Imaging movement-related activity in medicated Parkin-associated and sporadic Parkinson's disease.
Identifieur interne : 001A35 ( Main/Exploration ); précédent : 001A34; suivant : 001A36Imaging movement-related activity in medicated Parkin-associated and sporadic Parkinson's disease.
Auteurs : Thilo Van Eimeren [Canada] ; Ferdinand Binkofski ; Carsten Buhmann ; Johann Hagenah ; Antonio P. Strafella ; Peter P. Pramstaller ; Hartwig R. Siebner ; Christine KleinSource :
- Parkinsonism & related disorders [ 1873-5126 ] ; 2010.
English descriptors
- KwdEn :
- Adult, Aged, Brain (physiopathology), Brain Mapping, Dyskinesias (genetics), Female, Humans, Image Interpretation, Computer-Assisted, Magnetic Resonance Imaging, Male, Middle Aged, Movement (physiology), Mutation, Parkinson Disease (genetics), Parkinson Disease (physiopathology), Ubiquitin-Protein Ligases (genetics).
- MESH :
- chemical , genetics : Ubiquitin-Protein Ligases.
- genetics : Dyskinesias, Parkinson Disease.
- physiology : Movement.
- physiopathology : Brain, Parkinson Disease.
- Adult, Aged, Brain Mapping, Female, Humans, Image Interpretation, Computer-Assisted, Magnetic Resonance Imaging, Male, Middle Aged, Mutation.
Abstract
Treatment-related motor complications such as dyskinesias are a major problem in the long-term management of Parkinson's disease (PD). In sporadic PD, a relatively early onset of the disease is known to be associated with an early development of dyskinesias. Although linked with early onset, patients with Parkin-associated PD often show a stable long-term response to dopaminergic therapy without developing treatment-induced motor complications. Therefore, we reasoned that this difference in vulnerability to develop dyskinesias under long-term dopaminergic therapy may be associated with differences in movement-related activation patterns in Parkin-associated compared to sporadic PD. To test this hypothesis, medicated non-dyskinetic patients with either Parkin-associated or sporadic PD underwent functional magnetic resonance imaging (fMRI) while performing externally specified or internally selected movements. Patients with Parkin-associated and sporadic PD showed no difference in movement-related activation patterns. Moreover, the covariates 'age' and 'disease duration' similarly influenced brain activation in both patient groups. The present finding suggests that a stable long-term motor response in some patients with Parkin-associated PD may not be related to differences in cortical recruitment. In conclusion, our findings corroborate a substantial pathophysiologic overlap between Parkin-associated and sporadic PD and lend further support to the notion that Parkin-associated PD is a suitable genetic model for sporadic PD.
DOI: 10.1016/j.parkreldis.2010.04.003
PubMed: 20434937
Affiliations:
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Le document en format XML
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<front><div type="abstract" xml:lang="en">Treatment-related motor complications such as dyskinesias are a major problem in the long-term management of Parkinson's disease (PD). In sporadic PD, a relatively early onset of the disease is known to be associated with an early development of dyskinesias. Although linked with early onset, patients with Parkin-associated PD often show a stable long-term response to dopaminergic therapy without developing treatment-induced motor complications. Therefore, we reasoned that this difference in vulnerability to develop dyskinesias under long-term dopaminergic therapy may be associated with differences in movement-related activation patterns in Parkin-associated compared to sporadic PD. To test this hypothesis, medicated non-dyskinetic patients with either Parkin-associated or sporadic PD underwent functional magnetic resonance imaging (fMRI) while performing externally specified or internally selected movements. Patients with Parkin-associated and sporadic PD showed no difference in movement-related activation patterns. Moreover, the covariates 'age' and 'disease duration' similarly influenced brain activation in both patient groups. The present finding suggests that a stable long-term motor response in some patients with Parkin-associated PD may not be related to differences in cortical recruitment. In conclusion, our findings corroborate a substantial pathophysiologic overlap between Parkin-associated and sporadic PD and lend further support to the notion that Parkin-associated PD is a suitable genetic model for sporadic PD.</div>
</front>
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<name sortKey="Hagenah, Johann" sort="Hagenah, Johann" uniqKey="Hagenah J" first="Johann" last="Hagenah">Johann Hagenah</name>
<name sortKey="Klein, Christine" sort="Klein, Christine" uniqKey="Klein C" first="Christine" last="Klein">Christine Klein</name>
<name sortKey="Pramstaller, Peter P" sort="Pramstaller, Peter P" uniqKey="Pramstaller P" first="Peter P" last="Pramstaller">Peter P. Pramstaller</name>
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<country name="Canada"><region name="Ontario"><name sortKey="Van Eimeren, Thilo" sort="Van Eimeren, Thilo" uniqKey="Van Eimeren T" first="Thilo" last="Van Eimeren">Thilo Van Eimeren</name>
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