We studied cerebral dopamine D2-receptor binding using [C]raclopride and PET in 18 previously untreated patients with Parkinson’s disease (PD) and 14 healthyvolunteer subjects. Sixteen patients were scanned before and after 3 to 4 months of stable oral therapy with either L-dopa (300 mg/d) (n = 7) or lisuride (0.8 to 1.2 mg/d) (n = 9). Two additional patients were investigated before and after a continuous IV infusion of L-dopa. In addition, we studied the effect of acute IV L-dopa and lisuride administration on C]raclopride binding in a healthy rhesus monkey. At baseline, PD patients showed higher uptake values in the putamen than did healthy subjects (<0.0001). Oral lisuride treatment lowered [11C]raclopride uptake in the putamen (-19%) and in the caudate nucleus (-15%) compared with baseline, but the differencedid not reach significance upon Bonferroni correction for multiple comparisons. However, putamen tracer uptake returned to baseline in two patients when we repeateraclopride scans 4 days after lisuride withdrawal. Oral L-dopa treatment did not induce changesin the putamen or caudate nucleus indices. Acute lisuride (25 %g) administration in a healthy monkey reduced striatal uptake values, but acute injection of L-dopa (300 mg) did not. The results suggest that lisuride blocks [11C]raclopride binding at dopamine D2-receptor sites and demonstrate that 3 to 4 months’ oral therapy with L-dopa or lisuride does not change striatal dopamine D2-receptor density in PD patients.
|Number of pages||5|
|Publication status||Published - 1994|
ASJC Scopus subject areas
- Arts and Humanities (miscellaneous)
- Clinical Neurology