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Cathy M. Stinear
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Journal Articles
Publisher: Journals Gateway
Journal of Cognitive Neuroscience (2016) 28 (7): 909–919.
Published: 01 July 2016
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Dopamine agonists can impair inhibitory control and cause impulse control disorders for those with Parkinson disease (PD), although mechanistically this is not well understood. In this study, we hypothesized that the extent of such drug effects on impulse control is related to specific dopamine gene polymorphisms. This double-blind, placebo-controlled study aimed to examine the effect of single doses of 0.5 and 1.0 mg of the dopamine agonist ropinirole on impulse control in healthy adults of typical age for PD onset. Impulse control was measured by stop signal RT on a response inhibition task and by an index of impulsive decision-making on the Balloon Analogue Risk Task. A dopamine genetic risk score quantified basal dopamine neurotransmission from the influence of five genes: catechol- O -methyltransferase, dopamine transporter, and those encoding receptors D1, D2, and D3. With placebo, impulse control was better for the high versus low genetic risk score groups. Ropinirole modulated impulse control in a manner dependent on genetic risk score. For the lower score group, both doses improved response inhibition (decreased stop signal RT) whereas the lower dose reduced impulsiveness in decision-making. Conversely, the higher score group showed a trend for worsened response inhibition on the lower dose whereas both doses increased impulsiveness in decision-making. The implications of the present findings are that genotyping can be used to predict impulse control and whether it will improve or worsen with the administration of dopamine agonists.
Journal Articles
Publisher: Journals Gateway
Journal of Cognitive Neuroscience (2010) 22 (7): 1479–1492.
Published: 01 July 2010
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An important aspect of cognitive control is the ability to respond with restraint. Here, we modeled this experimentally by measuring the degree of response slowing that occurs when people respond to an imperative stimulus in a context where they might suddenly need to stop the initiated response compared with a context in which they do not need to stop. We refer to the RT slowing that occurs as the “response delay effect.” We conjectured that this response delay effect could relate to one or more neurocognitive mechanism(s): partial response suppression (i.e., “active braking”), prolonged decision time, and slower response facilitation. These accounts make different predictions about motor system excitability and brain activation. To test which neurocognitive mechanisms underlie the response delay effect, we performed two studies with TMS and we reanalyzed fMRI data. The results suggest that the response delay effect is at least partly explained by active braking, possibly involving a mechanism that is similar to that used to stop responses completely. These results further our understanding of how people respond with restraint by pointing to proactive recruitment of a neurocognitive mechanism heretofore associated with outright stopping.
Journal Articles
Publisher: Journals Gateway
Journal of Cognitive Neuroscience (2009) 21 (6): 1193–1203.
Published: 01 June 2009
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Converging lines of evidence show that volitional movement prevention depends on the right prefrontal cortex (PFC), especially the right inferior frontal gyrus (IFG). Selective movement prevention refers to the rapid prevention of some, but not all, movement. It is unknown whether the IFG, or other prefrontal areas, are engaged when movement must be selectively prevented, and whether additional cortical areas are recruited. We used rapid event-related fMRI to investigate selective and nonselective movement prevention during performance of a temporally demanding anticipatory task. Most trials involved simultaneous index and middle finger extension. Randomly interspersed trials required the prevention of one, or both, finger movements. Regions of the right hemisphere, including the IFG, were active for selective and nonselective movement prevention, with an overlap in the inferior parietal cortex and the middle frontal gyrus. Selective movement prevention caused a significant delay in movement initiation of the other digit. These trials were associated with activation of the medial frontal cortex. The results provide support for a right-hemisphere network that temporarily “brakes” all movement preparation. When movement is selectively prevented, the supplementary motor cortex (SMA/pre-SMA) may participate in conflict resolution and subsequent reshaping of excitatory drive to the motor cortex.