Journal article
Smaller spared subcortical nuclei are associated with worse post-stroke sensorimotor outcomes in 28 cohorts worldwide
SL Liew, A Zavaliangos-Petropulu, N Schweighofer, N Jahanshad, CE Lang, KR Lohse, N Banaj, G Barisano, LA Baugh, AK Bhattacharya, B Bigjahan, MR Borich, LA Boyd, A Brodtmann, CM Buetefisch, WD Byblow, JM Cassidy, CC Charalambous, V Ciullo, AB Conforto Show all
Brain Communications | Published : 2021
Open access
Abstract
Up to two-thirds of stroke survivors experience persistent sensorimotor impairments. Recovery relies on the integrity of spared brain areas to compensate for damaged tissue. Deep grey matter structures play a critical role in the control and regulation of sensorimotor circuits. The goal of this work is to identify associations between volumes of spared subcortical nuclei and sensorimotor behaviour at different timepoints after stroke. We pooled high-resolution T1-weighted MRI brain scans and behavioural data in 828 individuals with unilateral stroke from 28 cohorts worldwide. Cross-sectional analyses using linear mixed-effects models related post-stroke sensorimotor behaviour to non-lesioned..
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Grants
Awarded by Natural Sciences and Engineering Research Council of Canada
Funding Acknowledgements
S.-L.L. was supported by National Institutes of Health (NIH) K01 HD091283; NIH R01 NS115845. N.S. was supported by NIH R56 NS100528. N.J. was supported by NIH R01 AG059874; NIH R01 MH117601. A.B. was supported by National Health and Medical Research Council of Australia GNT1020526; GNT1094974; Heart Foundation Future Leader Fellowship 100784. C.M.B was supported by NIH R21 HD067906; NIH R01 NS090677. W.D.B. was supported by the Health Research Council of New Zealand (09/164R; 14/136). J.M.C was supported by NIH R00 HD091375. A.B.C. was supported by NIH R01 NS076348; IIEP-2250-14. A.N.D. was supported by the Lone Star Stroke Research Consortium. N.E. was supported by Australian Research Council DE180100893. W.F. was supported by NIH P20 GM109040. C.A.H. was supported by NIH P20 GM109040. K.S.H. was supported by National Health and Medical Research Council of Australia #1088449; NIH R01 NS115845. B.H. was supported by National Health and Medical Research Council fellowship (1125054). S.A.K. was supported by VA1IK6RX003075; NIH P20 GM109040. B.K was supported by NIH R01 HD065438; NIH R56 NS100528. H.K. was supported by a BrightFocus Faculty Award. B.J.M. was supported by Canadian Partnership for Stroke Recovery; Canadian Institutes of Health Research; Natural Sciences and Engineering Research Council; Brain & Behavior Research Foundation. A.R.-M. was supported by Basque Government Elkartek MODULA; H2020-EIC-FETPROACT-2019 MAIA 951910, Bundesministerium fur Bildung und Forschung BMBF AMORSA (FKZ 16SV7754); and the FortuneProgram of the University of Tubingen (2452-0-0/1). F.P. was supported by the Italian Ministry of Health, Grants RC 2016, 2017, 2018, 2019. K.P.R. was supported by NIH R21 HD067906; NIH R01 NS090677. H.M.S. was supported by NIH R01 NS110696; NIH R01 LM013316; NIH K02 NS104207. N.J.S. was supported by NIH U54 GM104941; NIH P20 GM109040. S.R.S. was supported by the European Research Council (ERC, Grant number 759370). G.S. was supported by Italian Ministry of Health grant RC 15-16-17-18-19-20/A. C.M.S was supported by the Health Research Council of New Zealand. L.T.W. was supported by the South-Eastern Norway Regional Health Authority (2014097, 2015044, 2015073); the Norwegian ExtraFoundation for Health and Rehabilitation (2015/FO5146); the Research Council of Norway (249795, 262372); and the European Research Council under the European Union's Horizon 2020 Research and Innovation program (ERC StG, Grant 802998). G.F.W. was supported by the Department of Veterans Affairs RR&D Program. S.L.W. was supported by NIH R01 NS115845, R01HD095975. S.C.C. was supported by NIH U01 NS086872, R01 NR015591, and R01 HD095457. P.M.T. was supported by NIH U54 EB020403.