In an influential study, de la Fuente-Fernandez et al. (2001)
scanned patients with PD using PET and a labelled
dopaminergic agonist ([11C] raclopride) which binds to
dopamine D2/D3 receptors. The striatal raclopride binding
potential of patients with PD was measured under two
conditions: (1) a placebo-controlled, blinded study in which
the patients did not know when they were receiving placebo or
active drug (apomorphine, a dopamine receptor agonist) – all
patients received both placebo and active drug; (2) an open
study in the same patients without placebo (baseline). When
placebo was administered, a significant decrease raclopride
binding potential was found in the striatum (caudate nucleus
and putamen) compared with baseline observations (Fig. 3).
The decrease in raclopride binding capacity correlated with
improvement in clinical symptoms. It is noteworthy that the
magnitude of the placebo response was comparable to that of
apomorphine. Moreover, there were no differences in the
striatal raclopride binding potential between this group of
patients when studied without placebo and another group of
patients matched for age and severity of parkinsonism and
examined solely in an open manner.