Apathy and impaired emotional facial recognition networks overlap in Parkinson's disease: a PET study with conjunction analyses.
Identifieur interne : 000A67 ( Main/Merge ); précédent : 000A66; suivant : 000A68Apathy and impaired emotional facial recognition networks overlap in Parkinson's disease: a PET study with conjunction analyses.
Auteurs : Gabriel Robert [France] ; Florence Le Jeune [France] ; Thibault Dondaine [France] ; Sophie Drapier [France] ; Julie Péron [Suisse] ; Clément Lozachmeur [France] ; Paul Sauleau [France] ; Jean-François Houvenaghel [France] ; David Travers [France] ; Bruno Millet [France] ; Marc Vérin [France] ; Dominique Drapier [France]Source :
- Journal of neurology, neurosurgery, and psychiatry [ 1468-330X ] ; 2014.
English descriptors
- KwdEn :
- Aged, Apathy (physiology), Brain Mapping, Facial Expression, Fluorodeoxyglucose F18, Frontal Lobe (physiopathology), Gyrus Cinguli (physiopathology), Humans, Image Processing, Computer-Assisted, Middle Aged, Parkinson Disease (physiopathology), Parkinson Disease (psychology), Positron-Emission Tomography, Recognition (Psychology) (physiology).
- MESH :
- chemical : Fluorodeoxyglucose F18.
- physiology : Apathy, Recognition (Psychology).
- physiopathology : Frontal Lobe, Gyrus Cinguli, Parkinson Disease.
- psychology : Parkinson Disease.
- Aged, Brain Mapping, Facial Expression, Humans, Image Processing, Computer-Assisted, Middle Aged, Positron-Emission Tomography.
Abstract
Apathy is a disabling non-motor symptom that is frequently observed in Parkinson's disease (PD). Its description and physiopathology suggest that it is partially mediated by emotional impairment, but this research issue has never been addressed at a clinical and metabolic level. We therefore conducted a metabolic study using (18)fluorodeoxyglucose positron emission tomography ((18)FDG PET) in 36 PD patients without depression and dementia. Apathy was assessed on the Apathy Evaluation Scale (AES), and emotional facial recognition (EFR) performances (ie, percentage of correct responses) were calculated for each patient. Confounding factors such as age, antiparkinsonian and antidepressant medication, global cognitive functions and depressive symptoms were controlled for. We found a significant negative correlation between AES scores and performances on the EFR task. The apathy network was characterised by increased metabolism within the left posterior cingulate (PC) cortex (Brodmann area (BA) 31). The impaired EFR network was characterised by decreased metabolism within the bilateral PC gyrus (BA 31), right superior frontal gyrus (BAs 10, 9 and 6) and left superior frontal gyrus (BA 10 and 11). By applying conjunction analyses to both networks, we identified the right premotor cortex (BA 6), right orbitofrontal cortex (BA 10), left middle frontal gyrus (BA 8) and left posterior cingulate gyrus (BA 31) as the structures supporting the association between apathy and impaired EFR. These results confirm that apathy in PD is partially mediated by impaired EFR, opening up new prospects for alleviating apathy in PD, such as emotional rehabilitation.
Url:
DOI: 10.1136/jnnp-2013-307025
PubMed: 24403280
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pubmed:24403280Le document en format XML
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<term>Apathy (physiology)</term>
<term>Brain Mapping</term>
<term>Facial Expression</term>
<term>Fluorodeoxyglucose F18</term>
<term>Frontal Lobe (physiopathology)</term>
<term>Gyrus Cinguli (physiopathology)</term>
<term>Humans</term>
<term>Image Processing, Computer-Assisted</term>
<term>Middle Aged</term>
<term>Parkinson Disease (physiopathology)</term>
<term>Parkinson Disease (psychology)</term>
<term>Positron-Emission Tomography</term>
<term>Recognition (Psychology) (physiology)</term>
</keywords>
<keywords scheme="MESH" type="chemical" xml:lang="en"><term>Fluorodeoxyglucose F18</term>
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<keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Apathy</term>
<term>Recognition (Psychology)</term>
</keywords>
<keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Frontal Lobe</term>
<term>Gyrus Cinguli</term>
<term>Parkinson Disease</term>
</keywords>
<keywords scheme="MESH" qualifier="psychology" xml:lang="en"><term>Parkinson Disease</term>
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<term>Brain Mapping</term>
<term>Facial Expression</term>
<term>Humans</term>
<term>Image Processing, Computer-Assisted</term>
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<front><div type="abstract" xml:lang="en">Apathy is a disabling non-motor symptom that is frequently observed in Parkinson's disease (PD). Its description and physiopathology suggest that it is partially mediated by emotional impairment, but this research issue has never been addressed at a clinical and metabolic level. We therefore conducted a metabolic study using (18)fluorodeoxyglucose positron emission tomography ((18)FDG PET) in 36 PD patients without depression and dementia. Apathy was assessed on the Apathy Evaluation Scale (AES), and emotional facial recognition (EFR) performances (ie, percentage of correct responses) were calculated for each patient. Confounding factors such as age, antiparkinsonian and antidepressant medication, global cognitive functions and depressive symptoms were controlled for. We found a significant negative correlation between AES scores and performances on the EFR task. The apathy network was characterised by increased metabolism within the left posterior cingulate (PC) cortex (Brodmann area (BA) 31). The impaired EFR network was characterised by decreased metabolism within the bilateral PC gyrus (BA 31), right superior frontal gyrus (BAs 10, 9 and 6) and left superior frontal gyrus (BA 10 and 11). By applying conjunction analyses to both networks, we identified the right premotor cortex (BA 6), right orbitofrontal cortex (BA 10), left middle frontal gyrus (BA 8) and left posterior cingulate gyrus (BA 31) as the structures supporting the association between apathy and impaired EFR. These results confirm that apathy in PD is partially mediated by impaired EFR, opening up new prospects for alleviating apathy in PD, such as emotional rehabilitation.</div>
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<idno type="DOI">10.1136/jnnp-2013-307025</idno>
<series><title level="j">Journal of Neurology, Neurosurgery and Psychiatry</title>
<idno type="ISSN">0022-3050</idno>
<imprint><date type="datePub">2014-09-30</date>
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<front><div type="abstract" xml:lang="en">Apathy is a disabling non-motor symptom that is frequently observed in Parkinson's disease (PD). Its description and physiopathology suggest that it is partially mediated by emotional impairment, but this research issue has never been addressed at a clinical and metabolic level. We therefore conducted a metabolic study using (18)fluorodeoxyglucose positron emission tomography ((18)FDG PET) in 36 PD patients without depression and dementia. Apathy was assessed on the Apathy Evaluation Scale (AES), and emotional facial recognition (EFR) performances (ie, percentage of correct responses) were calculated for each patient. Confounding factors such as age, antiparkinsonian and antidepressant medication, global cognitive functions and depressive symptoms were controlled for. We found a significant negative correlation between AES scores and performances on the EFR task. The apathy network was characterised by increased metabolism within the left posterior cingulate (PC) cortex (Brodmann area (BA) 31). The impaired EFR network was characterised by decreased metabolism within the bilateral PC gyrus (BA 31), right superior frontal gyrus (BAs 10, 9 and 6) and left superior frontal gyrus (BA 10 and 11). By applying conjunction analyses to both networks, we identified the right premotor cortex (BA 6), right orbitofrontal cortex (BA 10), left middle frontal gyrus (BA 8) and left posterior cingulate gyrus (BA 31) as the structures supporting the association between apathy and impaired EFR. These results confirm that apathy in PD is partially mediated by impaired EFR, opening up new prospects for alleviating apathy in PD, such as emotional rehabilitation.</div>
</front>
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<country xml:lang="fr">France</country>
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<author><name sortKey="Millet, Bruno" sort="Millet, Bruno" uniqKey="Millet B" first="Bruno" last="Millet">Bruno Millet</name>
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<country xml:lang="fr">France</country>
<wicri:regionArea>Behavior and Basal Ganglia host team 4712, University of Rennes 1, Rennes, France Department of Psychiatry, Rennes University Hospital, Guillaume Régnier Hospital Centre, Rennes</wicri:regionArea>
<placeName><region type="region">Région Bretagne</region>
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<settlement type="city">Rennes</settlement>
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<author><name sortKey="Le Jeune, Florence" sort="Le Jeune, Florence" uniqKey="Le Jeune F" first="Florence" last="Le Jeune">Florence Le Jeune</name>
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<country xml:lang="fr">France</country>
<wicri:regionArea>Behavior and Basal Ganglia host team 4712, University of Rennes 1, Rennes, France Department of Nuclear Medicine, Rennes University Hospital, Eugene Marquis Hospital Centre, Rennes</wicri:regionArea>
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<author><name sortKey="Dondaine, Thibault" sort="Dondaine, Thibault" uniqKey="Dondaine T" first="Thibault" last="Dondaine">Thibault Dondaine</name>
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<country xml:lang="fr">France</country>
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</author>
<author><name sortKey="Houvenaghel, Jean Francois" sort="Houvenaghel, Jean Francois" uniqKey="Houvenaghel J" first="Jean-François" last="Houvenaghel">Jean-François Houvenaghel</name>
<affiliation wicri:level="3"><nlm:affiliation>Behavior and Basal Ganglia host team 4712, University of Rennes 1, Rennes, France Department of Neurology, Rennes University Hospital, Rennes, France.</nlm:affiliation>
<country xml:lang="fr">France</country>
<wicri:regionArea>Behavior and Basal Ganglia host team 4712, University of Rennes 1, Rennes, France Department of Neurology, Rennes University Hospital, Rennes</wicri:regionArea>
<placeName><region type="region">Région Bretagne</region>
<region type="old region">Région Bretagne</region>
<settlement type="city">Rennes</settlement>
</placeName>
</affiliation>
</author>
<author><name sortKey="Travers, David" sort="Travers, David" uniqKey="Travers D" first="David" last="Travers">David Travers</name>
<affiliation wicri:level="3"><nlm:affiliation>Behavior and Basal Ganglia host team 4712, University of Rennes 1, Rennes, France Department of Psychiatry, Rennes University Hospital, Guillaume Régnier Hospital Centre, Rennes, France.</nlm:affiliation>
<country xml:lang="fr">France</country>
<wicri:regionArea>Behavior and Basal Ganglia host team 4712, University of Rennes 1, Rennes, France Department of Psychiatry, Rennes University Hospital, Guillaume Régnier Hospital Centre, Rennes</wicri:regionArea>
<placeName><region type="region">Région Bretagne</region>
<region type="old region">Région Bretagne</region>
<settlement type="city">Rennes</settlement>
</placeName>
</affiliation>
</author>
<author><name sortKey="Millet, Bruno" sort="Millet, Bruno" uniqKey="Millet B" first="Bruno" last="Millet">Bruno Millet</name>
<affiliation wicri:level="3"><nlm:affiliation>Behavior and Basal Ganglia host team 4712, University of Rennes 1, Rennes, France Department of Psychiatry, Rennes University Hospital, Guillaume Régnier Hospital Centre, Rennes, France.</nlm:affiliation>
<country xml:lang="fr">France</country>
<wicri:regionArea>Behavior and Basal Ganglia host team 4712, University of Rennes 1, Rennes, France Department of Psychiatry, Rennes University Hospital, Guillaume Régnier Hospital Centre, Rennes</wicri:regionArea>
<placeName><region type="region">Région Bretagne</region>
<region type="old region">Région Bretagne</region>
<settlement type="city">Rennes</settlement>
</placeName>
</affiliation>
</author>
<author><name sortKey="Verin, Marc" sort="Verin, Marc" uniqKey="Verin M" first="Marc" last="Vérin">Marc Vérin</name>
<affiliation wicri:level="3"><nlm:affiliation>Behavior and Basal Ganglia host team 4712, University of Rennes 1, Rennes, France Department of Neurology, Rennes University Hospital, Rennes, France.</nlm:affiliation>
<country xml:lang="fr">France</country>
<wicri:regionArea>Behavior and Basal Ganglia host team 4712, University of Rennes 1, Rennes, France Department of Neurology, Rennes University Hospital, Rennes</wicri:regionArea>
<placeName><region type="region">Région Bretagne</region>
<region type="old region">Région Bretagne</region>
<settlement type="city">Rennes</settlement>
</placeName>
</affiliation>
</author>
<author><name sortKey="Drapier, Dominique" sort="Drapier, Dominique" uniqKey="Drapier D" first="Dominique" last="Drapier">Dominique Drapier</name>
<affiliation wicri:level="3"><nlm:affiliation>Behavior and Basal Ganglia host team 4712, University of Rennes 1, Rennes, France Department of Psychiatry, Rennes University Hospital, Guillaume Régnier Hospital Centre, Rennes, France.</nlm:affiliation>
<country xml:lang="fr">France</country>
<wicri:regionArea>Behavior and Basal Ganglia host team 4712, University of Rennes 1, Rennes, France Department of Psychiatry, Rennes University Hospital, Guillaume Régnier Hospital Centre, Rennes</wicri:regionArea>
<placeName><region type="region">Région Bretagne</region>
<region type="old region">Région Bretagne</region>
<settlement type="city">Rennes</settlement>
</placeName>
</affiliation>
</author>
</analytic>
<series><title level="j">Journal of neurology, neurosurgery, and psychiatry</title>
<idno type="eISSN">1468-330X</idno>
<imprint><date when="2014" type="published">2014</date>
</imprint>
</series>
</biblStruct>
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</fileDesc>
<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged</term>
<term>Apathy (physiology)</term>
<term>Brain Mapping</term>
<term>Facial Expression</term>
<term>Fluorodeoxyglucose F18</term>
<term>Frontal Lobe (physiopathology)</term>
<term>Gyrus Cinguli (physiopathology)</term>
<term>Humans</term>
<term>Image Processing, Computer-Assisted</term>
<term>Middle Aged</term>
<term>Parkinson Disease (physiopathology)</term>
<term>Parkinson Disease (psychology)</term>
<term>Positron-Emission Tomography</term>
<term>Recognition (Psychology) (physiology)</term>
</keywords>
<keywords scheme="MESH" type="chemical" xml:lang="en"><term>Fluorodeoxyglucose F18</term>
</keywords>
<keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Apathy</term>
<term>Recognition (Psychology)</term>
</keywords>
<keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Frontal Lobe</term>
<term>Gyrus Cinguli</term>
<term>Parkinson Disease</term>
</keywords>
<keywords scheme="MESH" qualifier="psychology" xml:lang="en"><term>Parkinson Disease</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Aged</term>
<term>Brain Mapping</term>
<term>Facial Expression</term>
<term>Humans</term>
<term>Image Processing, Computer-Assisted</term>
<term>Middle Aged</term>
<term>Positron-Emission Tomography</term>
</keywords>
</textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en">Apathy is a disabling non-motor symptom that is frequently observed in Parkinson's disease (PD). Its description and physiopathology suggest that it is partially mediated by emotional impairment, but this research issue has never been addressed at a clinical and metabolic level. We therefore conducted a metabolic study using (18)fluorodeoxyglucose positron emission tomography ((18)FDG PET) in 36 PD patients without depression and dementia. Apathy was assessed on the Apathy Evaluation Scale (AES), and emotional facial recognition (EFR) performances (ie, percentage of correct responses) were calculated for each patient. Confounding factors such as age, antiparkinsonian and antidepressant medication, global cognitive functions and depressive symptoms were controlled for. We found a significant negative correlation between AES scores and performances on the EFR task. The apathy network was characterised by increased metabolism within the left posterior cingulate (PC) cortex (Brodmann area (BA) 31). The impaired EFR network was characterised by decreased metabolism within the bilateral PC gyrus (BA 31), right superior frontal gyrus (BAs 10, 9 and 6) and left superior frontal gyrus (BA 10 and 11). By applying conjunction analyses to both networks, we identified the right premotor cortex (BA 6), right orbitofrontal cortex (BA 10), left middle frontal gyrus (BA 8) and left posterior cingulate gyrus (BA 31) as the structures supporting the association between apathy and impaired EFR. These results confirm that apathy in PD is partially mediated by impaired EFR, opening up new prospects for alleviating apathy in PD, such as emotional rehabilitation.</div>
</front>
</TEI>
</PubMed>
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