Brain dopaminergic modulation associated with executive function in Parkinson's disease
Identifieur interne : 002419 ( Main/Curation ); précédent : 002418; suivant : 002420Brain dopaminergic modulation associated with executive function in Parkinson's disease
Auteurs : Karim Farid [France] ; Igor Sibon [France] ; Dominique Guehl [France] ; Emmanuel Cuny [France] ; Pierre Burbaud [France] ; Michèle Allard [France]Source :
- Movement Disorders [ 0885-3185 ] ; 2009-10-15.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
- Aged, Antiparkinson Agents (pharmacology), Antiparkinson Agents (therapeutic use), Brain (blood supply), Brain (drug effects), Brain (physiopathology), Brain Mapping, Cognition Disorders (drug therapy), Cognition Disorders (etiology), Dopamine (metabolism), Encephalon, Executive Function (drug effects), Executive Function (physiology), Executive function, Female, Humans, Image Processing, Computer-Assisted (methods), Levodopa (pharmacology), Levodopa (therapeutic use), Magnetic Resonance Imaging (methods), Male, Middle Aged, Modulation, Nervous system diseases, Neuropsychological Tests, Nuclear magnetic resonance imaging, Oxygen (blood), Parkinson Disease (complications), Parkinson Disease (drug therapy), Parkinson Disease (pathology), Parkinson disease, Parkinson's disease, dopaminergic cortical modulation, executive function, fMRI.
- MESH :
- chemical , blood : Oxygen.
- chemical , metabolism : Dopamine.
- chemical , pharmacology : Antiparkinson Agents, Levodopa.
- chemical , therapeutic use : Antiparkinson Agents, Levodopa.
- blood supply : Brain.
- complications : Parkinson Disease.
- drug effects : Brain, Executive Function.
- drug therapy : Cognition Disorders, Parkinson Disease.
- etiology : Cognition Disorders.
- methods : Image Processing, Computer-Assisted, Magnetic Resonance Imaging.
- pathology : Parkinson Disease.
- physiology : Executive Function.
- physiopathology : Brain.
- Aged, Brain Mapping, Female, Humans, Male, Middle Aged, Neuropsychological Tests.
Abstract
The progressive development of deficits in executive functions, including action planning, is a well‐known complication of Parkinson's disease. A dysfunction of the prefrontal lobe, which is known to be involved in the control of inhibitory processes, could explain the difficulties in initiating behavior or inhibiting ongoing actions in patients with PD. The strong dopaminergic innervation of the prefrontal cortex raises questions about the putative effects of dopa therapy on this cognitive impairment. In the present study, we used fMRI to examine the functional influence of dopa therapy on neural activity during a go/no‐go task in nine patients with and without levodopa treatment and in matched controls. Whereas the patient and control subjects exhibited the same performance during the go/no‐go task, different patterns of brain activation were observed depending on the dopaminergic status. The drug‐off state was characterized by more widely distributed brain activity, mainly in the bilateral caudate. Levodopa did not fully restore normal brain activation and induced changes in the pattern of cingulate cortex activity, which was more pronounced in the rostral part in the drug‐off state and in the caudal part after levodopa intake. These results support the idea of a critical role for dopamine in the control of executive functions in patients with PD. © 2009 Movement Disorder Society
Url:
DOI: 10.1002/mds.22709
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<front><div type="abstract" xml:lang="en">The progressive development of deficits in executive functions, including action planning, is a well‐known complication of Parkinson's disease. A dysfunction of the prefrontal lobe, which is known to be involved in the control of inhibitory processes, could explain the difficulties in initiating behavior or inhibiting ongoing actions in patients with PD. The strong dopaminergic innervation of the prefrontal cortex raises questions about the putative effects of dopa therapy on this cognitive impairment. In the present study, we used fMRI to examine the functional influence of dopa therapy on neural activity during a go/no‐go task in nine patients with and without levodopa treatment and in matched controls. Whereas the patient and control subjects exhibited the same performance during the go/no‐go task, different patterns of brain activation were observed depending on the dopaminergic status. The drug‐off state was characterized by more widely distributed brain activity, mainly in the bilateral caudate. Levodopa did not fully restore normal brain activation and induced changes in the pattern of cingulate cortex activity, which was more pronounced in the rostral part in the drug‐off state and in the caudal part after levodopa intake. These results support the idea of a critical role for dopamine in the control of executive functions in patients with PD. © 2009 Movement Disorder Society</div>
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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Brain Dopaminergic Modulation Associated with Executive Function in Parkinson's Disease</title>
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<placeName><settlement type="city">Bordeaux</settlement>
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<author><name sortKey="Guehl, Dominique" sort="Guehl, Dominique" uniqKey="Guehl D" first="Dominique" last="Guehl">Dominique Guehl</name>
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<placeName><settlement type="city">Bordeaux</settlement>
</placeName>
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</author>
<author><name sortKey="Allard, Michele" sort="Allard, Michele" uniqKey="Allard M" first="Michèle" last="Allard">Michèle Allard</name>
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<placeName><settlement type="city">Bordeaux</settlement>
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<placeName><settlement type="city">Bordeaux</settlement>
</placeName>
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<country>France</country>
<placeName><settlement type="city">Bordeaux</settlement>
</placeName>
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<placeName><settlement type="city">Paris</settlement>
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</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="2009">2009</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>Encephalon</term>
<term>Executive function</term>
<term>Modulation</term>
<term>Nervous system diseases</term>
<term>Nuclear magnetic resonance imaging</term>
<term>Parkinson disease</term>
</keywords>
<keywords scheme="Pascal" xml:lang="fr"><term>Maladie de Parkinson</term>
<term>Pathologie du système nerveux</term>
<term>Encéphale</term>
<term>Modulation</term>
<term>Fonction exécutive</term>
<term>Imagerie RMN</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en">The progressive development of deficits in executive functions, including action planning, is a well-known complication of Parkinson's disease. A dysfunction of the prefrontal lobe, which is known to be involved in the control of inhibitory processes, could explain the difficulties in initiating behavior or inhibiting ongoing actions in patients with PD. The strong dopaminergic innervation of the prefrontal cortex raises questions about the putative effects of dopa therapy on this cognitive impairment. In the present study, we used fMRI to examine the functional influence of dopa therapy on neural activity during a go/no-go task in nine patients with and without levodopa treatment and in matched controls. Whereas the patient and control subjects exhibited the same performance during the go/no-go task, different patterns of brain activation were observed depending on the dopaminergic status. The drug-off state was characterized by more widely distributed brain activity, mainly in the bilateral caudate. Levodopa did not fully restore normal brain activation and induced changes in the pattern of cingulate cortex activity, which was more pronounced in the rostral part in the drug-off state and in the caudal part after levodopa intake. These results support the idea of a critical role for dopamine in the control of executive functions in patients with PD.</div>
</front>
</TEI>
</INIST>
<ISTEX><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Brain dopaminergic modulation associated with executive function in Parkinson's disease</title>
<author><name sortKey="Farid, Karim" sort="Farid, Karim" uniqKey="Farid K" first="Karim" last="Farid">Karim Farid</name>
</author>
<author><name sortKey="Sibon, Igor" sort="Sibon, Igor" uniqKey="Sibon I" first="Igor" last="Sibon">Igor Sibon</name>
</author>
<author><name sortKey="Guehl, Dominique" sort="Guehl, Dominique" uniqKey="Guehl D" first="Dominique" last="Guehl">Dominique Guehl</name>
</author>
<author><name sortKey="Cuny, Emmanuel" sort="Cuny, Emmanuel" uniqKey="Cuny E" first="Emmanuel" last="Cuny">Emmanuel Cuny</name>
</author>
<author><name sortKey="Burbaud, Pierre" sort="Burbaud, Pierre" uniqKey="Burbaud P" first="Pierre" last="Burbaud">Pierre Burbaud</name>
</author>
<author><name sortKey="Allard, Michele" sort="Allard, Michele" uniqKey="Allard M" first="Michèle" last="Allard">Michèle Allard</name>
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<idno type="RBID">ISTEX:0C62DB0B5BE49F52ECB956002CAA2B853993A84F</idno>
<date when="2009" year="2009">2009</date>
<idno type="doi">10.1002/mds.22709</idno>
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</placeName>
</affiliation>
<affiliation wicri:level="1"><country xml:lang="fr">France</country>
<wicri:regionArea>CHU de Bordeaux, Bordeaux</wicri:regionArea>
<placeName><settlement type="city">Bordeaux</settlement>
</placeName>
</affiliation>
<affiliation wicri:level="1"><country xml:lang="fr">France</country>
<wicri:regionArea>Université Bordeaux 2, Bordeaux</wicri:regionArea>
<placeName><settlement type="city">Bordeaux</settlement>
</placeName>
</affiliation>
</author>
<author><name sortKey="Sibon, Igor" sort="Sibon, Igor" uniqKey="Sibon I" first="Igor" last="Sibon">Igor Sibon</name>
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<placeName><settlement type="city">Bordeaux</settlement>
</placeName>
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<affiliation wicri:level="1"><country xml:lang="fr">France</country>
<wicri:regionArea>Université Bordeaux 2, Bordeaux</wicri:regionArea>
<placeName><settlement type="city">Bordeaux</settlement>
</placeName>
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</author>
<author><name sortKey="Guehl, Dominique" sort="Guehl, Dominique" uniqKey="Guehl D" first="Dominique" last="Guehl">Dominique Guehl</name>
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<wicri:regionArea>CHU de Bordeaux, Bordeaux</wicri:regionArea>
<placeName><settlement type="city">Bordeaux</settlement>
</placeName>
</affiliation>
<affiliation wicri:level="1"><country xml:lang="fr">France</country>
<wicri:regionArea>Université Bordeaux 2, Bordeaux</wicri:regionArea>
<placeName><settlement type="city">Bordeaux</settlement>
</placeName>
</affiliation>
<affiliation wicri:level="1"><country xml:lang="fr">France</country>
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<author><name sortKey="Cuny, Emmanuel" sort="Cuny, Emmanuel" uniqKey="Cuny E" first="Emmanuel" last="Cuny">Emmanuel Cuny</name>
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<placeName><settlement type="city">Bordeaux</settlement>
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<author><name sortKey="Burbaud, Pierre" sort="Burbaud, Pierre" uniqKey="Burbaud P" first="Pierre" last="Burbaud">Pierre Burbaud</name>
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<author><name sortKey="Allard, Michele" sort="Allard, Michele" uniqKey="Allard M" first="Michèle" last="Allard">Michèle Allard</name>
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<series><title level="j">Movement Disorders</title>
<title level="j" type="abbrev">Mov. Disord.</title>
<idno type="ISSN">0885-3185</idno>
<idno type="eISSN">1531-8257</idno>
<imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher>
<pubPlace>Hoboken</pubPlace>
<date type="published" when="2009-10-15">2009-10-15</date>
<biblScope unit="vol">24</biblScope>
<biblScope unit="issue">13</biblScope>
<biblScope unit="page" from="1962">1962</biblScope>
<biblScope unit="page" to="1969">1969</biblScope>
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<idno type="ISSN">0885-3185</idno>
</series>
<idno type="istex">0C62DB0B5BE49F52ECB956002CAA2B853993A84F</idno>
<idno type="DOI">10.1002/mds.22709</idno>
<idno type="ArticleID">MDS22709</idno>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged</term>
<term>Antiparkinson Agents (pharmacology)</term>
<term>Antiparkinson Agents (therapeutic use)</term>
<term>Brain (blood supply)</term>
<term>Brain (drug effects)</term>
<term>Brain (physiopathology)</term>
<term>Brain Mapping</term>
<term>Cognition Disorders (drug therapy)</term>
<term>Cognition Disorders (etiology)</term>
<term>Dopamine (metabolism)</term>
<term>Executive Function (drug effects)</term>
<term>Executive Function (physiology)</term>
<term>Female</term>
<term>Humans</term>
<term>Image Processing, Computer-Assisted (methods)</term>
<term>Levodopa (pharmacology)</term>
<term>Levodopa (therapeutic use)</term>
<term>Magnetic Resonance Imaging (methods)</term>
<term>Male</term>
<term>Middle Aged</term>
<term>Neuropsychological Tests</term>
<term>Oxygen (blood)</term>
<term>Parkinson Disease (complications)</term>
<term>Parkinson Disease (drug therapy)</term>
<term>Parkinson Disease (pathology)</term>
<term>Parkinson's disease</term>
<term>dopaminergic cortical modulation</term>
<term>executive function</term>
<term>fMRI</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="blood" xml:lang="en"><term>Oxygen</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Dopamine</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Antiparkinson Agents</term>
<term>Levodopa</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Antiparkinson Agents</term>
<term>Levodopa</term>
</keywords>
<keywords scheme="MESH" qualifier="blood supply" xml:lang="en"><term>Brain</term>
</keywords>
<keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Parkinson Disease</term>
</keywords>
<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Brain</term>
<term>Executive Function</term>
</keywords>
<keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Cognition Disorders</term>
<term>Parkinson Disease</term>
</keywords>
<keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Cognition Disorders</term>
</keywords>
<keywords scheme="MESH" qualifier="methods" xml:lang="en"><term>Image Processing, Computer-Assisted</term>
<term>Magnetic Resonance Imaging</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Parkinson Disease</term>
</keywords>
<keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Executive Function</term>
</keywords>
<keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Brain</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Aged</term>
<term>Brain Mapping</term>
<term>Female</term>
<term>Humans</term>
<term>Male</term>
<term>Middle Aged</term>
<term>Neuropsychological Tests</term>
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<front><div type="abstract" xml:lang="en">The progressive development of deficits in executive functions, including action planning, is a well‐known complication of Parkinson's disease. A dysfunction of the prefrontal lobe, which is known to be involved in the control of inhibitory processes, could explain the difficulties in initiating behavior or inhibiting ongoing actions in patients with PD. The strong dopaminergic innervation of the prefrontal cortex raises questions about the putative effects of dopa therapy on this cognitive impairment. In the present study, we used fMRI to examine the functional influence of dopa therapy on neural activity during a go/no‐go task in nine patients with and without levodopa treatment and in matched controls. Whereas the patient and control subjects exhibited the same performance during the go/no‐go task, different patterns of brain activation were observed depending on the dopaminergic status. The drug‐off state was characterized by more widely distributed brain activity, mainly in the bilateral caudate. Levodopa did not fully restore normal brain activation and induced changes in the pattern of cingulate cortex activity, which was more pronounced in the rostral part in the drug‐off state and in the caudal part after levodopa intake. These results support the idea of a critical role for dopamine in the control of executive functions in patients with PD. © 2009 Movement Disorder Society</div>
</front>
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