Chronic Stroke Sensorimotor Impairment Is Related to Smaller Hippocampal Volumes: An ENIGMA Analysis: An ENIGMA Analysis

Artemis Zavaliangos‐Petropulu, Bethany Lo, Miranda R. Donnelly, Nicolas Schweighofer, Keith Lohse, Neda Jahanshad, Giuseppe Barisano, Nerisa Banaj, Michael R. Borich, Lara A. Boyd, Cathrin M. Buetefisch, Winston D. Byblow, Jessica M. Cassidy, Charalambos C. Charalambous, Adriana B. Conforto, Julie A. DiCarlo, Adrienne N. Dula, Natalia Egorova‐Brumley, Mark R. Etherton, Wuwei FengKelene A. Fercho, Fatemeh Geranmayeh, Colleen A. Hanlon, Kathryn S. Hayward, Brenton Hordacre, Steven A. Kautz, Mohamed Salah Khlif, Hosung Kim, Amy Kuceyeski, David J. Lin, Jingchun Liu, Martin Lotze, Bradley J. MacIntosh, John L. Margetis, Feroze B. Mohamed, Fabrizio Piras, Ander Ramos‐Murguialday, Kate P. Revill, Pamela S. Roberts, Andrew D. Robertson, Heidi M. Schambra, Na Jin Seo, Mark S. Shiroishi, Cathy M. Stinear, Surjo R. Soekadar, Gianfranco Spalletta, Myriam Taga, Wai Kwong Tang, Gregory T. Thielman, Daniela Vecchio, Nick S. Ward, Lars T. Westlye, Emilio Werden, Carolee Winstein, George F. Wittenberg, Steven L. Wolf, Kristin A. Wong, Chunshui Yu, Amy Brodtmann, Steven C. Cramer, Paul M. Thompson, Sook‐Lei Liew, Artemis Zavaliangos-Petropulu, Natalia Egorova-Brumley, Ander Ramos-Murguialday

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Resumen

Background. Persistent sensorimotor impairments after stroke can negatively impact quality of life. The hippocampus is vulnerable to poststroke secondary degeneration and is involved in sensorimotor behavior but has not been widely studied within the context of poststroke upper‐limb sensorimotor impairment. We investigated associations between non‐lesioned hippocampal volume and upper limb sensorimotor impairment in people with chronic stroke, hypothesizing that smaller ipsilesional hippocampal volumes would be associated with greater sensorimotor impairment. Methods and Results. Cross‐sectional T1‐weighted magnetic resonance images of the brain were pooled from 357 participants with chronic stroke from 18 research cohorts of the ENIGMA (Enhancing NeuoImaging Genetics through Meta‐Analysis) Stroke Recovery Working Group. Sensorimotor impairment was estimated from the FMA‐UE (Fugl‐Meyer Assessment of Upper Extremity). Robust mixed‐effects linear models were used to test associations between poststroke sensorimotor impairment and hippocampal volumes (ipsilesional and contralesional separately; Bonferroni‐corrected, P<0.025), controlling for age, sex, lesion volume, and lesioned hemisphere. In exploratory analyses, we tested for a sensorimotor impairment and sex interaction and relationships between lesion volume, sensorimotor damage, and hippocampal volume. Greater sensorimotor impairment was significantly associated with ipsilesional (P=0.005; β=0.16) but not contralesional (P=0.96; β=0.003) hippocampal volume, independent of lesion volume and other covariates (P=0.001; β=0.26). Women showed progressively worsening sensorimotor impairment with smaller ipsilesional (P=0.008; β=−0.26) and contralesional (P=0.006; β=−0.27) hippocampal volumes compared with men. Hippocampal volume was associated with lesion size (P<0.001; β=−0.21) and extent of sensorimotor damage (P=0.003; β=−0.15). Conclusions. The present study identifies novel associations between chronic poststroke sensorimotor impairment and ipsilesional hippocampal volume that are not caused by lesion size and may be stronger in women.
Idioma originalInglés
Número de artículoe025109
PublicaciónJournal of the American Heart Association
Volumen11
N.º10
DOI
EstadoPublicada - 17 may 2022

Palabras clave

  • Sensorimotor impairment

Project and Funding Information

  • Funding Info
  • S.-L.L. is supported by NIH K01 HD091283; NIH R01 NS115845. A.B. and M.S.K. are supported by National Health and Medical Research Council (NHMRC) GNT1020526, GNT1045617 (A.B.), GNT1094974, and Heart Foundation Future Leader Fellowship 100784 (A.B.). P.M.T. is supported by NIH U54 EB020403. L.A.B. is supported by the Canadian Institutes of Health Research (CIHR). C.M.B. is supported by NIH R21 HD067906. W.D.B. is supported by the Heath Research Council of New Zealand. J.M.C. is supported by NIH R00HD091375. A.B.C. is supported by NIH R01NS076348-01, Hospital Israelita Albert Einstein 2250-14, CNPq/305568/2016-7. A.N.D. is supported by funding provided by the Texas Legislature to the Lone Star Stroke Clinical Trial Network. Its contents are solely the responsibility of the authors and do not necessarily represent the of ficial views of the Government of the United States or the State of Texas. N.E.-B. is supported by Australian Research Council NIH DE180100893. W.F. is sup ported by NIH

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