H2(15)O PET activation studies enable the brain systems involved in controlling different aspects of motor function to be defined. In Parkinson's disease (PD) freely chosen limb movements are performed slowly. This bradykinesia is associated with selective underactivity of the supplementary motor area and dorsal prefrontal cortex, frontal association areas that receive subcortical input principally from the basal ganglia. At the same time there is compensatory overactivity of the lateral premotor and parietal cortex, areas that have a primary role in facilitating motor responses to visual and auditory cues. This finding explains why PD patients find it easier to perform cued as opposed to freely chosen actions. Levels of activation of the supplementary motor area and dorsal prefrontal cortex in PD can be restored with dopaminergic medication, implants of fetal mesencephalic tissue, internal pallidotomy or high frequency electrical subthalamic stimulation. Activation studies suggest that Parkinsonian rest tremor arises from a combination of inappropriate overactivity of cerebellar connections and loss of dopaminergic function. When tremor is relieved by ventral thalamotomy or thalamic stimulation this cerebellar overactivity is corrected but at the expense of reducing levels of primary motor cortex activation. It has been hypothesised that dyskinesias in PD arise due to altered dopamine receptor binding following chronic exposure to levodopa stimulation. Functional imaging findings, however, are against this hypothesis and rather suggest that downstream increases in basal ganglia opioid neurotransmission are more likely to be relevant.