechanisms of microhemorrhage development, further studies of experimental neuropathology are needed to determine causal relationships.
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Yan, Shenqiang, Yi Chen, Xuting Zhang, David S. Liebeskind, and Min Lou. "New Microbleeds After Thrombolysis." Medicine 93, no. 20 (2014): e99. http://dx.doi.org/10.1097/md.0000000000000099.
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Hilal, Saima, Monica Saini, Chuen Seng Tan, et al. "Cerebral Microbleeds and Cognition." Alzheimer Disease & Associated Disorders 28, no. 2 (2014): 106–12. http://dx.doi.org/10.1097/wad.0000000000000015.
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Galli, Silvio, Emelyne Muzard, Ansoumane Camara, Elizabeth Meideros de Bustos, and Thierry Moulin. "De drôle de microbleeds." Revue Neurologique 168 (April 2012): A127. http://dx.doi.org/10.1016/j.neurol.2012.01.326.
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Lee, Juyoun, Eun Hee Sohn, Eungseok Oh, and Ae Young Lee. "Characteristics of Cerebral Microbleeds." Dementia and Neurocognitive Disorders 17, no. 3 (2018): 73. http://dx.doi.org/10.12779/dnd.2018.17.3.73.
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Selim, Magdy, and Hans-Christoph Diener. "Atrial Fibrillation and Microbleeds." Stroke 48, no. 10 (2017): 2660–64. http://dx.doi.org/10.1161/strokeaha.117.017085.
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Dichgans, Martin, Markus Holtmannspötter, Jürgen Herzog, Nils Peters, Michael Bergmann, and Tarek A. Yousry. "Cerebral Microbleeds in CADASIL." Stroke 33, no. 1 (2002): 67–71. http://dx.doi.org/10.1161/hs0102.100885.
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Yagi, Takuya, Fumie Konoeda, Ikuko Mizuta, Toshiki Mizuno, and Norihiro Suzuki. "Increasing Microbleeds in CADASIL." European Neurology 69, no. 6 (2013): 352–53. http://dx.doi.org/10.1159/000348720.
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Linn, J. "Imaging of Cerebral Microbleeds." Clinical Neuroradiology 25, S2 (2015): 167–75. http://dx.doi.org/10.1007/s00062-015-0458-z.
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Stephenson, Joan. "Aspirin and Brain Microbleeds." JAMA 301, no. 19 (2009): 1977. http://dx.doi.org/10.1001/jama.2009.689.
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Fisher, Mark. "Cerebral Microbleeds and Thrombolysis." JAMA Neurology 73, no. 6 (2016): 632. http://dx.doi.org/10.1001/jamaneurol.2016.0576.
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