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Hugh S. Markus - One of the best experts on this subject based on the ideXlab platform.
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predicting dementia in cerebral Small Vessel Disease using an automatic diffusion tensor image segmentation technique
Stroke, 2019Co-Authors: Owen A Williams, Robin G. Morris, Hugh S. Markus, Andrew J Lawrence, Andrew D Mackinnon, Thomas R Barrick, Christian Lambert, Philip Benjamin, Eva Zeestraten, Rebecca A. CharltonAbstract:Background and Purpose— Cerebral Small Vessel Disease (SVD) is the most common cause of vascular cognitive impairment, with a significant proportion of cases going on to develop dementia. We explor...
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longitudinal patterns of leukoaraiosis and brain atrophy in symptomatic Small Vessel Disease
Brain, 2016Co-Authors: Christian Lambert, Andrew J Lawrence, Thomas R Barrick, Philip Benjamin, Eva Zeestraten, Hugh S. MarkusAbstract:Cerebral Small Vessel Disease is a common condition associated with lacunar stroke, cognitive impairment and significant functional morbidity. White matter hyperintensities and brain atrophy, seen on magnetic resonance imaging, are correlated with increasing Disease severity. However, how the two are related remains an open question. To better define the relationship between white matter hyperintensity growth and brain atrophy, we applied a semi-automated magnetic resonance imaging segmentation analysis pipeline to a 3-year longitudinal cohort of 99 subjects with symptomatic Small Vessel Disease, who were followed-up for ≥1 years. Using a novel two-stage warping pipeline with tissue repair step, voxel-by-voxel rate of change maps were calculated for each tissue class (grey matter, white matter, white matter hyperintensities and lacunes) for each individual. These maps capture both the distribution of Disease and spatial information showing local rates of growth and atrophy. These were analysed to answer three primary questions: first, is there a relationship between whole brain atrophy and magnetic resonance imaging markers of Small Vessel Disease (white matter hyperintensities or lacune volume)? Second, is there regional variation within the cerebral white matter in the rate of white matter hyperintensity progression? Finally, are there regionally specific relationships between the rates of white matter hyperintensity progression and cortical grey matter atrophy? We demonstrate that the rates of white matter hyperintensity expansion and grey matter atrophy are strongly correlated (Pearson's R = -0.69, P < 1 × 10(-7)), and significant grey matter loss and whole brain atrophy occurs annually (P < 0.05). Additionally, the rate of white matter hyperintensity growth was heterogeneous, occurring more rapidly within long association fasciculi. Using voxel-based quantification (family-wise error corrected P < 0.05), we show the rate of white matter hyperintensity progression is associated with increases in cortical grey matter atrophy rates, in the medial-frontal, orbito-frontal, parietal and occipital regions. Conversely, increased rates of global grey matter atrophy are significantly associated with faster white matter hyperintensity growth in the frontal and parietal regions. Together, these results link the progression of white matter hyperintensities with increasing rates of regional grey matter atrophy, and demonstrate that grey matter atrophy is the major contributor to whole brain atrophy in symptomatic cerebral Small Vessel Disease. These measures provide novel insights into the longitudinal pathogenesis of Small Vessel Disease, and imply that therapies aimed at reducing progression of white matter hyperintensities via end-arteriole damage may protect against secondary brain atrophy and consequent functional morbidity.
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progression of mri markers in cerebral Small Vessel Disease sample size considerations for clinical trials
Journal of Cerebral Blood Flow and Metabolism, 2016Co-Authors: Philip Benjamin, Bhavini Patel, Andrew J Lawrence, Andrew D Mackinnon, Thomas R Barrick, Christian Lambert, Eva Zeestraten, Irina Chis Ster, Owen A Williams, Hugh S. MarkusAbstract:Detecting treatment efficacy using cognitive change in trials of cerebral Small Vessel Disease (SVD) has been challenging, making the use of surrogate markers such as magnetic resonance imaging (MR...
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cerebral microbleeds and cognition in patients with symptomatic Small Vessel Disease
Stroke, 2013Co-Authors: Bhavini Patel, Robin G. Morris, Andrew J Lawrence, Ai Wern Chung, Philip Rich, Andrew D Mackinnon, Thomas R Barrick, Hugh S. MarkusAbstract:Background and Purpose—Cerebral microbleeds (CMBs) are common in cerebral Small Vessel Disease. They may cause cognitive impairment, possibly via white matter tract disruption but previous studies have produced inconsistent results. We determined whether CMB number and location are associated with impaired cognition in symptomatic Small Vessel Disease and whether any association was independent of other magnetic resonance imaging markers of Small Vessel Disease. Methods—One hundred sixteen patients with lacunar stroke and radiological leukoaraiosis were studied. Neuropsychological assessment was performed. CMBs on gradient echo images were assessed using the Brain Observer Microbleed Rating Scale criteria. Magnetic resonance imaging measures, including diffusion tensor imaging, were also analyzed. Associations between cognitive function and the presence, number, and location of CMBs were determined. Results—CMBs were present in 46 (39.7%) patients. CMB number correlated weakly with executive function (r=0...
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Depressive Symptoms as a Predictor of Quality of Life in Cerebral Small Vessel Disease, Acting Independently of Disability; a Study in Both Sporadic Small Vessel Disease and Cadasil
International Journal of Stroke, 2012Co-Authors: Rebecca L. Brookes, Thomas A. Willis, Bhavini Patel, Robin G. Morris, Hugh S. MarkusAbstract:BackgroundCerebral Small Vessel Disease causes lacunar stroke, and more recently has been implicated as a cause of depression. Factors causing reduced quality of life in Small Vessel Disease, including the relative contributions of disability and depressive symptoms, remain uncertain.MethodsOne hundred patients with Small Vessel Disease and 55 controls completed the Stroke-Specific Quality of Life scale. The protocol was repeated in 40 patients with the young-onset genetic form of Small Vessel Disease, cerebral autosomal dominant arteriopathy with sub-cortical infarcts and leukoencephalopathy, and 35 controls. Disability, activities of daily living, cognition and depression were measured.ResultsQuality of life was significantly lower in Small Vessel Disease versus controls: mean (standard deviation), 196·8 (35·2) vs. 226·8 (15·3), P < ·0001. Depressive symptoms were the major predictor of quality of life, explaining 52·9% of variance. The only other independent predictor was disability, explaining an addi...
Joanna M Wardlaw - One of the best experts on this subject based on the ideXlab platform.
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Small Vessel Disease mechanisms and clinical implications
Lancet Neurology, 2019Co-Authors: Joanna M Wardlaw, Colin Smith, Martin DichgansAbstract:Summary Small Vessel Disease is a disorder of cerebral microVessels that causes white matter hyperintensities and several other common abnormalities (eg, recent Small subcortical infarcts and lacunes) seen on brain imaging. Despite being a common cause of stroke and vascular dementia, the underlying pathogenesis is poorly understood. Research in humans has identified several manifestations of cerebral microVessel endothelial dysfunction including blood–brain barrier dysfunction, impaired vasodilation, Vessel stiffening, dysfunctional blood flow and interstitial fluid drainage, white matter rarefaction, ischaemia, inflammation, myelin damage, and secondary neurodegeneration. These brain abnormalities are more dynamic and widespread than previously thought. Relationships between lesions and symptoms are highly variable but poorly understood. Major challenges are the determination of which vascular dysfunctions are most important in pathogenesis, which abnormalities are reversible, and why lesion progression and symptomatology are so variable. This knowledge will help to identify potential targets for intervention and improve risk prediction for individuals with Small Vessel Disease.
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The relation between total cerebral Small Vessel Disease burden and gait impairment in patients with minor stroke
International Journal of Stroke, 2017Co-Authors: Caroline M.j. Loos, Julie Staals, Stephen Makin, Caroline A. Mchutchison, Vera Cvoro, Francesca M. Chappell, Martin S. Dennis, Robert J. Van Oostenbrugge, Joanna M WardlawAbstract:Background and aimsIndividual MRI markers of cerebral Small Vessel Disease are associated with gait impairment. The impact of total cerebral Small Vessel Disease-related brain damage, expressed by ...
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cerebral blood flow in Small Vessel Disease a systematic review and meta analysis
Journal of Cerebral Blood Flow and Metabolism, 2016Co-Authors: Michael J Thrippleton, Stephen Makin, Ian Marshall, Mirjam I Geerlings, Anton J M De Craen, Mark A Van Buchem, Joanna M WardlawAbstract:White matter hyperintensities are frequent on neuroimaging of older people and are a key feature of cerebral Small Vessel Disease. They are commonly attributed to chronic hypoperfusion, although wh...
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pharmacological treatment and prevention of cerebral Small Vessel Disease a review of potential interventions
International Journal of Stroke, 2015Co-Authors: Philip M W Bath, Joanna M WardlawAbstract:Small Vessel Disease encompasses lacunar stroke, white matter hyperintensities, lacunes and microbleeds. It causes a quarter of all ischemic strokes, is the commonest cause of vascular dementia, and the cause is incompletely understood. Vascular prophylaxis, as appropriate for large artery Disease and cardioembolism, includes antithrombotics, and blood pressure and lipid lowering; however, these strategies may not be effective for Small Vessel Disease, or are already used routinely so precluding further detailed study. Further, intensive antiplatelet therapy is known to be hazardous in Small Vessel Disease through enhanced bleeding. Whether acetylcholinesterase inhibitors, which delay the progression of Alzheimer's dementia, are relevant in Small Vessel Disease remains unclear. Potential prophylactic and treatment strategies might be those that target brain microvascular endothelium and the blood brain barrier, microvascular function and neuroinflammation. Potential interventions include endothelin antagonists, neurotrophins, nitric oxide donors and phosphodiesterase 5 inhibitors, peroxisome proliferator-activated receptor-gamma agonists, and prostacyclin mimics and phosphodiesterase 3 inhibitors. Several drugs that have relevant properties are licensed for other disorders, offering the possibility of drug repurposing. Others are in development. Since influencing multiple targets may be most effective, using multiple agents and/or those that have multiple effects may be preferable. We focus on potential Small Vessel Disease mechanistic targets, summarize drugs that have relevant actions, and review data available from randomized trials on their actions and on the available evidence for their use in lacunar stroke.
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blood brain barrier and cerebral Small Vessel Disease
Journal of the Neurological Sciences, 2010Co-Authors: Joanna M WardlawAbstract:Abstract Increasing evidence from neuro and retinal imaging, neuropathology, epidemiology and experimental models suggests that the primary underlying initiating cause of cerebral Small Vessel Disease is the derangement of the blood-brain barrier. This may start some years before the first symptoms, leads to the Small Vessel structural changes (Vessel wall thickening, disorganisation and eventual breakdown) and perivascular changes (oedema, enlarged perivascular spaces, tissue damage interpreted as “infarcts”) and is fundamentally different to traditional “ischaemic” mechanisms, although Small Vessel occlusion due to thrombus formation on damaged Vessel walls may be a late secondary phenomenon. Space limits a detailed discussion of the epidemiology and experimental evidence, so this brief review will focus on neuroimaging evidence and summarise the appearances, risk factors and associations of different components of cerebral Small Vessel Disease as identified on imaging, discuss potential causes and, in particular, the evidence that disordered blood-brain barrier precipitates or worsens progression of cerebral Small Vessel Disease. This mechanism may also play a role in other common disorders of ageing such as Alzheimer's Disease.
Monique M B Breteler - One of the best experts on this subject based on the ideXlab platform.
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arterial stiffness and cerebral Small Vessel Disease the rotterdam scan study
Stroke, 2012Co-Authors: Marielle M F Poels, Meike W Vernooij, Albert Hofman, Aad Van Der Lugt, Monique M B Breteler, Keren Zaccai, Germaine C Verwoert, Jacqueline C M Witteman, Francesco U S Mattaceraso, Arfan M IkramAbstract:Background and Purpose—Aging and vascular risk factors contribute to arterial stiffening. Increased arterial stiffness exposes the Small Vessels in the brain to abnormal flow pulsations and, as such, may contribute to the pathogenesis of cerebral Small Vessel Disease. In a population-based study, we investigated the association between arterial stiffness, as measured by aortic pulse wave velocity (aPWV), and Small Vessel Disease. Methods—Overall, 1460 participants (mean age, 58.2 years) underwent aPWV measurement and brain MRI scanning. We calculated aPWV by measuring time differences and distances between pulse waves in the carotid and femoral arteries. Using automated MRI analysis, we obtained white matter lesion volumes. Infarcts and microbleeds were rated visually. We used linear and logistic regression models to associate aPWV with Small Vessel Disease, adjusting for age, sex, mean arterial pressure, and heart rate and additionally for cardiovascular risk factors. Subsequently, we explored associatio...
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brain tissue volumes and Small Vessel Disease in relation to the risk of mortality
Neurobiology of Aging, 2009Co-Authors: Arfan M Ikram, Meike W Vernooij, Albert Hofman, Henri A Vrooman, Monique M B BretelerAbstract:Abstract Brain atrophy and Small Vessel Disease increase the risk of dementia and stroke. In a population-based cohort study (n = 490; 60–90 years) we investigated how volumetric measures of atrophy and Small Vessel Disease were related to mortality and whether this was independent of incident dementia or stroke. Brain volume and hippocampal volume were considered as measures of atrophy, whereas white matter lesions (WML) and lacunar infarcts reflected Small Vessel Disease. We first investigated all-cause mortality in the whole cohort. In subsequent analyses we censored persons at incident dementia or incident stroke. Finally, we separately investigated cardiovascular mortality. The average follow-up was 8.4 years, during which 191 persons died. Brain atrophy and hippocampal atrophy, as well as WML increased the risk of death. The risks associated with hippocampal atrophy attenuated when censoring persons at incident dementia, but not at incident stroke. Censoring at either incident dementia or stroke did not change the risk associated with brain atrophy and WML. Moreover, WML were particularly associated with cardiovascular mortality.
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kidney function is related to cerebral Small Vessel Disease
Stroke, 2008Co-Authors: Arfan M Ikram, Meike W Vernooij, Albert Hofman, Wiro J Niessen, Aad Van Der Lugt, Monique M B BretelerAbstract:Background and Purpose— Poor kidney function, as measured by glomerular filtration rate (GFR), is closely associated with presence of glomerular Small Vessel Disease. Given the hemodynamic similarities between the vascular beds of the kidney and the brain, we hypothesized an association between kidney function and markers of cerebral Small Vessel Disease on MRI. We investigated this association in a population-based study of elderly persons. Methods— We measured GFR using the Cockcroft-Gault equation in 484 participants (60 to 90 years of age) from the Rotterdam Scan Study. Using automated MRI-analysis we measured global as well as lobar and deep volumes of gray matter and white matter, and volume of WML. Lacunar infarcts were rated visually. Volumes of deep white matter and WML and presence of lacunar infarcts reflected cerebral Small Vessel Disease. We used linear and logistic regression models to investigate the association between GFR and brain imaging parameters. Analyses were adjusted for age, sex, ...
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retinal Vessel diameters and cerebral Small Vessel Disease the rotterdam scan study
Brain, 2006Co-Authors: Kamran M Ikram, Albert Hofman, Monique M B Breteler, Frank Jan De Jong, Ewoud J Van Dijk, Niels D Prins, Paulus T V M De JongAbstract:The direct visualization of retinal Vessels provides a unique opportunity to study cerebral Small Vessel Disease, because these Vessels share many features. It was reported that persons with Smaller retinal arteriolar-to-venular ratio tended to have more white matter lesions on MRI. It is unclear whether this is due to arteriolar narrowing or venular dilatation. We investigated whether Smaller arteriolar or larger venular diameters or both were related to severity and progression of cerebral Small Vessel Disease. We studied 490 persons (60Â?90 years) without dementia from a population-based cohort study. At baseline (1990Â?1993), retinal arteriolar and venular diameters were measured on digitized images of one eye of each participant. In 1995Â?1996, participants underwent cerebral MRI scanning. We rated the severity of periventricular white matter lesions on a 9-point scale, approximated a total subcortical white matter lesion volume (range: 0Â?29.5 ml) and rated the presence of lacunar infarcts. On average 3.3 years later, 279 persons had a second MRI. Changes in periventricular and subcortical white matter lesions were rated with a semi-quantitative scale, and progression was classified as no, minor and marked. An incident infarct was a new infarct on the follow-up MRI. Neither venular nor arteriolar diameters were related to the severity of cerebral Small Vessel Disease. Larger venular diameters were, however, associated with a marked progression of cerebral Small Vessel Disease. Age and gender adjusted odds ratios (ORs) per standard deviation increase were 1.71 [95% confidence interval (CI): 1.11Â?2.61] for periventricular, 1.72 (95% CI: 1.09Â?2.71) for subcortical white matter lesion progression and 1.59 (95% CI: 1.06Â?2.39) for incident lacunar infarcts. These associations were independent of other cardiovascular risk factors. Only the OR for incident lacunar infarcts was attenuated (1.24; 95% CI: 0.72Â?2.12). No association was observed between arteriolar diameters and progression of cerebral Small Vessel Disease. In conclusion, retinal venular dilatation was related to progression of cerebral Small Vessel Disease. The mechanisms underlying venular dilatation deserve more attention, as they may provide new clues into the pathophysiology of cerebral Small Vessel Disease.
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cerebral Small Vessel Disease and decline in information processing speed executive function and memory
Brain, 2005Co-Authors: Niels D Prins, Albert Hofman, Ewoud J Van Dijk, Sarah E Vermeer, Peter J Koudstaal, Tom Den Heijer, Jellemer Jolles, Monique M B BretelerAbstract:Cerebral Small-Vessel Disease is common in older people and may contribute to the development of dementia. The objective of the present study was to evaluate the relationship between measures of cerebral Small-Vessel Disease on MRI and the rate of decline in specific cognitive domains in participants from the prospective, population-based Rotterdam Scan Study. Participants were 60-90 years of age and free from dementia at baseline in 1995-1996. White matter lesions (WML), cerebral infarcts and generalized brain atrophy were assessed on the baseline MRI. We performed neuropsychological testing at baseline and repeatedly in 1999-2000 and in 2001-2003. We used random-effects models for repeated measures to examine the association between quantitative MRI measures and rate of decline in measures of global cognitive function, information processing speed, executive function and memory. There were a total of 2266 assessments for the 832 participants in the study, with an average time from the initial to last assessment of 5.2 years. Increasing severity of periventricular WML and generalized brain atrophy and the presence of brain infarcts on MRI were associated with a steeper decline in cognitive function. These structural brain changes were specifically associated with decline in information processing speed and executive function. The associations between MRI measures of cerebral Small-Vessel Disease and cognitive decline did not change after additional adjustment for vascular risk factors or depressed mood. After exclusion of participants with an incident stroke, some of the associations of periventricular WML, brain infarcts and generalized brain atrophy with measures of information processing speed and executive function were no longer significant. This may indicate that stroke plays an intermediate role in the relationship between cerebral Small-Vessel Disease and cognitive decline. Our results suggest that in older people cerebral Small-Vessel Disease may contribute to cognitive decline by affecting information processing speed and executive function.
Albert Hofman - One of the best experts on this subject based on the ideXlab platform.
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cerebral Small Vessel Disease is related to disturbed 24 h activity rhythms a population based study
European Journal of Neurology, 2015Co-Authors: Lisette A Zuurbier, Meike W Vernooij, Albert Hofman, M A Ikram, Annemarie I Luik, E J W Van Someren, Henning TiemeierAbstract:Background and purpose: Cerebral Small Vessel Disease is common in elderly persons. Patients with dementia or stroke frequently have cerebral Small Vessel Disease and often experience disturbances in the sleep-wake rhythm. It is unknown whether cerebral Small Vessel Disease is related to disturbances in sleep and 24-h activity rhythms. Methods: This study was conducted in the Rotterdam Study. A total of 970 community-dwelling persons (mean age 59.2 years) underwent brain magnetic resonance imaging and actigraphy. Cerebral Small Vessel Disease was defined as white matter lesions (total volume in millilitres) and the presence of cerebral microbleeds and lacunar infarcts. Twenty-four hour activity rhythms and sleep were measured with actigraphy by estimating the instability and fragmentation of the activity rhythm and total sleep time. Sleep quality was assessed with the Pittsburgh Sleep Quality Index. White matter lesions, instability, fragmentation and sleep quality were standardized for analyses. Results: Higher white matter lesion volume (B = 0.09 per SD, 95% confidence interval 0.02; 0.15) and cerebral microbleeds (B = 0.19 per SD, 95% confidence interval 0.02; 0.37) were significantly related to more fragmented 24-h activity rhythms. None of the Small Vessel Disease markers was related to total sleep time or sleep quality. Conclusions: White matter lesion volume and the presence of cerebral microbleeds are related to disturbed activity rhythms. This suggests that subclinical brain damage affects the 24-h activity rhythm.
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kidney function and cerebral Small Vessel Disease in the general population
International Journal of Stroke, 2015Co-Authors: Saloua Akoudad, Arfan M Ikram, Albert Hofman, Aad Van Der Lugt, Peter J Koudstaal, Sanaz Sedaghat, Meike W VernooijAbstract:BackgroundAnatomic and hemodynamic similarities between renal and cerebral Vessels suggest a tight link between kidney Disease and brain Disease. Although several distinct markers are used to identify subclinical kidney and brain Disease, a comprehensive assessment of how these markers link damage at both end organs is lacking.AimTo investigate whether measures of kidney function were associated with cerebral Small Vessel Disease on MRI.MethodsIn 2526 participants of the population-based Rotterdam Study, we measured urinary albumin-to-creatinine ratio, and estimated glomerular filtration rate based on serum creatinine and cystatin C. All participants underwent brain magnetic resonance imaging. We assessed presence of cerebral Small Vessel Disease by calculating white matter lesion volumes and rating the presence of lacunes and cerebral microbleeds. We used multivariable linear and logistic regression to investigate the association between kidney function and cerebral Small Vessel Disease.ResultsWorse kidn...
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arterial stiffness and cerebral Small Vessel Disease the rotterdam scan study
Stroke, 2012Co-Authors: Marielle M F Poels, Meike W Vernooij, Albert Hofman, Aad Van Der Lugt, Monique M B Breteler, Keren Zaccai, Germaine C Verwoert, Jacqueline C M Witteman, Francesco U S Mattaceraso, Arfan M IkramAbstract:Background and Purpose—Aging and vascular risk factors contribute to arterial stiffening. Increased arterial stiffness exposes the Small Vessels in the brain to abnormal flow pulsations and, as such, may contribute to the pathogenesis of cerebral Small Vessel Disease. In a population-based study, we investigated the association between arterial stiffness, as measured by aortic pulse wave velocity (aPWV), and Small Vessel Disease. Methods—Overall, 1460 participants (mean age, 58.2 years) underwent aPWV measurement and brain MRI scanning. We calculated aPWV by measuring time differences and distances between pulse waves in the carotid and femoral arteries. Using automated MRI analysis, we obtained white matter lesion volumes. Infarcts and microbleeds were rated visually. We used linear and logistic regression models to associate aPWV with Small Vessel Disease, adjusting for age, sex, mean arterial pressure, and heart rate and additionally for cardiovascular risk factors. Subsequently, we explored associatio...
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brain tissue volumes and Small Vessel Disease in relation to the risk of mortality
Neurobiology of Aging, 2009Co-Authors: Arfan M Ikram, Meike W Vernooij, Albert Hofman, Henri A Vrooman, Monique M B BretelerAbstract:Abstract Brain atrophy and Small Vessel Disease increase the risk of dementia and stroke. In a population-based cohort study (n = 490; 60–90 years) we investigated how volumetric measures of atrophy and Small Vessel Disease were related to mortality and whether this was independent of incident dementia or stroke. Brain volume and hippocampal volume were considered as measures of atrophy, whereas white matter lesions (WML) and lacunar infarcts reflected Small Vessel Disease. We first investigated all-cause mortality in the whole cohort. In subsequent analyses we censored persons at incident dementia or incident stroke. Finally, we separately investigated cardiovascular mortality. The average follow-up was 8.4 years, during which 191 persons died. Brain atrophy and hippocampal atrophy, as well as WML increased the risk of death. The risks associated with hippocampal atrophy attenuated when censoring persons at incident dementia, but not at incident stroke. Censoring at either incident dementia or stroke did not change the risk associated with brain atrophy and WML. Moreover, WML were particularly associated with cardiovascular mortality.
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kidney function is related to cerebral Small Vessel Disease
Stroke, 2008Co-Authors: Arfan M Ikram, Meike W Vernooij, Albert Hofman, Wiro J Niessen, Aad Van Der Lugt, Monique M B BretelerAbstract:Background and Purpose— Poor kidney function, as measured by glomerular filtration rate (GFR), is closely associated with presence of glomerular Small Vessel Disease. Given the hemodynamic similarities between the vascular beds of the kidney and the brain, we hypothesized an association between kidney function and markers of cerebral Small Vessel Disease on MRI. We investigated this association in a population-based study of elderly persons. Methods— We measured GFR using the Cockcroft-Gault equation in 484 participants (60 to 90 years of age) from the Rotterdam Scan Study. Using automated MRI-analysis we measured global as well as lobar and deep volumes of gray matter and white matter, and volume of WML. Lacunar infarcts were rated visually. Volumes of deep white matter and WML and presence of lacunar infarcts reflected cerebral Small Vessel Disease. We used linear and logistic regression models to investigate the association between GFR and brain imaging parameters. Analyses were adjusted for age, sex, ...
Bhavini Patel - One of the best experts on this subject based on the ideXlab platform.
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progression of mri markers in cerebral Small Vessel Disease sample size considerations for clinical trials
Journal of Cerebral Blood Flow and Metabolism, 2016Co-Authors: Philip Benjamin, Bhavini Patel, Andrew J Lawrence, Andrew D Mackinnon, Thomas R Barrick, Christian Lambert, Eva Zeestraten, Irina Chis Ster, Owen A Williams, Hugh S. MarkusAbstract:Detecting treatment efficacy using cognitive change in trials of cerebral Small Vessel Disease (SVD) has been challenging, making the use of surrogate markers such as magnetic resonance imaging (MR...
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cerebral microbleeds and cognition in patients with symptomatic Small Vessel Disease
Stroke, 2013Co-Authors: Bhavini Patel, Robin G. Morris, Andrew J Lawrence, Ai Wern Chung, Philip Rich, Andrew D Mackinnon, Thomas R Barrick, Hugh S. MarkusAbstract:Background and Purpose—Cerebral microbleeds (CMBs) are common in cerebral Small Vessel Disease. They may cause cognitive impairment, possibly via white matter tract disruption but previous studies have produced inconsistent results. We determined whether CMB number and location are associated with impaired cognition in symptomatic Small Vessel Disease and whether any association was independent of other magnetic resonance imaging markers of Small Vessel Disease. Methods—One hundred sixteen patients with lacunar stroke and radiological leukoaraiosis were studied. Neuropsychological assessment was performed. CMBs on gradient echo images were assessed using the Brain Observer Microbleed Rating Scale criteria. Magnetic resonance imaging measures, including diffusion tensor imaging, were also analyzed. Associations between cognitive function and the presence, number, and location of CMBs were determined. Results—CMBs were present in 46 (39.7%) patients. CMB number correlated weakly with executive function (r=0...
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Depressive Symptoms as a Predictor of Quality of Life in Cerebral Small Vessel Disease, Acting Independently of Disability; a Study in Both Sporadic Small Vessel Disease and Cadasil
International Journal of Stroke, 2012Co-Authors: Rebecca L. Brookes, Thomas A. Willis, Bhavini Patel, Robin G. Morris, Hugh S. MarkusAbstract:BackgroundCerebral Small Vessel Disease causes lacunar stroke, and more recently has been implicated as a cause of depression. Factors causing reduced quality of life in Small Vessel Disease, including the relative contributions of disability and depressive symptoms, remain uncertain.MethodsOne hundred patients with Small Vessel Disease and 55 controls completed the Stroke-Specific Quality of Life scale. The protocol was repeated in 40 patients with the young-onset genetic form of Small Vessel Disease, cerebral autosomal dominant arteriopathy with sub-cortical infarcts and leukoencephalopathy, and 35 controls. Disability, activities of daily living, cognition and depression were measured.ResultsQuality of life was significantly lower in Small Vessel Disease versus controls: mean (standard deviation), 196·8 (35·2) vs. 226·8 (15·3), P < ·0001. Depressive symptoms were the major predictor of quality of life, explaining 52·9% of variance. The only other independent predictor was disability, explaining an addi...
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magnetic resonance imaging in cerebral Small Vessel Disease and its use as a surrogate Disease marker
International Journal of Stroke, 2011Co-Authors: Bhavini Patel, Hugh S. MarkusAbstract:Cerebral Small Vessel Disease is an important cause of vascular cognitive impairment and dementia. On brain imaging, discrete lacunar infarcts and/or more diffuse regions of white matter hyperintensities or leucoaraiosis are seen. Magnetic resonance imaging plays a crucial role in diagnosis, and advanced magnetic resonance imaging techniques are providing new information on Disease mechanisms and offering potential as surrogate Disease markers. Longitudinal studies have demonstrated detectable progression of lesion load over short time periods, and weak correlations with cognition. Stronger correlations with cognition have been found with diffusion tensor imaging, which is more sensitive to white matter tract structure, supporting a role for disconnection in the pathogenesis of cognitive impairment. Brain volume also consistently correlates with cognition in asymptomatic Small Vessel Disease, sporadic Small Vessel Disease, and Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoenc...
