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      Neuroimaging standards for research into small vessel disease and its contribution to ageing and neurodegeneration

      a , b , c , * , e , f , g , h , e , i , j , k , l , m , n , o , p , q , r , d , s , t , v , w , x , y , z , aa , ab , ac , x , v , u , ad , b , ae , af , ag , s , ah , ** , STandards for ReportIng Vascular changes on nEuroimaging (STRIVE v1)

      Lancet Neurology

      Lancet Pub. Group

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          Cerebral small vessel disease (SVD) is a common accompaniment of ageing. Features seen on neuroimaging include recent small subcortical infarcts, lacunes, white matter hyperintensities, perivascular spaces, microbleeds, and brain atrophy. SVD can present as a stroke or cognitive decline, or can have few or no symptoms. SVD frequently coexists with neurodegenerative disease, and can exacerbate cognitive deficits, physical disabilities, and other symptoms of neurodegeneration. Terminology and definitions for imaging the features of SVD vary widely, which is also true for protocols for image acquisition and image analysis. This lack of consistency hampers progress in identifying the contribution of SVD to the pathophysiology and clinical features of common neurodegenerative diseases. We are an international working group from the Centres of Excellence in Neurodegeneration. We completed a structured process to develop definitions and imaging standards for markers and consequences of SVD. We aimed to achieve the following: first, to provide a common advisory about terms and definitions for features visible on MRI; second, to suggest minimum standards for image acquisition and analysis; third, to agree on standards for scientific reporting of changes related to SVD on neuroimaging; and fourth, to review emerging imaging methods for detection and quantification of preclinical manifestations of SVD. Our findings and recommendations apply to research studies, and can be used in the clinical setting to standardise image interpretation, acquisition, and reporting. This Position Paper summarises the main outcomes of this international effort to provide the STandards for ReportIng Vascular changes on nEuroimaging (STRIVE).

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          Vascular contributions to cognitive impairment and dementia: a statement for healthcare professionals from the american heart association/american stroke association.

          This scientific statement provides an overview of the evidence on vascular contributions to cognitive impairment and dementia. Vascular contributions to cognitive impairment and dementia of later life are common. Definitions of vascular cognitive impairment (VCI), neuropathology, basic science and pathophysiological aspects, role of neuroimaging and vascular and other associated risk factors, and potential opportunities for prevention and treatment are reviewed. This statement serves as an overall guide for practitioners to gain a better understanding of VCI and dementia, prevention, and treatment. Writing group members were nominated by the writing group co-chairs on the basis of their previous work in relevant topic areas and were approved by the American Heart Association Stroke Council Scientific Statement Oversight Committee, the Council on Epidemiology and Prevention, and the Manuscript Oversight Committee. The writing group used systematic literature reviews (primarily covering publications from 1990 to May 1, 2010), previously published guidelines, personal files, and expert opinion to summarize existing evidence, indicate gaps in current knowledge, and, when appropriate, formulate recommendations using standard American Heart Association criteria. All members of the writing group had the opportunity to comment on the recommendations and approved the final version of this document. After peer review by the American Heart Association, as well as review by the Stroke Council leadership, Council on Epidemiology and Prevention Council, and Scientific Statements Oversight Committee, the statement was approved by the American Heart Association Science Advisory and Coordinating Committee. The construct of VCI has been introduced to capture the entire spectrum of cognitive disorders associated with all forms of cerebral vascular brain injury-not solely stroke-ranging from mild cognitive impairment through fully developed dementia. Dysfunction of the neurovascular unit and mechanisms regulating cerebral blood flow are likely to be important components of the pathophysiological processes underlying VCI. Cerebral amyloid angiopathy is emerging as an important marker of risk for Alzheimer disease, microinfarction, microhemorrhage and macrohemorrhage of the brain, and VCI. The neuropathology of cognitive impairment in later life is often a mixture of Alzheimer disease and microvascular brain damage, which may overlap and synergize to heighten the risk of cognitive impairment. In this regard, magnetic resonance imaging and other neuroimaging techniques play an important role in the definition and detection of VCI and provide evidence that subcortical forms of VCI with white matter hyperintensities and small deep infarcts are common. In many cases, risk markers for VCI are the same as traditional risk factors for stroke. These risks may include but are not limited to atrial fibrillation, hypertension, diabetes mellitus, and hypercholesterolemia. Furthermore, these same vascular risk factors may be risk markers for Alzheimer disease. Carotid intimal-medial thickness and arterial stiffness are emerging as markers of arterial aging and may serve as risk markers for VCI. Currently, no specific treatments for VCI have been approved by the US Food and Drug Administration. However, detection and control of the traditional risk factors for stroke and cardiovascular disease may be effective in the prevention of VCI, even in older people. Vascular contributions to cognitive impairment and dementia are important. Understanding of VCI has evolved substantially in recent years, based on preclinical, neuropathologic, neuroimaging, physiological, and epidemiological studies. Transdisciplinary, translational, and transactional approaches are recommended to further our understanding of this entity and to better characterize its neuropsychological profile. There is a need for prospective, quantitative, clinical-pathological-neuroimaging studies to improve knowledge of the pathological basis of neuroimaging change and the complex interplay between vascular and Alzheimer disease pathologies in the evolution of clinical VCI and Alzheimer disease. Long-term vascular risk marker interventional studies beginning as early as midlife may be required to prevent or postpone the onset of VCI and Alzheimer disease. Studies of intensive reduction of vascular risk factors in high-risk groups are another important avenue of research.
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            Cerebral small vessel disease: from pathogenesis and clinical characteristics to therapeutic challenges.

            The term cerebral small vessel disease refers to a group of pathological processes with various aetiologies that affect the small arteries, arterioles, venules, and capillaries of the brain. Age-related and hypertension-related small vessel diseases and cerebral amyloid angiopathy are the most common forms. The consequences of small vessel disease on the brain parenchyma are mainly lesions located in the subcortical structures such as lacunar infarcts, white matter lesions, large haemorrhages, and microbleeds. Because lacunar infarcts and white matter lesions are easily detected by neuroimaging, whereas small vessels are not, the term small vessel disease is frequently used to describe the parenchyma lesions rather than the underlying small vessel alterations. This classification, however, restricts the definition of small vessel disease to ischaemic lesions and might be misleading. Small vessel disease has an important role in cerebrovascular disease and is a leading cause of cognitive decline and functional loss in the elderly. Small vessel disease should be a main target for preventive and treatment strategies, but all types of presentation and complications should be taken into account. Copyright 2010 Elsevier Ltd. All rights reserved.
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              Is Open Access

              The clinical importance of white matter hyperintensities on brain magnetic resonance imaging: systematic review and meta-analysis

              Objectives To review the evidence for an association of white matter hyperintensities with risk of stroke, cognitive decline, dementia, and death. Design Systematic review and meta-analysis. Data sources PubMed from 1966 to 23 November 2009. Study selection Prospective longitudinal studies that used magnetic resonance imaging and assessed the impact of white matter hyperintensities on risk of incident stroke, cognitive decline, dementia, and death, and, for the meta-analysis, studies that provided risk estimates for a categorical measure of white matter hyperintensities, assessing the impact of these lesions on risk of stroke, dementia, and death. Data extraction Population studied, duration of follow-up, method used to measure white matter hyperintensities, definition of the outcome, and measure of the association of white matter hyperintensities with the outcome. Data synthesis 46 longitudinal studies evaluated the association of white matter hyperintensities with risk of stroke (n=12), cognitive decline (n=19), dementia (n=17), and death (n=10). 22 studies could be included in a meta-analysis (nine of stroke, nine of dementia, eight of death). White matter hyperintensities were associated with an increased risk of stroke (hazard ratio 3.3, 95% confidence interval 2.6 to 4.4), dementia (1.9, 1.3 to 2.8), and death (2.0, 1.6 to 2.7). An association of white matter hyperintensities with a faster decline in global cognitive performance, executive function, and processing speed was also suggested. Conclusion White matter hyperintensities predict an increased risk of stroke, dementia, and death. Therefore white matter hyperintensities indicate an increased risk of cerebrovascular events when identified as part of diagnostic investigations, and support their use as an intermediate marker in a research setting. Their discovery should prompt detailed screening for risk factors of stroke and dementia.

                Author and article information

                Lancet Neurol
                Lancet Neurol
                Lancet Neurology
                Lancet Pub. Group
                1 August 2013
                August 2013
                : 12
                : 8
                : 822-838
                Neuroimaging Sciences, University of Edinburgh, Edinburgh, UK
                Centre for Clinical Brain Sciences, University of Edinburgh, Edinburgh, UK
                Centre for Cognitive Ageing and Cognitive Epidemiology, University of Edinburgh, Edinburgh, UK
                Brain Research Imaging Centre, University of Edinburgh, Edinburgh, UK
                Departments of Clinical Neurosciences and Radiology, Hotchkiss Brain Institute, University of Calgary and Seaman Family MR Research Centre, Calgary, AL, Canada
                Department of Neurology, Rudolf Magnus Institute of Neuroscience, UMC Utrecht, Utrecht, Netherlands
                Department of Neurology, Lille University Hospital, Lille, France
                Department of Neurology, Medical University of Graz, Graz, Austria
                University of Sydney and George Institute for Global Health, Westmead Hospital, University of Sydney, Sydney, NSW, Australia
                Department of Psychiatry, University of Cambridge, Addenbrooke's Hospital, Cambridge, UK
                Department of Radiology and Nuclear Medicine, VU University Medical Centre, Amsterdam, Netherlands
                Department of Medicine, Division of Neurology, Brain Research Centre, University of British Columbia, Vancouver, BC, Canada
                Sunnybrook Health Sciences Centre, Toronto, ON, Canada
                Cambridge Institute of Public Health, School of Clinical Medicine, Cambridge, UK
                German Center for Neurodegenerative diseases, Bonn, Germany
                Service de Neurologie, Hopital Lariboisiere, INSERM, Université Denis Diderot, Paris, France
                Department of Neurology, University of California at Davis, Sacramento, CA, USA
                Department of Neurology, Radboud University Nijmegen Medical Centre, Donders Institute for Brain, Cognition and Behaviour, Nijmegen, Netherlands
                Institute for Stroke and Dementia Research, Klinikum der Universität München, Ludwig-Maximilians-Universität, Munich, Germany
                Department of Neurodegeneration, Dementia Research Centre, Institute of Neurology, University College London, London, UK
                Stroke Research Group, Department of Brain Repair and Rehabilitation, Institute of Neurology, University College London, London, UK
                Massachusetts General Hospital, Stroke Research Center, Boston, MA, USA
                Department of Clinical Neurological Sciences, Western University, London, ON, Canada
                German Center for Neurodegenerative Diseases (DZNE) Rostock and Greifswald, Rostock, Germany
                Division of Neurology, Department of Medicine and Therapeutics, Prince of Wales Hospital, Chinese University of Hong Kong, Hong Kong Special Administrative Region, China
                Department of Neurology, School of Mental Health and Neuroscience, and Cardiovascular Research Institute Maastricht, Maastricht University Medical Center, Maastricht, Netherlands
                Azienda Universitario Ospedaliera Careggi, Department of Neuroscience, Pharmacology and Child's Health (NEUROFARBA), University of Florence, Florence, Italy
                Department of Biomedical Magnetic Resonance, Faculty for Natural Sciences, Institute for Experimental Physics, Otto-von-Guericke UniversityMagdeburg, Magdeburg, Germany
                Newcastle University, Newcastle upon Tyne, UK
                Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore
                Department of Radiology, Leiden University Medical Center, Leiden, Netherlands
                Department of Clinical Sciences, Section of Neurology, Skåne University Hospital, Lund, Sweden
                Saint Mary's Health Care, Hauenstein Neuroscience Center, Grand Rapids, MI, USA
                Munich Cluster for Systems Neurology (SyNergy), Munich, Germany
                Author notes
                [* ]Correspondence to: Prof Joanna M Wardlaw, Division of Neuroimaging Sciences, University of Edinburgh, Western General Hospital, Edinburgh, EH4 2XU, UK joanna.wardlaw@
                [** ]Prof M Dichgans, Institute for Stroke and Dementia Research, Klinikum der Universität, Munich, Germany martin.dichgans@
                © 2013 Elsevier Ltd. All rights reserved.

                This document may be redistributed and reused, subject to certain conditions.

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