[18F]FDOPA PET and clinical features in parkinsonism due to manganism
Identifieur interne : 001387 ( Main/Exploration ); précédent : 001386; suivant : 001388[18F]FDOPA PET and clinical features in parkinsonism due to manganism
Auteurs : Brad A. Racette [États-Unis] ; Jo Ann Antenor [États-Unis] ; Lori Mcgee-Minnich [États-Unis] ; Stephen M. Moerlein [États-Unis] ; Tom O. Videen [États-Unis] ; Vikas Kotagal [États-Unis] ; Joel S. Perlmutter [États-Unis]Source :
- Movement Disorders [ 0885-3185 ] ; 2005-04.
English descriptors
- KwdEn :
Abstract
Manganese exposure reportedly causes a clinically and pathophysiologically distinct syndrome from idiopathic Parkinson's disease (PD). We describe the clinical features and results of positron emission tomography with 6‐[18F]fluorodopa ([18F]FDOPA PET) of a patient with parkinsonism occurring in the setting of elevated blood manganese. The patient developed parkinsonism associated with elevated serum manganese from hepatic dysfunction. [18F]FDOPA PET demonstrated relatively symmetric and severely reduced [18F]FDOPA levels in the posterior putamen compared to controls. The globus pallidum interna had increased signal on T1‐weighted magnetic resonance imaging (MRI) images. We conclude that elevated manganese exposure may be associated with reduced striatal [18F]FDOPA uptake, and MRI may reveal selective abnormality within the internal segment of the pallidum. This case suggests that the clinical and pathophysiological features of manganese‐associated parkinsonism may overlap with that of PD. © 2005 Movement Disorder Society
Url:
DOI: 10.1002/mds.20381
Affiliations:
- États-Unis
- Missouri (État)
- Saint-Louis (Missouri)
- École de médecine (Université Washington de Saint-Louis)
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<front><div type="abstract" xml:lang="en">Manganese exposure reportedly causes a clinically and pathophysiologically distinct syndrome from idiopathic Parkinson's disease (PD). We describe the clinical features and results of positron emission tomography with 6‐[18F]fluorodopa ([18F]FDOPA PET) of a patient with parkinsonism occurring in the setting of elevated blood manganese. The patient developed parkinsonism associated with elevated serum manganese from hepatic dysfunction. [18F]FDOPA PET demonstrated relatively symmetric and severely reduced [18F]FDOPA levels in the posterior putamen compared to controls. The globus pallidum interna had increased signal on T1‐weighted magnetic resonance imaging (MRI) images. We conclude that elevated manganese exposure may be associated with reduced striatal [18F]FDOPA uptake, and MRI may reveal selective abnormality within the internal segment of the pallidum. This case suggests that the clinical and pathophysiological features of manganese‐associated parkinsonism may overlap with that of PD. © 2005 Movement Disorder Society</div>
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