Research Article Dopaminergic Modulation of Medial Prefrontal Cortex Deactivation in Parkinson Depression Anders H. Andersen, 1,2 Charles D. Smith, 2,3,4 John T. Slevin, 3,5 Richard J. Kryscio, 4,6,7 Catherine A. Martin, 8 Frederick A. Schmitt, 3,4,8,9 and Lee X. Blonder 3,4,9 1 Department of Anatomy and Neurobiology, University of Kentucky, Lexington, KY 40536, USA 2 Magnetic Resonance Imaging and Spectroscopy Center, University of Kentucky, Lexington, KY 40536, USA 3 Department of Neurology, University of Kentucky, Lexington, KY 40536, USA 4 Sanders-Brown Center on Aging, University of Kentucky, Lexington, KY 40536, USA 5 Veterans Administration Medical Center, Lexington, KY 40502, USA 6 Department of Statistics, University of Kentucky, Lexington, KY 40536, USA 7 Department of Biostatistics, University of Kentucky, Lexington, KY 40536, USA 8 Department of Psychiatry, University of Kentucky, Lexington, KY 40536, USA 9 Department of Behavioral Science, University of Kentucky, Lexington, KY 40536, USA Correspondence should be addressed to Anders H. Andersen; anders@uky.edu Received 28 July 2015; Accepted 25 November 2015 Academic Editor: Marjan Jahanshahi Copyright © 2015 Anders H. Andersen et al. Tis is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Parkinson’s disease (PD) is associated with emotional abnormalities. Dopaminergic medications ameliorate Parkinsonian motor symptoms, but less is known regarding the impact of dopaminergic agents on afective processing, particularly in depressed PD (dPD) patients. Te aim of this study was to examine the efects of dopaminergic pharmacotherapy on brain activation to emotional stimuli in depressed versus nondepressed Parkinson disease (ndPD) patients. Participants included 18 ndPD patients (11 men, 7 women) and 10 dPD patients (7 men, 3 women). Patients viewed photographs of emotional faces during functional MRI. Scans were performed while the patient was taking anti-Parkinson medication and the day afer medication had been temporarily discontinued. Results indicate that dopaminergic medications have opposite efects in the prefrontal cortex depending upon depression status. DPD patients show greater deactivation in the ventromedial prefrontal cortex (VMPFC) on dopaminergic medications than of, while ndPD patients show greater deactivation in this region of drugs. Te VMPFC is in the default-mode network (DMN). DMN activity is negatively correlated with activity in brain systems used for external visual attention. Tus dopaminergic medications may promote increased attention to external visual stimuli among dPD patients but impede normal suppression of DMN activity during external stimulation among ndPD patients. 1. Introduction Parkinson’s disease (PD) is characterized by tremor, muscular rigidity, and bradykinesia. Individuals with PD also experi- ence nonmotor symptoms, such as impairments in cognitive and emotional processing, including depression, anxiety, and apathy (see Blonder and Slevin [1] for a review). Although dopaminergic drugs show considerable efcacy in treating PD motor symptoms, dopaminergic pharmacotherapy may have variable efects on cognitive and afective processing depending upon the mood state of the PD patient. In particular, Blonder et al. [2] found that depressed PD (dPD) patients performed more poorly on neuropsychological tests of working memory and facial afect recognition while on dopaminergic medications than while of. Nondepressed PD (ndPD) patients showed the opposite pattern. Functional neuroimaging studies of dPD patients have shown abnormalities in the caudate, orbitofrontal cortex, medial frontal cortex, anterior cingulate, limbic system, and thalamus [3–7]. Few studies have examined regional Hindawi Publishing Corporation Parkinson’s Disease Volume 2015, Article ID 513452, 11 pages http://dx.doi.org/10.1155/2015/513452