Executive processes in Parkinson's disease: FDG-PET and network analysis.
Identifieur interne : 000451 ( Ncbi/Curation ); précédent : 000450; suivant : 000452Executive processes in Parkinson's disease: FDG-PET and network analysis.
Auteurs : Catherine Lozza [France] ; Jean-Claude Baron ; David Eidelberg ; Marc J. Mentis ; Maren Carbon ; Rose-Marie MariéSource :
- Human brain mapping [ 1065-9471 ] ; 2004.
English descriptors
- KwdEn :
- Adult, Aged, Brain (diagnostic imaging), Brain (metabolism), Brain (physiopathology), Corpus Striatum (diagnostic imaging), Corpus Striatum (metabolism), Corpus Striatum (physiopathology), Female, Fluorodeoxyglucose F18, Frontal Lobe (diagnostic imaging), Frontal Lobe (metabolism), Frontal Lobe (physiopathology), Humans, Male, Middle Aged, Movement (physiology), Nerve Net (diagnostic imaging), Nerve Net (metabolism), Nerve Net (physiopathology), Neural Networks (Computer), Neural Pathways (diagnostic imaging), Neural Pathways (metabolism), Neural Pathways (physiopathology), Parkinson Disease (diagnostic imaging), Parkinson Disease (metabolism), Parkinson Disease (physiopathology), Tomography, Emission-Computed.
- MESH :
- chemical : Fluorodeoxyglucose F18.
- diagnostic imaging : Brain, Corpus Striatum, Frontal Lobe, Nerve Net, Neural Pathways, Parkinson Disease.
- metabolism : Brain, Corpus Striatum, Frontal Lobe, Nerve Net, Neural Pathways, Parkinson Disease.
- physiology : Movement.
- physiopathology : Brain, Corpus Striatum, Frontal Lobe, Nerve Net, Neural Pathways, Parkinson Disease.
- Adult, Aged, Female, Humans, Male, Middle Aged, Neural Networks (Computer), Tomography, Emission-Computed.
Abstract
It is assumed widely that the clinical expression of Parkinson's Disease (PD), both motor and cognitive, is subtended by topographically distributed brain networks. However, little is known about the functional neuroanatomy of executive dysfunction in PD. Our objective was to validate further in a PD group the use of network analysis to assess the relationship between executive processes and pathological disorganization of frontostriatal networks. We studied 15 patients with idiopathic PD, and 7 age-matched normal controls, using resting [(18)F]fluorodeoxyglucose (FDG) and high-resolution positron emission tomography (PET). We carried out network analysis on regional metabolic data to identify specific covariation patterns associated with motor and executive dysfunction. We detected two independent patterns relating respectively to the two clinical abnormalities. The first pattern (principal component 1) was topographically similar to that described previously in other PD populations. Subject scores for this pattern discriminated patients from controls and correlated significantly with bradykinesia ratings (P = 0.013, r = 0.655) in PD patients. The second pattern (principal component 2) was characterized by relative ventromedial frontal, hippocampal, and striatal hypometabolism, associated with mediodorsal thalamic hypermetabolism. In the PD group, scores from this pattern correlated with scores on the conditional associative learning (CAL; P = 0.01, r = 0.690) and the Brown Peterson paradigm (BPP; P = 0.017, r = -0.651) tests, respectively assessing strategy and planning, and working memory. According to these findings, the networks subserving bradykinesia and executive dysfunction in PD seems to be topographically distinct and to involve different aspects of subcortico-cortical processing.
DOI: 10.1002/hbm.20033
PubMed: 15195290
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pubmed:15195290Le document en format XML
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<front><div type="abstract" xml:lang="en">It is assumed widely that the clinical expression of Parkinson's Disease (PD), both motor and cognitive, is subtended by topographically distributed brain networks. However, little is known about the functional neuroanatomy of executive dysfunction in PD. Our objective was to validate further in a PD group the use of network analysis to assess the relationship between executive processes and pathological disorganization of frontostriatal networks. We studied 15 patients with idiopathic PD, and 7 age-matched normal controls, using resting [(18)F]fluorodeoxyglucose (FDG) and high-resolution positron emission tomography (PET). We carried out network analysis on regional metabolic data to identify specific covariation patterns associated with motor and executive dysfunction. We detected two independent patterns relating respectively to the two clinical abnormalities. The first pattern (principal component 1) was topographically similar to that described previously in other PD populations. Subject scores for this pattern discriminated patients from controls and correlated significantly with bradykinesia ratings (P = 0.013, r = 0.655) in PD patients. The second pattern (principal component 2) was characterized by relative ventromedial frontal, hippocampal, and striatal hypometabolism, associated with mediodorsal thalamic hypermetabolism. In the PD group, scores from this pattern correlated with scores on the conditional associative learning (CAL; P = 0.01, r = 0.690) and the Brown Peterson paradigm (BPP; P = 0.017, r = -0.651) tests, respectively assessing strategy and planning, and working memory. According to these findings, the networks subserving bradykinesia and executive dysfunction in PD seems to be topographically distinct and to involve different aspects of subcortico-cortical processing.</div>
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