Abstract
ABSTRACTIntroductionDopamine agonist medication is one of the largest risk factors for development of problematic impulse control behaviours (ICBs) in people with Parkinson’s disease. The present study investigated the potential of dopamine gene profiling and individual performance on impulse control tasks to explain ICB severity.MethodsClinical, genetic and task performance data were entered into a mixed-effects linear regression model for people with Parkinson’s disease taking (n = 50) or not taking (n = 25) dopamine agonist medication. Severity of ICBs was captured via the Questionnaire for Impulsive-compulsive disorders in Parkinson’s disease Rating Scale. A cumulative dopamine genetic risk score (DGRS) was calculated for each participant from variance in five dopamine-regulating genes. Objective measures of impulsive action and impulsive choice were measured on the Anticipatory Response Inhibition Task and Balloon Analogue Risk Task, respectively.ResultsFor participants on dopamine agonist medication, task performance reflecting greater impulsive choice (p = .014), and to a trend level greater impulsive action (p = .056), as well as a longer history of DA medication (p < .001) all predicted increased ICB severity. DGRS however, did not predict ICB severity (p = .708). No variables could explain ICB severity in the non-agonist group.ConclusionsOur task-derived measures of impulse control have the potential to predict ICB severity in people with Parkinson’s and warrant further investigation to determine whether they can be used to monitor ICB changes over time. The DGRS appears better suited to predicting the incidence, rather than severity, of ICBs on agonist medication.
Publisher
Cold Spring Harbor Laboratory