Limb‐kinetic apraxia in corticobasal degeneration: Clinical and kinematic features
Identifieur interne : 000093 ( Istex/Corpus ); précédent : 000092; suivant : 000094Limb‐kinetic apraxia in corticobasal degeneration: Clinical and kinematic features
Auteurs : Ram N C. Leiguarda ; Marcelo Merello ; María Inés Nouzeilles ; Jorge Balej ; Alberto Rivero ; Martín NoguésSource :
- Movement Disorders [ 0885-3185 ] ; 2003-01.
English descriptors
Abstract
Current concepts regarding the organisation of the motor system indicate the existence of a frontoparietal circuit involved in prehension and manipulation, whose damage may result in a motor behavioural disorder strongly resembling the one originally described as limb‐kinetic apraxia. To determine the specific clinical and kinematic features of this distinctive praxic disorder, 5 patients with corticobasal degeneration (apraxic group), 5 with Parkinson's disease (nonapraxic group), and 10 control subjects were studied by a comprehensive apraxic battery, three‐dimensional motion analysis of manipulative movements and motor evoked potentials. A mathematical model [quality of movement coefficient (QMC)] was applied to quantify differential kinematic characteristics between elementary motor deficits and the praxic disorder. Transcranial magnetic stimulation was used to evaluate corticomotoneural projections and cortical inhibition. All five patients in the apraxic group exhibited a unilateral praxic deficit characterised by derangement of fractionated and segmental finger movements. QMC was significantly greater in apraxic than in nonapraxic patients (P < 0.02), revealing a chaotic movement with marked interfinger uncoordination. Conventional transcranial magnetic stimulation parameters were within normal limits in both groups of patients; however, the silent period was significantly shorter in the apraxic limb when compared with control subjects (P < 0.001). Limb‐kinetic apraxia is a distinctive disorder affecting the performance of finger and hand postures and movements over and above a corticospinal or basal ganglion deficit. Disruption of the frontoparietal circuit devoted to grasping and manipulation, together with defective cortical inhibition, which would also interfere with the selection and control of hand muscle activity, are the most likely underlying physiopathological mechanisms of limb‐kinetic apraxia in patients with corticobasal degeneration.
Url:
DOI: 10.1002/mds.10303
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ISTEX:AF9AEC18BFEDE3B317641409AA4901B36789A7EBLe document en format XML
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To determine the specific clinical and kinematic features of this distinctive praxic disorder, 5 patients with corticobasal degeneration (apraxic group), 5 with Parkinson's disease (nonapraxic group), and 10 control subjects were studied by a comprehensive apraxic battery, three‐dimensional motion analysis of manipulative movements and motor evoked potentials. A mathematical model [quality of movement coefficient (QMC)] was applied to quantify differential kinematic characteristics between elementary motor deficits and the praxic disorder. Transcranial magnetic stimulation was used to evaluate corticomotoneural projections and cortical inhibition. All five patients in the apraxic group exhibited a unilateral praxic deficit characterised by derangement of fractionated and segmental finger movements. QMC was significantly greater in apraxic than in nonapraxic patients (P < 0.02), revealing a chaotic movement with marked interfinger uncoordination. Conventional transcranial magnetic stimulation parameters were within normal limits in both groups of patients; however, the silent period was significantly shorter in the apraxic limb when compared with control subjects (P < 0.001). Limb‐kinetic apraxia is a distinctive disorder affecting the performance of finger and hand postures and movements over and above a corticospinal or basal ganglion deficit. Disruption of the frontoparietal circuit devoted to grasping and manipulation, together with defective cortical inhibition, which would also interfere with the selection and control of hand muscle activity, are the most likely underlying physiopathological mechanisms of limb‐kinetic apraxia in patients with corticobasal degeneration.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Ramón C. 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To determine the specific clinical and kinematic features of this distinctive praxic disorder, 5 patients with corticobasal degeneration (apraxic group), 5 with Parkinson's disease (nonapraxic group), and 10 control subjects were studied by a comprehensive apraxic battery, three‐dimensional motion analysis of manipulative movements and motor evoked potentials. A mathematical model [quality of movement coefficient (QMC)] was applied to quantify differential kinematic characteristics between elementary motor deficits and the praxic disorder. Transcranial magnetic stimulation was used to evaluate corticomotoneural projections and cortical inhibition. All five patients in the apraxic group exhibited a unilateral praxic deficit characterised by derangement of fractionated and segmental finger movements. QMC was significantly greater in apraxic than in nonapraxic patients (P > 0.02), revealing a chaotic movement with marked interfinger uncoordination. Conventional transcranial magnetic stimulation parameters were within normal limits in both groups of patients; however, the silent period was significantly shorter in the apraxic limb when compared with control subjects (P > 0.001). Limb‐kinetic apraxia is a distinctive disorder affecting the performance of finger and hand postures and movements over and above a corticospinal or basal ganglion deficit. 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To determine the specific clinical and kinematic features of this distinctive praxic disorder, 5 patients with corticobasal degeneration (apraxic group), 5 with Parkinson's disease (nonapraxic group), and 10 control subjects were studied by a comprehensive apraxic battery, three‐dimensional motion analysis of manipulative movements and motor evoked potentials. A mathematical model [quality of movement coefficient (QMC)] was applied to quantify differential kinematic characteristics between elementary motor deficits and the praxic disorder. Transcranial magnetic stimulation was used to evaluate corticomotoneural projections and cortical inhibition. All five patients in the apraxic group exhibited a unilateral praxic deficit characterised by derangement of fractionated and segmental finger movements. QMC was significantly greater in apraxic than in nonapraxic patients (P < 0.02), revealing a chaotic movement with marked interfinger uncoordination. Conventional transcranial magnetic stimulation parameters were within normal limits in both groups of patients; however, the silent period was significantly shorter in the apraxic limb when compared with control subjects (P < 0.001). Limb‐kinetic apraxia is a distinctive disorder affecting the performance of finger and hand postures and movements over and above a corticospinal or basal ganglion deficit. Disruption of the frontoparietal circuit devoted to grasping and manipulation, together with defective cortical inhibition, which would also interfere with the selection and control of hand muscle activity, are the most likely underlying physiopathological mechanisms of limb‐kinetic apraxia in patients with corticobasal degeneration.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>limb‐kinetic apraxia</term></item><item><term>grasping and manipulation</term></item><item><term>frontoparietal circuit</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>Article category</head><item><term>Research Article</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2002-02-04">Received</change><change when="2002-06-28">Registration</change><change when="2003-01">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/AF9AEC18BFEDE3B317641409AA4901B36789A7EB/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Wiley Subscription Services, Inc., A Wiley Company</publisherName><publisherLoc>New York</publisherLoc></publisherInfo><doi registered="yes">10.1002/(ISSN)1531-8257</doi><issn type="print">0885-3185</issn><issn type="electronic">1531-8257</issn><idGroup><id type="product" value="MDS"></id></idGroup><titleGroup><title type="main" xml:lang="en" sort="MOVEMENT DISORDERS">Movement Disorders</title><title type="subtitle">Official Journal of the Movement Disorder Society</title><title type="short">Mov. 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To determine the specific clinical and kinematic features of this distinctive praxic disorder, 5 patients with corticobasal degeneration (apraxic group), 5 with Parkinson's disease (nonapraxic group), and 10 control subjects were studied by a comprehensive apraxic battery, three‐dimensional motion analysis of manipulative movements and motor evoked potentials. A mathematical model [quality of movement coefficient (QMC)] was applied to quantify differential kinematic characteristics between elementary motor deficits and the praxic disorder. Transcranial magnetic stimulation was used to evaluate corticomotoneural projections and cortical inhibition. All five patients in the apraxic group exhibited a unilateral praxic deficit characterised by derangement of fractionated and segmental finger movements. QMC was significantly greater in apraxic than in nonapraxic patients (<i>P</i> < 0.02), revealing a chaotic movement with marked interfinger uncoordination. Conventional transcranial magnetic stimulation parameters were within normal limits in both groups of patients; however, the silent period was significantly shorter in the apraxic limb when compared with control subjects (<i>P</i> < 0.001). Limb‐kinetic apraxia is a distinctive disorder affecting the performance of finger and hand postures and movements over and above a corticospinal or basal ganglion deficit. Disruption of the frontoparietal circuit devoted to grasping and manipulation, together with defective cortical inhibition, which would also interfere with the selection and control of hand muscle activity, are the most likely underlying physiopathological mechanisms of limb‐kinetic apraxia in patients with corticobasal degeneration.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><!--Version 0.6 générée le 3-12-2015--><mods version="3.6"><titleInfo lang="en"><title>Limb‐kinetic apraxia in corticobasal degeneration: Clinical and kinematic features</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>Limb‐Kinetic Apraxia</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Limb‐kinetic apraxia in corticobasal degeneration: Clinical and kinematic features</title></titleInfo><name type="personal"><namePart type="given">Ramón C.</namePart><namePart type="family">Leiguarda</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Raúl Carrea Institute for Neurological Research (FLENI), Buenos Aires, Argentina</affiliation><description>Correspondence: Raúl Carrea Institute for Neurological Research (FLENI) Montañeses 2325, (1428) Buenos Aires, Argentina</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Marcelo</namePart><namePart type="family">Merello</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Raúl Carrea Institute for Neurological Research (FLENI), Buenos Aires, Argentina</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">María Inés</namePart><namePart type="family">Nouzeilles</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Raúl Carrea Institute for Neurological Research (FLENI), Buenos Aires, Argentina</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jorge</namePart><namePart type="family">Balej</namePart><namePart type="termsOfAddress">PhD</namePart><affiliation>Raúl Carrea Institute for Neurological Research (FLENI), Buenos Aires, Argentina</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Alberto</namePart><namePart type="family">Rivero</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Raúl Carrea Institute for Neurological Research (FLENI), Buenos Aires, Argentina</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Martín</namePart><namePart type="family">Nogués</namePart><namePart type="termsOfAddress">MD</namePart><affiliation>Raúl Carrea Institute for Neurological Research (FLENI), Buenos Aires, Argentina</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre authority="originalCategForm">article</genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">New York</placeTerm></place><dateIssued encoding="w3cdtf">2003-01</dateIssued><dateCaptured encoding="w3cdtf">2002-02-04</dateCaptured><dateValid encoding="w3cdtf">2002-06-28</dateValid><copyrightDate encoding="w3cdtf">2003</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="figures">2</extent><extent unit="tables">4</extent><extent unit="references">50</extent><extent unit="words">7704</extent></physicalDescription><abstract lang="en">Current concepts regarding the organisation of the motor system indicate the existence of a frontoparietal circuit involved in prehension and manipulation, whose damage may result in a motor behavioural disorder strongly resembling the one originally described as limb‐kinetic apraxia. To determine the specific clinical and kinematic features of this distinctive praxic disorder, 5 patients with corticobasal degeneration (apraxic group), 5 with Parkinson's disease (nonapraxic group), and 10 control subjects were studied by a comprehensive apraxic battery, three‐dimensional motion analysis of manipulative movements and motor evoked potentials. A mathematical model [quality of movement coefficient (QMC)] was applied to quantify differential kinematic characteristics between elementary motor deficits and the praxic disorder. Transcranial magnetic stimulation was used to evaluate corticomotoneural projections and cortical inhibition. All five patients in the apraxic group exhibited a unilateral praxic deficit characterised by derangement of fractionated and segmental finger movements. QMC was significantly greater in apraxic than in nonapraxic patients (P < 0.02), revealing a chaotic movement with marked interfinger uncoordination. Conventional transcranial magnetic stimulation parameters were within normal limits in both groups of patients; however, the silent period was significantly shorter in the apraxic limb when compared with control subjects (P < 0.001). Limb‐kinetic apraxia is a distinctive disorder affecting the performance of finger and hand postures and movements over and above a corticospinal or basal ganglion deficit. Disruption of the frontoparietal circuit devoted to grasping and manipulation, together with defective cortical inhibition, which would also interfere with the selection and control of hand muscle activity, are the most likely underlying physiopathological mechanisms of limb‐kinetic apraxia in patients with corticobasal degeneration.</abstract><subject lang="en"><genre>Keywords</genre><topic>limb‐kinetic apraxia</topic><topic>grasping and manipulation</topic><topic>frontoparietal circuit</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title><subTitle>Official Journal of the Movement Disorder Society</subTitle></titleInfo><titleInfo type="abbreviated"><title>Mov. Disord.</title></titleInfo><subject><genre>article category</genre><topic>Research Article</topic></subject><identifier type="ISSN">0885-3185</identifier><identifier type="eISSN">1531-8257</identifier><identifier type="DOI">10.1002/(ISSN)1531-8257</identifier><identifier type="PublisherID">MDS</identifier><part><date>2003</date><detail type="volume"><caption>vol.</caption><number>18</number></detail><detail type="issue"><caption>no.</caption><number>1</number></detail><extent unit="pages"><start>49</start><end>59</end><total>11</total></extent></part></relatedItem><identifier type="istex">AF9AEC18BFEDE3B317641409AA4901B36789A7EB</identifier><identifier type="DOI">10.1002/mds.10303</identifier><identifier type="ArticleID">MDS10303</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 2002 Movement Disorder Society</accessCondition><recordInfo><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin><recordContentSource>WILEY</recordContentSource></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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