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Brain Advance Access published online on April 7, 2005

Brain, doi:10.1093/brain/awh485
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© The Author (2005). Published by Oxford University Press on behalf of the Guarantors of Brain. All rights reserved. For Permissions, please email: journals.permissions@oupjournals.org
Received October 18, 2004
Revised January 24, 2005
Accepted February 21, 2005

Article

Voxel-wise analysis of [123I]{beta}-CIT SPECT differentiates the Parkinson variant of multiple system atrophy from idiopathic Parkinson's disease

Christoph Scherfler 1*, Klaus Seppi 1, Eveline Donnemiller 2, Georg Goebel 3, Christian Brenneis 1, Irene Virgolini 2, Gregor K. Wenning 1, and Werner Poewe 1

1 Department of Neurology, Innsbruck Medical University, Anichstrasse 35, 6020 Innsbruck, Austria
2 Department of Nuclear Medicine, Innsbruck Medical University, Anichstrasse 35, 6020 Innsbruck, Austria
3 Department of Medical Statistics, Informatics and Health Economics, Innsbruck Medical University, Anichstrasse 35, 6020 Innsbruck, Austria

* To whom correspondence should be addressed.
Christoph Scherfler, E-mail: christoph.scherfler{at}uibk.ac.at


   Abstract

To investigate the cerebral dopamine transporter status in the early stages of the parkinson-variant of multiple system atrophy (MSA-P), 15 patients with MSA-P and a disease duration up to 3 years were studied with [123I]{beta}-CIT single photon emission computed tomography (SPECT). Data were compared with 13 age-matched healthy control subjects and 15 patients with idiopathic Parkinson's disease (IPD), matched for age and disease duration. Parametric SPECT images of the specific-to-nondisplaceable equilibrium partition coefficient (V3''), which is proportional to the receptor density (Bmax) have been generated. To objectively localize focal changes in dopaminergic function throughout the entire brain volume without having to make an a priori hypothesis as to their location, statistical parametric mapping (SPM) was applied to our [123I]{beta}-CIT SPECT study. Both MSA-P and IPD patients showed significant decreases in striatal [123I]{beta}-CIT SPECT uptake. However, in MSA-P patients an additional reduction in midbrain [123I]{beta}-CIT signal was localized with SPM compared with control subjects (MSA-P, V3'': 0.89 ± 0.37 versus controls V3'': 1.81 ± 0.38; P < 0.001) and patients with IPD (V3'': 1.84 ± 0.26; P < 0.001). Stepwise linear discriminant analysis of mean [123I]{beta}-CIT uptake in the putamen, caudate and midbrain identified the caudate and midbrain as indices to classify correctly 95.2% of subjects as either normal, patients with MSA-P or IPD. Voxel-wise analysis of [123I]{beta}-CIT SPECT revealed more widespread decline of monoaminergic transporter availability in MSA-P compared with IPD, matching the underlying pathological features. We suggest that the quantification of midbrain DAT signal should be included in the routine clinical analysis of [123I]{beta}-CIT SPECT in patients with uncertain parkinsonism.

Keywords: [123I]{beta}-CIT SPECT; multiple system atrophy; idiopathic Parkinson's disease; statistical parametric mapping; discriminant analysis.
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