Modeling Reaching Impairment After Stroke Using a Population Vector Model of Movement Control That Incorporates Neural Firing-Rate Variability

The directional control of reaching after stroke was simulated by including cell death and firing-rate noise in a population vector model of movement control. In this model, cortical activity was assumed to cause the hand to move in the direction of a population vector, defined by a summation of res...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Neural computation 2003-11, Vol.15 (11), p.2619-2642
Hauptverfasser: Reinkensmeyer, David J., Iobbi, Mario G., Kahn, Leonard E., Kamper, Derek G., Takahashi, Craig D.
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
container_end_page 2642
container_issue 11
container_start_page 2619
container_title Neural computation
container_volume 15
creator Reinkensmeyer, David J.
Iobbi, Mario G.
Kahn, Leonard E.
Kamper, Derek G.
Takahashi, Craig D.
description The directional control of reaching after stroke was simulated by including cell death and firing-rate noise in a population vector model of movement control. In this model, cortical activity was assumed to cause the hand to move in the direction of a population vector, defined by a summation of responses from neurons with cosine directional tuning. Two types of directional error were analyzed: the between-target variability, defined as the standard deviation of the directional error across a wide range of target directions, and the within-target variability, defined as the standard deviation of the directional error for many reaches to a single target. Both between and within-target variability increased with increasing cell death. The increase in between-target variability arose because cell death caused a nonuniform distribution of preferred directions. The increase in within-target variability arose because the magnitude of the population vector decreased more quickly than its standard deviation for increasing cell death, provided appropriate levels of firing-rate noise were present. Comparisons to reaching data from 29 stroke subjects revealed similar increases in between and within-target variability as clinical impairment severity increased. Relationships between simulated cell death and impairment severity were derived using the between and within-target variability results. For both relationships, impairment severity increased similarly with decreasing percentage of surviving cells, consistent with results from previous imaging studies. These results demonstrate that a population vector model of movement control that incorporates cosine tuning, linear summation of unitary responses, firing-rate noise, and random cell death can account for some features of impaired arm movement after stroke.
doi_str_mv 10.1162/089976603322385090
format Article
fullrecord <record><control><sourceid>proquest_pasca</sourceid><recordid>TN_cdi_proquest_miscellaneous_71301967</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>19203148</sourcerecordid><originalsourceid>FETCH-LOGICAL-c399t-fe854ddac9a432a6c412a0a6f5ddb2dca1185c56d6b2cb781101e064dc9679293</originalsourceid><addsrcrecordid>eNqF0c1uFSEYBmBiNPZYvQEXho3upvIzMLBsTqyepP6kto27yTcMY6nMMAJj0pvwmmV6TtKFia4g8LwvCR9CLyk5oVSyt0Rp3UhJOGeMK0E0eYQ2VHBSKaW-PUabFVRFNEfoWUq3hBBJiXiKjmgtmkYJuUG_P4beejd9xxcWzM262Y0zuDjaKePTIduIv-YYflh8ldZbwF_CvHjILkz42pocIr7vwGEom1_2PrgNUwl5fHkDGe8mE-IcImSb8Ce7RPD4zMXSVl2UM3wN0UHnvMt3z9GTAXyyLw7rMbo6e3e5_VCdf36_256eV4ZrnavBKlH3PRgNNWcgTU0ZEJCD6PuO9QYoVcII2cuOma5RlBJqiax7o2WjmebH6M2-d47h52JTbkeXjPUeJhuW1DaUE1rsfyHVjHBaqwLZHpoYUop2aOfoRoh3LSXtOq7273GV0KtD-9KNtn-IHOZTwOsDgGTADxEm49KDE0UyurqTvRtdbm_DEqfye_96-Q_bTKvP</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>19203148</pqid></control><display><type>article</type><title>Modeling Reaching Impairment After Stroke Using a Population Vector Model of Movement Control That Incorporates Neural Firing-Rate Variability</title><source>MEDLINE</source><source>MIT Press Journals</source><creator>Reinkensmeyer, David J. ; Iobbi, Mario G. ; Kahn, Leonard E. ; Kamper, Derek G. ; Takahashi, Craig D.</creator><creatorcontrib>Reinkensmeyer, David J. ; Iobbi, Mario G. ; Kahn, Leonard E. ; Kamper, Derek G. ; Takahashi, Craig D.</creatorcontrib><description>The directional control of reaching after stroke was simulated by including cell death and firing-rate noise in a population vector model of movement control. In this model, cortical activity was assumed to cause the hand to move in the direction of a population vector, defined by a summation of responses from neurons with cosine directional tuning. Two types of directional error were analyzed: the between-target variability, defined as the standard deviation of the directional error across a wide range of target directions, and the within-target variability, defined as the standard deviation of the directional error for many reaches to a single target. Both between and within-target variability increased with increasing cell death. The increase in between-target variability arose because cell death caused a nonuniform distribution of preferred directions. The increase in within-target variability arose because the magnitude of the population vector decreased more quickly than its standard deviation for increasing cell death, provided appropriate levels of firing-rate noise were present. Comparisons to reaching data from 29 stroke subjects revealed similar increases in between and within-target variability as clinical impairment severity increased. Relationships between simulated cell death and impairment severity were derived using the between and within-target variability results. For both relationships, impairment severity increased similarly with decreasing percentage of surviving cells, consistent with results from previous imaging studies. These results demonstrate that a population vector model of movement control that incorporates cosine tuning, linear summation of unitary responses, firing-rate noise, and random cell death can account for some features of impaired arm movement after stroke.</description><identifier>ISSN: 0899-7667</identifier><identifier>EISSN: 1530-888X</identifier><identifier>DOI: 10.1162/089976603322385090</identifier><identifier>PMID: 14577856</identifier><language>eng</language><publisher>One Rogers Street, Cambridge, MA 02142-1209, USA: MIT Press</publisher><subject>Action Potentials - physiology ; Biological and medical sciences ; Cell Death - physiology ; Cell Survival - physiology ; Fundamental and applied biological sciences. Psychology ; General aspects. Models. Methods ; Humans ; Models, Neurological ; Movement - physiology ; Neurons - physiology ; Stroke - physiopathology ; Vertebrates: nervous system and sense organs</subject><ispartof>Neural computation, 2003-11, Vol.15 (11), p.2619-2642</ispartof><rights>2004 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c399t-fe854ddac9a432a6c412a0a6f5ddb2dca1185c56d6b2cb781101e064dc9679293</citedby><cites>FETCH-LOGICAL-c399t-fe854ddac9a432a6c412a0a6f5ddb2dca1185c56d6b2cb781101e064dc9679293</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://direct.mit.edu/neco/article/doi/10.1162/089976603322385090$$EHTML$$P50$$Gmit$$H</linktohtml><link.rule.ids>314,777,781,27905,27906,53990,53991</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&amp;idt=15145216$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/14577856$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Reinkensmeyer, David J.</creatorcontrib><creatorcontrib>Iobbi, Mario G.</creatorcontrib><creatorcontrib>Kahn, Leonard E.</creatorcontrib><creatorcontrib>Kamper, Derek G.</creatorcontrib><creatorcontrib>Takahashi, Craig D.</creatorcontrib><title>Modeling Reaching Impairment After Stroke Using a Population Vector Model of Movement Control That Incorporates Neural Firing-Rate Variability</title><title>Neural computation</title><addtitle>Neural Comput</addtitle><description>The directional control of reaching after stroke was simulated by including cell death and firing-rate noise in a population vector model of movement control. In this model, cortical activity was assumed to cause the hand to move in the direction of a population vector, defined by a summation of responses from neurons with cosine directional tuning. Two types of directional error were analyzed: the between-target variability, defined as the standard deviation of the directional error across a wide range of target directions, and the within-target variability, defined as the standard deviation of the directional error for many reaches to a single target. Both between and within-target variability increased with increasing cell death. The increase in between-target variability arose because cell death caused a nonuniform distribution of preferred directions. The increase in within-target variability arose because the magnitude of the population vector decreased more quickly than its standard deviation for increasing cell death, provided appropriate levels of firing-rate noise were present. Comparisons to reaching data from 29 stroke subjects revealed similar increases in between and within-target variability as clinical impairment severity increased. Relationships between simulated cell death and impairment severity were derived using the between and within-target variability results. For both relationships, impairment severity increased similarly with decreasing percentage of surviving cells, consistent with results from previous imaging studies. These results demonstrate that a population vector model of movement control that incorporates cosine tuning, linear summation of unitary responses, firing-rate noise, and random cell death can account for some features of impaired arm movement after stroke.</description><subject>Action Potentials - physiology</subject><subject>Biological and medical sciences</subject><subject>Cell Death - physiology</subject><subject>Cell Survival - physiology</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>General aspects. Models. Methods</subject><subject>Humans</subject><subject>Models, Neurological</subject><subject>Movement - physiology</subject><subject>Neurons - physiology</subject><subject>Stroke - physiopathology</subject><subject>Vertebrates: nervous system and sense organs</subject><issn>0899-7667</issn><issn>1530-888X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqF0c1uFSEYBmBiNPZYvQEXho3upvIzMLBsTqyepP6kto27yTcMY6nMMAJj0pvwmmV6TtKFia4g8LwvCR9CLyk5oVSyt0Rp3UhJOGeMK0E0eYQ2VHBSKaW-PUabFVRFNEfoWUq3hBBJiXiKjmgtmkYJuUG_P4beejd9xxcWzM262Y0zuDjaKePTIduIv-YYflh8ldZbwF_CvHjILkz42pocIr7vwGEom1_2PrgNUwl5fHkDGe8mE-IcImSb8Ce7RPD4zMXSVl2UM3wN0UHnvMt3z9GTAXyyLw7rMbo6e3e5_VCdf36_256eV4ZrnavBKlH3PRgNNWcgTU0ZEJCD6PuO9QYoVcII2cuOma5RlBJqiax7o2WjmebH6M2-d47h52JTbkeXjPUeJhuW1DaUE1rsfyHVjHBaqwLZHpoYUop2aOfoRoh3LSXtOq7273GV0KtD-9KNtn-IHOZTwOsDgGTADxEm49KDE0UyurqTvRtdbm_DEqfye_96-Q_bTKvP</recordid><startdate>20031101</startdate><enddate>20031101</enddate><creator>Reinkensmeyer, David J.</creator><creator>Iobbi, Mario G.</creator><creator>Kahn, Leonard E.</creator><creator>Kamper, Derek G.</creator><creator>Takahashi, Craig D.</creator><general>MIT Press</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7TK</scope><scope>7X8</scope></search><sort><creationdate>20031101</creationdate><title>Modeling Reaching Impairment After Stroke Using a Population Vector Model of Movement Control That Incorporates Neural Firing-Rate Variability</title><author>Reinkensmeyer, David J. ; Iobbi, Mario G. ; Kahn, Leonard E. ; Kamper, Derek G. ; Takahashi, Craig D.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c399t-fe854ddac9a432a6c412a0a6f5ddb2dca1185c56d6b2cb781101e064dc9679293</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Action Potentials - physiology</topic><topic>Biological and medical sciences</topic><topic>Cell Death - physiology</topic><topic>Cell Survival - physiology</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>General aspects. Models. Methods</topic><topic>Humans</topic><topic>Models, Neurological</topic><topic>Movement - physiology</topic><topic>Neurons - physiology</topic><topic>Stroke - physiopathology</topic><topic>Vertebrates: nervous system and sense organs</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Reinkensmeyer, David J.</creatorcontrib><creatorcontrib>Iobbi, Mario G.</creatorcontrib><creatorcontrib>Kahn, Leonard E.</creatorcontrib><creatorcontrib>Kamper, Derek G.</creatorcontrib><creatorcontrib>Takahashi, Craig D.</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Neural computation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Reinkensmeyer, David J.</au><au>Iobbi, Mario G.</au><au>Kahn, Leonard E.</au><au>Kamper, Derek G.</au><au>Takahashi, Craig D.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Modeling Reaching Impairment After Stroke Using a Population Vector Model of Movement Control That Incorporates Neural Firing-Rate Variability</atitle><jtitle>Neural computation</jtitle><addtitle>Neural Comput</addtitle><date>2003-11-01</date><risdate>2003</risdate><volume>15</volume><issue>11</issue><spage>2619</spage><epage>2642</epage><pages>2619-2642</pages><issn>0899-7667</issn><eissn>1530-888X</eissn><abstract>The directional control of reaching after stroke was simulated by including cell death and firing-rate noise in a population vector model of movement control. In this model, cortical activity was assumed to cause the hand to move in the direction of a population vector, defined by a summation of responses from neurons with cosine directional tuning. Two types of directional error were analyzed: the between-target variability, defined as the standard deviation of the directional error across a wide range of target directions, and the within-target variability, defined as the standard deviation of the directional error for many reaches to a single target. Both between and within-target variability increased with increasing cell death. The increase in between-target variability arose because cell death caused a nonuniform distribution of preferred directions. The increase in within-target variability arose because the magnitude of the population vector decreased more quickly than its standard deviation for increasing cell death, provided appropriate levels of firing-rate noise were present. Comparisons to reaching data from 29 stroke subjects revealed similar increases in between and within-target variability as clinical impairment severity increased. Relationships between simulated cell death and impairment severity were derived using the between and within-target variability results. For both relationships, impairment severity increased similarly with decreasing percentage of surviving cells, consistent with results from previous imaging studies. These results demonstrate that a population vector model of movement control that incorporates cosine tuning, linear summation of unitary responses, firing-rate noise, and random cell death can account for some features of impaired arm movement after stroke.</abstract><cop>One Rogers Street, Cambridge, MA 02142-1209, USA</cop><pub>MIT Press</pub><pmid>14577856</pmid><doi>10.1162/089976603322385090</doi><tpages>24</tpages></addata></record>
fulltext fulltext
identifier ISSN: 0899-7667
ispartof Neural computation, 2003-11, Vol.15 (11), p.2619-2642
issn 0899-7667
1530-888X
language eng
recordid cdi_proquest_miscellaneous_71301967
source MEDLINE; MIT Press Journals
subjects Action Potentials - physiology
Biological and medical sciences
Cell Death - physiology
Cell Survival - physiology
Fundamental and applied biological sciences. Psychology
General aspects. Models. Methods
Humans
Models, Neurological
Movement - physiology
Neurons - physiology
Stroke - physiopathology
Vertebrates: nervous system and sense organs
title Modeling Reaching Impairment After Stroke Using a Population Vector Model of Movement Control That Incorporates Neural Firing-Rate Variability
url https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-20T17%3A48%3A55IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pasca&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Modeling%20Reaching%20Impairment%20After%20Stroke%20Using%20a%20Population%20Vector%20Model%20of%20Movement%20Control%20That%20Incorporates%20Neural%20Firing-Rate%20Variability&rft.jtitle=Neural%20computation&rft.au=Reinkensmeyer,%20David%20J.&rft.date=2003-11-01&rft.volume=15&rft.issue=11&rft.spage=2619&rft.epage=2642&rft.pages=2619-2642&rft.issn=0899-7667&rft.eissn=1530-888X&rft_id=info:doi/10.1162/089976603322385090&rft_dat=%3Cproquest_pasca%3E19203148%3C/proquest_pasca%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=19203148&rft_id=info:pmid/14577856&rfr_iscdi=true