http://journals.sagepub.com/doi/abs/10.1177/1545968318779731
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Karin L. de Gooijer-van de Groep, MSc1
, Jurriaan H. de Groot, PhD1
, Hanneke van der Krogt, MD1
, , ,
1Leiden University Medical Center, Leiden, The Netherlands
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1Leiden University Medical Center, Leiden, The Netherlands
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1Leiden University Medical Center, Leiden, The Netherlands
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Erwin de Vlugt, PhD2
, J. Hans Arendzen, MD, PhD1
, Carel G. M. Meskers, MD, PhD34
, Karin L. de Gooijer-van de Groep, MSc1
, Jurriaan H. de Groot, PhD1
, Hanneke van der Krogt, MD1
, Erwin de Vlugt, PhD2
, J. Hans Arendzen, MD, PhD1
, Carel G. M. Meskers, MD, PhD34
...
2Delft University of Technology, Delft, Netherlands
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1Leiden University Medical Center, Leiden, The Netherlands
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3VU Medical Center, Amsterdam, Netherlands4Amsterdam Movement Sciences, Amsterdam, The Netherlands
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1Leiden University Medical Center, Leiden, The Netherlands
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1Leiden University Medical Center, Leiden, The Netherlands
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1Leiden University Medical Center, Leiden, The Netherlands
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2Delft University of Technology, Delft, Netherlands
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1Leiden University Medical Center, Leiden, The Netherlands
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3VU Medical Center, Amsterdam, Netherlands4Amsterdam Movement Sciences, Amsterdam, The Netherlands
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Article Information
Article first published online: June 25, 2018
https://doi.org/10.1177/1545968318779731
Karin L. de Gooijer-van de Groep, MSc1, Jurriaan H. de Groot, PhD1, Hanneke van der Krogt, MD1, Erwin de Vlugt, PhD2, J. Hans Arendzen, MD, PhD1, Carel G. M. Meskers, MD, PhD3, 4
1Leiden University Medical Center, Leiden, The Netherlands
2Delft University of Technology, Delft, Netherlands
3VU Medical Center, Amsterdam, Netherlands
4Amsterdam Movement Sciences, Amsterdam, The Netherlands
Corresponding Author: Karin L. de Gooijer-van de Groep, Department of Rehabilitation Medicine, Leiden University Medical Center, Postzone B0-Q, P.O. Box 9600, 2300 RC Leiden, the Netherlands. Email: k. l. de_gooijer-van_de_groep@lumc. nl
This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (http://www.creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage).
Abstract
Background. The mechanism and time course of increased wrist joint stiffness poststroke and clinically observed wrist flexion deformity is still not well understood. The components contributing to increased joint stiffness are of neural reflexive and peripheral tissue origin and quantified by reflexive torque and muscle slack length and stiffness coefficient parameters.
Objective. To investigate the time course of the components contributing to wrist joint stiffness during the first 26 weeks poststroke in a group of patients, stratified by prognosis and functional recovery of the upper extremity.
Methods. A total of 36 stroke patients were measured on 8 occasions within the first 26 weeks poststroke using ramp-and-hold rotations applied to the wrist joint by a robot manipulator. Neural reflexive and peripheral tissue components were estimated using an electromyography-driven antagonistic wrist model. Outcome was compared between groups cross-sectionally at 26 weeks poststroke and development over time was analyzed longitudinally.
Results. At 26 weeks poststroke, patients with poor recovery (Action Research Arm Test [ARAT] ≤9 points) showed a higher predicted reflexive torque of the flexors (P < .001) and reduced predicted slack length (P < .001) indicating shortened muscles contributing to higher peripheral tissue stiffness (P < .001), compared with patients with good recovery (ARAT ≥10 points). Significant differences in peripheral tissue stiffness between groups could be identified around weeks 4 and 5; for neural reflexive stiffness, this was the case around week 12.
Conclusions. We found onset of peripheral tissue stiffness to precede neural reflexive stiffness. Temporal identification of components contributing to joint stiffness after stroke may prompt longitudinal interventional studies to further evaluate and eventually prevent these phenomena.
Objective. To investigate the time course of the components contributing to wrist joint stiffness during the first 26 weeks poststroke in a group of patients, stratified by prognosis and functional recovery of the upper extremity.
Methods. A total of 36 stroke patients were measured on 8 occasions within the first 26 weeks poststroke using ramp-and-hold rotations applied to the wrist joint by a robot manipulator. Neural reflexive and peripheral tissue components were estimated using an electromyography-driven antagonistic wrist model. Outcome was compared between groups cross-sectionally at 26 weeks poststroke and development over time was analyzed longitudinally.
Results. At 26 weeks poststroke, patients with poor recovery (Action Research Arm Test [ARAT] ≤9 points) showed a higher predicted reflexive torque of the flexors (P < .001) and reduced predicted slack length (P < .001) indicating shortened muscles contributing to higher peripheral tissue stiffness (P < .001), compared with patients with good recovery (ARAT ≥10 points). Significant differences in peripheral tissue stiffness between groups could be identified around weeks 4 and 5; for neural reflexive stiffness, this was the case around week 12.
Conclusions. We found onset of peripheral tissue stiffness to precede neural reflexive stiffness. Temporal identification of components contributing to joint stiffness after stroke may prompt longitudinal interventional studies to further evaluate and eventually prevent these phenomena.
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