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William L Young - One of the best experts on this subject based on the ideXlab platform.
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hemorrhage rates from Brain Arteriovenous Malformation in patients with hereditary hemorrhagic telangiectasia
Stroke, 2015Co-Authors: Helen Kim, Charles E Mcculloch, William L Young, Michael T. Lawton, Timo Krings, Jeffrey Nelson, Karel G Terbrugge, Marie E Faughnan, Murali M Chakinala, James R GossageAbstract:Background and Purpose—Hereditary hemorrhagic telangiectasia (HHT) is a systemic disease characterized by mucocutaneous telangiectasias, epistaxis, and Arteriovenous Malformations (AVMs). Intracranial hemorrhage (ICH) rates in this population are not well described. We report ICH rates and characteristics in HHT patients with Brain AVMs (HHT-BAVMs). Methods—We studied the first 153 HHT-BAVM patients with follow-up data enrolled in the Brain Vascular Malformation Consortium HHT Project. We estimated ICH rates after BAVM diagnosis. Results—The majority of patients were women (58%) and white (98%). The mean age at BAVM diagnosis was 31±19 years (range, 0–70), with 61% of cases diagnosed on asymptomatic screening. Overall, 14% presented with ICH; among symptomatic cases, 37% presented ruptured. During 493 patient-years of follow-up, 5 ICH events occurred yielding a rate of 1.02% per year (95% confidence interval, 0.42–2.44%). ICH-free survival differed significantly by ICH presentation (P=0.003); ruptured cas...
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distinctive distribution of lymphocytes in unruptured and previously untreated Brain Arteriovenous Malformation
Neuroimmunology and Neuroinflammation, 2014Co-Authors: Yi Guo, Christopher P. Hess, William L Young, Helen Kim, Michael T. Lawton, Tarik Tihan, Yuanli ZhaoAbstract:Aim: To test the hypothesis that lymphocyte infiltration in Brain Arteriovenous Malformation (bAVM) is not associated with iron deposition (indicator of micro-hemorrhage). Methods: Sections of unruptured, previously untreated bAVM specimens ( n = 19) were stained immunohistochemically for T-lymphocytes (CD3 + ), B-lymphocytes (CD20 + ), plasma cells (CD138 + ) and macrophages (CD68 + ). Iron deposition was assessed by hematoxylin and eosin and Prussian blue stains. Superficial temporal arteries (STA) were used as control. Results: Both T-lymphocytes and macrophages were present in unruptured, previously untreated bAVM specimens, whereas few B cells and plasma cells were detected. Iron deposition was detected in 8 specimens (42%; 95% confidence intervals = 20-67%). The samples with iron deposition tended to have more macrophages than those without (666 ± 313 vs . 478 ± 174 cells/mm 2 ; P = 0.11). T-cells were clustered on the luminal side of the endothelial surface, on the vessel-wall, and in the perivascular regions. There was no correlation between T-lymphocyte load and iron deposition ( P = 0.88). No macrophages and lymphocytes were detected in STA controls. Conclusion: T-lymphocytes were present in bAVM specimens. Unlike macrophages, the load and location of T-lymphocytes were not associated with iron deposition, suggesting the possibility of an independent cell-mediated immunological mechanism in bAVM pathogenesis.
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untreated Brain Arteriovenous Malformation patient level meta analysis of hemorrhage predictors
Neurology, 2014Co-Authors: Rustam Alshahi Salman, Charles E Mcculloch, Christian Stapf, William L YoungAbstract:Objective: To identify risk factors for intracranial hemorrhage in the natural history course of Brain Arteriovenous Malformations (AVMs) using individual patient data meta-analysis of 4 existing cohorts. Methods: We harmonized data from Kaiser Permanente of Northern California (n = 856), University of California San Francisco (n = 787), Columbia University (n = 672), and the Scottish Intracranial Vascular Malformation Study (n = 210). We censored patients at first treatment, death, last visit, or 10-year follow-up, and performed stratified Cox regression analysis of time-to-hemorrhage after evaluating hemorrhagic presentation, sex, age at diagnosis, deep venous drainage, and AVM size as predictors. Multiple imputation was performed to assess impact of missing data. Results: A total of 141 hemorrhage events occurred during 6,074 patient-years of follow-up (annual rate of 2.3%, 95% confidence interval [CI] 2.0%–2.7%), higher for ruptured (4.8%, 3.9%–5.9%) than unruptured (1.3%, 1.0%–1.7%) AVMs at presentation. Hemorrhagic presentation (hazard ratio 3.86, 95% CI 2.42–6.14) and increasing age (1.34 per decade, 1.17–1.53) independently predicted hemorrhage and remained significant predictors in the imputed dataset. Female sex (1.49, 95% CI 0.96–2.30) and exclusively deep venous drainage (1.60, 0.95–2.68, p = 0.02 in imputed dataset) may be additional predictors. AVM size was not associated with intracerebral hemorrhage in multivariable models ( p > 0.5). Conclusion: This large, individual patient data meta-analysis identified hemorrhagic presentation and increasing age as independent predictors of hemorrhage during follow-up. Additional AVM cohort data may further improve precision of estimates, identify new risk factors, and allow validation of prediction models.
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novel Brain Arteriovenous Malformation mouse models for type 1 hereditary hemorrhagic telangiectasia
PLOS ONE, 2014Co-Authors: Eun-jung Choi, Wanqiu Chen, Kristine Jun, Helen M Arthur, William L YoungAbstract:Endoglin (ENG) is a causative gene of type 1 hereditary hemorrhagic telangiectasia (HHT1). HHT1 patients have a higher prevalence of Brain Arteriovenous Malformation (AVM) than the general population and patients with other HHT subtypes. The pathogenesis of Brain AVM in HHT1 patients is currently unknown and no specific medical therapy is available to treat patients. Proper animal models are crucial for identifying the underlying mechanisms for Brain AVM development and for testing new therapies. However, creating HHT1 Brain AVM models has been quite challenging because of difficulties related to deleting Eng-floxed sequence in Eng2fl/2fl mice. To create an HHT1 Brain AVM mouse model, we used several Cre transgenic mouse lines to delete Eng in different cell-types in Eng2fl/2fl mice: R26CreER (all cell types after tamoxifen treatment), SM22α-Cre (smooth muscle and endothelial cell) and LysM-Cre (lysozyme M-positive macrophage). An adeno-associated viral vector expressing vascular endothelial growth factor (AAV-VEGF) was injected into the Brain to induce focal angiogenesis. We found that SM22α-Cre-mediated Eng deletion in the embryo caused AVMs in the postnatal Brain, spinal cord, and intestines. Induction of Eng deletion in adult mice using R26CreER plus local VEGF stimulation induced the Brain AVM phenotype. In both models, Eng-null endothelial cells were detected in the Brain AVM lesions, and formed mosaicism with wildtype endothelial cells. However, LysM-Cre-mediated Eng deletion in the embryo did not cause AVM in the postnatal Brain even after VEGF stimulation. In this study, we report two novel HHT1 Brain AVM models that mimic many phenotypes of human Brain AVM and can thus be used for studying Brain AVM pathogenesis and testing new therapies. Further, our data indicate that macrophage Eng deletion is insufficient and that endothelial Eng homozygous deletion is required for HHT1 Brain AVM development.
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Induction of Brain Arteriovenous Malformation in the adult mouse.
Methods in molecular biology (Clifton N.J.), 2014Co-Authors: Wanqiu Chen, William L YoungAbstract:Brain Arteriovenous Malformations (bAVM) are tangles of abnormal, dilated vessels that directly shunt blood between the arteries and veins. The pathogenesis of bAVM is currently unknown. Patients with hereditary hemorrhagic telangiectasia (HHT) have a higher prevalence of bAVM than the general population. Animal models are important tools for dissecting the disease etiopathogenesis and for testing new therapies. Here, we introduce a method that induces the bAVM phenotype through regional deletion of activin-like kinase 1 (Alk1, the causal gene for HHT2) and vascular endothelial growth factor (VEGF) stimulation.
Michael T. Lawton - One of the best experts on this subject based on the ideXlab platform.
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effect of elevation of vascular endothelial growth factor level on exacerbation of hemorrhage in mouse Brain Arteriovenous Malformation
Journal of Neurosurgery, 2020Co-Authors: Philip Cheng, Wan Zhu, Lei Zhan, Sonali Shaligram, Espen J Walker, Shuntai Yang, Chaoliang Tang, Xiaonan Zhu, Michael T. LawtonAbstract:Author(s): Cheng, Philip; Ma, Li; Shaligram, Sonali; Walker, Espen J; Yang, Shun-Tai; Tang, Chaoliang; Zhu, Wan; Zhan, Lei; Li, Qiang; Zhu, Xiaonan; Lawton, Michael T; Su, Hua | Abstract: OBJECTIVE:A high level of vascular endothelial growth factor (VEGF) has been implicated in Brain Arteriovenous Malformation (bAVM) bleeding and rupture. However, direct evidence is missing. In this study the authors used a mouse bAVM model to test the hypothesis that elevation of focal VEGF levels in bAVMs exacerbates the severity of bAVM hemorrhage. METHODS:Brain AVMs were induced in adult mice in which activin receptor-like kinase 1 (Alk1, a gene that causes AVM) gene exons 4-6 were floxed by intrabasal ganglia injection of an adenoviral vector expressing Cre recombinase to induce Alk1 mutation and an adeno-associated viral vector expressing human VEGF (AAV-VEGF) to induce angiogenesis. Two doses of AAV-VEGF (5 × 109 [high] or 2 × 109 [low]) viral genomes were used. In addition, the common carotid artery and external jugular vein were anastomosed in a group of mice treated with low-dose AAV-VEGF 6 weeks after the model induction to induce cerebral venous hypertension (VH), because VH increases the VEGF level in the Brain. Brain samples were collected 8 weeks after the model induction. Hemorrhages in the bAVM lesions were quantified on Brain sections stained with Prussian blue, which detects iron deposition. VEGF levels were quantified in bAVM tissue by enzyme-linked immunosorbent assay. RESULTS:Compared to mice injected with a low dose of AAV-VEGF, the mice injected with a high dose had higher levels of VEGF (p = 0.003) and larger Prussian blue-positive areas in the bAVM lesion at 8 or 9 weeks after model induction (p = 0.002). VH increased bAVM hemorrhage in the low-dose AAV-VEGF group. The overall mortality in the high-dose AAV-VEGF group was 26.7%, whereas no mouse died in the low-dose AAV-VEGF group without VH. In contrast, VH caused a mortality of 50% in the low-dose AAV-VEGF group. CONCLUSIONS:Using mouse bAVM models, the authors provided direct evidence that elevation of the VEGF level increases bAVM hemorrhage and mouse mortality.
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abstract tp585 long term outcomes in unruptured Brain Arteriovenous Malformation patients the multicenter Arteriovenous Malformation research study mars
Stroke, 2019Co-Authors: Helen Kim, Christopher P. Hess, Steven W. Hetts, Rustam Alshahi Salman, Kelly D Flemming, Alexander C Flint, Timo Krings, Aki Laakso, Giuseppe Lanzino, Michael T. LawtonAbstract:Introduction: Accurately balancing risks of interventional treatment and intracranial hemorrhage (ICH) in the untreated course of unruptured Brain Arteriovenous Malformation (uBAVM) patients is cri...
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hemorrhage rates from Brain Arteriovenous Malformation in patients with hereditary hemorrhagic telangiectasia
Stroke, 2015Co-Authors: Helen Kim, Charles E Mcculloch, William L Young, Michael T. Lawton, Timo Krings, Jeffrey Nelson, Karel G Terbrugge, Marie E Faughnan, Murali M Chakinala, James R GossageAbstract:Background and Purpose—Hereditary hemorrhagic telangiectasia (HHT) is a systemic disease characterized by mucocutaneous telangiectasias, epistaxis, and Arteriovenous Malformations (AVMs). Intracranial hemorrhage (ICH) rates in this population are not well described. We report ICH rates and characteristics in HHT patients with Brain AVMs (HHT-BAVMs). Methods—We studied the first 153 HHT-BAVM patients with follow-up data enrolled in the Brain Vascular Malformation Consortium HHT Project. We estimated ICH rates after BAVM diagnosis. Results—The majority of patients were women (58%) and white (98%). The mean age at BAVM diagnosis was 31±19 years (range, 0–70), with 61% of cases diagnosed on asymptomatic screening. Overall, 14% presented with ICH; among symptomatic cases, 37% presented ruptured. During 493 patient-years of follow-up, 5 ICH events occurred yielding a rate of 1.02% per year (95% confidence interval, 0.42–2.44%). ICH-free survival differed significantly by ICH presentation (P=0.003); ruptured cas...
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abstract w p413 intravenous delivery of the aav9 sflt vector reverses the phenotype of spontaneously developed Brain Arteriovenous Malformation in mice
Stroke, 2015Co-Authors: Lei Mao, Fanxia Shen, Lei Zhan, Michael T. LawtonAbstract:Background and Purpose: Current therapies for Brain Arteriovenous Malformation (bAVM) are invasive and have potential treatment-related morbidity. Excessive vascular endothelial growth factor (VEGF) expression is one of the key players in bAVM pathophysiology. The soluble VEGF receptor 1 (sFLT) possesses an anti-angiogenic effect. We hypothesize that intravenous delivery of adeno-associated viral vector serotype 9 (AAV9) expressing sFLT reverses the bAVM phenotype. Methods: SM22α-Cre transgenic mice were crossed with endoglin (Eng)-floxed mice to delete Eng. More than 95% of SM22 α-Cre;Eng-floxed mice spontaneously developed bAVM at age of 5 weeks. AAV9-sFLT (1x1011 viral genomes) was injected into the jugular vein of 5-week-old mice. AAV9-GFP was used as vector control. Brain vascular structure was analyzed using latex vascular casting 4 weeks after vector injection. The success of gene delivery, lymphocyte infiltration and neuronal loss was analyzed in the Brain sections. Results: Due to the severity of the AVM lesion in this model, 3 of 9 AAV9-GFP-treated mice and 2 of 8 AAV9-sFLT-treated mice died during the 4-week treatment period. One paralyzed mouse in the AAV9-GFP group was euthanized before the treatment period ended. Only 1 of the 6 surviving mice in the AAV9-sFLT group had detectable bAVM, whereas all 5 mice in the AAV9-GFP group had it. GFP expression was detected in the bAVM lesion of AAV9-GFP-treated mice. Neither lymphocyte infiltration nor neuronal loss was observed. Conclusion: Because intravenous delivery of AAV9-sFLT reverses the bAVM phenotype without inducing intra-Brain lymphocyte filtration and neuronal loss, AAV-mediated sFLT delivery could thus be developed into a specific, non-invasive therapy for patients with bAVM.
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distinctive distribution of lymphocytes in unruptured and previously untreated Brain Arteriovenous Malformation
Neuroimmunology and Neuroinflammation, 2014Co-Authors: Yi Guo, Christopher P. Hess, William L Young, Helen Kim, Michael T. Lawton, Tarik Tihan, Yuanli ZhaoAbstract:Aim: To test the hypothesis that lymphocyte infiltration in Brain Arteriovenous Malformation (bAVM) is not associated with iron deposition (indicator of micro-hemorrhage). Methods: Sections of unruptured, previously untreated bAVM specimens ( n = 19) were stained immunohistochemically for T-lymphocytes (CD3 + ), B-lymphocytes (CD20 + ), plasma cells (CD138 + ) and macrophages (CD68 + ). Iron deposition was assessed by hematoxylin and eosin and Prussian blue stains. Superficial temporal arteries (STA) were used as control. Results: Both T-lymphocytes and macrophages were present in unruptured, previously untreated bAVM specimens, whereas few B cells and plasma cells were detected. Iron deposition was detected in 8 specimens (42%; 95% confidence intervals = 20-67%). The samples with iron deposition tended to have more macrophages than those without (666 ± 313 vs . 478 ± 174 cells/mm 2 ; P = 0.11). T-cells were clustered on the luminal side of the endothelial surface, on the vessel-wall, and in the perivascular regions. There was no correlation between T-lymphocyte load and iron deposition ( P = 0.88). No macrophages and lymphocytes were detected in STA controls. Conclusion: T-lymphocytes were present in bAVM specimens. Unlike macrophages, the load and location of T-lymphocytes were not associated with iron deposition, suggesting the possibility of an independent cell-mediated immunological mechanism in bAVM pathogenesis.
Helen Kim - One of the best experts on this subject based on the ideXlab platform.
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concurrent presentation of Brain Arteriovenous Malformation peripheral Arteriovenous Malformation and cerebellar astrocytoma case report
Interdisciplinary Neurosurgery, 2020Co-Authors: Ayushi Gautam, Ethan A. Winkler, Helen Kim, Christopher F Dowd, Zhengda Sun, Tarik Tihan, Timothy H Mccalmont, William Y Hoffman, Ilona J Frieden, Daniel L. CookeAbstract:Abstract Background We report a rare case of a 19-year-old female progressively affected by a peripheral Arteriovenous Malformation (pAVM), a midline cerebellar astrocytoma, and a Brain Arteriovenous Malformation (bAVM). Case description She presented with a pulsatile mass on her left cheek, which was classified as a pAVM through angiography. Following treatment with embolization and surgical resection, she returned with enlargement of the mass and imaging incidentally identified a cerebellar astrocytoma. Suboccipital craniotomy, C1 laminectomy, and endoscopic third ventriculostomy were subsequently performed. She was later treated again for growth of her pAVM, and angiography revealed the presence of a left temporal bAVM, which was resected via a pterional craniotomy. Conclusions Pathological staining identified activation of mTOR and RAS/MAPK pathway in the patient’s pAVM and bAVM tissue samples. Furthermore, genetic sequencing demonstrated an activating MAPK21 (K57N) mutation in the pAVM and a gain of distal chromosome 7q in the pilocytic astrocytoma. No germline mutation was identified to explain all pathologies. This case demonstrates the need for continued development and further integration of multi-disciplinary genetic, radiological, and neurological treatment teams to effectively care for such complex presentations.
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abstract tp585 long term outcomes in unruptured Brain Arteriovenous Malformation patients the multicenter Arteriovenous Malformation research study mars
Stroke, 2019Co-Authors: Helen Kim, Christopher P. Hess, Steven W. Hetts, Rustam Alshahi Salman, Kelly D Flemming, Alexander C Flint, Timo Krings, Aki Laakso, Giuseppe Lanzino, Michael T. LawtonAbstract:Introduction: Accurately balancing risks of interventional treatment and intracranial hemorrhage (ICH) in the untreated course of unruptured Brain Arteriovenous Malformation (uBAVM) patients is cri...
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predictors of intracranial hemorrhage volume and distribution in Brain Arteriovenous Malformation
Interventional Neuroradiology, 2018Co-Authors: A Nicholson, Helen Kim, Steven W. Hetts, Jeffrey Nelson, Matthew D Alexander, Stephanie Tse, Claude J Hemphill, Daniel L. CookeAbstract:Background and purposeDespite evidence regarding risk factors for Brain Arteriovenous Malformation (bAVM)-associated spontaneous intracranial hemorrhage (ICH), few data exist describing the spectrum of clinical outcomes that bAVM-associated ICH may manifest. This study aimed to identify the demographical, clinical, and bAVM anatomical variables associated with ICH volume and the presence of intraventricular hemorrhage (IVH) of ruptured bAVMs, two indicators of worse clinical outcome, to help better predict outcome for unruptured bAVMs.MethodsComputed tomography images (n = 169) of patients with ruptured bAVM in a prospectively maintained institutional database were retrospectively reviewed to calculate ICH volume and the presence or absence of IVH. Demographic, clinical, and bAVM characteristics information was summarized and analyzed with univariable and multivariable regression models to identify the associations of these features with ICH volume and the presence of IVH.ResultsPatient sex, exclusively d...
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Morbidity after Hemorrhage in Children with Untreated Brain Arteriovenous Malformation.
Cerebrovascular diseases (Basel Switzerland), 2017Co-Authors: Helen Kim, Xiaolin Chen, Yuanli ZhaoAbstract:Background: Children with untreated Brain Arteriovenous Malformations (bAVM) are at risk of encountering life-threatening hemorrhage very early in their lives. Th
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hemorrhage rates from Brain Arteriovenous Malformation in patients with hereditary hemorrhagic telangiectasia
Stroke, 2015Co-Authors: Helen Kim, Charles E Mcculloch, William L Young, Michael T. Lawton, Timo Krings, Jeffrey Nelson, Karel G Terbrugge, Marie E Faughnan, Murali M Chakinala, James R GossageAbstract:Background and Purpose—Hereditary hemorrhagic telangiectasia (HHT) is a systemic disease characterized by mucocutaneous telangiectasias, epistaxis, and Arteriovenous Malformations (AVMs). Intracranial hemorrhage (ICH) rates in this population are not well described. We report ICH rates and characteristics in HHT patients with Brain AVMs (HHT-BAVMs). Methods—We studied the first 153 HHT-BAVM patients with follow-up data enrolled in the Brain Vascular Malformation Consortium HHT Project. We estimated ICH rates after BAVM diagnosis. Results—The majority of patients were women (58%) and white (98%). The mean age at BAVM diagnosis was 31±19 years (range, 0–70), with 61% of cases diagnosed on asymptomatic screening. Overall, 14% presented with ICH; among symptomatic cases, 37% presented ruptured. During 493 patient-years of follow-up, 5 ICH events occurred yielding a rate of 1.02% per year (95% confidence interval, 0.42–2.44%). ICH-free survival differed significantly by ICH presentation (P=0.003); ruptured cas...
Frédéric Clarençon - One of the best experts on this subject based on the ideXlab platform.
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S100B Serum Elevation Predicts In-Hospital Mortality After Brain Arteriovenous Malformation Rupture
Stroke, 2019Co-Authors: Eimad Shotar, Caroline Amouyal, Alice Jacquens, Bertrand Mathon, Grégoire Boulouis, Denis Monneret, Kevin Premat, Stéphanie Lenck, Nader-antoine Sourour, Frédéric ClarençonAbstract:Background and Purpose- S100B protein serum elevation has been associated with poor prognosis in neurologically ill patients. The purpose of this study is to determine whether elevation of S100B is associated with increased in-hospital mortality after Brain Arteriovenous Malformation rupture. Methods- This is a retrospective study of patients admitted for Brain Arteriovenous Malformation rupture. The study population was divided into derivation and validation cohorts. Univariate followed by multivariate logistic regression was used to determine whether elevation of S100B serum levels above 0.5 µg/L during the first 48 hours after admission (S100Bmax48) was associated with in-hospital mortality. Results- Two hundred and three ruptures met inclusion criteria. Twenty-three led to in-hospital mortality (11%). Mean S100Bmax48 was 0.49±0.62 µg/L. In the derivation cohort (n=101 ruptures), multivariate analysis found Glasgow coma scale score ≤8 (odds ratio, 21; 95% CI, 2-216; 0.001) and an S100Bmax48>0.5 µg/L (odds ratio, 19; 95% CI, 2-188; P=0.001) to be associated with in-hospital mortality. When applied to the validation cohort (n=102 ruptures), the same model found only S100Bmax48>0.5 µg/L (odds ratio, 8; 95% CI, 1.5-44; P=0.01) to be associated with in-hospital mortality. Conclusions- Elevated S100B protein serum level is strongly associated with in-hospital mortality after Brain Arteriovenous Malformation rupture.
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s100b serum elevation predicts in hospital mortality after Brain Arteriovenous Malformation rupture
Stroke, 2019Co-Authors: Eimad Shotar, Caroline Amouyal, Alice Jacquens, Bertrand Mathon, Grégoire Boulouis, Denis Monneret, Kevin Premat, Stéphanie Lenck, Nader-antoine Sourour, Frédéric ClarençonAbstract:Background and Purpose— S100B protein serum elevation has been associated with poor prognosis in neurologically ill patients. The purpose of this study is to determine whether elevation of S100B is...
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retrospective study of long term outcome after Brain Arteriovenous Malformation rupture the rap score
Journal of Neurosurgery, 2018Co-Authors: Eimad Shotar, Nader-antoine Sourour, Jacques Chiras, Matthieu Debarre, Federico Di Maria, Joseph Gabrieli, Aurelien Nouet, Vincent Degos, Frédéric ClarençonAbstract:OBJECTIVE The authors aimed to design a score for stratifying patients with Brain Arteriovenous Malformation (BAVM) rupture, based on the likelihood of a poor long-term neurological outcome. METHODS The records of consecutive patients with BAVM hemorrhagic events who had been admitted over a period of 11 years were retrospectively reviewed. Independent predictors of a poor long-term outcome (modified Rankin Scale score ≥ 3) beyond 1 year after admission were identified. A risk stratification scale was developed and compared with the intracranial hemorrhage (ICH) score to predict poor outcome and inpatient mortality. RESULTS One hundred thirty-five patients with 139 independent hemorrhagic events related to BAVM rupture were included in this analysis. Multivariate logistic regression followed by stepwise analysis showed that consciousness level according to the Glasgow Coma Scale (OR 6.5, 95% CI 3.1–13.7, p < 10−3), hematoma volume (OR 1.8, 95% CI 1.2–2.8, p = 0.005), and intraventricular hemorrhage (OR 7....
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Elaboration of a semi-automated algorithm for Brain Arteriovenous Malformation segmentation: initial results
European radiology, 2014Co-Authors: Frédéric Clarençon, Franck Maizeroi-eugène, Damien Bresson, Flavien Maingreaud, Nader Sourour, Claude Couquet, David Ayoub, Jacques Chiras, Catherine Yardin, Charbel MounayerAbstract:Objectives The purpose of our study was to distinguish the different components of a Brain Arteriovenous Malformation (bAVM) on 3D rotational angiography (3D-RA) using a semi-automated segmentation algorithm.
Eimad Shotar - One of the best experts on this subject based on the ideXlab platform.
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S100B Serum Elevation Predicts In-Hospital Mortality After Brain Arteriovenous Malformation Rupture
Stroke, 2019Co-Authors: Eimad Shotar, Caroline Amouyal, Alice Jacquens, Bertrand Mathon, Grégoire Boulouis, Denis Monneret, Kevin Premat, Stéphanie Lenck, Nader-antoine Sourour, Frédéric ClarençonAbstract:Background and Purpose- S100B protein serum elevation has been associated with poor prognosis in neurologically ill patients. The purpose of this study is to determine whether elevation of S100B is associated with increased in-hospital mortality after Brain Arteriovenous Malformation rupture. Methods- This is a retrospective study of patients admitted for Brain Arteriovenous Malformation rupture. The study population was divided into derivation and validation cohorts. Univariate followed by multivariate logistic regression was used to determine whether elevation of S100B serum levels above 0.5 µg/L during the first 48 hours after admission (S100Bmax48) was associated with in-hospital mortality. Results- Two hundred and three ruptures met inclusion criteria. Twenty-three led to in-hospital mortality (11%). Mean S100Bmax48 was 0.49±0.62 µg/L. In the derivation cohort (n=101 ruptures), multivariate analysis found Glasgow coma scale score ≤8 (odds ratio, 21; 95% CI, 2-216; 0.001) and an S100Bmax48>0.5 µg/L (odds ratio, 19; 95% CI, 2-188; P=0.001) to be associated with in-hospital mortality. When applied to the validation cohort (n=102 ruptures), the same model found only S100Bmax48>0.5 µg/L (odds ratio, 8; 95% CI, 1.5-44; P=0.01) to be associated with in-hospital mortality. Conclusions- Elevated S100B protein serum level is strongly associated with in-hospital mortality after Brain Arteriovenous Malformation rupture.
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s100b serum elevation predicts in hospital mortality after Brain Arteriovenous Malformation rupture
Stroke, 2019Co-Authors: Eimad Shotar, Caroline Amouyal, Alice Jacquens, Bertrand Mathon, Grégoire Boulouis, Denis Monneret, Kevin Premat, Stéphanie Lenck, Nader-antoine Sourour, Frédéric ClarençonAbstract:Background and Purpose— S100B protein serum elevation has been associated with poor prognosis in neurologically ill patients. The purpose of this study is to determine whether elevation of S100B is...
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retrospective study of long term outcome after Brain Arteriovenous Malformation rupture the rap score
Journal of Neurosurgery, 2018Co-Authors: Eimad Shotar, Nader-antoine Sourour, Jacques Chiras, Matthieu Debarre, Federico Di Maria, Joseph Gabrieli, Aurelien Nouet, Vincent Degos, Frédéric ClarençonAbstract:OBJECTIVE The authors aimed to design a score for stratifying patients with Brain Arteriovenous Malformation (BAVM) rupture, based on the likelihood of a poor long-term neurological outcome. METHODS The records of consecutive patients with BAVM hemorrhagic events who had been admitted over a period of 11 years were retrospectively reviewed. Independent predictors of a poor long-term outcome (modified Rankin Scale score ≥ 3) beyond 1 year after admission were identified. A risk stratification scale was developed and compared with the intracranial hemorrhage (ICH) score to predict poor outcome and inpatient mortality. RESULTS One hundred thirty-five patients with 139 independent hemorrhagic events related to BAVM rupture were included in this analysis. Multivariate logistic regression followed by stepwise analysis showed that consciousness level according to the Glasgow Coma Scale (OR 6.5, 95% CI 3.1–13.7, p < 10−3), hematoma volume (OR 1.8, 95% CI 1.2–2.8, p = 0.005), and intraventricular hemorrhage (OR 7....