Binge Eating in Parkinson's Disease: Prevalence, Correlates and the Contribution of Deep Brain Stimulation

Dept. of Clinical & Health Psychology, University of Florida in Gainesville, FL, USA.
The Journal of neuropsychiatry and clinical neurosciences (Impact Factor: 2.82). 02/2011; 23(1):56-62. DOI: 10.1176/appi.neuropsych.23.1.56
Source: PubMed

ABSTRACT Of 96 Parkinson's disease patients surveyed at the University of Florida Movement Disorders Center, one (1%) met diagnostic criteria for binge-eating disorder. Eight (8.3%) exhibited subthreshold binge eating. Psychometric criteria classified problem gambling in 17.8%, hoarding in 8.3%, compulsive buying in 11.5%, hypersexuality in 1.0%, and mania in 1.0% of patients. More overeaters met psychometric criteria for at least one additional impulse-control disorder (67% versus 29%). No more overeaters than non-overeaters were taking a dopamine agonist (44% versus 41%). More overeaters had a history of subthalamic deep brain stimulation (DBS; 44% versus 14%). History of DBS was the only independent predictor of overeating.

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    • "The consequence is that we can only speculate here about the effects of STN-DBS on non-motor clinical disorders. Several non-motor manifestations of STN- DBS in PD patients have been described, including manic states and addictive behaviors (Funkiewiez et al., 2003; Kulisevsky et al., 2002; Mallet et al., 2007; Ulla et al., 2011; Zahodne et al., 2011). Regarding apathy, there is a debate about whether it is improved or aggravated by STN-DBS, which is confused by the fact that dopaminergic medication is usually reduced after electrode implantation (Chaudhuri and Schapira, 2009; Czernecki et al., 2008; Kirsch-Darrow et al., 2011; Le Jeune et al., 2009; Thobois et al., 2010). "
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    ABSTRACT: Rewards have various effects on human behavior and multiple representations in the human brain. Behaviorally, rewards notably enhance response vigor in incentive motivation paradigms and bias subsequent choices in instrumental learning paradigms. Neurally, rewards affect activity in different fronto-striatal regions attached to different motor effectors, for instance in left and right hemispheres for the two hands. Here we address the question of whether manipulating reward-related brain activity has local or general effects, with respect to behavioral paradigms and motor effectors. Neuronal activity was manipulated in a single hemisphere using unilateral deep brain stimulation (DBS) in patients with Parkinson's disease. Results suggest that DBS amplifies the representation of reward magnitude within the targeted hemisphere, so as to affect the behavior of the contralateral hand specifically. These unilateral DBS effects on behavior include both boosting incentive motivation and biasing instrumental choices. Furthermore, using computational modeling we show that DBS effects on incentive motivation can predict DBS effects on instrumental learning (or vice versa). Thus, we demonstrate the feasibility of causally manipulating reward-related neuronal activity in humans, in a manner that is specific to a class of motor effectors but that generalizes to different computational processes. As these findings proved independent from therapeutic effects on parkinsonian motor symptoms, they might provide insight into DBS impact on non-motor disorders, such as apathy or hypomania.
    Cortex 03/2013; 49(10). DOI:10.1016/j.cortex.2013.02.014 · 5.13 Impact Factor
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    • "Although numerous publications report weight gain, the motivational state of these patients has been rarely studied to favor instead metabolic or motor explanation. Interestingly, a recent report studying bingeeating in PD patients has highlighted the fact that the over-eaters were indeed those patients subjected to STN DBS (Zahodne et al., 2011). "
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    ABSTRACT: Since the early 90s, the subthalamic nucleus (STN) has started to be the subject of an increasing interest not only in the community of the basal ganglia scientists but also for neurosurgeons and neurologists, thanks to the development of the surgical treatment for Parkinson's disease. The involvement of the STN in cognitive and motivational processes has been demonstrated since, and psychiatrists are now considering this small structure as a possible target for the treatment of various disorders. In this review, we will address six questions to highlight (1) How increased knowledge has led us from a strictly motor model to an integrative one. (2) How knowledge acquired in animal models can be similar or (3) different from the effects observed in human patients. (4) How clinical trials are sometimes ahead of fundamental research carried out in animals, showing effects that could not be predicted on the basis of animal studies, thus questioning the relevance of some animal models, especially for psychiatric disorders. We will also address the possible future orientations (5) and how the use, or precaution not to use, certain key words in animal research dedicated to STN functions can lead to the omission of a certain amount of available data in the literature (6).
    Neuroscience 12/2011; 198:193-204. DOI:10.1016/j.neuroscience.2011.09.059 · 3.36 Impact Factor
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    ABSTRACT: Although the diagnosis of Parkinson disease (PD) still relies mainly on the appearance of its classical motor features of resting tremor, rigidity, bradykinesia, and postural instability, nonmotor manifestations in PD are now recognized as an integral component of this multisystem disorder. Nonmotor complications in PD occur commonly. The current understanding of cognitive dysfunction; neuropsychiatric manifestations including psychosis, impulsive control, and compulsive disorders, depression, anxiety and apathy; autonomic complications such as hypotension, erectile dysfunction, and urinary complications; sleep disorders and other nonmotor manifestations are summarized in this review. Nonmotor complications often carry a greater impact than motor features in PD. Therefore, heightened awareness and proper recognition of these features are critical in improving a Parkinson patient's quality of life.
    The Neurologist 01/2012; 18(1):1-16. DOI:10.1097/NRL.0b013e31823d7abb · 1.16 Impact Factor
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