La maladie de Parkinson au Canada (serveur d'exploration)

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JOINT AMPLITUDE AND CONNECTIVITY COMPENSATORY MECHANISMS IN PARKINSON'S DISEASE

Identifieur interne : 000842 ( PascalFrancis/Curation ); précédent : 000841; suivant : 000843

JOINT 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 :

RBID : Pascal:10-0271036

Descripteurs français

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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C01 01    ENG  @0 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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Pascal:10-0271036

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<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. 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.</div>
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<fC07 i1="01" i2="X" l="ENG">
<s0>Osteoarticular system</s0>
<s5>20</s5>
</fC07>
<fC07 i1="01" i2="X" l="SPA">
<s0>Sistema osteoarticular</s0>
<s5>20</s5>
</fC07>
<fC07 i1="02" i2="X" l="FRE">
<s0>Maladie dégénérative</s0>
<s5>21</s5>
</fC07>
<fC07 i1="02" i2="X" l="ENG">
<s0>Degenerative disease</s0>
<s5>21</s5>
</fC07>
<fC07 i1="02" i2="X" l="SPA">
<s0>Enfermedad degenerativa</s0>
<s5>21</s5>
</fC07>
<fC07 i1="03" i2="X" l="FRE">
<s0>Pathologie du système nerveux</s0>
<s5>22</s5>
</fC07>
<fC07 i1="03" i2="X" l="ENG">
<s0>Nervous system diseases</s0>
<s5>22</s5>
</fC07>
<fC07 i1="03" i2="X" l="SPA">
<s0>Sistema nervioso patología</s0>
<s5>22</s5>
</fC07>
<fC07 i1="04" i2="X" l="FRE">
<s0>Pathologie de l'encéphale</s0>
<s5>23</s5>
</fC07>
<fC07 i1="04" i2="X" l="ENG">
<s0>Cerebral disorder</s0>
<s5>23</s5>
</fC07>
<fC07 i1="04" i2="X" l="SPA">
<s0>Encéfalo patología</s0>
<s5>23</s5>
</fC07>
<fC07 i1="05" i2="X" l="FRE">
<s0>Syndrome extrapyramidal</s0>
<s5>24</s5>
</fC07>
<fC07 i1="05" i2="X" l="ENG">
<s0>Extrapyramidal syndrome</s0>
<s5>24</s5>
</fC07>
<fC07 i1="05" i2="X" l="SPA">
<s0>Extrapiramidal síndrome</s0>
<s5>24</s5>
</fC07>
<fC07 i1="06" i2="X" l="FRE">
<s0>Pathologie du système nerveux central</s0>
<s5>25</s5>
</fC07>
<fC07 i1="06" i2="X" l="ENG">
<s0>Central nervous system disease</s0>
<s5>25</s5>
</fC07>
<fC07 i1="06" i2="X" l="SPA">
<s0>Sistema nervosio central patología</s0>
<s5>25</s5>
</fC07>
<fN21>
<s1>172</s1>
</fN21>
<fN44 i1="01">
<s1>OTO</s1>
</fN44>
<fN82>
<s1>OTO</s1>
</fN82>
</pA>
</standard>
</inist>
</record>

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