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 Feng; Kelene 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

doi:10.1161/JAHA.121.025109

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 Feng

Kelene 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

Tecnologías médicas

University of Southern California
Washington University St. Louis
IRCCS Fondazione Santa Lucia - Roma
Emory University
University of British Columbia
The University of Auckland
University of North Carolina at Chapel Hill
University of Nicosia Medical School
Center for Neuroscience and Integrative Brain Research (CENIBRE)
Universidade de São Paulo
Hospital Israelita Albert Einstein
Massachusetts General Hospital
University of Texas at Austin
University of Melbourne
University of South Dakota
Federal Aviation Administration
Imperial College London
Wake Forest University
Florey Institute of Neuroscience and Mental Health
University of South Australia
Department of Veterans Affairs
Medical University of South Carolina
Cornell University
Tianjin Medical University
University of Greifswald
Sunnybrook Health Sciences Centre
University of Toronto
Thomas Jefferson University
University of Tübingen
Cedars-Sinai Medical Center
University of Waterloo
New York University
Charité – Universitätsmedizin Berlin
Chinese University of Hong Kong
University of Sciences in Philadelphia
University College London
University of Oslo
University of Pittsburgh
VA Medical Center
University of California at Los Angeles
California Rehabilitation Hospital

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10 Citas (Scopus)

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 original	Inglés
Número de artículo	e025109
Publicación	Journal of the American Heart Association
Volumen	11
N.º	10
DOI	https://doi.org/10.1161/JAHA.121.025109
Estado	Publicada - 17 may 2022

ODS de las Naciones Unidas

Este resultado contribuye a los siguientes Objetivos de Desarrollo Sostenible

ODS 3: Salud y bienestar

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Sensorimotor impairment

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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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Zavaliangos‐Petropulu, A., Lo, B., Donnelly, M. R., Schweighofer, N., Lohse, K., Jahanshad, N., Barisano, G., Banaj, N., Borich, M. R., Boyd, L. A., Buetefisch, C. M., Byblow, W. D., Cassidy, J. M., Charalambous, C. C., Conforto, A. B., DiCarlo, J. A., Dula, A. N., Egorova‐Brumley, N., Etherton, M. R., ... Ramos-Murguialday, A. (2022). Chronic Stroke Sensorimotor Impairment Is Related to Smaller Hippocampal Volumes: An ENIGMA Analysis: An ENIGMA Analysis. Journal of the American Heart Association, 11(10), Artículo e025109. https://doi.org/10.1161/JAHA.121.025109

@article{55e38d1899bf476797eefe7b492a734c,

title = "Chronic Stroke Sensorimotor Impairment Is Related to Smaller Hippocampal Volumes: An ENIGMA Analysis: An ENIGMA Analysis",

abstract = "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.",

keywords = "Sensorimotor impairment, Sensorimotor impairment, Hippocampus, MRI, Stroke",

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

note = "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 P20 GM109040. F.G. is supported by Wellcome Trust (093957). B.H. is funded by and NHMRC fellowship (1125054). S.A.K is supported by NIH P20 HD109040. F.B. is supported by Italian Ministry of Health, RC 20, 21. N.S. is supported by NIH R21NS120274. N.J.S. is supported by NIH/National Institute of General Medical Sciences (NIGMS) 2P20GM109040-06, U54-GM104941. S.R.S. is supported by European Research Council (ERC) (NGBMI, 759370). G.S. is supported by Italian Ministry of Health RC 18-19-20-21A. M.T. is sup ported by National Institute of Neurological Disorders and Stroke (NINDS) R01 NS110696. G.T.T. is supported by Temple University sub-award of NIH R24 –NHLBI (Dr Mickey Selzer) Center for Experimental Neurorehabilitation Training. N.J.S. is funded by NIH/National Institute of Child Health and Human Development (NICHD) 1R01HD094731-01A1.",

year = "2022",

month = may,

day = "17",

doi = "10.1161/JAHA.121.025109",

language = "English",

volume = "11",

journal = "Journal of the American Heart Association",

issn = "2047-9980",

publisher = "Wiley-Blackwell Publishing Ltd",

number = "10",

}

Zavaliangos‐Petropulu, A, Lo, B, Donnelly, MR, Schweighofer, N, Lohse, K, Jahanshad, N, Barisano, G, Banaj, N, Borich, MR, Boyd, LA, Buetefisch, CM, Byblow, WD, Cassidy, JM, Charalambous, CC, Conforto, AB, DiCarlo, JA, Dula, AN, Egorova‐Brumley, N, Etherton, MR, Feng, W, Fercho, KA, Geranmayeh, F, Hanlon, CA, Hayward, KS, Hordacre, B, Kautz, SA, Khlif, MS, Kim, H, Kuceyeski, A, Lin, DJ, Liu, J, Lotze, M, MacIntosh, BJ, Margetis, JL, Mohamed, FB, Piras, F, Ramos‐Murguialday, A, Revill, KP, Roberts, PS, Robertson, AD, Schambra, HM, Seo, NJ, Shiroishi, MS, Stinear, CM, Soekadar, SR, Spalletta, G, Taga, M, Tang, WK, Thielman, GT, Vecchio, D, Ward, NS, Westlye, LT, Werden, E, Winstein, C, Wittenberg, GF, Wolf, SL, Wong, KA, Yu, C, Brodtmann, A, Cramer, SC, Thompson, PM, Liew, SL, Zavaliangos-Petropulu, A, Egorova-Brumley, N & Ramos-Murguialday, A 2022, 'Chronic Stroke Sensorimotor Impairment Is Related to Smaller Hippocampal Volumes: An ENIGMA Analysis: An ENIGMA Analysis', Journal of the American Heart Association, vol. 11, n.º 10, e025109. https://doi.org/10.1161/JAHA.121.025109

Chronic Stroke Sensorimotor Impairment Is Related to Smaller Hippocampal Volumes: An ENIGMA Analysis: An ENIGMA Analysis. / Zavaliangos‐Petropulu, Artemis; Lo, Bethany; Donnelly, Miranda R. et al.
En: Journal of the American Heart Association, Vol. 11, N.º 10, e025109, 17.05.2022.

Producción científica: Contribución a una revista › Artículo › revisión exhaustiva

TY - JOUR

T1 - Chronic Stroke Sensorimotor Impairment Is Related to Smaller Hippocampal Volumes: An ENIGMA Analysis

T2 - An ENIGMA Analysis

AU - Zavaliangos‐Petropulu, Artemis

AU - Lo, Bethany

AU - Donnelly, Miranda R.

AU - Schweighofer, Nicolas

AU - Lohse, Keith

AU - Jahanshad, Neda

AU - Barisano, Giuseppe

AU - Banaj, Nerisa

AU - Borich, Michael R.

AU - Boyd, Lara A.

AU - Buetefisch, Cathrin M.

AU - Byblow, Winston D.

AU - Cassidy, Jessica M.

AU - Charalambous, Charalambos C.

AU - Conforto, Adriana B.

AU - DiCarlo, Julie A.

AU - Dula, Adrienne N.

AU - Egorova‐Brumley, Natalia

AU - Etherton, Mark R.

AU - Feng, Wuwei

AU - Fercho, Kelene A.

AU - Geranmayeh, Fatemeh

AU - Hanlon, Colleen A.

AU - Hayward, Kathryn S.

AU - Hordacre, Brenton

AU - Kautz, Steven A.

AU - Khlif, Mohamed Salah

AU - Kim, Hosung

AU - Kuceyeski, Amy

AU - Lin, David J.

AU - Liu, Jingchun

AU - Lotze, Martin

AU - MacIntosh, Bradley J.

AU - Margetis, John L.

AU - Mohamed, Feroze B.

AU - Piras, Fabrizio

AU - Ramos‐Murguialday, Ander

AU - Revill, Kate P.

AU - Roberts, Pamela S.

AU - Robertson, Andrew D.

AU - Schambra, Heidi M.

AU - Seo, Na Jin

AU - Shiroishi, Mark S.

AU - Stinear, Cathy M.

AU - Soekadar, Surjo R.

AU - Spalletta, Gianfranco

AU - Taga, Myriam

AU - Tang, Wai Kwong

AU - Thielman, Gregory T.

AU - Vecchio, Daniela

AU - Ward, Nick S.

AU - Westlye, Lars T.

AU - Werden, Emilio

AU - Winstein, Carolee

AU - Wittenberg, George F.

AU - Wolf, Steven L.

AU - Wong, Kristin A.

AU - Yu, Chunshui

AU - Brodtmann, Amy

AU - Cramer, Steven C.

AU - Thompson, Paul M.

AU - Liew, Sook‐Lei

AU - Zavaliangos-Petropulu, Artemis

AU - Egorova-Brumley, Natalia

AU - Ramos-Murguialday, Ander

N1 - 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 P20 GM109040. F.G. is supported by Wellcome Trust (093957). B.H. is funded by and NHMRC fellowship (1125054). S.A.K is supported by NIH P20 HD109040. F.B. is supported by Italian Ministry of Health, RC 20, 21. N.S. is supported by NIH R21NS120274. N.J.S. is supported by NIH/National Institute of General Medical Sciences (NIGMS) 2P20GM109040-06, U54-GM104941. S.R.S. is supported by European Research Council (ERC) (NGBMI, 759370). G.S. is supported by Italian Ministry of Health RC 18-19-20-21A. M.T. is sup ported by National Institute of Neurological Disorders and Stroke (NINDS) R01 NS110696. G.T.T. is supported by Temple University sub-award of NIH R24 –NHLBI (Dr Mickey Selzer) Center for Experimental Neurorehabilitation Training. N.J.S. is funded by NIH/National Institute of Child Health and Human Development (NICHD) 1R01HD094731-01A1.

PY - 2022/5/17

Y1 - 2022/5/17

N2 - 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.

AB - 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.

KW - Sensorimotor impairment

KW - Hippocampus

KW - MRI

KW - Stroke

UR - https://www.scopus.com/pages/publications/85130644416

U2 - 10.1161/JAHA.121.025109

DO - 10.1161/JAHA.121.025109

M3 - Article

C2 - 35574963

SN - 2047-9980

VL - 11

JO - Journal of the American Heart Association

JF - Journal of the American Heart Association

IS - 10

M1 - e025109

ER -

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

Resumen

ODS de las Naciones Unidas

Palabras clave

Project and Funding Information

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