Relevant bibliographies by topics / Microbleeds

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  1. Journal articles
  2. Dissertations / Theses
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  4. Book chapters
  5. Conference papers
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Academic literature on the topic 'Microbleeds'

Author: Grafiati
Published: 4 June 2021
Last updated: 5 July 2023

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Journal articles on the topic "Microbleeds"

1

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 < 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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Dissertations / Theses on the topic "Microbleeds"

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Asl, Babak Ghafary. "A Computer Aided Detection System for Cerebral Microbleeds in Brain MRI." Thesis, Blekinge Tekniska Högskola, Sektionen för ingenjörsvetenskap, 2012. http://urn.kb.se/resolve?urn=urn:nbn:se:bth-6053.

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Advances in MR technology have improved the potential for visualization of small lesions in brain images. This has resulted in the opportunity to detect cerebral microbleeds (CMBs), small hemorrhages in the brain that are known to be associated with risk of ischemic stroke and intracerebral bleeding. Currently, no computerized method is available for fully- or semi-automated detection of CMBs. In this paper, we propose a CAD system for the detection of CMBs to speed up visual analysis in population-based studies. Our method consists of three steps: (i) skull-stripping (ii) initial candidate selection (iii) reduction of false-positives using a two layer classi cation and (iv) determining the anatomical location of CMBs. The training and test sets consist of 156 subjects (448 CMBs) and 81 subjects (183 CMBs), respectively. The geometrical, intensity-based and local image descriptor features were used in the classi cation steps. The training and test sets consist of 156 subjects (448 CMBs) and 81 subjects (183 CMBs), respectively. The sensitivity for CMB detection was 90% with, on average, 4 false-positives per subject.
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Momeni, Saba. "Synthetic data generation for machine learning to improve Microbleeds detection from MRI images." Thesis, Griffith University, 2022. http://hdl.handle.net/10072/417201.

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Cerebral Microbleeds (CMB) are small chronic brain haemorrhages, known as paramagnetic blood products, and likely caused by structural abnormalities of the small vessels. The concept of CMB is primarily a radiological construct describing small MRI signal voids. They are often present with cerebrovascular disease, dementia, Alzheimer’s disease, and normal aging people. Substantial progress has been made in recent years, in developing MRI methodologies showing CMB, such as susceptibility-weighted imaging (SWI) which is sensitive to differences in tissue magnetic susceptibility. In SWI, residual paramagnetic blood products appear with a lower intensity and are therefore suitable for detecting CMB, showing as hypointense amorphous small semi-spherical blobs. However, on visual inspection of SWI scans, CMB appearance can easily be confounded with small blood vessels cross-sections. The detection of CMB from MRI is clinically important and has generated increasing interest as an imaging marker of vessel diseases and cognitive dysfunctions. Being subjective, time-consuming, and high missing rates are some critical challenges of human rating. Computer-aided algorithms are being proposed to detect CMB for different MRI modalities with the aim of increasing sensitivity and reducing the number of false positives. However, the lack of ground truth leads to the imbalanced data problem and overfitting. To cope with the lack of dataset, traditional data augmentation methods, undersampling, cost-sensitive matrices are employed to mitigate the imbalanced data during classifier training. There are some problems behind with these applied solutions. Undersampling could omit some informative negative samples, traditional data augmentation methods are highly dependent on the diversity and availability of the ground truth, and the cost-sensitive matrix is not a general solution. Data privacy is a critical issue in medical research and it is essential to highlight that research and public health activities need to be carried out in ways that protect individuals’ privacy. Therefore, the demand to generate synthetic data is increasing. This thesis proposes a synthetic CMB generation model independent of the ground truth availability, and with the capability of being adaptable to new MRI modalities. The second aim is to improve CMB classification by using synthetic CMB in the classifier to achieve high sensitivity with low false positives. To propose our synthetic CMB generation model, we exploited our limited ground truth from SWI MRI images. Some features such as location, intensity, size and shape were extracted to get intuition from real CMB. The Gaussian mixture model was applied to distinguish background and outliers and extract a binary CMB mask to compute volume. To have information about the Microbleeds’ location, we defined our tissue mask including gray matter, white matter, ventricle, and cerebrospinal fluid to compute distance distribution and CMB proportion for each region. For shape, and intensity, the average of all real CMB and minimum intensity values was computed. After analysing the real CMB’s characteristics, we proposed our analytical model to generate synthetic CMB. The model is based on the hypothesis that the rCMB are Gaussian-like structures, elongated in z direction, and spreading all over the brain with low-intensity value. There are some benefits to using an analytical model. The model can cover the diversity of the CMB in location and shape by adding random parameters. In addition, any classifier could be trained only on the synthetic data and tested on the real limited lesions. Extensive validation and testing experiments become possible by using synthetic data. The dataset with 37,000 synthetic lesions is publicly available for the research community. To evaluate the generalization of our proposed analytical model, we applied the model to QSM images for the same patients. The main contribution is that our proposed analytical model can be applied to another MRI modality without extensive parameter changes when CMB appears with different contracts. CMB classification shows improvements over traditional data augmentation from QSM images. The conditional generative adversarial network is another model that we exploited for the synthetic CMB generation that forms the main contribution in this thesis. Our proposed model is independent of any MRI imaging parameters. It can learn the effect of the CMB on the surrounding tissue. Synthetic Microbleeds could be generated with shape diversity related to any desire locations in the brain, and the model can be applied to a new dataset and improve the CMB classification for an unseen dataset with different MRI parameters, and disease categories with limited ground truth.<br>Thesis (PhD Doctorate)<br>Doctor of Philosophy (PhD)<br>School of Eng & Built Env<br>Science, Environment, Engineering and Technology<br>Full Text
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Mori, Nobuyuki. "Microbleeds in moyamoya disease: susceptibility-weighted imaging versus T2*-weighted imaging at 3T." Kyoto University, 2009. http://hdl.handle.net/2433/124278.

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Dannenberg, Steffen [Verfasser]. "Number of cerebral microbleeds and risk of intracerebral hemorrhage after intravenous thrombolysis / Steffen Dannenberg." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2016. http://d-nb.info/1082237167/34.

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Taber, Samantha Jeanne Stearns [Verfasser]. "Associations between cerebral microbleeds and lipids in first time ischemic stroke patients / Samantha Jeanne Stearns Taber." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2018. http://d-nb.info/1160514852/34.

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Taber, Samantha [Verfasser]. "Associations between cerebral microbleeds and lipids in first time ischemic stroke patients / Samantha Jeanne Stearns Taber." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2018. http://d-nb.info/1160514852/34.

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Kaaouana, Takoua. "Detection and characterization of cerebral microbleeds : application in clinical imaging sequences on large populations of subjects." Thesis, Paris 6, 2015. http://www.theses.fr/2015PA066456/document.

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Les micro-saignements cérébraux (MSC) sont des dépôts d’hémosidérine particulièrement visibles sur des séquences IRM sensibles à la susceptibilité magnétique, comme par exemple la séquence en écho de gradient pondérée (GRE) en T2*. Néanmoins, leur détection in-vivo à partir de l’image d'amplitude GRE T2* obtenue en routine clinique est peu exacte et très sensible aux paramètres d’acquisition. Une détection automatique des MSC permettrait d’augmenter la portée et la pertinence de cette séquence, mais il est avant tout nécessaire de mieux caractériser les MSC pour augmenter la spécificité de détection. Cette thèse présente une nouvelle méthode pour extraire l’information d’intérêt (la carte champ interne) à partir d’images de phase obtenues avec les mêmes acquisitions cliniques GRE T2*. En effet, l’image de phase T2* contient directement une information sur la susceptibilité et pourrait donc améliorer la détection des MSC. Cette méthode a été évaluée avec succès sur des données multicentriques de qualité compatible avec la routine clinique pour des sujets avec un nombre très variable de MSC et a permis de différencier les MSC des micro-calcifications. Une étude de validation a également été menée pour évaluer l’utilité clinique de la carte de champ interne pour la détection par un expert, par rapport à d’autres types d’images et reconstructions utilisées en clinique. Elle a montré une amélioration de la spécificité. La thèse comprend également une preuve de concept d’une méthode d’identification automatique utilisant l’information provenant de plusieurs types d’image et de reconstruction afin d’augmenter la spécificité de l’identification. L’évaluation est menée sur les sujets précédemment décrits. Cette preuve de concept est basée sur un algorithme d’apprentissage supervisé ; cela consiste à combiner les informations issues des différents types d’image à partir desquels des descripteurs d’intensités et de forme ont été extraits pour créer un modèle de prédiction permettant discriminer les MSC<br>CMBs, small hypo-intense foci with a maximum diameter of 10 millimeters, were first thought clinically silent. They are now considered as an imaging marker of cerebral small vessel diseases and their clinical involvement is increasingly recognized; they may be associated with an increased risk of hemorrhagic stroke, ischemia and dementia such as Alzheimer's disease. However, their relation with pathology and its causality remains largely to be understood, partly because of their tricky characterization in-vivo. Large scale studies or meta-analyses are made difficult because their identification varies with MRI sequence parameters and suffers from reproducibility issues and is time-consuming. Automatic identification methods have been proposed to address these issues but they all require manual post processing selection steps, because of a very high number of false positives. This suggests that a better characterization of CMBs may be the key to improve their detection, as it would allow better identifying them from misleading structures and lesions.This PhD focused on achieving a better characterization of CMBs to better detect them with an automatic method. It covers multiple aspects to improve CMBs identification. First, MR phase image was taken into account in addition to the standard MR magnitude image, because of its sensitivity to CMBs. A new MR phase image processing technique was thus developed to obtain the magnetic field of interest free of contamination from background sources in datasets equivalent to clinical routine. A comparison study was carried-out to evaluate the outcome of this tool for CMBs detection in a standardized dataset in a clinical environment. A proof-of-concept is given to illustrate the advantages of new features for automatically identifying CMBs
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Gregoire, S. M. F. "Cerebral microbleeds as a marker of small vessel disease : new insights from neuro-imaging and clinical studies in stroke patients." Thesis, University College London (University of London), 2014. http://discovery.ucl.ac.uk/1437813/.

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Introduction: A portfolio of studies is presented aimed at understanding the clinical and pathophysiological significance of cerebral microbleeds (CMBs) in stroke patients. CMBs are the radiological marker of microscopic haemosiderin deposits on iron-sensitiveMRI sequences (mainly gradient-recalled echo [GRE] T2* MRI). They are common in patients with cerebrovascular disease and are hypothesised to be a biomarker for brain small vessel diseases, including hypertensive arteriopathy and cerebral amyloid angiopathy (CAA). Important questions relating to CMBs include their use as a prognostic marker for antithrombotic-related intracerebral haemorrhage (ICH) and cognitive impairment. Our aims were to address the pathophysiological and clinical relevance of CMBs using longitudinal, case-control and cross-sectional studies. Methods: Patients were ascertained from prospective databases of admissions to the stroke service at the National Hospital for Neurology and Neurosurgery and at University College London Hospital’s (UCLH) NHS Trust. Magnetic resonance imaging data was collected and analysed for markers of small vessel disease including CMBs. Clinical and radiological associations of CMBs were determined using appropriate statistical tests. Objectives: First, ways of improving microbleed detection and reporting were explored through the development of a visual rating scale (theMicrobleed Anatomical Rating Scale, MARS) aimed at reliably rating CMBs. Second, the prognostic relevance of CMBs was investigated for antiplatelet-related ICH in a case-comparison study. Third, the detection of new CMBs over time and the factors that influence this were explored. Fourth, the impact of CMBs on cognitive impairment was studied in a cross-sectional study. Finally, the association between CMBs and acute silent ischaemia on diffusion-weighted MRI was investigated via a multi-centre cross-sectional MRI study of patients with ICH. Main findings: 1. MARS is a reliable scale with good intra- and inter-rater agreement for rating CMBs presence and number in any brain location. 2. Lobar CMBs, especially if numerous, are a risk factor for antiplatelet-related ICH independent of the extent of white matter changes. 3. CMBs accumulate over time in stroke patients, and the risk is related to baseline systolic blood pressure. 4. Lobar CMBs are an independent predictor of frontal executive impairment; this suggests that CAA is a potential underlying contributor to cognitive impairment. 5. Silent acute infarcts are frequent in patients within 3 months of ICH, especially in those with probable CAA, and are associated with markers of small vessel disease severity, including CMBs. Conclusion: These studies provide new information on detection, clinical impact and associations of CMBs in stroke patients. They suggest that CMBs have useful roles in understanding pathophysiology, diagnosis and prognosis in patients with small vessel diseases. Further studies are required to determine the direct therapeutic consequences of CMBs, but the present work suggests several promising areas for future research.
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Chen, Yaohua. "Maladie d’Alzheimer : influence des microhémorragies, du sexe et de la modulation pharmacologique : données cliniques et expérimentales." Thesis, Lille 2, 2018. http://www.theses.fr/2018LIL2S043/document.

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La maladie d'Alzheimer (MA) est un processus multifactoriel. La dysfonction vasculaire pourrait être impliquée dans sa progression. Les microhémorragies cérébrales (MH) sont fréquentes chez les patients atteints de MA, et pourraient jouer un rôle clé dans le lien qui relie la dysfonction vasculaire à la MA. Le sexe pourrait également impacter sur la sévérité des lésions. Les statines ont été proposées en prévention de maladies neurodégénératives dont la MA. Leur intérêt est encore débattu mais ces molécules ont une action pléiotrope. Ce travail a pour objectif d'étudier l'impact des lésions microhémorragiques sur le déclin cognitif dans la MA, le rôle du sexe et la modulation pharmacologique par Atorvastatine, dans une perspective translationnelle,i.e. en considérant à la fois l'aspect expérimental chez l'animal et l'aspect clinique. Pour la partie expérimentale, nous avons étudié à partir d'un modèle original de MH chez les souris femelles saines et pathologiques. La MHC est créée par injection stéréotaxique de Collagénase (0,8|uUI/|iL). L'atorvastatine est administrée dans l'alimentation quotidienne des rongeurs(5mg/Kg/J). Le suivi était multimodal à trois temps différents : six semaines, six mois et douze mois après la chirurgie. Au plan clinique, nous avons étudié une base de données de patients atteints de la MA, suivis de façon standardisée. Notre travail a mis en évidence, dans une approche translationnelle, un impact cognitif et non cognitif des MHs, en présence ou non d'une maladie d'Alzheimer chez le sexe féminin. Nos résultats tendent à confirmer l'intérêt de l'atorvastatine dans la neuroprotection, grâce à ses effets pléiotropes. D'une manière générale,notre travail souligne, une fois de plus, l'intérêt d'une prise en charge personnalisée, et précoce de la MA<br>The physiopathology of Alzheimer disease (AD) is complex. Associated factors, in particular at the vascular level with damaged small blood vessels, might be involved. Cerebral microbleeds(CMB) in particular, could be one of the key contributing factor in AD. The cumulative evidence suggested a sex-specific patterns of disease. Furthermore, statins might be interesting by pleitropic effects. The objectives of this study was to evaluate the interaction between vascular and neurodegenerative lesions in Alzheimer, the influence of sex, and the pharmacological modulation by atorvastatin. This experimental model is designed in a multimodal approach to ensure its scientific relevance and to fit with clinical research. The third objective is indeed to confront theresulting experimental data to the clinical data of cohorts of Alzheimer patients. With an original model of CMB in female mice, we folio wed-up them from 1.5 months to 12 months postsurgery.For the clinical part, we studied patients with AD from a database of a tertiary memory center, with standardized framework. In a translational way, we observed a cognitive and a non cognitiveimpact of CMBs, differently in wild-type mice and in diseased mice. Different outcome was noticed for young female mice. And Atorvastatine offered a mild neuroprotection particularly in presymptomatic stage. Finally, the mechanism implied will be studied, in particular the inflammatory pathway, and will help to propose targeted pharmacological modulation in order to prevent or limit the impact of CMB on AD, by offering a personalized approach
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Pasquini, Marta. "Hémorragies cérébrales non traumatiques et traitements antithrombotiques." Thesis, Lille 2, 2015. http://www.theses.fr/2015LIL2S064/document.

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L’augmentation de la prévalence des hémorragies cérébrales (HC) sous traitement antithrombotique constitue un problème de Santé Publique à cause du mauvais pronostic vital et fonctionnel et du risque compétitif de récidive hémorragique ou ischémique chez les survivants, qui pose le problème d’une prévention secondaire adaptée._x000D_L’objectif de la thèse était d’étudier l’impact des traitements antithrombotiques sur le pronostic des HC. Le terme d’HC, entendu au sens large, regroupe les HC spontanées et les microhémorragies cérébrales.La première partie avait comme objectif de comparer les caractéristiques des HC survenant avec ou sans traitement par antagonistes de la vitamine K (AVK), stratifiant l’analyse selon la localisation de l’HC. L’analyse a porté sur 545 patients de la cohorte Lilloise (PITCH), parmi lesquels 83 (15%) étaient sous AVK. La prise d’un traitement par AVK n’influençait pas la localisation de l’HC, mais était prédictive d’HC plus volumineuses (25 ml vs 12 ; p=0.002) chez les victimes d’HC non lobaire, alors que aucune différence existait en cas d’HC lobaire (26 ml vs 30; p=0.507). Ces résultats suggèrent que l’impact des AVK diffère en fonction de la localisation de l’HC et de la vasculopathie sous-jacente.La deuxième partie avait comme objectif d’analyser l’impact du traitement antithrombotique sur l’apparition de nouvelles microhémorragies cérébrales stratifiant l’analyse selon la localisation de l’HC. L’étude a porté sur 168 survivants à 6 mois d’une HC (cohorte PITCH) ayant bénéficié d’une IRM cérébrale 1.5T lors de l’HC et durant le suivi. Lors de l’HC, 89 (53%) patients présentaient des microhémorragies, et 80 (48%) ont développé des microhémorragies durant le suivi. La présence sur la première IRM de microhémorragies (aOR 2,3; IC 95%1,2-4,3), leur position mixte, lobaire et profonde (aOR 3.7; IC95% 1,7-8,3), et la présence de séquelles de macrohémorragies (aOR 6,8; IC95% 2,8-16,7), étaient associées à l’apparition de microhémorragies. Chez les patients avec HC non lobaire, l’apparition de microhémorragies était associée à l’utilisation d’un traitement antithrombotique durant le suivi (aOR 2,9 ; IC95% 1,1-7,3) et avec l’apparition de lacunes (aOR: 2,9; 95%CI 1,0-7,8). Chez les patients avec HC lobaire, l’apparition de microhémorragies était associée à l’apparition de macrohémorragie (aOR 9.8 ; IC95% 1,1-88,8). Ces résultats suggèrent que l’impact des traitements antithrombotiques diffère en fonction de la vasculopathie sous-jacente.La troisième partie avait comme objectif de : (i) comparer les proportions de survivants d’une HC ayant une indication formelle au traitement antithrombotique chez lesquels ce traitement était repris à la sorite ; (ii) identifier les caractéristiques associées à la reprise du traitement antithrombotique, au sein de 5 cohortes européennes (Lille, n=542; Utrecht, n=389 ; Amsterdam, n= 403 ; Londres, n=667 ; Lothian, n=137). Un traitement antithrombotique était recommencé chez 96 (20%) des 469 survivants ayant une indication formelle, mais en proportions différentes dans les 5 cohortes (Lille 18%, Utrecht 45%, Amsterdam 30% ; Londres 11% ; Lothian 15%; p&lt;0.001). Nous n’avons retrouvé aucun autre facteur prédictif de reprise du traitement antithrombotique en dehors de la cohorte d’origine. Ces résultats montrent que la décision de reprise du traitement antithrombotique ne repose pas sur des critères reproductibles, et soulignent la nécessité de réaliser des essais randomisés.La quatrième partie, actuellement en cours, prévoit d’évaluer chez ces mêmes patients (survivants d’une HC ayant une indication formelle au traitement antithrombotique) le risque de récidive hémorragique ou ischémique en fonction de la reprise ou de l’arrêt du traitement antithrombotique. Il s’agit d’une étude observationnelle portant sur 274 patients de 4 cohortes Européennes, avec un suivi d’environ 2.5 ans. L’analyse statistique est en cours<br>The proportion of patients who are taking antithrombotic drugs at the time they suffer a spontaneous intracerebral hemorrhage (ICH) is increasing over time, and this is a major issue in public health because of the poor prognosis of patients. Also, the decision to restart or not antithrombotic drugs in survivors is still a clinical dilemma. _x000D_The aim of this work was to evaluate the impact of antithrombotic drugs on ICH prognosis. The term ICH regroups (i) spontaneous ICH and (ii) cerebral microbleeds (CMBs).As a first step, we compared baseline characteristics of 545 consecutive patients with ICH included in the PITCH cohort (Lille, France), receiving or not Vitamin K Antagonists (VKAs) at the time of ICH, stratifying the analysis according to the ICH location (lobar vs non lobar). VKAs-ICH accounted for 83 patients (15%). The use of VKAs did not influence ICH location, but influenced ICH volume: in non lobar ICH, VKAs use was associated with larger ICH volumes (25 ml versus 12 ml, p=0.002). In lobar ICH, no difference was observed (26ml versus 30ml; p=0.507). The different impact of VKAs on ICH volumes according to location suggests a different susceptibility of the underlying vasculopathies to VKAs.As a second step, we aimed to evaluate the impact of antithrombotic drugs on the incidence of CMBs in 168 ICH survivors from the PITCH cohort who underwent 1.5T Magnetic resonance imaging (MRI) at ICH onset and during follow-up, stratifying the analysis according to the index ICH location. At the time of ICH, 89 (53%) patients had CMBs at ICH onset, and 80 (48%) showed new CMBs during follow-up. Predictors of incident CMBs were the presence on the first MRI of: at least 1 CMB (aOR 2.3; 95% CI: 1.2-4.3), old macro-hemorrhage (aOR 6.8; 95%CI 2.8-16.7), and CMBs in mixed location (aOR 3.7; 95%CI 1.7-8.3). In non lobar ICH, incident CMBs were associated with incident lacunes (aOR: 2.9; 95%CI 1.0-7.8) and with the use of antiplatelet agents (aOR 2.9; 95%CI 1.1-7.3). In lobar ICH, incident CMBs were associated with incident macro-hemorrhage (aOR 9.8; 95%CI 1.1-88.8). These results suggest that the impact of antithrombotic drugs differs according to the index ICH location, and therefore according to the underlying vasculpathy.The third step consisted in comparing the characteristics and proportions of patients taking antithrombotic drugs at ICH discharge in five European cohorts (Lille, France, n=542; Utrecht, The Netherlands, n=389; Amsterdam, The Netherlands, n=403; multicenter UK cohort, n=667; Lothian, Scotland, n=137). We then identified characteristics associated with restarting. Antithrombotic drugs were restarted in 96 (20%) of the 469 survivors who had an indication for antithrombotic drugs (secondary prevention or atrial fibrillation), but in different proportions according to the cohort of origin (Lille 18%, Utrecht 45%, Amsterdam 30%, CROMIS-2 ICH 11%, Lothian 15%; p&lt;0.001). We did not find other consistent associations with restarting antithrombotic drugs. The variation in clinical practice in restarting antithrombotic drugs after ICH supports the need for randomized controlled trials.In the fourth step, we aim to analyse the risk of ICH recurrences or ischemic events in the same population of patients (ICH survivors who suffered from ICH while on antithrombotic drugs because of secondary prevention or atrial fibrillation) according to the antithrombotic drug status during follow-up. We included 274 patients from 4 European cohorts, with a median follow-up of 2.5 years. Statistical analysis is ongoing
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Books on the topic "Microbleeds"

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Werring, David J., ed. Cerebral Microbleeds. Cambridge University Press, 2009. http://dx.doi.org/10.1017/cbo9780511974892.

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Cerebral microbleeds: From pathophysiology to clinical practice. Cambridge University Press, 2011.

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Werring, David J. Cerebral Microbleeds: Pathophysiology to Clinical Practice. Cambridge University Press, 2011.

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Werring, David J. Cerebral Microbleeds: Pathophysiology to Clinical Practice. Cambridge University Press, 2011.

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Werring, David J. Cerebral Microbleeds: Pathophysiology to Clinical Practice. Cambridge University Press, 2011.

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Werring, David J. Cerebral Microbleeds: Pathophysiology to Clinical Practice. Cambridge University Press, 2011.

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Book chapters on the topic "Microbleeds"

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Hendrikse, Jeroen. "Previous Microbleeds." In This is Our Brain. Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-10-4148-8_7.

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Ayaz, Muhammad, Alexander Boikov, Grant McAuley, et al. "Imaging Cerebral Microbleeds with SWI." In Susceptibility Weighted Imaging in MRI. John Wiley & Sons, Inc., 2011. http://dx.doi.org/10.1002/9780470905203.ch12.

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Lee, JungSeok, and Mark Fisher. "Cerebral Microbleeds and Thrombolysis for Acute Ischemic Stroke." In Springer Series in Translational Stroke Research. Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-45345-3_21.

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Zhao, Meng, Chen Jin, Lingmin Jin, Shenghua Teng, and Zuoyong Li. "Cerebral Microbleeds Detection Based on 3D Convolutional Neural Network." In Machine Learning for Cyber Security. Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-62223-7_14.

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Viswanathan, Anand, Hugues Chabriat, and Steven M. Greenberg. "Cerebral Microbleeds, Small-Vessel Disease of the Brain, Hypertension, and Cognition." In Hypertension and Stroke. Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-29152-9_17.

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Viswanathan, Anand, Hugues Chabriat, and Steven M. Greenberg. "Cerebral Microbleeds, Small-Vessel Disease of the Brain, Hypertension, and Cognition." In Hypertension and Stroke. Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-010-6_14.

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Hong, Jin, and Jie Liu. "Cerebral Microbleeds Detection via Convolutional Neural Network with and Without Batch Normalization." In Frontiers in Intelligent Computing: Theory and Applications. Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-13-9920-6_16.

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Momeni, Saba, Amir Fazllolahi, Pierrick Bourgeat, et al. "Data Augmentation Using Synthetic Lesions Improves Machine Learning Detection of Microbleeds from MRI." In Simulation and Synthesis in Medical Imaging. Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-030-00536-8_2.

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Liu, Hangfan, Tanweer Rashid, Jeffrey Ware, et al. "Adaptive Squeeze-and-Shrink Image Denoising for Improving Deep Detection of Cerebral Microbleeds." In Medical Image Computing and Computer Assisted Intervention – MICCAI 2021. Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-87231-1_26.

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Kim, Jun-Ho, Mohammed A. Al-masni, Seul Lee, Haejoon Lee, and Dong-Hyun Kim. "Cerebral Microbleeds Detection Using a 3D Feature Fused Region Proposal Network with Hard Sample Prototype Learning." In Lecture Notes in Computer Science. Springer Nature Switzerland, 2022. http://dx.doi.org/10.1007/978-3-031-16431-6_43.

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Conference papers on the topic "Microbleeds"

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Tajudin, Amin Sabirin, Siti Noraini Sulaiman, Iza Sazanita Isa, Zainal Hisham Che Soh, Noor Khairiah A. Karim, and Ibrahim Lutfi Shuaib. "Microbleeds detection using watershed-driven active contour." In 2017 7th IEEE International Conference on Control System, Computing and Engineering (ICCSCE). IEEE, 2017. http://dx.doi.org/10.1109/iccsce.2017.8284427.

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Tajudin, Amin Sabirin, Siti Noraini Sulaiman, Iza Sazanita Isa, and Noor Khairiah A. Karim. "Cerebral microbleeds (CMB) from MRI brain images: Review paper." In 2016 6th IEEE International Conference on Control System, Computing and Engineering (ICCSCE). IEEE, 2016. http://dx.doi.org/10.1109/iccsce.2016.7893634.

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Tajudin, Amin Sabirin, Siti Noraini Sulaiman, Iza Sazanita Isa, et al. "An improved watershed segmentation technique for microbleeds detection in MRI images." In 2017 International Conference on Electrical, Electronics and System Engineering (ICEESE). IEEE, 2017. http://dx.doi.org/10.1109/iceese.2017.8298394.

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Ghafaryasl, Babak, Fedde van der Lijn, Marielle Poels, et al. "A computer aided detection system for cerebral microbleeds in brain MRI." In 2012 IEEE 9th International Symposium on Biomedical Imaging (ISBI 2012). IEEE, 2012. http://dx.doi.org/10.1109/isbi.2012.6235503.

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Chen, Hao, Lequan Yu, Qi Dou, Lin Shi, Vincent C. T. Mok, and Pheng Ann Heng. "Automatic detection of cerebral microbleeds via deep learning based 3D feature representation." In 2015 IEEE 12th International Symposium on Biomedical Imaging (ISBI 2015). IEEE, 2015. http://dx.doi.org/10.1109/isbi.2015.7163984.

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Hong, Jin, and Zhihai Lu. "Cerebral Microbleeds Detection via Discrete Wavelet Transform and Back Propagation Neural Network." In Proceedings of the 2nd International Conference on Social Science, Public Health and Education (SSPHE 2018). Atlantis Press, 2019. http://dx.doi.org/10.2991/ssphe-18.2019.54.

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Saber, H., J. Saver, V. Szeder, et al. "P-016 Association of cerebral microbleeds and clinical outcomes following endovascular stroke therapy." In SNIS 18TH ANNUAL MEETING. BMJ Publishing Group Ltd., 2021. http://dx.doi.org/10.1136/neurintsurg-2021-snis.52.

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Kuijf, Hugo J., Jeroen de Bresser, Geert Jan Biessels, Max A. Viergever, and Koen L. Vincken. "Detecting cerebral microbleeds in 7.0 T MR images using the radial symmetry transform." In 2011 8th IEEE International Symposium on Biomedical Imaging (ISBI 2011). IEEE, 2011. http://dx.doi.org/10.1109/isbi.2011.5872516.

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Mao, Hejiao, Ning Su, Jiangxia Zhang, et al. "Basal ganglia and brainstem located cerebral microbleeds contribute to gait impairment (P4-11.016)." In 2023 Annual Meeting Abstracts. Lippincott Williams & Wilkins, 2023. http://dx.doi.org/10.1212/wnl.0000000000202515.

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Qi Dou, Hao Chen, Lequan Yu, et al. "Automatic cerebral microbleeds detection from MR images via Independent Subspace Analysis based hierarchical features." In 2015 37th Annual International Conference of the IEEE Engineering in Medicine and Biology Society (EMBC). IEEE, 2015. http://dx.doi.org/10.1109/embc.2015.7320232.

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Reports on the topic "Microbleeds"

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Cheng, Yu-Chung N. Development and Testing of Iron Based Phantoms as Standards for the Diagnosis of Microbleeds and Oxygen Saturation with Applications in Dementia, Stroke, and Traumatic Brain Injury. Defense Technical Information Center, 2013. http://dx.doi.org/10.21236/ada601806.

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