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...
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Veröffentlicht in: | Neural computation 2003-11, Vol.15 (11), p.2619-2642 |
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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 |
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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>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=15145216$$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> |
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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 |
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