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Intrinsic and reflex stiffness in normal and spastic, spinal cord injured subjects
Mechanical changes underlying spastic hypertonia were explored using a parallel cascade system identification technique to evaluate the relative contributions of intrinsic and reflex mechanisms to dynamic ankle stiffness in healthy subjects (controls) and spastic, spinal cord injured (SCI) patients....
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Published in: | Experimental brain research 2001-12, Vol.141 (4), p.446-459 |
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description | Mechanical changes underlying spastic hypertonia were explored using a parallel cascade system identification technique to evaluate the relative contributions of intrinsic and reflex mechanisms to dynamic ankle stiffness in healthy subjects (controls) and spastic, spinal cord injured (SCI) patients. We examined the modulation of the gain and dynamics of these components with ankle angle for both passive and active conditions. Four main findings emerged. First, intrinsic and reflex stiffness dynamics were qualitatively similar in SCI patients and controls. Intrinsic stiffness dynamics were well modeled by a linear second-order model relating intrinsic torque to joint position, while reflex stiffness dynamics were accurately described by a linear, third-order system relating half-wave rectified velocity to reflex torque. Differences between the two groups were evident in the values of four parameters, the elastic and viscous parameters for intrinsic stiffness and the gain and first-order cut-off frequency for reflex stiffness. Second, reflex stiffness was substantially increased in SCI patients, where it generated as much as 40% of the total torque variance, compared with controls, where reflex contributions never exceeded 7%. Third, differences between SCI patients and controls depended strongly on joint position, becoming larger as the ankle was dorsiflexed. At full plantarflexion, there was no difference between SCI and control subjects; in the mid-range, reflex stiffness was abnormally high in SCI patients; at full dorsiflexion, both reflex and intrinsic stiffness were larger than normal. Fourth, differences between SCI and control subjects were smaller during the active than the passive condition, because intrinsic stiffness increased more in controls than SCI subjects; nevertheless, reflex gain remained abnormally high in SCI patients. These results elucidate the nature and origins of the mechanical abnormalities associated with hypertonia and provide a better understanding of its functional and clinical implications. |
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M ; BARBEAU, H ; LADOUCEUR, M ; KEARNEY, R. E</creator><creatorcontrib>MIRBAGHERI, M. M ; BARBEAU, H ; LADOUCEUR, M ; KEARNEY, R. E</creatorcontrib><description>Mechanical changes underlying spastic hypertonia were explored using a parallel cascade system identification technique to evaluate the relative contributions of intrinsic and reflex mechanisms to dynamic ankle stiffness in healthy subjects (controls) and spastic, spinal cord injured (SCI) patients. We examined the modulation of the gain and dynamics of these components with ankle angle for both passive and active conditions. Four main findings emerged. First, intrinsic and reflex stiffness dynamics were qualitatively similar in SCI patients and controls. Intrinsic stiffness dynamics were well modeled by a linear second-order model relating intrinsic torque to joint position, while reflex stiffness dynamics were accurately described by a linear, third-order system relating half-wave rectified velocity to reflex torque. Differences between the two groups were evident in the values of four parameters, the elastic and viscous parameters for intrinsic stiffness and the gain and first-order cut-off frequency for reflex stiffness. Second, reflex stiffness was substantially increased in SCI patients, where it generated as much as 40% of the total torque variance, compared with controls, where reflex contributions never exceeded 7%. Third, differences between SCI patients and controls depended strongly on joint position, becoming larger as the ankle was dorsiflexed. At full plantarflexion, there was no difference between SCI and control subjects; in the mid-range, reflex stiffness was abnormally high in SCI patients; at full dorsiflexion, both reflex and intrinsic stiffness were larger than normal. Fourth, differences between SCI and control subjects were smaller during the active than the passive condition, because intrinsic stiffness increased more in controls than SCI subjects; nevertheless, reflex gain remained abnormally high in SCI patients. These results elucidate the nature and origins of the mechanical abnormalities associated with hypertonia and provide a better understanding of its functional and clinical implications.</description><identifier>ISSN: 0014-4819</identifier><identifier>EISSN: 1432-1106</identifier><identifier>DOI: 10.1007/s00221-001-0901-z</identifier><identifier>PMID: 11810139</identifier><identifier>CODEN: EXBRAP</identifier><language>eng</language><publisher>Berlin: Springer</publisher><subject>Adult ; Ankle ; Ankle Joint - physiopathology ; Biological and medical sciences ; Diseases of striated muscles. Neuromuscular diseases ; Female ; Humans ; hypertonia ; Linear Models ; Male ; Medical sciences ; Middle Aged ; Movement - physiology ; Muscle Contraction - physiology ; Muscle Spasticity - pathology ; Muscle Spasticity - physiopathology ; Muscle Tonus - physiology ; Muscle, Skeletal - innervation ; Muscle, Skeletal - physiology ; Neurology ; Patients ; Posture - physiology ; Range of Motion, Articular - physiology ; Reference Values ; Reflex - physiology ; Spinal cord ; Spinal cord injuries ; Spinal Cord Injuries - physiopathology ; Torque</subject><ispartof>Experimental brain research, 2001-12, Vol.141 (4), p.446-459</ispartof><rights>2002 INIST-CNRS</rights><rights>Springer-Verlag 2001.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c421t-63108559b95ea7a06f0230fcc5731db4cb7d272c9486b22870b8b3bb0486e9153</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/2717189339/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$H</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2717189339?pq-origsite=primo$$EHTML$$P50$$Gproquest$$H</linktohtml><link.rule.ids>314,780,784,21394,27924,27925,33611,33612,43733,74221</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=14116754$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11810139$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>MIRBAGHERI, M. M</creatorcontrib><creatorcontrib>BARBEAU, H</creatorcontrib><creatorcontrib>LADOUCEUR, M</creatorcontrib><creatorcontrib>KEARNEY, R. E</creatorcontrib><title>Intrinsic and reflex stiffness in normal and spastic, spinal cord injured subjects</title><title>Experimental brain research</title><addtitle>Exp Brain Res</addtitle><description>Mechanical changes underlying spastic hypertonia were explored using a parallel cascade system identification technique to evaluate the relative contributions of intrinsic and reflex mechanisms to dynamic ankle stiffness in healthy subjects (controls) and spastic, spinal cord injured (SCI) patients. We examined the modulation of the gain and dynamics of these components with ankle angle for both passive and active conditions. Four main findings emerged. First, intrinsic and reflex stiffness dynamics were qualitatively similar in SCI patients and controls. Intrinsic stiffness dynamics were well modeled by a linear second-order model relating intrinsic torque to joint position, while reflex stiffness dynamics were accurately described by a linear, third-order system relating half-wave rectified velocity to reflex torque. Differences between the two groups were evident in the values of four parameters, the elastic and viscous parameters for intrinsic stiffness and the gain and first-order cut-off frequency for reflex stiffness. Second, reflex stiffness was substantially increased in SCI patients, where it generated as much as 40% of the total torque variance, compared with controls, where reflex contributions never exceeded 7%. Third, differences between SCI patients and controls depended strongly on joint position, becoming larger as the ankle was dorsiflexed. At full plantarflexion, there was no difference between SCI and control subjects; in the mid-range, reflex stiffness was abnormally high in SCI patients; at full dorsiflexion, both reflex and intrinsic stiffness were larger than normal. Fourth, differences between SCI and control subjects were smaller during the active than the passive condition, because intrinsic stiffness increased more in controls than SCI subjects; nevertheless, reflex gain remained abnormally high in SCI patients. These results elucidate the nature and origins of the mechanical abnormalities associated with hypertonia and provide a better understanding of its functional and clinical implications.</description><subject>Adult</subject><subject>Ankle</subject><subject>Ankle Joint - physiopathology</subject><subject>Biological and medical sciences</subject><subject>Diseases of striated muscles. Neuromuscular diseases</subject><subject>Female</subject><subject>Humans</subject><subject>hypertonia</subject><subject>Linear Models</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Movement - physiology</subject><subject>Muscle Contraction - physiology</subject><subject>Muscle Spasticity - pathology</subject><subject>Muscle Spasticity - physiopathology</subject><subject>Muscle Tonus - physiology</subject><subject>Muscle, Skeletal - innervation</subject><subject>Muscle, Skeletal - physiology</subject><subject>Neurology</subject><subject>Patients</subject><subject>Posture - physiology</subject><subject>Range of Motion, Articular - physiology</subject><subject>Reference Values</subject><subject>Reflex - physiology</subject><subject>Spinal cord</subject><subject>Spinal cord injuries</subject><subject>Spinal Cord Injuries - physiopathology</subject><subject>Torque</subject><issn>0014-4819</issn><issn>1432-1106</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><sourceid>ALSLI</sourceid><sourceid>M2R</sourceid><recordid>eNpdkF1L5DAUhsOirOPHD9ibpSB6ZfWcpG2SSxG_QBBEr0OSptChk87mtKD-ejM7A4IX-Th5n3MID2N_EC4RQF4RAOdYAuSl8_b5iy2wErxEhGaPLXJQlZVCfcAOiZabUkj4zQ4QFQIKvWAvj3FKfaTeFza2RQrdEN4Lmvqui4Go6GMRx7Syw_-Y1jZH_iJf-pjf_JjajCznFHI4u2XwEx2z_c4OFE525xF7u7t9vXkon57vH2-un0pfcZzKRiCoutZO18FKC00HXEDnfS0Ftq7yTrZccq8r1TjOlQSnnHAOch001uKInW_nrtP4bw40mVVPPgyDjWGcyaASNWqFGTz9AS7HOeX_k-ESJSothM4UbimfRqIswqxTv7LpwyCYjW6z1W2yRrPRbT5zz9_d5NmtQvvdsfObgbMdYMnboUs2-p6-uQqxkXUlvgCW04aB</recordid><startdate>20011201</startdate><enddate>20011201</enddate><creator>MIRBAGHERI, M. 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Neuromuscular diseases</topic><topic>Female</topic><topic>Humans</topic><topic>hypertonia</topic><topic>Linear Models</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Movement - physiology</topic><topic>Muscle Contraction - physiology</topic><topic>Muscle Spasticity - pathology</topic><topic>Muscle Spasticity - physiopathology</topic><topic>Muscle Tonus - physiology</topic><topic>Muscle, Skeletal - innervation</topic><topic>Muscle, Skeletal - physiology</topic><topic>Neurology</topic><topic>Patients</topic><topic>Posture - physiology</topic><topic>Range of Motion, Articular - physiology</topic><topic>Reference Values</topic><topic>Reflex - physiology</topic><topic>Spinal cord</topic><topic>Spinal cord injuries</topic><topic>Spinal Cord Injuries - physiopathology</topic><topic>Torque</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>MIRBAGHERI, M. 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M</au><au>BARBEAU, H</au><au>LADOUCEUR, M</au><au>KEARNEY, R. E</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Intrinsic and reflex stiffness in normal and spastic, spinal cord injured subjects</atitle><jtitle>Experimental brain research</jtitle><addtitle>Exp Brain Res</addtitle><date>2001-12-01</date><risdate>2001</risdate><volume>141</volume><issue>4</issue><spage>446</spage><epage>459</epage><pages>446-459</pages><issn>0014-4819</issn><eissn>1432-1106</eissn><coden>EXBRAP</coden><abstract>Mechanical changes underlying spastic hypertonia were explored using a parallel cascade system identification technique to evaluate the relative contributions of intrinsic and reflex mechanisms to dynamic ankle stiffness in healthy subjects (controls) and spastic, spinal cord injured (SCI) patients. We examined the modulation of the gain and dynamics of these components with ankle angle for both passive and active conditions. Four main findings emerged. First, intrinsic and reflex stiffness dynamics were qualitatively similar in SCI patients and controls. Intrinsic stiffness dynamics were well modeled by a linear second-order model relating intrinsic torque to joint position, while reflex stiffness dynamics were accurately described by a linear, third-order system relating half-wave rectified velocity to reflex torque. Differences between the two groups were evident in the values of four parameters, the elastic and viscous parameters for intrinsic stiffness and the gain and first-order cut-off frequency for reflex stiffness. Second, reflex stiffness was substantially increased in SCI patients, where it generated as much as 40% of the total torque variance, compared with controls, where reflex contributions never exceeded 7%. Third, differences between SCI patients and controls depended strongly on joint position, becoming larger as the ankle was dorsiflexed. At full plantarflexion, there was no difference between SCI and control subjects; in the mid-range, reflex stiffness was abnormally high in SCI patients; at full dorsiflexion, both reflex and intrinsic stiffness were larger than normal. Fourth, differences between SCI and control subjects were smaller during the active than the passive condition, because intrinsic stiffness increased more in controls than SCI subjects; nevertheless, reflex gain remained abnormally high in SCI patients. These results elucidate the nature and origins of the mechanical abnormalities associated with hypertonia and provide a better understanding of its functional and clinical implications.</abstract><cop>Berlin</cop><pub>Springer</pub><pmid>11810139</pmid><doi>10.1007/s00221-001-0901-z</doi><tpages>14</tpages></addata></record> |
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subjects | Adult Ankle Ankle Joint - physiopathology Biological and medical sciences Diseases of striated muscles. Neuromuscular diseases Female Humans hypertonia Linear Models Male Medical sciences Middle Aged Movement - physiology Muscle Contraction - physiology Muscle Spasticity - pathology Muscle Spasticity - physiopathology Muscle Tonus - physiology Muscle, Skeletal - innervation Muscle, Skeletal - physiology Neurology Patients Posture - physiology Range of Motion, Articular - physiology Reference Values Reflex - physiology Spinal cord Spinal cord injuries Spinal Cord Injuries - physiopathology Torque |
title | Intrinsic and reflex stiffness in normal and spastic, spinal cord injured subjects |
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