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. Author manuscript; available in PMC: 2011 Jun 1.
Published in final edited form as: Ann Neurol. 2010 Jun;67(6):715–725. doi: 10.1002/ana.21995

TABLE. PD Imaging Studies of Striatal or Putaminal Dopaminergic Deficits at Time of Symptom Onset.

AUTHOR YEAR N MODALITY LIGAND STRIATUM (% LOSS) PUTAMEN (% LOSS) ANALYSIS
LEVODOPA METABOLISM
Morrish et al 1995 11 PET [18F]DOPA --- 20-43 HY I (IPSI vs CONTRA)
Morrish et al 1998 32 PET [18F]DOPA --- 25 REGRESSION
Lee et al 2000 13 (HY I) PET [18F]DOPA --- 38-52 HY I (IPSI vs CONTRA)
Hilker et al 2005 31 PET [18F]DOPA --- 31 REGRESSION
DOPAMINE TRANSPORTER BINDING
Tissingh et al 1998 8 (HY I) SPECT [123I]β-CIT 39-51 51-64 HY I (IPSI vs CONTRA)
Lee et al 2000 13 (HY I) PET [11C]MP --- 56-71 HY I (IPSI vs CONTRA)
Schwartz et al 2004 6 SPECT [123I]IPT 43 56 REGRESSION
VESICULAR MONOAMINE TRANSPORTER BINDING
Lee et al 2000 13 (HY I) PET [11C]DTBZ 51-62 HY I (IPSI vs CONTRA)

In each study, the degree of dopaminergic terminal loss in whole striatum or putamen was determined either by regression analysis with back extrapolation to Time = 0, or by determination of the loss on the side ipsilateral (IPSI) to symptoms in comparison to the side contralateral (CONTRA) to symptoms in patients with unilateral PD (Hoehn and Yahr Stage I (HY I)). β-CIT: 2β-carbomethoxy-3 β -(4-iodophenyl); MP: methylphenidate; IPT: N-(3-iodopropene-2-yl)-2β - carbomethoxy-3β -(chlorophenyl); DTBZ: dihydrotetrabenazine.