Competitions are part and parcel of daily life and require people to invest time and energy to gain advantage over others and to avoid (the risk of) falling behind. Whereas the behavioral mechanisms underlying competition are well documented, its neurocognitive underpinnings remain poorly understood. We addressed this using neuroimaging and computational modeling of individual investment decisions aimed at exploiting one's counterpart (“attack”) or at protecting against exploitation by one's counterpart (“defense”). Analyses revealed that during attack relative to defense (i) individuals invest less and are less successful; (ii) computations of expected reward are strategically more sophisticated (reasoning level k = 4 vs. k = 3 during defense); (iii) ventral striatum activity tracks reward prediction errors; (iv) risk prediction errors were not correlated with neural activity in either ROI or whole-brain analyses; and (v) successful exploitation correlated with neural activity in the bilateral ventral striatum, left OFC, left anterior insula, left TPJ, and lateral occipital cortex. We conclude that, in economic contests, coming out ahead (vs. not falling behind) involves sophisticated strategic reasoning that engages both reward and value computation areas and areas associated with theory of mind.

Goal-directed behavior requires control over automatic behavior, for example, when goal-irrelevant information from the environment captures an inappropriate response and conflicts with the correct, goal-relevant action. Neural oscillations in the theta band (∼6 Hz) measured at midfrontal electrodes are thought to form an important substrate of the detection and subsequent resolution of response conflict. Here, we examined the extent to which response conflict and associated theta-band activity depend on the visual stimulus feature dimension that triggers the conflict. We used a feature-based Simon task to manipulate conflict by motion direction and stimulus color. Analyses were focused on individual differences in behavioral response conflict elicited across different stimulus dimensions and their relationship to conflict-related midfrontal theta. We first confirmed the presence of response conflict elicited by task-irrelevant motion and stimulus color, demonstrating the usefulness of our modified version of the Simon task to assess different sensory origins of response conflict. Despite titrating overall task performance, we observed large individual differences in the behavioral manifestations of response conflict elicited by the different visual dimensions. These behavioral conflict effects were mirrored in a dimension-specific relationship with conflict-related midfrontal theta power, such that, for each dimension, individual midfrontal theta power was generally higher when experienced response conflict was high. Finally, exploratory analyses of interregional functional connectivity suggested a role for phase synchronization between frontal and parietal scalp sites in modulating experienced conflict when color was the task-relevant visual dimension. Highlighting the importance of an individual differences approach in cognitive neuroscience, these results reveal large individual differences in experienced response conflict depending on the source of visual interference, which are predicted by conflict-related midfrontal theta power.

Action selection often requires the transformation of visual information into motor plans. Preventing premature responses may entail the suppression of visual input and/or of prepared muscle activity. This study examined how the quality of visual information affects frontobasal ganglia (BG) routes associated with response selection and inhibition. Human fMRI data were collected from a stop task with visually degraded or intact face stimuli. During go trials, degraded spatial frequency information reduced the speed of information accumulation and response cautiousness. Effective connectivity analysis of the fMRI data showed action selection to emerge through the classic direct and indirect BG pathways, with inputs deriving form both prefrontal and visual regions. When stimuli were degraded, visual and prefrontal regions processing the stimulus information increased connectivity strengths toward BG, whereas regions evaluating visual scene content or response strategies reduced connectivity toward BG. Response inhibition during stop trials recruited the indirect and hyperdirect BG pathways, with input from visual and prefrontal regions. Importantly, when stimuli were nondegraded and processed fast, the optimal stop model contained additional connections from prefrontal to visual cortex. Individual differences analysis revealed that stronger prefrontal-to-visual connectivity covaried with faster inhibition times. Therefore, prefrontal-to-visual cortex connections appear to suppress the fast flow of visual input for the go task, such that the inhibition process can finish before the selection process. These results indicate response selection and inhibition within the BG to emerge through the interplay of top–down adjustments from prefrontal and bottom–up input from sensory cortex.

Goal-directed action control comes into play when selecting between competing action alternatives. Response capture reflects the susceptibility of the motor system to incitement by task-irrelevant action impulses; the subsequent selective suppression of incorrect action impulses aims to counteract response capture and facilitate the desired response. The goal of this experiment was to clarify physiological mechanisms of response capture and suppression of action impulses during conflict at the level of the motor system. We administered single-pulse TMS at various intervals preceding speeded choice responses. The correct response side was designated by stimulus color, whereas stimulus location (which could match or conflict with response side) was to be ignored. TMS pulses triggered motor evoked potential and silent period, providing sensitive indices of cortico-spinal excitation and inhibition. Motor evoked potential data showed the typical progressive increase in cortico-spinal motor excitability leading up to the imminent (correct) response, which started earlier on nonconflict than on conflict trials. On conflict trials, the irrelevant stimulus location captured the incorrect response, as expressed by an early and transient rise in excitability. Silent period data showed that, already early during the response process, inhibition of the incorrect response was stronger for conflict than for nonconflict trials. Furthermore, inhibition decreased over time for nonconflict trials facilitating the imminent correct response while maintaining higher levels of inhibition on conflict trials. In conclusion, dynamic patterns of cortico-spinal excitability provide unique physiological evidence for the expression and selective suppression of action impulses captured by competing action alternatives.

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.

Cognitive control allows us to adjust to environmental changes. The medial frontal cortex (MFC) is thought to detect conflicts and recruit additional resources from other brain areas including the lateral prefrontal cortices. Here we investigated how the MFC acts in concert with visual, motor, and lateral prefrontal cortices to support adaptations of goal-directed behavior. Physiologically, these interactions may occur through local and long-range synchronized oscillation dynamics, particularly in the theta range (4–8 Hz). A speeded flanker task allowed us to investigate conflict-type-specific control networks for perceptual and response conflicts. Theta power over MFC was sensitive to both perceptual and response conflict. Interareal theta phase synchrony, however, indicated a selective enhancement specific for response conflicts between MFC and left frontal cortex as well as between MFC and the presumed motor cortex contralateral to the response hand. These findings suggest that MFC theta-band activity is both generally involved in conflict processing and specifically involved in linking a neural network controlling response conflict.

Frontal oscillatory dynamics in the theta (4–8 Hz) and beta (20–30 Hz) frequency bands have been implicated in cognitive control processes. Here we investigated the changes in coordinated activity within and between frontal brain areas during feedback-based response learning. In a time estimation task, participants learned to press a button after specific, randomly selected time intervals (300–2000 msec) using the feedback after each button press (correct, too fast, too slow). Consistent with previous findings, theta-band activity over medial frontal scalp sites (presumably reflecting medial frontal cortex activity) was stronger after negative feedback, whereas beta-band activity was stronger after positive feedback. Theta-band power predicted learning only after negative feedback, and beta-band power predicted learning after positive and negative feedback. Furthermore, negative feedback increased theta-band intersite phase synchrony (a millisecond resolution measure of functional connectivity) among right lateral prefrontal, medial frontal, and sensorimotor sites. These results demonstrate the importance of frontal theta- and beta-band oscillations and intersite communication in the realization of reinforcement learning.

The ability to interact with a constantly changing environment requires a balance between maintaining the currently relevant working memory content and being sensitive to potentially relevant new information that should be given priority access to working memory. Mesocortical dopamine projections to frontal brain areas modulate working memory maintenance and flexibility. Recent neurocognitive and neurocomputational work suggests that dopamine release is transiently enhanced by induced positive affect. This ERP study investigated the role of positive affect in different aspects of information processing: in proactive control (context maintenance and updating), reactive control (flexible adaptation to incoming task-relevant information), and evaluative control in an AX -CPT task. Subjects responded to a target probe if it was preceded by a specific cue. Induced positive affect influenced the reactive and evaluative components of control (indexed by the N2 elicited by the target and by the error-related negativity elicited after incorrect responses, respectively), whereas cue-induced proactive preparation and maintenance processes remained largely unaffected (as reflected in the P3b and the contingent negative variation components of the ERP).

The presupplementary motor area (pre-SMA) is considered key in contributing to voluntary action selection during response conflict. Here we test whether individual differences in the ability to select appropriate actions in the face of strong (conscious) and weak (virtually unconscious) distracting alternatives are related to individual variability in pre-SMA anatomy. To this end, we scanned 58 participants, who performed a masked priming task in which conflicting response tendencies were elicited either consciously (through primes that were weakly masked) or virtually unconsciously (strongly masked primes), with structural magnetic resonance imaging. Voxel-based morphometry revealed that individual differences in pre-SMA gray-matter density are related to subjects' ability to voluntary select the correct action in the face of conflict, irrespective of the awareness level of conflict-inducing stimuli. These results link structural anatomy to individual differences in cognitive control ability, and provide support for the role of the pre-SMA in the selection of appropriate actions in situations of response conflict. Furthermore, these results suggest that flexible and voluntary behavior requires efficiently dealing with competing response tendencies, even those that are activated automatically and unconsciously.

Cognitive control allows humans to overrule and inhibit habitual responses to optimize performance in challenging situations. Contradicting traditional views, recent studies suggest that cognitive control processes can be initiated unconsciously. To further capture the relation between consciousness and cognitive control, we studied the dynamics of inhibitory control processes when triggered consciously versus unconsciously in a modified version of the stop task. Attempts to inhibit an imminent response were often successful after unmasked (visible) stop signals. Masked (invisible) stop signals rarely succeeded in instigating overt inhibition but did trigger slowing down of response times. Masked stop signals elicited a sequence of distinct ERP components that were also observed on unmasked stop signals. The N2 component correlated with the efficiency of inhibitory control when elicited by unmasked stop signals and with the magnitude of slowdown when elicited by masked stop signals. Thus, the N2 likely reflects the initiation of inhibitory control, irrespective of conscious awareness. The P3 component was much reduced in amplitude and duration on masked versus unmasked stop trials. These patterns of differences and similarities between conscious and unconscious cognitive control processes are discussed in a framework that differentiates between feedforward and feedback connections in yielding conscious experience.

Processing irrelevant visual information sometimes activates incorrect response impulses. The engagement of cognitive control mechanisms to suppress these impulses and make proactive adjustments to reduce the future impact of incorrect impulses may rely on the integrity of frontal–basal ganglia circuitry. Using a Simon task, we investigated the effects of basal ganglia dysfunction produced by Parkinson's disease (PD) on both on-line (within-trial) and proactive (between-trial) control efforts to reduce interference produced by the activation of an incorrect response. As a novel feature, we applied distributional analyses, guided by the activation–suppression model, to differentiate the strength of incorrect response activation and the proficiency of suppression engaged to counter this activation. For situations requiring on-line control, PD ( n = 52) and healthy control ( n = 30) groups showed similar mean interference effects (i.e., Simon effects) on reaction time (RT) and accuracy. Distributional analyses showed that although the strength of incorrect response impulses was similar between the groups PD patients were less proficient at suppressing these impulses. Both groups demonstrated equivalent and effective proactive control of response interference on mean RT and accuracy rates. However, PD patients were less effective at reducing the strength of incorrect response activation proactively. Among PD patients, motor symptom severity was associated with difficulties in on-line, but not in proactive, control of response impulses. These results suggest that basal ganglia dysfunction produced by PD has selective effects on cognitive control mechanisms engaged to resolve response conflict, with primary deficits in the on-line suppression of incorrect responses occurring in the context of a relatively spared ability to adjust control proactively to minimize future conflict.

The ability to stop ongoing motor responses in a split-second is a vital element of human cognitive control and flexibility that relies in large part on prefrontal cortex. We used the stop-signal paradigm to elucidate the engagement of primary motor cortex (M1) in inhibiting an ongoing voluntary motor response. The stop-signal paradigm taps the ability to flexibly countermand ongoing voluntary behavior upon presentation of a stop signal. We applied single-pulse TMS to M1 at several intervals following the stop signal to track the time course of excitability of the motor system related to generating and stopping a manual response. Electromyography recorded from the flexor pollicis brevis allowed quantification of the excitability of the corticospinal tract and the involvement of intracortical GABA B ergic circuits within M1, indexed respectively by the amplitude of the motor-evoked potential and the duration of the late part of the cortical silent period (SP). The results extend our knowledge of the neural basis of inhibitory control in three ways. First, the results revealed a dynamic interplay between response activation and stopping processes at M1 level during stop-signal inhibition of an ongoing response. Second, increased excitability of inhibitory interneurons that drives SP prolongation was evident as early as 134 msec following the instruction to stop. Third, this pattern was followed by a stop-related reduction of corticospinal excitability implemented around 180 after the stop signal. These findings point to the recruitment of GABA B ergic intracortical inhibitory circuits within M1 in stop-signal inhibition and support the notion of stopping as an active act of control.

Functional magnetic resonance imaging (fMRI) methods may help in understanding processes of response capture and response inhibition in conflict tasks, such as the Simon task. However, data-driven approaches thus far have not yielded consistent insights into these processes. Here, a theory-driven approach is introduced that capitalizes on individual differences in the processes of central interest. Based on the so-called activation-suppression model, specific behavioral parameters for each individual derived from reaction time (RT) distribution analysis were computed and entered into model-based fMRI analyses. These parameters correspond closely to the processes of inappropriate location-driven response activation (capture) and the subsequent inhibition of this activation as detailed by the model. Data from 24 participants revealed activation in the pre-supplementary motor area, which covaried with the RT distribution measure of response capture. Activation in the right inferior frontal cortex was found to covary with the RT distribution measure of response inhibition. These results, which are consistent against the backdrop of the larger literature on cognitive control, could have been derived neither from the standard data-driven fMRI approach, nor from inspecting overall mean RT alone.