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      Longitudinal Progression of White Matter Hyperintensity Severity in Chronic Stroke Aphasia

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          Abstract

          Objective

          To determine whether longitudinal progression of small vessel disease in chronic stroke survivors is associated with longitudinal worsening of chronic aphasia severity.

          Design

          A longitudinal retrospective study. Severity of white matter hyperintensities (WMHs) as a marker for small vessel disease was assessed on fluid-attenuated inversion recovery (FLAIR) scans using the Fazekas scale, with ratings for deep WMHs (DWMHs) and periventricular WMHs (PVHs).

          Setting

          University research laboratories.

          Participants

          This study includes data from 49 chronic stroke survivors with aphasia (N=49; 15 women, 34 men, age range=32-81 years, >6 months post-stroke, stroke type: [46 ischemic, 3 hemorrhagic], community dwelling). All participants completed the Western Aphasia Battery-Revised (WAB) and had FLAIR scans at 2 timepoints (average years between timepoints: 1.87 years, SD=3.21 years).

          Interventions

          Not applicable.

          Main Outcome Measures

          Change in white matter hyperintensity severity (calculated using the Fazekas scale) and change in aphasia severity (difference in Western Aphasia Battery scores) were calculated between timepoints. Separate stepwise regression models were used to identify predictors of WMH severity change, with lesion volume, age, time between timepoints, body mass index (BMI), and presence of diabetes as independent variables. Additional stepwise regression models investigated predictors of change in aphasia severity, with PVH change, DWMH change, lesion volume, time between timepoints, and age as independent predictors.

          Results

          22.5% of participants (11/49) had increased WMH severity. Increased BMI was associated with increases in PVH severity ( P=.007), whereas the presence of diabetes was associated with increased DWMH severity ( P=.002). Twenty-five percent of participants had increased aphasia severity which was significantly associated with increased severity of PVH ( P<.001, 16.8% variance explained).

          Conclusion

          Increased small vessel disease burden is associated with contributing to chronic changes in aphasia severity. These findings support the idea that good cardiovascular risk factor control may play an important role in the prevention of long-term worsening of aphasic symptoms.

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          Most cited references79

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          Unified segmentation.

          A probabilistic framework is presented that enables image registration, tissue classification, and bias correction to be combined within the same generative model. A derivation of a log-likelihood objective function for the unified model is provided. The model is based on a mixture of Gaussians and is extended to incorporate a smooth intensity variation and nonlinear registration with tissue probability maps. A strategy for optimising the model parameters is described, along with the requisite partial derivatives of the objective function.
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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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              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

                Contributors
                Journal
                Arch Rehabil Res Clin Transl
                Arch Rehabil Res Clin Transl
                Archives of Rehabilitation Research and Clinical Translation
                Elsevier
                2590-1095
                05 October 2023
                December 2023
                05 October 2023
                : 5
                : 4
                : 100302
                Affiliations
                [a ]Department of Communication Sciences and Disorders, University of South Carolina, Columbia, SC
                [b ]Department of Psychology, University of South Carolina, Columbia, SC
                [c ]Department of Neurology, Medical University of South Carolina, Charleston, SC
                [d ]Department of Neurology, Emory University, Atlanta, GA
                Author notes
                [* ]Corresponding author Natalie Busby, 915 Greene Street, Columbia, SC 29209. hethern@ 123456mailbox.sc.edu
                Article
                S2590-1095(23)00064-2 100302
                10.1016/j.arrct.2023.100302
                10757197
                d0ab4c5b-793f-414d-93b1-d3ee649f91b9
                © 2023 The Authors

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                Categories
                Original Research

                aphasia,cardiovascular risk factors,rehabilitation,small vessel disease,stroke,white matter hyperintensities

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