Trait impulsivity and response-inhibition in Parkinson Disease. An fMRI study.

IntroductionDopamine agonists and levodopa have been implicated in impulse-control disorder (ICD) development since they can induce alterations in the frontostriatal network that manage reward and mediate impulse monitoring and control. The aim the study was to explore the response-inhibition performance and the neural correlates of inhibition in Parkinsons disease (PD) patients that varied on self-reported trait impulsivity.\n\nMethodsTen cognitively non-impaired patients with PD were recruited. They underwent a neurological evaluation, a neuropsychological assessment and questionnaires on behavioral mood changes. The Barratt Impulsiveness Scale (BISS-11) provided an integrated measure of trait impulsivity. During an fMRI acquisition, each subject was asked to perform a GO-NOGO task. Associations between BOLD response of the whole brain during the response-inhibition task and trait impulsivity were investigated.\n\nResultsPatients with greater scores on BIS-11 had greater activation of the bilateral presupplementary motor area (pre-SMA), bilateral anterior insula, right anterior cingulate cortex, and right temporal parietal junction (TPJ) during response-inhibition. Moreover, a significant association between higher impulsivity scores and worse performance was present (p= 0.038).\n\nConclusionsOur results suggest that deficit in inhibitory processes may affect everyday life, causing impulsive conduct, which is generally detrimental for PD patients. The strong association between BIS-11 scores, MPFC, pre-SMA and TPJ suggests that greater engagement of that network was needed to maintain behavioral inhibition in more impulsive PD patients. Indeed, neuroimaging of brain activity during GO-NOGO task may be useful in characterizing the clinical profile while evaluating the treatment options.\n\nFinancial disclosure/Conflict of interest concerning the research related to the manuscript: No conflicts of interest/ financial disclosures considering all the authors.\n\nFunding sources: this research was not funded by any commercial or governmental agency.