JOINT AMPLITUDE AND CONNECTIVITY COMPENSATORY MECHANISMS IN PARKINSON'S DISEASE
Identifieur interne : 000334 ( PascalFrancis/Checkpoint ); précédent : 000333; suivant : 000335JOINT AMPLITUDE AND CONNECTIVITY COMPENSATORY MECHANISMS IN PARKINSON'S DISEASE
Auteurs : S. J. Palmer [Canada] ; J. Li [Canada] ; Z. J. Wang [Canada] ; M. J. Mckeown [Canada]Source :
- Neuroscience [ 0306-4522 ] ; 2010.
Descripteurs français
- Pascal (Inist)
English descriptors
Abstract
Neuroimaging studies in Parkinson's disease (PD) have previously demonstrated several regions of hypo- and hyper-activation during voluntary movement. How these patterns of amplitude changes at multiple discrete foci relate to changes within functional networks recruited by a given task is unclear. Changes in both amplitude and connectivity have both been individually shown within the striato-thalamo-cortical (STC) loop in PD, as well as other regions, most consistently in the cerebellum and primary motor cortex. We have previously shown overactivation of the cerebellum and motor cortex in PD subjects off medication during a visuo-motor tracking task performed at three frequencies. Here, we show that this change in activation amplitude is also accompanied by significant changes in functional connectivity between regions of interest (ROIs), with enhanced connectivity within the cerebello-thalamo-cortical (CTC) loop as well as increased inter-hemispheric communication between several basal ganglia structures. Although changes in activation amplitude were influenced by the frequency of movement performed in the tracking task, functional connectivity changes were robustly present across all three task frequencies performed, suggesting that functional connectivity analysis in PD may be a more sensitive means of detecting plastic changes which are relatively invariant to the particulars of the experimental task. Additionally, we demonstrate amplitude and connectivity changes in structures that are typically active during the resting state, or "default-mode," in PD. Unlike in STC/CTC loops, where the direction of change was the same for amplitude and connectivity, default-mode regions showed increased amplitude but decreased connectivity. Our results further support that the CTC is recruited in PD to compensate for dysfunctional basal ganglia circuits, and that this recruitment involves both amplitude and connectivity changes. The differing relationship between amplitude and connectivity changes within individual loops highlights the importance of jointly examining them in order to fully elucidate functional changes in Parkinson's disease.
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J." last="Palmer">S. J. Palmer</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Department of Neuroscience, University of British Columbia</s1><s2>Vancouver, BC</s2><s3>CAN</s3><sZ>1 aut.</sZ></inist:fA14><country>Canada</country><wicri:noRegion>Vancouver, BC</wicri:noRegion></affiliation><affiliation wicri:level="1"><inist:fA14 i1="02"><s1>Pacific Parkinson's Research Centre</s1><s2>Vancouver, BC</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>4 aut.</sZ></inist:fA14><country>Canada</country><wicri:noRegion>Pacific Parkinson's Research Centre</wicri:noRegion></affiliation></author><author><name sortKey="Li, J" sort="Li, J" uniqKey="Li J" first="J." last="Li">J. Li</name><affiliation wicri:level="1"><inist:fA14 i1="03"><s1>Department of Electrical and Computer Engineering, University of British Columbia</s1><s2>Vancouver, BC</s2><s3>CAN</s3><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ></inist:fA14><country>Canada</country><wicri:noRegion>Vancouver, BC</wicri:noRegion></affiliation></author><author><name sortKey="Wang, Z J" sort="Wang, Z J" uniqKey="Wang Z" first="Z. J." last="Wang">Z. J. Wang</name><affiliation wicri:level="1"><inist:fA14 i1="03"><s1>Department of Electrical and Computer Engineering, University of British Columbia</s1><s2>Vancouver, BC</s2><s3>CAN</s3><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ></inist:fA14><country>Canada</country><wicri:noRegion>Vancouver, BC</wicri:noRegion></affiliation></author><author><name sortKey="Mckeown, M J" sort="Mckeown, M J" uniqKey="Mckeown M" first="M. J." last="Mckeown">M. J. Mckeown</name><affiliation wicri:level="1"><inist:fA14 i1="02"><s1>Pacific Parkinson's Research Centre</s1><s2>Vancouver, BC</s2><s3>CAN</s3><sZ>1 aut.</sZ><sZ>4 aut.</sZ></inist:fA14><country>Canada</country><wicri:noRegion>Pacific Parkinson's Research Centre</wicri:noRegion></affiliation><affiliation wicri:level="1"><inist:fA14 i1="03"><s1>Department of Electrical and Computer Engineering, University of British Columbia</s1><s2>Vancouver, BC</s2><s3>CAN</s3><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ></inist:fA14><country>Canada</country><wicri:noRegion>Vancouver, BC</wicri:noRegion></affiliation><affiliation wicri:level="1"><inist:fA14 i1="04"><s1>Department of Medicine (Neurology), University of British Columbia</s1><s2>Vancouver, BC</s2><s3>CAN</s3><sZ>4 aut.</sZ></inist:fA14><country>Canada</country><wicri:noRegion>Vancouver, BC</wicri:noRegion></affiliation><affiliation wicri:level="1"><inist:fA14 i1="05"><s1>Brain Research Centre, University of British Columbia</s1><s2>Vancouver, BC</s2><s3>CAN</s3><sZ>4 aut.</sZ></inist:fA14><country>Canada</country><wicri:noRegion>Vancouver, BC</wicri:noRegion></affiliation></author></analytic><series><title level="j" type="main">Neuroscience</title><title level="j" type="abbreviated">Neuroscience</title><idno type="ISSN">0306-4522</idno><imprint><date when="2010">2010</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">Neuroscience</title><title level="j" type="abbreviated">Neuroscience</title><idno type="ISSN">0306-4522</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Functional imaging</term><term>Joint</term><term>Nuclear magnetic resonance imaging</term><term>Parkinson disease</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Articulation</term><term>Imagerie RMN</term><term>Imagerie fonctionnelle</term><term>Maladie de Parkinson</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Neuroimaging studies in Parkinson's disease (PD) have previously demonstrated several regions of hypo- and hyper-activation during voluntary movement. How these patterns of amplitude changes at multiple discrete foci relate to changes within functional networks recruited by a given task is unclear. Changes in both amplitude and connectivity have both been individually shown within the striato-thalamo-cortical (STC) loop in PD, as well as other regions, most consistently in the cerebellum and primary motor cortex. We have previously shown overactivation of the cerebellum and motor cortex in PD subjects off medication during a visuo-motor tracking task performed at three frequencies. Here, we show that this change in activation amplitude is also accompanied by significant changes in functional connectivity between regions of interest (ROIs), with enhanced connectivity within the cerebello-thalamo-cortical (CTC) loop as well as increased inter-hemispheric communication between several basal ganglia structures. Although changes in activation amplitude were influenced by the frequency of movement performed in the tracking task, functional connectivity changes were robustly present across all three task frequencies performed, suggesting that functional connectivity analysis in PD may be a more sensitive means of detecting plastic changes which are relatively invariant to the particulars of the experimental task. Additionally, we demonstrate amplitude and connectivity changes in structures that are typically active during the resting state, or "default-mode," in PD. Unlike in STC/CTC loops, where the direction of change was the same for amplitude and connectivity, default-mode regions showed increased amplitude but decreased connectivity. Our results further support that the CTC is recruited in PD to compensate for dysfunctional basal ganglia circuits, and that this recruitment involves both amplitude and connectivity changes. 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Unlike in STC/CTC loops, where the direction of change was the same for amplitude and connectivity, default-mode regions showed increased amplitude but decreased connectivity. Our results further support that the CTC is recruited in PD to compensate for dysfunctional basal ganglia circuits, and that this recruitment involves both amplitude and connectivity changes. 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J." last="Palmer">S. J. Palmer</name></noRegion><name sortKey="Li, J" sort="Li, J" uniqKey="Li J" first="J." last="Li">J. Li</name><name sortKey="Mckeown, M J" sort="Mckeown, M J" uniqKey="Mckeown M" first="M. J." last="Mckeown">M. J. Mckeown</name><name sortKey="Mckeown, M J" sort="Mckeown, M J" uniqKey="Mckeown M" first="M. J." last="Mckeown">M. J. Mckeown</name><name sortKey="Mckeown, M J" sort="Mckeown, M J" uniqKey="Mckeown M" first="M. J." last="Mckeown">M. J. Mckeown</name><name sortKey="Mckeown, M J" sort="Mckeown, M J" uniqKey="Mckeown M" first="M. J." last="Mckeown">M. J. Mckeown</name><name sortKey="Palmer, S J" sort="Palmer, S J" uniqKey="Palmer S" first="S. J." last="Palmer">S. J. Palmer</name><name sortKey="Wang, Z J" sort="Wang, Z J" uniqKey="Wang Z" first="Z. J." last="Wang">Z. J. Wang</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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