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Resting state neurophysiology of agonist-antagonist myoneural interface in persons with transtibial amputation

The agonist-antagonist myoneural interface (AMI) is a novel amputation surgery that preserves sensorimotor signaling mechanisms of the central-peripheral nervous systems. Our first neuroimaging study investigating AMI subjects (Srinivasan et al., Sci. Transl. Med. 2020) focused on task-based neural...

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Autores principales: Chicos, Laura, Rangaprakash, D., Barry, Robert, Herr, Hugh
Formato: Online Artículo Texto
Lenguaje:English
Publicado: American Journal Experts 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9934762/
https://www.ncbi.nlm.nih.gov/pubmed/36798194
http://dx.doi.org/10.21203/rs.3.rs-2362961/v1
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author Chicos, Laura
Rangaprakash, D.
Barry, Robert
Herr, Hugh
author_facet Chicos, Laura
Rangaprakash, D.
Barry, Robert
Herr, Hugh
author_sort Chicos, Laura
collection PubMed
description The agonist-antagonist myoneural interface (AMI) is a novel amputation surgery that preserves sensorimotor signaling mechanisms of the central-peripheral nervous systems. Our first neuroimaging study investigating AMI subjects (Srinivasan et al., Sci. Transl. Med. 2020) focused on task-based neural signatures, and showed evidence of proprioceptive feedback to the central nervous system. The study of resting state neural activity helps non-invasively characterize the neural patterns that prime task response. In this first study on resting state fMRI in AMI subjects, we compared resting state functional connectivity in patients with transtibial AMI (n=12) and traditional (n=7) amputations, as well as biologically intact control subjects (n=10). We hypothesized that the AMI surgery will induce functional network reorganization that significantly differs from the traditional amputation surgery and also more closely resembles the neural configuration of controls. We found AMI subjects to have lower connectivity with salience and motor seed regions compared to traditional amputees. Additionally, with connections affected in traditional amputees, AMI subjects exhibited a connectivity pattern more closely resembling controls. Lastly, sensorimotor connectivity in amputee cohorts was significantly associated with phantom sensation (R(2)=0.7, p=0.0008). These findings provide researchers and clinicians with a critical mechanistic understanding of the effects of the AMI surgery on the brain at rest, spearheading future research towards improved prosthetic control and embodiment.
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spelling pubmed-99347622023-02-17 Resting state neurophysiology of agonist-antagonist myoneural interface in persons with transtibial amputation Chicos, Laura Rangaprakash, D. Barry, Robert Herr, Hugh Res Sq Article The agonist-antagonist myoneural interface (AMI) is a novel amputation surgery that preserves sensorimotor signaling mechanisms of the central-peripheral nervous systems. Our first neuroimaging study investigating AMI subjects (Srinivasan et al., Sci. Transl. Med. 2020) focused on task-based neural signatures, and showed evidence of proprioceptive feedback to the central nervous system. The study of resting state neural activity helps non-invasively characterize the neural patterns that prime task response. In this first study on resting state fMRI in AMI subjects, we compared resting state functional connectivity in patients with transtibial AMI (n=12) and traditional (n=7) amputations, as well as biologically intact control subjects (n=10). We hypothesized that the AMI surgery will induce functional network reorganization that significantly differs from the traditional amputation surgery and also more closely resembles the neural configuration of controls. We found AMI subjects to have lower connectivity with salience and motor seed regions compared to traditional amputees. Additionally, with connections affected in traditional amputees, AMI subjects exhibited a connectivity pattern more closely resembling controls. Lastly, sensorimotor connectivity in amputee cohorts was significantly associated with phantom sensation (R(2)=0.7, p=0.0008). These findings provide researchers and clinicians with a critical mechanistic understanding of the effects of the AMI surgery on the brain at rest, spearheading future research towards improved prosthetic control and embodiment. American Journal Experts 2023-02-09 /pmc/articles/PMC9934762/ /pubmed/36798194 http://dx.doi.org/10.21203/rs.3.rs-2362961/v1 Text en https://creativecommons.org/licenses/by/4.0/This work is licensed under a Creative Commons Attribution 4.0 International License (https://creativecommons.org/licenses/by/4.0/) , which allows reusers to distribute, remix, adapt, and build upon the material in any medium or format, so long as attribution is given to the creator. The license allows for commercial use. https://creativecommons.org/licenses/by/4.0/License: This work is licensed under a Creative Commons Attribution 4.0 International License. Read Full License (https://creativecommons.org/licenses/by/4.0/)
spellingShingle Article
Chicos, Laura
Rangaprakash, D.
Barry, Robert
Herr, Hugh
Resting state neurophysiology of agonist-antagonist myoneural interface in persons with transtibial amputation
title Resting state neurophysiology of agonist-antagonist myoneural interface in persons with transtibial amputation
title_full Resting state neurophysiology of agonist-antagonist myoneural interface in persons with transtibial amputation
title_fullStr Resting state neurophysiology of agonist-antagonist myoneural interface in persons with transtibial amputation
title_full_unstemmed Resting state neurophysiology of agonist-antagonist myoneural interface in persons with transtibial amputation
title_short Resting state neurophysiology of agonist-antagonist myoneural interface in persons with transtibial amputation
title_sort resting state neurophysiology of agonist-antagonist myoneural interface in persons with transtibial amputation
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9934762/
https://www.ncbi.nlm.nih.gov/pubmed/36798194
http://dx.doi.org/10.21203/rs.3.rs-2362961/v1
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