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Monosymptomatic resting tremor and Parkinson's disease: A multitracer positron emission tomographic study
Author(s) -
Ghaemi Mehran,
Raethjen Jan,
Hilker Rüdiger,
Rudolf Jobst,
Sobesky Jan,
Deuschl Günther,
Heiss WolfDieter
Publication year - 2002
Publication title -
movement disorders
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.352
H-Index - 198
eISSN - 1531-8257
pISSN - 0885-3185
DOI - 10.1002/mds.10125
Subject(s) - putamen , positron emission tomography , parkinson's disease , medicine , magnetic resonance imaging , nuclear medicine , resting tremor , central nervous system disease , essential tremor , binding potential , red nucleus , hyperintensity , psychology , radiology , disease , physical medicine and rehabilitation , nucleus , psychiatry
We sought to elucidate the relationship between monosymptomatic resting tremor (mRT) and Parkinson's disease (PD). We studied eight mRT patients (mean Hoehn and Yahr [H&Y], 1.1 ± 0.4), eight patients with PD (mean H&Y, 1.5 ± 0.8), who showed all three classic parkinsonian symptoms, and seven age‐matched healthy subjects. Subjects underwent cerebral magnetic resonance imaging (MRI) and multitracer positron emission tomography (PET) with 6‐[ 18 F]fluoro‐ L ‐dopa ( F ‐dopa), [ 18 F]fluorodeoxyglucose (FDG), and [ 11 C]raclopride (RACLO). PD and mRT patients did not show significant differences in F ‐dopa‐, RACLO‐, or FDG‐PET scans. In F ‐dopa‐ and RACLO‐PET, significant differences between the pooled patient data and control subjects were found for the following regions: anterior and posterior putamen ipsilateral and contralateral to the more affected body side, and ipsilateral and contralateral putaminal gradients of the K i values. Furthermore, we found a difference for the normalized glucose values of the whole cerebellum between the control group (0.94 ± 0.06) and PD patients (1.01 ± 0.04; P < 0.05) but not for the mRT group (0.97 ± 0.03). Our findings indicate that monosymptomatic resting tremor represents a phenotype of Parkinson's disease, with a nearly identical striatal dopaminergic deficit and postsynaptic D2‐receptor upregulation in both patient groups. We suggest that the cerebellar metabolic hyperactivity in PD is closer related to akinesia and rigidity rather than to tremor. © 2002 Movement Disorder Society