Early stage idiopathic Parkinson’s disease (PD) is characterized by the three classic motor symptoms: rigidity, tremor, and bradykinesia. The core pathological hallmark of PD is the progressive loss of dopamine (DA) neurons in the ventrolateral tier of the substantia nigra pars compacta which primarily projects to the dorsal striatum (Fearnley and Lees, 1991; Kish, Shannak, and Hornykiewicz, 1988). The severely DA depleted dorsal striatum sends efferents, via the nigrostriatal pathway, to the supplementary motor area and distinct areas of the PFC, namely the dorsolateral PFC and ventrolateral PFC (Middleton and Strick, 2000a; Middleton and Strick, 2000b). Less severely affected are direct dopaminergic projections from the ventral tegmental area (VTA) to the PFC via the mesocortical pathway (Uhl, Hedreen, and Price, 1985). Due to the strong reciprocal connections between the striatum and specific areas of the frontal cortex, PD pathology results in a host of executive deficits, such as planning, attentional set-shifting, and working memory. These cognitive deficits are similar, but not identical, to ones observed with frontal lobe damage (Owen et al., 1992). This set of slides describes the executive deficits after frontal lobe lesions, and then compares them to the executive deficits seen in PD.