La maladie de Parkinson en France (serveur d'exploration)

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Cortical motor reorganization in akinetic patients with Parkinson's disease: A functional MRI study

Identifieur interne : 003C01 ( Main/Curation ); précédent : 003C00; suivant : 003C02

Cortical motor reorganization in akinetic patients with Parkinson's disease: A functional MRI study

Auteurs : U. Sabatini [France] ; K. Boulanouar [France, Italie] ; N. Fabre [France] ; F. Martin [France] ; C. Carel [France] ; C. Colonnese [Italie] ; L. Bozzao [Italie] ; I. Berry [France] ; J. L. Montastruc [France] ; F. Chollet [France] ; O. Rascol [France]

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RBID : Pascal:00-0094277

Descripteurs français

English descriptors

Abstract

Using functional MRI (fMRI), we have studied the changes induced by the performance of a complex sequential motor task in the cortical areas of six akinetic patients with Parkinson's disease and six normal subjects. Compared with the normal subjects, the patients with Parkinson's disease exhibited a relatively decreased fMRI signal in the rostral part of the supplementary motor area (SMA) and in the right dorsolateral prefrontal cortex, as previously shown in PET studies. Concomitantly, the same patients exhibited a significant bilateral relative increase in fMRI signal in the primary sensorimotor cortex, lateral premotor cortex, inferior parietal cortex, caudal part of the SMA and anterior cingulate cortex. These fMRI data confirm that the frontal hypoactivation observed in patients with Parkinson's disease is restricted to the rostral part of the SMA and to the dorsolateral prefrontal cortex. These results also show that, apart from the lateral premotor and parietal cortices, increased fMRI signals can be found in other cortical motor areas of these patients, including the posterior SMA, the anterior cingulate cortex and the primary sensorimotor cortices, which are then likely to participate in the same putative attempt by the dopamine-denervated brain to recruit parallel motor circuits in order to overcome the functional deficit of the striatocortical motor loops.

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Pascal:00-0094277

Le document en format XML

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<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
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<sZ>8 aut.</sZ>
<sZ>10 aut.</sZ>
<sZ>11 aut.</sZ>
</inist:fA14>
<country>France</country>
<wicri:noRegion>University Hospital of Toulouse</wicri:noRegion>
<wicri:noRegion>INSERM U455, University Hospital of Toulouse</wicri:noRegion>
</affiliation>
<affiliation wicri:level="1">
<inist:fA14 i1="03">
<s1>Department of Neurology, University Hospital of Toulouse</s1>
<s3>FRA</s3>
<sZ>3 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>10 aut.</sZ>
</inist:fA14>
<country>France</country>
<wicri:noRegion>University Hospital of Toulouse</wicri:noRegion>
<wicri:noRegion>Department of Neurology, University Hospital of Toulouse</wicri:noRegion>
</affiliation>
</author>
<author>
<name sortKey="Rascol, O" sort="Rascol, O" uniqKey="Rascol O" first="O." last="Rascol">O. Rascol</name>
<affiliation wicri:level="1">
<inist:fA14 i1="01">
<s1>INSERM U455, University Hospital of Toulouse</s1>
<s3>FRA</s3>
<sZ>1 aut.</sZ>
<sZ>2 aut.</sZ>
<sZ>3 aut.</sZ>
<sZ>4 aut.</sZ>
<sZ>5 aut.</sZ>
<sZ>8 aut.</sZ>
<sZ>10 aut.</sZ>
<sZ>11 aut.</sZ>
</inist:fA14>
<country>France</country>
<wicri:noRegion>University Hospital of Toulouse</wicri:noRegion>
<wicri:noRegion>INSERM U455, University Hospital of Toulouse</wicri:noRegion>
</affiliation>
<affiliation wicri:level="1">
<inist:fA14 i1="05">
<s1>Department of Clinical Pharmacology and Clinical Investigation Center, University Hospital of Toulouse</s1>
<s3>FRA</s3>
<sZ>9 aut.</sZ>
<sZ>11 aut.</sZ>
</inist:fA14>
<country>France</country>
<wicri:noRegion>University Hospital of Toulouse</wicri:noRegion>
<wicri:noRegion>Department of Clinical Pharmacology and Clinical Investigation Center, University Hospital of Toulouse</wicri:noRegion>
</affiliation>
</author>
</analytic>
<series>
<title level="j" type="main">Brain</title>
<title level="j" type="abbreviated">Brain</title>
<idno type="ISSN">0006-8950</idno>
<imprint>
<date when="2000">2000</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
<seriesStmt>
<title level="j" type="main">Brain</title>
<title level="j" type="abbreviated">Brain</title>
<idno type="ISSN">0006-8950</idno>
</seriesStmt>
</fileDesc>
<profileDesc>
<textClass>
<keywords scheme="KwdEn" xml:lang="en">
<term>Akinesia</term>
<term>Cartography</term>
<term>Elderly</term>
<term>Exploration</term>
<term>Motor cortex</term>
<term>Motricity</term>
<term>Nuclear magnetic resonance imaging</term>
<term>Parkinson disease</term>
<term>Supplementary motor area</term>
</keywords>
<keywords scheme="Pascal" xml:lang="fr">
<term>Parkinson maladie</term>
<term>Akinésie</term>
<term>Imagerie RMN</term>
<term>Cortex moteur</term>
<term>Aire motrice supplémentaire</term>
<term>Motricité</term>
<term>Cartographie</term>
<term>Exploration</term>
<term>Personne âgée</term>
</keywords>
<keywords scheme="Wicri" type="topic" xml:lang="fr">
<term>Cartographie</term>
<term>Personne âgée</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front>
<div type="abstract" xml:lang="en">Using functional MRI (fMRI), we have studied the changes induced by the performance of a complex sequential motor task in the cortical areas of six akinetic patients with Parkinson's disease and six normal subjects. Compared with the normal subjects, the patients with Parkinson's disease exhibited a relatively decreased fMRI signal in the rostral part of the supplementary motor area (SMA) and in the right dorsolateral prefrontal cortex, as previously shown in PET studies. Concomitantly, the same patients exhibited a significant bilateral relative increase in fMRI signal in the primary sensorimotor cortex, lateral premotor cortex, inferior parietal cortex, caudal part of the SMA and anterior cingulate cortex. These fMRI data confirm that the frontal hypoactivation observed in patients with Parkinson's disease is restricted to the rostral part of the SMA and to the dorsolateral prefrontal cortex. These results also show that, apart from the lateral premotor and parietal cortices, increased fMRI signals can be found in other cortical motor areas of these patients, including the posterior SMA, the anterior cingulate cortex and the primary sensorimotor cortices, which are then likely to participate in the same putative attempt by the dopamine-denervated brain to recruit parallel motor circuits in order to overcome the functional deficit of the striatocortical motor loops.</div>
</front>
</TEI>
</record>

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