Limb-kinetic apraxia in corticobasal degeneration: Clinical and kinematic features
Identifieur interne : 002417 ( PascalFrancis/Checkpoint ); précédent : 002416; suivant : 002418Limb-kinetic apraxia in corticobasal degeneration: Clinical and kinematic features
Auteurs : Ramon C. Leiguarda [Argentine] ; Marcelo Merello [Argentine] ; Maria Inés Nouzeilles [Argentine] ; Jorge Balej [Argentine] ; Alberto Rivero [Argentine] ; Martin Nogues [Argentine]Source :
- Movement disorders [ 0885-3185 ] ; 2003.
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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.
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Leiguarda</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Raúl Carrea Institute for Neurological Research (FLENI)</s1><s2>Buenos Aires</s2><s3>ARG</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ><sZ>6 aut.</sZ></inist:fA14><country>Argentine</country><wicri:noRegion>Raúl Carrea Institute for Neurological Research (FLENI)</wicri:noRegion></affiliation></author><author><name sortKey="Merello, Marcelo" sort="Merello, Marcelo" uniqKey="Merello M" first="Marcelo" last="Merello">Marcelo Merello</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Raúl Carrea Institute for Neurological Research (FLENI)</s1><s2>Buenos Aires</s2><s3>ARG</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ><sZ>6 aut.</sZ></inist:fA14><country>Argentine</country><wicri:noRegion>Raúl Carrea Institute for Neurological Research (FLENI)</wicri:noRegion></affiliation></author><author><name sortKey="Nouzeilles, Maria Ines" sort="Nouzeilles, Maria Ines" uniqKey="Nouzeilles M" first="Maria Inés" last="Nouzeilles">Maria Inés Nouzeilles</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Raúl Carrea Institute for Neurological Research (FLENI)</s1><s2>Buenos Aires</s2><s3>ARG</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ><sZ>6 aut.</sZ></inist:fA14><country>Argentine</country><wicri:noRegion>Raúl Carrea Institute for Neurological Research (FLENI)</wicri:noRegion></affiliation></author><author><name sortKey="Balej, Jorge" sort="Balej, Jorge" uniqKey="Balej J" first="Jorge" last="Balej">Jorge Balej</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Raúl Carrea Institute for Neurological Research (FLENI)</s1><s2>Buenos Aires</s2><s3>ARG</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ><sZ>6 aut.</sZ></inist:fA14><country>Argentine</country><wicri:noRegion>Raúl Carrea Institute for Neurological Research (FLENI)</wicri:noRegion></affiliation></author><author><name sortKey="Rivero, Alberto" sort="Rivero, Alberto" uniqKey="Rivero A" first="Alberto" last="Rivero">Alberto Rivero</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Raúl Carrea Institute for Neurological Research (FLENI)</s1><s2>Buenos Aires</s2><s3>ARG</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ><sZ>6 aut.</sZ></inist:fA14><country>Argentine</country><wicri:noRegion>Raúl Carrea Institute for Neurological Research (FLENI)</wicri:noRegion></affiliation></author><author><name sortKey="Nogues, Martin" sort="Nogues, Martin" uniqKey="Nogues M" first="Martin" last="Nogues">Martin Nogues</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Raúl Carrea Institute for Neurological Research (FLENI)</s1><s2>Buenos Aires</s2><s3>ARG</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ><sZ>6 aut.</sZ></inist:fA14><country>Argentine</country><wicri:noRegion>Raúl Carrea Institute for Neurological Research (FLENI)</wicri:noRegion></affiliation></author></analytic><series><title level="j" type="main">Movement disorders</title><title level="j" type="abbreviated">Mov. disord.</title><idno type="ISSN">0885-3185</idno><imprint><date when="2003">2003</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">Movement disorders</title><title level="j" type="abbreviated">Mov. disord.</title><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Apraxia</term><term>Basal ganglion</term><term>Cerebral cortex</term><term>Complication</term><term>Degeneration</term><term>Elderly</term><term>Gripping</term><term>Kinematics</term><term>Limb</term><term>Magnetic stimulus</term><term>Pathogenesis</term><term>Transcranial route</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Dégénérescence</term><term>Cortex cérébral</term><term>Noyau gris central</term><term>Apraxie</term><term>Membre</term><term>Cinématique</term><term>Stimulus magnétique</term><term>Voie transcrânienne</term><term>Préhension</term><term>Complication</term><term>Pathogénie</term><term>Personne âgée</term></keywords><keywords scheme="Wicri" type="topic" xml:lang="fr"><term>Personne âgée</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml: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.</div></front></TEI><inist><standard h6="B"><pA><fA01 i1="01" i2="1"><s0>0885-3185</s0></fA01><fA03 i2="1"><s0>Mov. disord.</s0></fA03><fA05><s2>18</s2></fA05><fA06><s2>1</s2></fA06><fA08 i1="01" i2="1" l="ENG"><s1>Limb-kinetic apraxia in corticobasal degeneration: Clinical and kinematic features</s1></fA08><fA11 i1="01" i2="1"><s1>LEIGUARDA (Ramon C.)</s1></fA11><fA11 i1="02" i2="1"><s1>MERELLO (Marcelo)</s1></fA11><fA11 i1="03" i2="1"><s1>NOUZEILLES (Maria Inés)</s1></fA11><fA11 i1="04" i2="1"><s1>BALEJ (Jorge)</s1></fA11><fA11 i1="05" i2="1"><s1>RIVERO (Alberto)</s1></fA11><fA11 i1="06" i2="1"><s1>NOGUES (Martin)</s1></fA11><fA14 i1="01"><s1>Raúl Carrea Institute for Neurological Research (FLENI)</s1><s2>Buenos Aires</s2><s3>ARG</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ><sZ>6 aut.</sZ></fA14><fA20><s1>49-59</s1></fA20><fA21><s1>2003</s1></fA21><fA23 i1="01"><s0>ENG</s0></fA23><fA43 i1="01"><s1>INIST</s1><s2>20953</s2><s5>354000103916060050</s5></fA43><fA44><s0>0000</s0><s1>© 2003 INIST-CNRS. All rights reserved.</s1></fA44><fA45><s0>50 ref.</s0></fA45><fA47 i1="01" i2="1"><s0>03-0149886</s0></fA47><fA60><s1>P</s1></fA60><fA61><s0>A</s0></fA61><fA64 i1="01" i2="1"><s0>Movement disorders</s0></fA64><fA66 i1="01"><s0>USA</s0></fA66><fC01 i1="01" l="ENG"><s0>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.</s0></fC01><fC02 i1="01" i2="X"><s0>002B17G</s0></fC02><fC02 i1="02" i2="X"><s0>235</s0></fC02><fC03 i1="01" i2="X" l="FRE"><s0>Dégénérescence</s0><s5>01</s5></fC03><fC03 i1="01" i2="X" l="ENG"><s0>Degeneration</s0><s5>01</s5></fC03><fC03 i1="01" i2="X" l="SPA"><s0>Degeneración</s0><s5>01</s5></fC03><fC03 i1="02" i2="X" l="FRE"><s0>Cortex cérébral</s0><s5>02</s5></fC03><fC03 i1="02" i2="X" l="ENG"><s0>Cerebral cortex</s0><s5>02</s5></fC03><fC03 i1="02" i2="X" l="SPA"><s0>Corteza cerebral</s0><s5>02</s5></fC03><fC03 i1="03" i2="X" l="FRE"><s0>Noyau gris central</s0><s5>03</s5></fC03><fC03 i1="03" i2="X" l="ENG"><s0>Basal ganglion</s0><s5>03</s5></fC03><fC03 i1="03" i2="X" l="SPA"><s0>Núcleo basal</s0><s5>03</s5></fC03><fC03 i1="04" i2="X" l="FRE"><s0>Apraxie</s0><s5>04</s5></fC03><fC03 i1="04" i2="X" l="ENG"><s0>Apraxia</s0><s5>04</s5></fC03><fC03 i1="04" i2="X" l="SPA"><s0>Apraxia</s0><s5>04</s5></fC03><fC03 i1="05" i2="X" l="FRE"><s0>Membre</s0><s5>05</s5></fC03><fC03 i1="05" i2="X" l="ENG"><s0>Limb</s0><s5>05</s5></fC03><fC03 i1="05" i2="X" l="SPA"><s0>Miembro</s0><s5>05</s5></fC03><fC03 i1="06" i2="X" l="FRE"><s0>Cinématique</s0><s5>07</s5></fC03><fC03 i1="06" i2="X" l="ENG"><s0>Kinematics</s0><s5>07</s5></fC03><fC03 i1="06" i2="X" l="SPA"><s0>Cinemática</s0><s5>07</s5></fC03><fC03 i1="07" i2="X" l="FRE"><s0>Stimulus magnétique</s0><s5>10</s5></fC03><fC03 i1="07" i2="X" l="ENG"><s0>Magnetic stimulus</s0><s5>10</s5></fC03><fC03 i1="07" i2="X" l="SPA"><s0>Estímulo magnético</s0><s5>10</s5></fC03><fC03 i1="08" i2="X" l="FRE"><s0>Voie transcrânienne</s0><s5>11</s5></fC03><fC03 i1="08" i2="X" l="ENG"><s0>Transcranial route</s0><s5>11</s5></fC03><fC03 i1="08" i2="X" l="SPA"><s0>Vía transcraneana</s0><s5>11</s5></fC03><fC03 i1="09" i2="X" l="FRE"><s0>Préhension</s0><s5>13</s5></fC03><fC03 i1="09" i2="X" l="ENG"><s0>Gripping</s0><s5>13</s5></fC03><fC03 i1="09" i2="X" l="SPA"><s0>Prension</s0><s5>13</s5></fC03><fC03 i1="10" i2="X" l="FRE"><s0>Complication</s0><s5>17</s5></fC03><fC03 i1="10" i2="X" l="ENG"><s0>Complication</s0><s5>17</s5></fC03><fC03 i1="10" i2="X" l="SPA"><s0>Complicación</s0><s5>17</s5></fC03><fC03 i1="11" i2="X" l="FRE"><s0>Pathogénie</s0><s5>18</s5></fC03><fC03 i1="11" i2="X" l="ENG"><s0>Pathogenesis</s0><s5>18</s5></fC03><fC03 i1="11" i2="X" l="SPA"><s0>Patogenia</s0><s5>18</s5></fC03><fC03 i1="12" i2="X" l="FRE"><s0>Personne âgée</s0><s5>20</s5></fC03><fC03 i1="12" i2="X" l="ENG"><s0>Elderly</s0><s5>20</s5></fC03><fC03 i1="12" i2="X" l="SPA"><s0>Anciano</s0><s5>20</s5></fC03><fC07 i1="01" i2="X" l="FRE"><s0>Homme</s0></fC07><fC07 i1="01" i2="X" l="ENG"><s0>Human</s0></fC07><fC07 i1="01" i2="X" l="SPA"><s0>Hombre</s0></fC07><fC07 i1="02" i2="X" l="FRE"><s0>Système nerveux pathologie</s0><s5>37</s5></fC07><fC07 i1="02" i2="X" l="ENG"><s0>Nervous system diseases</s0><s5>37</s5></fC07><fC07 i1="02" i2="X" l="SPA"><s0>Sistema nervioso patología</s0><s5>37</s5></fC07><fC07 i1="03" i2="X" l="FRE"><s0>Système nerveux central pathologie</s0><s5>38</s5></fC07><fC07 i1="03" i2="X" l="ENG"><s0>Central nervous system disease</s0><s5>38</s5></fC07><fC07 i1="03" i2="X" l="SPA"><s0>Sistema nervosio central patología</s0><s5>38</s5></fC07><fC07 i1="04" i2="X" l="FRE"><s0>Encéphale pathologie</s0><s5>39</s5></fC07><fC07 i1="04" i2="X" l="ENG"><s0>Cerebral disorder</s0><s5>39</s5></fC07><fC07 i1="04" i2="X" l="SPA"><s0>Encéfalo patología</s0><s5>39</s5></fC07><fC07 i1="05" i2="X" l="FRE"><s0>Maladie dégénérative</s0><s5>40</s5></fC07><fC07 i1="05" i2="X" l="ENG"><s0>Degenerative disease</s0><s5>40</s5></fC07><fC07 i1="05" i2="X" l="SPA"><s0>Enfermedad degenerativa</s0><s5>40</s5></fC07><fC07 i1="06" i2="X" l="FRE"><s0>Trouble neurologique</s0><s5>45</s5></fC07><fC07 i1="06" i2="X" l="ENG"><s0>Neurological disorder</s0><s5>45</s5></fC07><fC07 i1="06" i2="X" l="SPA"><s0>Trastorno neurológico</s0><s5>45</s5></fC07><fC07 i1="07" i2="X" l="FRE"><s0>Electrodiagnostic</s0><s5>61</s5></fC07><fC07 i1="07" i2="X" l="ENG"><s0>Electrodiagnosis</s0><s5>61</s5></fC07><fC07 i1="07" i2="X" l="SPA"><s0>Electrodiagnóstico</s0><s5>61</s5></fC07><fN21><s1>083</s1></fN21><fN82><s1>PSI</s1></fN82></pA></standard></inist><affiliations><list><country><li>Argentine</li></country></list><tree><country name="Argentine"><noRegion><name sortKey="Leiguarda, Ramon C" sort="Leiguarda, Ramon C" uniqKey="Leiguarda R" first="Ramon C." last="Leiguarda">Ramon C. Leiguarda</name></noRegion><name sortKey="Balej, Jorge" sort="Balej, Jorge" uniqKey="Balej J" first="Jorge" last="Balej">Jorge Balej</name><name sortKey="Merello, Marcelo" sort="Merello, Marcelo" uniqKey="Merello M" first="Marcelo" last="Merello">Marcelo Merello</name><name sortKey="Nogues, Martin" sort="Nogues, Martin" uniqKey="Nogues M" first="Martin" last="Nogues">Martin Nogues</name><name sortKey="Nouzeilles, Maria Ines" sort="Nouzeilles, Maria Ines" uniqKey="Nouzeilles M" first="Maria Inés" last="Nouzeilles">Maria Inés Nouzeilles</name><name sortKey="Rivero, Alberto" sort="Rivero, Alberto" uniqKey="Rivero A" first="Alberto" last="Rivero">Alberto Rivero</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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