“…Given this connectivity between the striatum and the DLPFC, it is not surprising that PD-related dysfunction in the striatum can lead to impairments in those cognitive processes dependent on the DLPFC, namely, executive functioning (Mega et al, 1994; Rinne et al, 2000). Studies have found a range of executive functioning deficits in individuals with PD, including working memory (Farina et al, 2000; Owen et al, 1992; Owen et al, 1995; Postle et al, 1997), planning and problem-solving ability (Culbertson et al, 2004; Hanes et al, 1996; Lewis et al, 2003;), verbal fluency (Azuma et al, 2003; Green et al, 2002; Gurd, 1995; Hanes et al, 1996; Stefanova et al, 2001), and set-shifting (Bondi et al, 1993; Dirksen et al, 2006; Farina et al, 2000; Green et al, 2002; Hayes et al, 1998; Lange et al, 1992; Owen et al, 1992; Stamenovic et al, 2004), although findings of frontal deficits have not been entirely consistent (Farina et al, 2000; Gabrieli et al, 1996; Levin et al, 1989; Rogers et al, 1998), possibly due to heterogeneity in samples. It has been suggested that these executive functioning deficits are direct effects of dopamine dysregulation, and neuroimaging studies using both PD and nonclinical populations have linked markers of dopamine and functional activation in both the striatum and the prefrontal cortex to performance on executive functioning tasks (Backman et al, 2000; Brück et al, 2001; Cropley et al, 2006; Lewis et al, 2003; Marie et al, 1999; Rinne et al, 2000; Sawamoto et al, 2008; van Beilen et al, 2008; Volkow et al, 1998).…”