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      Association of Cerebral Small Vessel Disease Burden and Health-Related Quality of Life after Acute Ischemic Stroke

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          Abstract

          Objective: Cerebral small vessel disease (SVD) is associated with increased mortality, disability and cognitive decline, depression in stroke survivors. This study examined the association between SVD burden, defined by a combination of SVD markers, and health-related quality of life (HRQoL) in acute ischemic stroke.

          Methods: Patients admitted with acute ischemic stroke of any etiology were prospectively screened between January 2010 to December 2014 and enrolled in the study if they met study entry criteria. HRQoL was evaluated with the 12-item Stroke Specific Quality of Life (SSQoL) at 3 months after the onset of acute ischemic stroke. SVD was ascertained by the presence of any of the SVD markers including lacune, white matter hyperintensities (WMH), cerebral microbleeds (CMB) and enlarged perivascular spaces (EPVS) in the basal ganglia or their combinations on brain magnetic resonance imaging (MRI). The presence of each individual marker scored 1 point and was summed up to generate an ordinal “SVD score” (0–4) capturing total SVD burden. Linear regression was used to determine the associations between SVD burden and HRQoL.

          Results: Of the743 acute ischemic stroke patients that formed he study sample (mean age: 66.3 ± 10.6 years; 41.7% women), 49.3%, 22.5%, 16.0%, 9.2% and 3.1% had SVD scores of 0, 1, 2, 3 and 4, respectively. After adjusting for demographic, clinical and imaging variables, the SVD score was independently associated with lower overall score of SSQoL ( B = −1.39, SE = 0.56, p = 0.01), and its domains of mobility ( B = −0.41, SE = 0.10, p < 0.001) and vision ( B = −0.12, SE = 0.06, p = 0.03). Acute infract volume ( B = −1.44, SE = 0.54, p = 0.01), functional independence ( B = 5.69, SE = 0.34, p < 0.001) and anxious ( B = −1.13, SE = 0.23, p < 0.001) and depressive symptoms ( B = −3.41, SE = 0.22, p < 0.001) were also the significant predictors of the overall score of SSQoL.

          Conclusion: The brain’s SVD burden predicts lower HRQoL, predominantly in domains of mobility and vision at 3 months after acute ischemic stroke. The evaluation of SVD burden could facilitate developing individual treatment strategies.

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          Most cited references 29

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          MR signal abnormalities at 1.5 T in Alzheimer's dementia and normal aging.

          The type, frequency, and extent of MR signal abnormalities in Alzheimer's disease and normal aging are a subject of controversy. With a 1.5-MR unit we studied 12 Alzheimer patients, four subjects suffering from multiinfarct dementia and nine age-matched controls. Punctate or early confluent high-signal abnormalities in the deep white matter, noted in 60% of both Alzheimer patients and controls, were unrelated to the presence of hypertension or other vascular risk factors. A significant number of Alzheimer patients exhibited a more extensive smooth "halo" of periventricular hyperintensity when compared with controls (p = .024). Widespread deep white-matter hyperintensity (two patients) and extensive, irregular periventricular hyperintensity (three patients) were seen in multiinfarct dementia. Areas of high signal intensity affecting hippocampal and sylvian cortex were also present in five Alzheimer and two multiinfarct dementia patients, but absent in controls. Discrete, small foci of deep white-matter hyperintensity are not characteristic of Alzheimer's disease nor do they appear to imply a vascular cause for the dementing illness. The frequently observed "halo" of periventricular hyperintensity in Alzheimer's disease may be of diagnostic importance. High-signal abnormalities in specific cortical regions are likely to reflect disease processes localized to those structures.
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            Neuroimaging standards for research into small vessel disease and its contribution to ageing and neurodegeneration

            Summary 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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              Mechanisms of sporadic cerebral small vessel disease: insights from neuroimaging.

              The term cerebral small vessel disease (SVD) describes a range of neuroimaging, pathological, and associated clinical features. Clinical features range from none, to discrete focal neurological symptoms (eg, stroke), to insidious global neurological dysfunction and dementia. The burden on public health is substantial. The pathogenesis of SVD is largely unknown. Although the pathological processes leading to the arteriolar disease are associated with vascular risk factors and are believed to result from an intrinsic cerebral arteriolar occlusive disease, little is known about how these processes result in brain disease, how SVD lesions contribute to neurological or cognitive symptoms, and the association with risk factors. Pathology often shows end-stage disease, which makes identification of the earliest stages difficult. Neuroimaging provides considerable insights; although the small vessels are not easily seen themselves, the effects of their malfunction on the brain can be tracked with detailed brain imaging. We discuss potential mechanisms, detectable with neuroimaging, that might better fit the available evidence and provide testable hypotheses for future study. Copyright © 2013 Elsevier Ltd. All rights reserved.
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                Author and article information

                Affiliations
                1Department of Psychiatry, The Chinese University of Hong Kong , Hong Kong, China
                2Department of Neurology, Dongguan People’s Hospital , Dongguan, China
                3Department of Imaging and Interventional Radiology, The Chinese University of Hong Kong , Hong Kong, China
                4Department of Medicine and Therapeutics, The Chinese University of Hong Kong , Hong Kong, China
                5Australia/Marian Centre, University of Notre Dame , Perth, WA, Australia
                6Department of Rehabilitation, Sagamihara Minami Hospital , Sagamihara, Japan
                7Shenzhen Research Institute, The Chinese University of Hong Kong , Shenzhen, China
                Author notes

                Edited by: Philip P. Foster, University of Texas Health Science Center at Houston, United States

                Reviewed by: Lei Liu, University of Florida, United States; Hale Z. Toklu, University of Central Florida College of Medicine, United States; Susanne Asenbaum-Nan, NÖ Landesklinikenholding, Austria

                *Correspondence: Wai-Kwong Tang tangwk@ 123456cuhk.edu.hk
                Contributors
                Journal
                Front Aging Neurosci
                Front Aging Neurosci
                Front. Aging Neurosci.
                Frontiers in Aging Neuroscience
                Frontiers Media S.A.
                1663-4365
                13 November 2017
                2017
                : 9
                5693845 10.3389/fnagi.2017.00372
                Copyright © 2017 Liang, Chen, Deng, Mok, Wang, Ungvari, Chu, Kamiya and Tang.

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                Counts
                Figures: 1, Tables: 3, Equations: 0, References: 29, Pages: 7, Words: 5801
                Funding
                Funded by: National Natural Science Foundation of China 10.13039/501100001809
                Award ID: 81371460
                Categories
                Neuroscience
                Original Research

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