title: Progression of dopamine transporter decline in patients with the Parkinson variant of multiple system atrophy: a voxel-based analysis of [123I]β-CIT SPECT.
abstract: OBJECTIVE
  We characterized the progression of dopamine transporter (DAT) decline in the striatum and extrastriatal regions including the midbrain and pons of patients with the Parkinson variant of multiple system atrophy (MSA-P) and compared longitudinally collected SPECT results with those in a cohort of patients with Parkinson's disease (PD).
  
  
  METHODS
  Eight patients with MSA-P (age 60.4 ± 7.7 years, disease duration 2.4 ± 1 years, UPDRS-III motor score 39.7 ± 4.7), and 11 patients with PD (age 61.2 ± 6.4 years, disease duration 2.4 ± 1.1 years, UPDRS-III motor score 18.9 ± 7.6) underwent a baseline and follow-up [(123)I]β-CIT SPECT investigation within a time period of 1.3 years. Statistical parametric mapping (SPM) and a repetitive ANOVA design were used to objectively localize the decline in DAT availability without having to make an a priori hypothesis as to its location.
  
  
  RESULTS
  SPM localized significant reductions in [(123)I]β-CIT uptake in the dorsal brainstem of MSA-P patients compared to PD patients (p < 0.001) at baseline. Additional reductions in the DAT signal were localized in the caudate and anterior putamen of patients with MSA-P patients compared to PD patients at the follow-up examination (p < 0.001). Relative decline in tracer binding was evident in the caudate and anterior putamen of MSA-P patients compared to PD patients in the longitudinal analysis (p < 0.05), whereas no significant relative signal alteration was observed in the brainstem.
  
  
  CONCLUSIONS
  In contrast to PD, the relatively higher rate of signal reduction in the caudate and anterior putamen is consistent with the faster disease progression reported in MSA-P. At baseline, the tracer uptake in the brainstem was already at very low levels in the MSA-P patients compared to that in healthy control subjects and did not progress any further, suggesting that the degeneration of monoaminergic neurons is almost complete early in the disease course.
authors.affiliation: Department of Neurology, Innsbruck Medical University, Anichstrasse 35, 6020 Innsbruck, Austria. Michael.Nocker@i-med.ac.at
authors.forename: Michael
authors.initials: M
authors.lastname: Nocker
authors.forename: Klaus
authors.initials: K
authors.lastname: Seppi
authors.forename: Eveline
authors.initials: E
authors.lastname: Donnemiller
authors.forename: Irene
authors.initials: I
authors.lastname: Virgolini
authors.forename: Gregor K
authors.initials: GK
authors.lastname: Wenning
authors.forename: Werner
authors.initials: W
authors.lastname: Poewe
authors.forename: Christoph
authors.initials: C
authors.lastname: Scherfler
mesh_terms: D001921:Brain / Q000000981:diagnostic imaging / Q000378:metabolism / Q000503:physiopathology; D003042:Cocaine / Q000031:analogs & derivatives*; D050483:Dopamine Plasma Membrane Transport Proteins / Q000378:metabolism*; D005260:Female; D006801:Humans; D007090:Image Interpretation, Computer-Assisted; D008297:Male; D008875:Middle Aged; D009043:Motor Activity; D019578:Multiple System Atrophy / Q000150:complications*; D010300:Parkinson Disease / Q000150:complications / Q000000981:diagnostic imaging* / Q000378:metabolism* / Q000503:physiopathology; D013997:Time Factors; D015899:Tomography, Emission-Computed, Single-Photon
chemical_list: D050483:Dopamine Plasma Membrane Transport Proteins; C069723:2beta-carbomethoxy-3beta-(4-iodophenyl)tropane; D003042:Cocaine