Dopamine agonists and the suppression of impulsive motor actions in Parkinson disease.

Journal Article (Clinical Trial;Journal Article)

The suppression of spontaneous motor impulses is an essential facet of cognitive control that is linked to frontal-BG circuitry. BG dysfunction caused by Parkinson disease (PD) disrupts the proficiency of action suppression, but how pharmacotherapy for PD impacts impulsive motor control is poorly understood. Dopamine agonists improve motor symptoms of PD but can also provoke impulsive-compulsive behaviors (ICB). We investigated whether dopamine agonist medication has a beneficial or detrimental effect on impulsive action control in 38 PD patients, half of whom had current ICB. Participants performed the Simon conflict task, which measures susceptibility to acting on spontaneous action impulses as well as the proficiency of suppressing these impulses. Compared with an off-agonist state, patients on their agonists were no more susceptible to reacting impulsively but were less proficient at suppressing the interference from the activation of impulsive actions. Importantly, agonist effects depended on baseline performance in the off-agonist state; more proficient suppressors off agonist experienced a reduction in suppression on agonist, whereas less-proficient suppressors off agonist showed improved suppression on agonist. Patients with active ICB were actually less susceptible to making fast, impulsive response errors than patients without ICB, suggesting that behavioral problems in this subset of patients may be less related to impulsivity in motor control. Our findings provide further evidence that dopamine agonist medication impacts specific cognitive control processes and that the direction of its effects depends on individual differences in performance off medication.

Full Text

Duke Authors

Cited Authors

  • Wylie, SA; Claassen, DO; Huizenga, HM; Schewel, KD; Ridderinkhof, KR; Bashore, TR; van den Wildenberg, WPM

Published Date

  • August 2012

Published In

Volume / Issue

  • 24 / 8

Start / End Page

  • 1709 - 1724

PubMed ID

  • 22571461

Pubmed Central ID

  • PMC3657467

Electronic International Standard Serial Number (EISSN)

  • 1530-8898

International Standard Serial Number (ISSN)

  • 0898-929X

Digital Object Identifier (DOI)

  • 10.1162/jocn_a_00241


  • eng