Cognitive control & the anterior cingulate cortex: Necessity & coherence

The functional organization of human medial frontal cortex (MFC) is a subject of intense study. Using fMRI, the MFC has been associated with diverse psychological processes, including motor function, cognitive control, affect, and social cognition. However, there have been few large-scale efforts to comprehensively map specific psychological functions to subregions of medial frontal anatomy. Here we applied a meta-analytic data-driven approach to nearly 10,000 fMRI studies to identify putatively separable regions of MFC and determine which psychological states preferentially recruit their activation. We identified regions at several spatial scales on the basis of meta-analytic coactivation, revealing three broad functional zones along a rostrocaudal axis composed of 2-4 smaller subregions each. Multivariate classification analyses aimed at identifying the psychological functions most strongly predictive of activity in each region revealed a tripartite division within MFC, with each zone displaying a relatively distinct functional signature. The posterior zone was associated preferentially with motor function, the middle zone with cognitive control, pain, and affect, and the anterior with reward, social processing, and episodic memory. Within each zone, the more fine-grained subregions showed distinct, but subtler, variations in psychological function. These results provide hypotheses about the functional organization of medial prefrontal cortex that can be tested explicitly in future studies. Activation of medial frontal cortex in fMRI studies is associated with a wide range of psychological states ranging from cognitive control to pain. However, this high rate of activation makes it challenging to determine how these various processes are topologically organized across medial frontal anatomy. We conducted a meta-analysis across nearly 10,000 studies to comprehensively map psychological states to discrete subregions in medial frontal cortex using relatively unbiased data-driven methods. This approach revealed three distinct zones that differed substantially in function, each of which were further subdivided into 2-4 smaller subregions that showed additional functional variation. Each individual region was recruited by multiple psychological states, suggesting subregions of medial frontal cortex are functionally heterogeneous.

Goal-directed behavior has been shown to be affected by consciously and subliminally induced conflicts. Both types of conflict conjointly modulate behavioral performance, but the underlying neuronal mechanisms have remained unclear. While cognitive control is linked to oscillations in the theta frequency band, there are several mechanisms via which theta oscillations may enable cognitive control: via the coordination and synchronization of a large and complex neuronal network and/or via local processes within the medial frontal cortex. We, therefore, investigated this issue with a focus on theta oscillations and the underlying neuronal networks. For this purpose, n = 40 healthy young participants performed a conflict paradigm that combines conscious and subliminal distractors while an EEG was recorded. The data show that separate processes modulate the theta-based activation and organization of cognitive control networks: EEG beamforming analyses showed that variations in theta band power generated in the supplementary motor area reflected the need for control and task-relevant goal shielding, as both conflicts as well as their conjoint effect on behavior increased theta power. Yet, large networks were not modulated by this and graph theoretical analyses of the efficiency (i.e. small worldness) of theta-driven networks did not reflect the need for control. Instead, theta network efficiency was decreased by subliminal conflicts only. This dissociation suggests that while both kinds of conflict require control and goal shielding, which are induced by an increase in theta band power and modulate processes in the medial frontal cortex, only non-conscious conflicts diminish the efficiency of theta-driven large-scale networks.

The detection of a conflict between relevant and irrelevant information on a given trial typically results in a smaller conflict effect on the next trial. This sequential effect has been interpreted as an expression of cognitive control implemented to resolve conflict. In this context, 2 different but related issues have received increasing attention in the literature. The first issue is whether the detection of motor conflict is necessary to induce cognitive control or, alternatively, whether the detection of perceptual conflict is sufficient. The second issue concerns whether awareness of the conflict is necessary to induce cognitive control. Here, we address both issues in a single design. Our reaction-time (RT) results indicate that conflict-driven control is domain-specific. The detection of perceptual conflict on the previous trial selectively reduces perceptual conflict on the next trial. Similarly, the detection of motor conflict on the previous trial selectively reduces motor conflict on the next trial. For errors, adaptive control seemed to be more general: The detection of perceptual or motor conflict on the previous trial reduced the frequency of errors on response-conflict trials. Furthermore, unconsciously triggered conflict adaptation was observed, but not systematically. Results on errors provide some evidence that sensitivity to an unconscious conflict on the previous trial reduces the frequency of errors on the current trial. For RT analyses however, unconscious conflict appeared not to be sufficient to induce cognitive control. This pattern of results is in line with previous studies examining the role of consciousness in conflict adaptation. (PsycINFO Database Record

Morphometric gray matter differences of the medial frontal cortex influence the social Simon effect

Making sense of all the conflict: A theoretical review and critique of conflict-related ERPs

Summary“Near-miss” events, where unsuccessful outcomes are proximal to the jackpot, increase gambling propensity and may be associated with the addictiveness of gambling, but little is known about the neurocognitive mechanisms that underlie their potency. Using a simplified slot machine task, we measured behavioral and neural responses to gambling outcomes. Compared to “full-misses,” near-misses were experienced as less pleasant, but increased desire to play. This effect was restricted to trials where the subject had personal control over arranging their gamble. Near-miss outcomes recruited striatal and insula circuitry that also responded to monetary wins; in addition, near-miss-related activity in the rostral anterior cingulate cortex varied as a function of personal control. Insula activity to near-misses correlated with self-report ratings as well as a questionnaire measure of gambling propensity. These data indicate that near-misses invigorate gambling through the anomalous recruitment of reward circuitry, despite the objective lack of monetary reinforcement on these trials.

Reward-predictive stimuli can increase an automatic response tendency, which needs to be counteracted by effortful response inhibition when this tendency is inappropriate for the current task. Here we investigated how the human brain implements this dynamic process by adopting a reward-modulated Simon task while acquiring EEG and fMRI data in separate sessions. In the Simon task, a lateral target stimulus triggers an automatic response tendency of the spatially corresponding hand, which needs to be overcome if the activated hand is opposite to what the task requires, thereby delaying the response. We associated high or low reward with different targets, the location of which could be congruent or incongruent with the correct response hand. High-reward targets elicited larger Simon effects than low-reward targets, suggesting an increase in the automatic response tendency induced by the stimulus location. This tendency was accompanied by modulations of the lateralized readiness potential over the motor cortex, and was inhibited soon after if the high-reward targets were incongruent with the correct response hand. Moreover, this process was accompanied by enhanced theta oscillations in medial frontal cortex and enhanced activity in a frontobasal ganglia network. With dynamical causal modeling, we further demonstrated that the connection from presupplementary motor area (pre-SMA) to right inferior frontal cortex (rIFC) played a crucial role in modulating the reward-modulated response inhibition. Our results support a dynamic neural model of reward-induced response activation and inhibition, and shed light on the neural communication between reward and cognitive control in generating adaptive behaviors.

Action sets and decisions in the medial frontal cortex

In the following article, Kim et al.1 attempted to understand the factors that influence outcomes in the resection of the medial frontal lobes. As the authors indicate in their introduction, since Penfield and Welch,2 neurosurgeons treating epilepsy have noted this interesting phenomenon of temporary postoperative deficits in motor and possibly speech function associated with resection of the medial frontal cortex immediately anterior to the central gyrus. The term “supplementary motor area,” or SMA, has been used to describe this region. They detail their experience in treating 43 adults with a variety of pathological lesions of the medial frontal lobe as a means of controlling pharmacoresistant epilepsy. They found that transient new neurological deficits occurred in approximately half of their patients and that these deficits affected a mixture of motor, sensory, and speech functions. Only 3 (7%) of the 43 patients had what they considered to be permanent deficits, and all deficits involved motor loss: 1 case involving the upper extremity; 1 case, the lower extremity; and 1 case, the upper and lower extremities. While this series adds a significant number of patients to the literature on this important topic, it does not yet give neurosurgeons what they would like to know regarding surgery in this brain region. What has been difficult to determine is which patients are more likely to experience these deficits and, even more importantly, which patients are at higher risk for permanent deficits. Kim et al. found that, in general terms, patients who demonstrated temporary deficits had resections that were farther posterior (true SMA) and more inferior, including the cingulate gyrus. The authors performed a multivariate analysis and found that resection of the cingulate gyrus was the only factor that was predictive of a new deficit.1 There were no predictors of which patients would have permanent deficits, possibly because the risk was so low (7%). Nevertheless, these data should be helpful to surgeons who are planning to resect medial frontal cortex, both for the treatment of pharmacoresistant epilepsy and for the resection of cortical brain tumors. Like the findings of Kim et al., the review by Rostomily et al.3 indicated that permanent deficits are exceedingly rare. Similarly, Tate et al.4 described a large series of patients who had undergone resection of lesions from the cingulate gyrus. Once again, permanent deficits were exceedingly rare, and temporary deficits were more likely to occur if SMA tissue was also resected, which implies that although resection of the cingulate gyrus is a factor, it is not the only explanation for new deficits. The take-home message from this series of cases is that patients and families should be informed in advance about the possibility of new, probably transient deficits when this region of the brain is approached, and a 50% likelihood seems reasonable. What the report by Kim et al. does not do is help us to understand whether there was something different about the injury in cases in which permanent deficits developed. For example, could there have been a vascular injury that caused damage to primary motor cortex (for example, a pericallosal arterial branch or a venous infarction), or is there something intrinsically different about the SMA in a small subset of patients? Presumably, with enough experience and with the addition of tools such as functional MRI and fiber tract imaging, these questions will eventually be answered. Until then, surgeons must give patients as much advance information as possible and continue to wait expectantly each time an SMA syndrome occurs to see if the deficits resolve. (http://thejns.org/doi/abs/10.3171/2013.1.JNS121986)

The glucagon-like peptide 1 (GLP-1) receptor agonist is used for the treatment of type 2 diabetes (DM2) as it improves glycemic control, reduces appetite and body weight. It is also related to altered brain responses to food stimuli, but its effects on intrinsic brain connectivity are unknown. With the goal of better understanding GLP-1's role in the intrinsic brain connectivity of DM2 patients, functional resonance imaging (fMRI) data of resting-state networks relevant for eating behavior was analyzed in two studies. In both, all images were acquired after an overnight fast (8-12 hours). Study 1 aimed to investigate the acute effect of GLP-1 blockade on functional connectivity. On two separate days, fMRI data was acquired from 20 DM2 patients and 20 healthy controls, first under saline infusion and thereafter under GLP-1 antagonist infusion. Study 2 aimed to investigate, in DM2 patients, if there were any between treatment differences in intrinsic connectivity when comparing GLP-1 receptor agonist liraglutide with insulin glargine. The same DM2 participants in study 1 were thus treated in random order for 12 weeks with liraglutide and insulin glargine, fMRI data was collected at the start of treatment, after 10 days and after 12 weeks. Study 1 results showed that, during saline infusion, DM2 patients had greater connectivity compared to controls in the left insula and operculum, which related to greater GLP-1 mediated weightloss after 10 days and 12 weeks. Also, connectivity was greater in DM2 patients versus controls in the frontal pole, frontal medial cortex, anterior cingulate and paracingulate giry, which related to less GLP-1 mediated weight-loss after 10 days (all PFWE < 0.05). There was no effect on connectivity for GLP-1 antagonist, and no long-term differences between treatments (all PFWE < 0.05). In conclusion, baseline resting-state connectivity was shown to be related to GLP-1 mediated weightchange, with greater frontal connectivity relating to less weight loss during GLP-1 treatment, while higher left insula connectivity correlated to greater weight loss PUC-Rio -Certificao Digital N 1712306/CA during GLP-1 treatment, indicating a relationship between baseline intrinsic connectivity in these regions and weight loss during GLP-1 treatment.

Patients with obstructive sleep apnea (OSA) show significant white matter injury; whether that injury represents myelin or axonal damage is unclear. The objective was to examine myelin and axonal changes in patients with newly diagnosed OSA over control subjects. Cross-sectional study. University-based medical center. Twenty-three newly-diagnosed, treatment-naïve OSA and 23 age- and sex-matched control subjects. None. Radial and axial diffusivity maps, calculated from diffusion tensor imaging data (3.0 Tesla MRI scanner), indicating diffusion perpendicular (myelin status) or parallel (axonal status) to fibers, respectively, were normalized, smoothed, and compared between groups (analysis of covariance; covariate: age). Global brain radial and axial diffusivity values, and global brain volume with myelin and axonal changes were determined, and region-of-interest analyses performed in areas of significant differences between groups based on voxel-based procedures. Global radial and axial diffusivity values were significantly reduced in OSA versus control subjects (radial, P = 0.004; axial, P = 0.019), with radial (myelin) diffusivity reduced more than axial (axonal), and more left-sided reduction for both measures. Localized declines for myelin and axonal measures appeared in the dorsal and ventral medulla, cerebellar cortex and deep nuclei, basal ganglia, hippocampus, amygdala, corpus callosum, insula, cingulate and medial frontal cortices, and other cortical areas (P < 0.005), all regions mediating functions affected in OSA. Fiber injury appears in critical medullary respiratory regulatory sites, as well as cognitive and autonomic control areas. Myelin is more affected in newly diagnosed OSA than axons, and primarily on the left side, possibly from the increased myelin sensitivity to hypoxia and asymmetric perfusion.

The present event-related potential study investigated the correlates of decision making in relation to the amount of response conflict. In a gambling paradigm, response conflict was introduced by giving participants the option to either gamble or pass. Second, the odds and gains in each trial were manipulated to make the decision to gamble or pass determined or underdetermined. Underdetermined trials included an extra conflict. The N2 was modulated by the mere presence of conflict. In contrast to both conflict monitoring and inhibition theories for N2, these results suggest that an enhancement in N2 reflects the mere detection of conflicting alternatives. The P3 showed a fronto-central increase in amplitude in trials including two forms of response conflict compared to trials including only one conflict. These findings suggest that P3 reflects part of the conflict resolution processes.

Cognitive reward control recruits medial and lateral frontal cortices, which are also involved in cognitive emotion regulation: A coordinate-based meta-analysis of fMRI studies

Stochastic optimal control for aircraft conflict resolution under wind uncertainty

The distinction between intuitive and analytic thinking is common in psychology. However, while often being quite clear on the characteristics of the two processes (‘Type 1’ processes are fast, autonomous, intuitive, etc. and ‘Type 2’ processes are slow, deliberative, analytic, etc.), dual-process theorists have been heavily criticized for being unclear on the factors that determine when an individual will think analytically or rely on their intuition. We address this issue by introducing a three-stage model that elucidates the bottom-up factors that cause individuals to engage Type 2 processing. According to the model, multiple Type 1 processes may be cued by a stimulus (Stage 1), leading to the potential for conflict detection (Stage 2). If successful, conflict detection leads to Type 2 processing (Stage 3), which may take the form of rationalization (i.e., the Type 1 output is verified post hoc) or decoupling (i.e., the Type 1 output is falsified). We tested key aspects of the model using a novel base-rate task where stereotypes and base-rate probabilities cued the same (non-conflict problems) or different (conflict problems) responses about group membership. Our results support two key predictions derived from the model: (1) conflict detection and decoupling are dissociable sources of Type 2 processing and (2) conflict detection sometimes fails. We argue that considering the potential stages of reasoning allows us to distinguish early (conflict detection) and late (decoupling) sources of analytic thought. Errors may occur at both stages and, as a consequence, bias arises from both conflict monitoring and decoupling failures.