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| Fältnamn | Indikatorer | Metadata |
|---|---|---|
| 000 | 06698naa a2201021 4500 | |
| 001 | oai:gup.ub.gu.se/322134 | |
| 003 | SwePub | |
| 008 | 240528s2022 | |||||||||||000 ||eng| | |
| 024 | 7 | a https://gup.ub.gu.se/publication/3221342 URI |
| 024 | 7 | a https://doi.org/10.1212/wnl.00000000002009262 DOI |
| 040 | a (SwePub)gu | |
| 041 | a eng | |
| 042 | 9 SwePub | |
| 072 | 7 | a ref2 swepub-contenttype |
| 072 | 7 | a art2 swepub-publicationtype |
| 100 | 1 | a Bonkhoff, A. K.4 aut |
| 245 | 1 0 | a Association of Stroke Lesion Pattern and White Matter Hyperintensity Burden With Stroke Severity and Outcome |
| 264 | c 2022-07-08 | |
| 264 | 1 | b Ovid Technologies (Wolters Kluwer Health),c 2022 |
| 520 | a Background and Objectives To examine whether high white matter hyperintensity (WMH) burden is associated with greater stroke severity and worse functional outcomes in lesion pattern-specific ways. Methods MR neuroimaging and NIH Stroke Scale data at index stroke and the modified Rankin Scale (mRS) score at 3-6 months after stroke were obtained from the MRI-Genetics Interface Exploration study of patients with acute ischemic stroke (AIS). Individual WMH volume was automatically derived from fluid-attenuated inversion recovery images. Stroke lesions were automatically segmented from diffusion-weighted imaging (DWI) images, parcellated into atlas-defined brain regions and further condensed to 10 lesion patterns via machine learning-based dimensionality reduction. Stroke lesion effects on AIS severity and unfavorable outcomes (mRS score >2) were modeled within purpose-built Bayesian linear and logistic regression frameworks. Interaction effects between stroke lesions and a high vs lowWMHburden were integrated via hierarchical model structures. Models were adjusted for age, age2, sex, total DWI lesion and WMH volumes, and comorbidities. Data were split into derivation and validation cohorts. Results A total of 928 patients with AIS contributed to acute stroke severity analyses (age: 64.8 [14.5] years, 40% women) and 698 patients to long-term functional outcome analyses (age: 65.9 [14.7] years, 41% women). Stroke severity was mainly explained by lesions focused on bilateral subcortical and left hemispherically pronounced cortical regions across patients with both a high and low WMH burden. Lesions centered on left-hemispheric insular, opercular, and inferior frontal regions and lesions affecting right-hemispheric temporoparietal regions had more pronounced effects on stroke severity in case of high compared with low WMH burden. Unfavorable outcomes were predominantly explained by lesions in bilateral subcortical regions. In difference to the lesion location-specific WMH effects on stroke severity, higher WMH burden increased the odds of unfavorable outcomes independent of lesion location. Discussion Higher WMH burden may be associated with an increased stroke severity in case of stroke lesions involving left-hemispheric insular, opercular, and inferior frontal regions (potentially linked to language functions) and right-hemispheric temporoparietal regions (potentially linked to attention). Our findings suggest that patients with specific constellations of WMH burden and lesion locations may have greater benefits from acute recanalization treatments. Future clinical studies are warranted to systematically assess this assumption and guide more tailored treatment decisions. | |
| 650 | 7 | a MEDICIN OCH HÄLSOVETENSKAPx Klinisk medicinx Neurologi0 (SwePub)302072 hsv//swe |
| 650 | 7 | a MEDICAL AND HEALTH SCIENCESx Clinical Medicinex Neurology0 (SwePub)302072 hsv//eng |
| 653 | a network | |
| 653 | a topography | |
| 653 | a genetics | |
| 653 | a neglect | |
| 653 | a mri | |
| 653 | a Neurosciences & Neurology | |
| 700 | 1 | a Hong, S. M.4 aut |
| 700 | 1 | a Bretzner, M.4 aut |
| 700 | 1 | a Schirmer, M. D.4 aut |
| 700 | 1 | a Regenhardt, R. W.4 aut |
| 700 | 1 | a Arsava, E. M.4 aut |
| 700 | 1 | a Donahue, K.4 aut |
| 700 | 1 | a Nardin, M.4 aut |
| 700 | 1 | a Dalca, A.4 aut |
| 700 | 1 | a Giese, A. K.4 aut |
| 700 | 1 | a Etherton, M. R.4 aut |
| 700 | 1 | a Hancock, B. L.4 aut |
| 700 | 1 | a Mocking, S. J. T.4 aut |
| 700 | 1 | a McIntosh, E.4 aut |
| 700 | 1 | a Attia, J.4 aut |
| 700 | 1 | a Benavente, O.4 aut |
| 700 | 1 | a Cole, J. W.4 aut |
| 700 | 1 | a Donatti, A.4 aut |
| 700 | 1 | a Griessenauer, C.4 aut |
| 700 | 1 | a Heitsch, L.4 aut |
| 700 | 1 | a Holmegaard, Lukasu Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi, sektionen för klinisk neurovetenskap,Institute of Neuroscience and Physiology, Department of Clinical Neuroscience4 aut0 (Swepub:gu)xhollu |
| 700 | 1 | a Jood, Katarina,d 1966u Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi, sektionen för klinisk neurovetenskap,Institute of Neuroscience and Physiology, Department of Clinical Neuroscience4 aut0 (Swepub:gu)xjooka |
| 700 | 1 | a Jimenez-Conde, J.4 aut |
| 700 | 1 | a Kittner, S.4 aut |
| 700 | 1 | a Lemmens, R.4 aut |
| 700 | 1 | a Levi, C.4 aut |
| 700 | 1 | a McDonough, C. W.4 aut |
| 700 | 1 | a Meschia, J.4 aut |
| 700 | 1 | a Phuah, C. L.4 aut |
| 700 | 1 | a Rolfs, A.4 aut |
| 700 | 1 | a Ropele, S.4 aut |
| 700 | 1 | a Rosand, J.4 aut |
| 700 | 1 | a Roquer, J.4 aut |
| 700 | 1 | a Rundek, T.4 aut |
| 700 | 1 | a Sacco, R. L.4 aut |
| 700 | 1 | a Schmidt, R.4 aut |
| 700 | 1 | a Sharma, P.4 aut |
| 700 | 1 | a Slowik, A.4 aut |
| 700 | 1 | a Soederholm, M.4 aut |
| 700 | 1 | a Sousa, A.4 aut |
| 700 | 1 | a Stanne, T. M.4 aut |
| 700 | 1 | a Strbian, D.4 aut |
| 700 | 1 | a Tatlisumak, Turgutu Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi, sektionen för klinisk neurovetenskap,Institute of Neuroscience and Physiology, Department of Clinical Neuroscience4 aut0 (Swepub:gu)xtatlt |
| 700 | 1 | a Thijs, V.4 aut |
| 700 | 1 | a Vagal, A.4 aut |
| 700 | 1 | a Wasselius, J.4 aut |
| 700 | 1 | a Woo, D.4 aut |
| 700 | 1 | a Zand, R.4 aut |
| 700 | 1 | a McArdle, P.4 aut |
| 700 | 1 | a Worrall, B. B.4 aut |
| 700 | 1 | a Jern, C.4 aut |
| 700 | 1 | a Lindgren, A. G.4 aut |
| 700 | 1 | a Maguire, J.4 aut |
| 700 | 1 | a Golland, P.4 aut |
| 700 | 1 | a Bzdok, D.4 aut |
| 700 | 1 | a Wu, O.4 aut |
| 700 | 1 | a Rost, N. S.4 aut |
| 710 | 2 | a Göteborgs universitetb Institutionen för neurovetenskap och fysiologi, sektionen för klinisk neurovetenskap4 org |
| 773 | 0 | t NEUROLOGYd : Ovid Technologies (Wolters Kluwer Health)g 99:13q 99:13x 0028-3878x 1526-632X |
| 856 | 4 8 | u https://gup.ub.gu.se/publication/322134 |
| 856 | 4 8 | u https://doi.org/10.1212/wnl.0000000000200926 |
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