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The molecular imaging of central nervous metabolic disturbances using fluorodeoxyglucose-positron emission tomography (FDG-PET) has been one of the major additions to the armamentarium for non-invasive evaluation of neurodegenerative and neuroinflammatory diseases.1 However, FDG-PET is a rather unspecific method that cannot distinguish between the different causes of hypermetabolism in given cortical or subcortical regions (eg, relative hyperactivation or inflammation). FDG-PET has gained the highest impact in the evaluation of neurodegenerative disease where given patterns of hypometabolism correlate very well with neuropsychological and clinical features.2 Nevertheless, using statistical parametric mapping, relatively increased glucose consumption …
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