The overarching goal of the current project is increased understanding of emotional processes in Parkinson's disease. Parkinson's disease (PD) is one of the most common neurodegenerative disorders of late life. It is caused by progressive dopaminergic depletion with motor, cognitive, and emotional changes. While advances have been made with respect to motor symptoms, emotional and neuropsychiatric changes (depression, apathy, anxiety) are prevalent and can be the some of the most disturbing, disabling, and complex aspects of the disorder. Findings from four recent studies of emotional responding have found that non-demented Parkinson patients without psychiatric co-morbidities exhibited blunted physiologic reactivity to aversive pictures as indexed by the startle eyeblink response (Bowers et al., 2006;Miller et al., 2009;Zahodne et al., 2011) or an event related potential component of motivated attention, the late positive potential, LPP (Dietz et al., 2011a). This reduced reactivity to unpleasant stimuli was not due to medication, depression, perceptual difficulties, or failure to generate basic startle or electrocortical activity. One interpretation of this emotional blunting relates to dopaminergic gating and inhibition of the amygdala, a key limbic structure in the emotion processing cascade. In light of these findings, the aims of the present study are to learn whether Parkinson patients can upregulate their responses to emotional stimuli and whether success in doing so is related to integrity of frontal-executive function. To address this aim, two approaches for amplifying emotional reactivity will be taken, one that is more active and self-directed (auto-evoked) and another that is more passive (exo-evoked). Both approaches have been associated with increased physiologic reactivity in healthy controls, as indexed by electrocortical responses (Moser et al., 2009, 2010;Foti &Hajcak, 2008;McNamara et al., 2009). In the current research, non-demented, non-depressed Parkinson patients and healthy controls will participate in two separate studies. Parkinson patients will be psychometrically classified into two cognitive subgroups based on neurocognitive measures: executively impaired (PD-exec) and cognitively normal (PD). During testing, participants will view standardized sets of neutral and emotional pictures while startle eyeblink responses and EEG are recorded. One study will involve use of self-directed regulation strategies to increase reactivity to emotional pictures, and the other study will involve passive listening to narratives that alter subsequent semantic meaning. Primary dependent variables will be amplitude of LPP, startle eyeblink and verbal ratings of valence and arousal. The major hypothesis is that effective regulation of physiologic reactivity to emotional stimuli by PD patients will depend on the integrity of frontal-executive systems. Parkinson patients in the cognitively normal subgroup will show changes in emotional reactivity regardless of active or more passive regulation approaches, whereas PD patients with executive disturbance will benefit only in the passive condition. Relationship to disease variables and neuropsychiatric factors (apathy, anxiety) will be examined. The proposed research will be the first to test whether Parkinson patients can benefit from techniques for bolstering their physiological and emotional reactivity. If predictions are met, the obtained findings may have broad implications for emotional enhancement in Parkinson disease.
This study examines emotional blunting in patients with Parkinson disease and focuses on nonpharmacologic techniques to bolster emotional reactivity. This study has potential treatment implications for improving apathy symptoms in Parkinson disease.
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|Jones, Jacob D; Butterfield, London C; Song, Woojin et al. (2015) Anxiety and Depression Are Better Correlates of Parkinson's Disease Quality of Life Than Apathy. J Neuropsychiatry Clin Neurosci 27:213-8|
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|Zahodne, Laura B; Marsiske, Michael; Bowers, Dawn (2013) A latent class analysis of psychological disturbance in Parkinson's disease. Int J Geriatr Psychiatry 28:1054-60|
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