Several hypotheses are emerging regarding the role of the parkinsonian lesions: parkinsonian dopaminergic lesions can increase levodopa-treated D3 receptor (D3R) expression in dorsal striatal regions; relative sparing or abberant neurodegeneration of dopaminergic limbic regions might be associated with differential motor, cognitive, and limbic effects of dopamine agonist therapy (appendix); and differential involvement of the parkinsonian lesion on striatal subregions might have an effect on the severity and latency of impulse control disorders or levodopa- induced dyskinesias (panel 1; appendix).