PET studies and motor complications in Parkinson's disease

Parkinson's disease (PD) patients with motor complications show a greater reduction in putamen [(18)F]dopa uptake on positron emission tomography (PET) compared with sustained responders to L-dopa, although individual ranges overlap considerably. This implies that, although loss of putamen dopamine storage predisposes motor complications in PD, it cannot be the only factor determining timing of onset. Additional PET studies suggest that loss of striatal dopamine storage capacity along with pulsatile exposure to exogenous L-dopa results in pathologically raised synaptic dopamine levels and deranged basal ganglia opioid transmission. This, rather than altered dopamine receptor binding, then causes inappropriate overactivity of basal ganglia-frontal projections, resulting in breakthrough involuntary movements.