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Fluorodeoxyglucose positron emission tomography in Richardson's syndrome and progressive supranuclear palsy-parkinsonism

✍ Scribed by Karin Srulijes; Matthias Reimold; Rajka M. Liscic; Sarah Bauer; Elisabeth Dietzel; Inga Liepelt-Scarfone; Daniela Berg; Walter Maetzler


Book ID
102945957
Publisher
John Wiley and Sons
Year
2011
Tongue
English
Weight
1006 KB
Volume
27
Category
Article
ISSN
0885-3185

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✦ Synopsis


Abstract

Background:

We hypothesized that postural instability and cognitive decline in patients with Richardson's syndrome could be a consequence of reduced thalamic and frontal metabolism. Severe Parkinsonian signs in patients with progressive supranuclear palsy‐parkinsonism may be reflected by alterations in putaminal metabolism.

Methods:

Eleven patients with Richardson's syndrome, 8 patients with progressive supranuclear palsy‐parkinsonism, 12 with Parkinson's disease, and 10 controls underwent clinical assessment and fluorodeoxyglucose positron emission tomography (PET).

Results:

Richardson's syndrome patients showed pronounced thalamic hypometabolism, and patients with progressive supranuclear palsy‐parkinsonism pronounced putaminal hypometabolism, compared to all other investigated groups. The putamen/thalamus uptake ratio differentiated progressive supranuclear palsy‐parkinsonism from Richardson's syndrome (area under the curve = 0.86) and from Parkinson's disease (area under the curve = 0.80) with acceptable accuracy. Frontal hypometabolism was predominantly found in Richardson's syndrome patients.

Conclusions:

Richardson's syndrome, progressive supranuclear palsy‐parkinsonism and Parkinson's disease showed different metabolic patterns in fluorodeoxyglucose PET. © 2011 Movement Disorder Society


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