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Clinical Trial
. 2001 Jun;22(6):721-5.
doi: 10.1097/00006231-200106000-00017.

Striatal dopamine transporter binding in early to moderately advanced Parkinson's disease: monitoring of disease progression over 2 years

Affiliations
Clinical Trial

Striatal dopamine transporter binding in early to moderately advanced Parkinson's disease: monitoring of disease progression over 2 years

M Chouker et al. Nucl Med Commun. 2001 Jun.

Abstract

Imaging of striatal dopamine transporter binding allows differentiation between patients with Parkinson's disease and controls. We investigated the use of this technique to monitor disease progression. We used N-(3-iodopropen-2-yl)-2beta-carbomethoxy-3beta-(4-chlorophenyl) tropane (IPT) and single photon emission computed tomography (SPECT) to determine dopamine transporter function in eight patients with Parkinson's disease Hoehn and Yahr stage I to III over time. Patients were recruited from the movement disorder clinic and were studied at entry and after a follow-up period of 1 and 2 years. Specific striatal IPT binding was measured with a manual region of interest technique. At entry, all patients showed a reduction of striatal IPT uptake of approximately 50% compared to controls, with a mean striatum to background ratio of 3.61 +/- 0.72 (controls, 7.34 +/- 1.18). Putamen to background ratios were initially measured as 2.42 +/- 0.74 and caudate to background ratios as 5.00 +/- 0.73 (controls, 6.46 +/- 1.22 for putamen and 8.58 +/- 1.36 for caudate). Specific striatal IPT binding decreased by a mean of 6.6% in the first year and another 5.3% in the second year. Changes of specific IPT binding over time were similar in caudate and putamen. In patients with clinically asymmetric disease, differences between the rate of decline in the ipsilateral and contralateral sides could not be detected. The findings suggest that IPT SPECT can quantify the reduction of dopamine transporter binding over time. This technique seems to be a useful tool in monitoring the intra-individual progression of dopaminergic cell loss in patients with Parkinson's disease and may help to follow the effects of putative neuroprotective drugs in future clinical trials.

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