| Abstract No.: | A-C1084 |
| Country: | Canada |
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| Title: | PATHOLOGICAL GAMBLING IN PARKINSON’S DISEASE PATIENTS: BRAIN ACTIVATION, BETTING STRATEGIES, AND PERSONALITY TRAITS DIFFER FROM CONTROLS. |
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| Authors/Affiliations: | 2 Crystal Erickson*; 1 Michel Panisset; 1 Brigitte Stemmer; 2 Alain Dagher;
1 Centre Hopsitalier de l’Université de Montréal, QC, Canada; 2 Montreal Neurological Institute, McGill University, QC, Canada
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| Content: | Objectives: Parkinson’s disease (PD) is associated with depletion of dopamine (DA) in the nigrostriatal and, to a lesser extent, mesocorticolimbic DA pathways. Recent evidence suggests that administration of Levodopa and/or DA agonists, which attenuate the motor deficits in PD, can also cause behavioural/psychological side effects including drug addiction, compulsive behaviour, and pathological gambling (PG). In fact, dopamine replacement therapy has been found to cause abnormal impulse control in some PD patients, while normal reasoning remains intact. Since, impulsivity is thought to be the primary personality trait mediating vulnerability to many impulse-control disorders one theory of why only a subset of PD patients are vulnerable is that individual differences in basal (pre-morbid) impulsivity traits underlie the aberrant behaviour resulting from treatment. The purpose of this study was to investigate inter-individual differences in personality traits and neural responses to gambling between PD patients who are an are not susceptible to treatment induced addictions.
Materials/Methods: Two groups of PD patients, those who had in the past developed PG in response to dopaminergic treatment (PGPD, n=7) and those who did not (n=6), played a gambling task in which they were required to make either a high bet ($3) or a low bet ($1) on card hands with different probabilities of winning. Subjects played the game while undergoing fMRI scanning. PGPD patients were no longer suffering from PG at the time of testing.
Results: PGPD’s showed a shift toward higher bets as compared to controls. In other words, PGPDs were more likely to bet high on risky hands than did controls, supporting our lab’s previous findings in PGs without PD. PGPD’s tended to score higher on traits of impulsivity, novelty seeking, risk avoidance, depression, and reward dependence. In light of the fact that the PG behaviour was induced by pharmacological treatment in all cases, we assessed current and past PG tendencies using the Yale-Brown Obsessive-Compulsive (YBOCS) scale modified for PG. We found significantly lower YBOCS scores in the post-gambling period. Our results also show that, even among the PGPD group, there were significant inter-individual differences in betting profiles. This further supports findings from Cools et al. (Cerebral Cortex, 2001, 11:1136-43), who found the direction and extent of dopaminergic effects vary across individuals and tasks.
Conclusions: The results suggest that PD patients susceptible to treatment induced PG tend to score higher on measures of impulsivity and novelty seeking, and tend toward more risky behavior, even after the PG condition has been resolved. Young, healthy controls show significant activation in the Nucleus Accumbens (NAc) and Ventral Tegmental Area (VTA) in response to the anticipation and feedback of winning, while PD patients do not. Therefore, our study, while still preliminary, suggests that PDPG patients differ from PD controls in traits of impulsivity, novelty seeking and risky behaviour while PD patients in general differ from young, healthy controls in NAc and VTA activation in response to the gambling task. |
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