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Neuroimaging Markers of Motor and Nonmotor Features of Parkinson's Disease: An 18FFluorodeoxyglucose Positron Emission Computed Tomography Study
Neuroimaging Markers of Motor and Nonmotor Features of Parkinson's Disease: An 18FFluorodeoxyglucose Positron Emission Computed Tomography Study
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Neuroimaging Markers of Motor and Nonmotor Features of Parkinson's Disease: An 18FFluorodeoxyglucose Positron Emission Computed Tomography Study
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Neuroimaging Markers of Motor and Nonmotor Features of Parkinson's Disease: An 18FFluorodeoxyglucose Positron Emission Computed Tomography Study
Neuroimaging Markers of Motor and Nonmotor Features of Parkinson's Disease: An 18FFluorodeoxyglucose Positron Emission Computed Tomography Study

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Neuroimaging Markers of Motor and Nonmotor Features of Parkinson's Disease: An 18FFluorodeoxyglucose Positron Emission Computed Tomography Study
Neuroimaging Markers of Motor and Nonmotor Features of Parkinson's Disease: An 18FFluorodeoxyglucose Positron Emission Computed Tomography Study
Journal Article

Neuroimaging Markers of Motor and Nonmotor Features of Parkinson's Disease: An 18FFluorodeoxyglucose Positron Emission Computed Tomography Study

2013
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Overview
Aim: We sought to identify markers of motor and nonmotor function in Parkinson's disease (PD) using advanced neuroimaging techniques in subjects with PD. Methods: We enrolled 26 nondemented PD subjects and 12 control subjects. All subjects underwent [ 18 F]fluorodeoxyglucose positron emission computed tomography (FDG-PET) and magnetic resonance imaging, and a complete neuropsychological battery. Results: FDG-PET of subjects with PD revealed significant metabolic elevations in the bilateral posterior lentiform nucleus, posterior cingulate, and parahippocampus, and metabolic reductions in the bilateral temporoparietal association cortex and occipital lobe versus controls. PD subjects had significant reductions in executive/attention function, memory/verbal learning, and speed of thinking, and significantly increased depression, anxiety and apathy scores compared with controls. Motor dysfunction correlated with increased metabolism in the posterior lentiform nucleus, pons, and cerebellum, and decreased metabolism in the temporoparietal lobe. Cognitive dysfunction correlated with increased posterior cingulate metabolism and decreased temporoparietal lobe metabolism. Depressive symptoms correlated with increased amygdala metabolism; anxiety scores correlated with decreased caudate metabolism, and apathy scores correlated with increased metabolism in the anterior cingulate and orbitofrontal lobe and decreased metabolism in the temporoparietal association cortex. Conclusions: Our findings showed that motor, cognitive, and emotional dysfunction in PD are associated with distinct patterns of cerebral metabolic changes.