The Role of Anatomic Connectivity in Inhibitory Control Revealed by Combining Connectome-based Lesion-symptom Mapping with Event-related Potentials.

Inhibitory control refers to the ability to suppress cognitive or motor processes. Current neurocognitive models indicate that this function mainly involves the anterior cingulate cortex and the inferior frontal cortex. However, how the communication between these areas influence inhibitory control performance and their functional response remains unknown. We addressed this question by injecting behavioral and electrophysiological markers of inhibitory control recorded during a Go/NoGo task as the 'symptoms' in a connectome-based lesion-symptom mapping approach in a sample of 96 first unilateral stroke patients. This approach enables us to identify the white matter tracts whose disruption by the lesions causally influences brain functional activity during inhibitory control. We found a central role of left frontotemporal and frontobasal intrahemispheric connections, as well as of the connections between the left temporoparietal and right temporal areas in inhibitory control performance. We also found that connections between the left temporal and right superior parietal areas modulate the conflict-related N2 event-related potential component and between the left temporal parietal area and right temporal and occipital areas for the inhibition P3 component. Our study supports the role of a distributed bilateral network in inhibitory control and reveals that combining lesion-symptom mapping approaches with functional indices of cognitive processes could shed new light on post-stroke functional reorganization. It may further help to refine the interpretation of classical electrophysiological markers of executive control in stroke patients.

Reduction in sugar drink valuation and consumption with gamified executive control training.

The overvaluation of high-energy, palatable food cues contributes to unhealthy eating and being overweight. Reducing the valuation of unhealthy food may thus constitute a powerful lever to improve eating habits and conditions characterized by unhealthy eating. We conducted a double-blind, placebo-controlled, randomized intervention trial assessing the efficacy of a five to twenty days online cognitive training intervention to reduce sugary drink perceived palatability and consumption. Our intervention involved a recently identified action-to-valuation mechanism of action, in which the repeated inhibition of prepotent motor responses to hedonic food cues in a Go/NoGo (GNG) and an attentional bias modification (ABM) task eventually reduces their valuation and intake. Confirming our hypotheses, the experimental intervention with consistent (100%) mapping between motor inhibition and the targeted unhealthy sugary drinks cues induced a larger decrease in their valuation than the control intervention with inconsistent (50%) mapping (- 27.6% vs. - 19%), and a larger increase of the (water) items associated with response execution (+ 11% vs + 4.2%). Exploratory analyses suggest that the effect of training on unhealthy items valuation may persist for at least one month. Against our hypothesis, we observed equivalent reductions in self-reported consumption of sugary drinks following the two interventions (exp: - 27% vs. ctrl: - 19%, BF01 = 4.7), suggesting a dose-independent effect of motor inhibition on self-reported consumption. Our collective results corroborate the robustness and large size of the devaluation effects induced by response inhibition on palatable items, but challenge the assumption of a linear relationship between such effects and the actual consumption of the target items. PROTOCOL REGISTRATION: The stage 1 protocol for this Registered Report was accepted in principle on 30/03/2021. The protocol, as accepted by the journal, can be found at: https://doi.org/10.17605/OSF.IO/5ESMP .

Mental flexibility depends on a largely distributed white matter network: Causal evidence from connectome-based lesion-symptom mapping.

Mental flexibility (MF) refers to the capacity to dynamically switch from one task to another. Current neurocognitive models suggest that since this function requires interactions between multiple remote brain areas, the integrity of the anatomic tracts connecting these brain areas is necessary to maintain performance. We tested this hypothesis by assessing with a connectome-based lesion-symptom mapping approach the effects of white matter lesions on the brain's structural connectome and their association with performance on the trail making test, a neuropsychological test of MF, in a sample of 167 first unilateral stroke patients. We found associations between MF deficits and damage of i) left lateralized fronto-temporo-parietal connections and interhemispheric connections between left temporo-parietal and right parietal areas; ii) left cortico-basal connections; and iii) left cortico-pontine connections. We further identified a relationship between MF and white matter disconnections within cortical areas composing the cognitive control, default mode and attention functional networks. These results for a central role of white matter integrity in MF extend current literature by providing causal evidence for a functional interdependence among the regional cortical and subcortical structures composing the MF network. Our results further emphasize the necessity to consider connectomics in lesion-symptom mapping analyses to establish comprehensive neurocognitive models of high-order cognitive functions.

Predictors for Returning to Paid Work after Transient Ischemic Attack and Minor Ischemic Stroke.

This study aims to determine which factors within the first week after a first-ever transient ischemic attack (TIA) or minor ischemic stroke (MIS) are associated with stroke survivors' ability to return to either partial or full time paid external work (RTpW). In this single-center prospective cohort study, we recruited 88 patients with first-ever TIA or MIS (NIHSS ≤ 5). Bivariate analyses were conducted between patients that did (RTpW) or did not return to paid work (noRTpW) within 7 days after stroke onset and at 3-months follow-up. Then, we conducted multivariate logistic and negative binomial regression analyses assessing (i) which factors are associated with RTpW at 3 months (ii) the likelihood that patients would RTpW at 3 months and (iii) the number of months necessary to RTpW. Overall, 43.2% of the patients did not RTpW at 3 months. At 3-months follow-up, higher anxiety/depression and fatigue-related disabilities were associated with noRTpW. Multivariate analysis showed that higher NIHSS scores at onset and hyperlipidemia (LDL cholesterol > 2.6 mmol/L or statins at stroke onset) were associated with noRTpW at 3 months. Stroke severity and/or newly diagnosed hypercholesterolemia at stroke onset in TIA or MIS patients were associated with not returning to paid work at 3 months.

Neural correlates of expectations-induced effects of caffeine intake on executive functions.

Placebo effects are defined as the beneficial subjective or behavioral outcomes of an intervention that are not attributable to its inherent properties; Placebo effects thus follow from individuals' expectations about the effects of the intervention. The present study aimed at examining how expectations influence neurocognitive processes. We addressed this question by contrasting three double-blinded within-subjects experimental conditions in which participants were given decaffeinated coffee, while being told they had received caffeinated (condition i) or decaffeinated coffee (ii), and given caffeinated coffee while being told they had received decaffeinated coffee (iii). After each of these three interventions, performance and electroencephalogram was recorded at rest as well as during sustained attention Rapid Visual Information Processing task (RVIP) and a Go/NoGo motor inhibitory control task. We first aimed to confirm previous findings for caffeine-induced enhancement on these executive components and on their associated electrophysiological indexes (The Attention-P3 component, response conflict NoGo-N2 and inhibition NoGo-P3 components (ii vs iii contrast); and then to test the hypotheses that expectations also induce these effects (i vs ii), although with a weaker amplitude (i vs iii). We did not confirm any of our hypotheses for caffeine-induced behavioral improvements and thus did not test the effect of caffeine-related expectations. At the electrophysiological level, however, we confirmed that caffeine increased the Attention-P3 and NoGo-P3 components amplitude but did not confirm an effect on the response-conflict N2 component. We did not confirm that expectations influence any of the investigated electrophysiological indices, but we confirmed that the Attention-P3 Global Field Power values were larger for the caffeine compared to the expectations conditions. We conclude that previously identified behavioral effect size of caffeine and of the related expectations for sustained attention and inhibitory control may have been overestimated, and that caffeine primarily influences the cognitive processes and brain areas supporting attention allocation. Finally, we confirm that caffeine-related expectations induce smaller effects than the substance itself.

Experience with opioids does not modify the brain network involved in expectations of placebo analgesia.

Placebo analgesia (PA) is defined as a psychobiological phenomenon triggered by the information surrounding an analgesic drug instead of its inherent pharmacological properties. PA is hypothesized to be formed through either verbal suggestions or conditioning. The present study aims at disentangling the neural correlates of expectations effects with or without conditioning through prior experience using the model of PA. We addressed this question by recruiting two groups of individuals holding comparable verbally-induced expectations regarding morphine analgesia but either (i) with or (ii) without prior experience with opioids. We then contrasted the two groups' neurocognitive response to acute heat-pain induction following the injection of sham morphine using electroencephalography (EEG). Topographic ERP analyses of the N2 and P2 pain evoked potential components allowed to test the hypothesis that PA involves distinct neural networks when induced by expectations with or without prior experience. First, we confirmed that the two groups showed corresponding expectations of morphine analgesia (Hedges' gs < .4 positive control criteria, gs = .37 observed difference), and that our intervention induced a medium-sized PA (Hedges' gav ≥ .5 positive control, gav = .6 observed PA). We then tested our hypothesis on the recruitment of different PA-associated brain networks in individuals with versus without prior experience with opioids and found no evidence for a topographic N2 and P2 ERP components difference between the two groups. Our results thus suggest that in the presence of verbally-induced expectations, modifications in the PA-associated brain activity by conditioning are either absent or very small.

Proactive inhibition is not modified by deep brain stimulation for Parkinson's disease: An electrical neuroimaging study.

In predictable contexts, motor inhibitory control can be deployed before the actual need for response suppression. The brain functional underpinnings of proactive inhibition, and notably the role of basal ganglia, are not entirely identified. We investigated the effects of deep brain stimulation of the subthalamic nucleus or internal globus pallidus on proactive inhibition in patients with Parkinson's disease. They completed a cued go/no-go proactive inhibition task ON and (unilateral) OFF stimulation while EEG was recorded. We found no behavioural effect of either subthalamic nucleus or internal globus pallidus deep brain stimulation on proactive inhibition, despite a general improvement of motor performance with subthalamic nucleus stimulation. In the non-operated and subthalamic nucleus group, we identified periods of topographic EEG modulation by the level of proactive inhibition. In the subthalamic nucleus group, source estimation analysis suggested the initial involvement of bilateral frontal and occipital areas, followed by a right lateralized fronto-basal network, and finally of right premotor and left parietal regions. Our results confirm the overall preservation of proactive inhibition capacities in both subthalamic nucleus and internal globus pallidus deep brain stimulation, and suggest a partly segregated network for proactive inhibition, with a preferential recruitment of the indirect pathway.

Modifying food items valuation and weight with gamified executive control training.

Recent lines of research suggest that repeated executive control of motor responses to food items modifies their perceived value and in turn their consumption. Cognitive interventions involving the practice of motor control and attentional tasks have thus been advanced as potential approach to improve eating habits. Yet, their efficacy remains debated, notably due to a lack of proper control for the effects of expectations. We examined whether a one-month intervention combining the practice of Go/NoGo and Cue approach training modified the perceived palatability of food items (i.e. decrease in unhealthy and increase in healthy food items' palatability ratings), and in turn participants' weights. We assessed our hypotheses with a parallel, double-blind, randomized controlled trial. Motivation and adherence to the intervention were maximized by a professional-level gamification of the training tasks. The control intervention differed from the experimental intervention only in the biasing of the stimulus-response mapping rules, enabling to balance expectations between the two groups and thus to conclude on the causal influence of motoric control on items valuation. We found a larger decrease of the unhealthy items' palatability ratings in the experimental (20.6%) than control group (13.1%). However, we did not find any increase of the healthy items' ratings or weight loss. Overall, the present registered report confirms that the repeated inhibition of motor responses to food cues, together with the development of attentional biases away from these cues, reduces their perceived value.

Randomized-controlled trial of response inhibition training for individuals with PTSD and impaired response inhibition.

Deficits in response inhibition, defined as an inability to stop a behavior that is no longer relevant, are characteristic of posttraumatic stress disorder (PTSD). Given that impaired response inhibition is associated with worse symptom recovery and accumulating evidence pointing to the effectiveness of cognitive control trainings in reducing PTSD symptoms, individuals with moderate to severe PTSD total severity (Posttraumatic Diagnostic Scale total score ≥ 21) and pre-training response inhibition deficits (M ≤ 75% successful inhibition on the Go/No-go) completed a 3-h, adaptive Go/No-go training designed to improve ability to withhold prepotent motor responses. Then forty-nine participants were randomized to an adaptive response inhibition training (n = 24, M = 19.27 years, SD = 0.70) or a waitlist condition (n = 25, M = 18.31 years, SD = 4.80). Behavioral response inhibition and self-reported trauma-related symptoms were assessed at pre- and post-training. Response inhibition training was associated with improved response inhibition on an untrained transfer Stop-Signal task and symptom reduction in PTSD compared to a waitlist group, at post-training. There was, however, reduced inhibition on a modified Go/No-go task from pre-to post-training. Overall, response inhibition deficits and PTSD symptoms are amenable to top-down remediation using response inhibition training. Our study provides preliminary evidence for the feasibility of response inhibition training in a PTSD sample characterized by response inhibition deficits.

Aging Modulates Prefrontal Plasticity Induced by Executive Control Training.

While declines in inhibitory control, the capacity to suppress unwanted neurocognitive processes, represent a hallmark of healthy aging, whether this function is susceptible to training-induced plasticity in older populations remains largely unresolved. We addressed this question with a randomized controlled trial investigating the changes in behavior and electrical neuroimaging activity induced by a 3-week adaptive gamified Go/NoGo inhibitory control training (ICT). Performance improvements were accompanied by the development of more impulsive response strategies, but did not generalize to impulsivity traits nor quality of life. As compared with a 2-back working-memory training, the ICT in the older adults resulted in a purely quantitative reduction in the strength of the activity in a medial and ventrolateral prefrontal network over the 400 ms P3 inhibition-related event-related potentials component. However, as compared with young adults, the ICT induced distinct configurational modifications in older adults' 200 ms N2 conflict monitoring medial-frontal functional network. Hence, while older populations show preserved capacities for training-induced plasticity in executive control, aging interacts with the underlying plastic brain mechanisms. Training improves the efficiency of the inhibition process in older adults, but its effects differ from those in young adults at the level of the coping with inhibition demands.

Brain structural evidence for a frontal pole specialization in glossolalia.

Glossolalia is defined as the ritual oral production of phoneme sequences without recognizable semantic content. The functional underpinnings of glossolalia, and notably whether it consists of a highly specific or ordinary behavior, remain largely unresolved. We addressed this question by measuring the structural brain remodeling associated with the extensive practice of glossolalia in thirty experts. This approach enabled us to circumvent the limitations of functional imaging to reveal the neural correlates of behaviors elicited in specific contexts and involving movements incompatible with most imaging methods. Whole-brain regression analyses of glossolalia expertise with indices of grey and white matter structure revealed positive associations between practice time and grey matter volume within the left frontal pole and the right middle frontal gyrus. These findings suggest that glossolalia involves a degree of neurocognitive specialization, though not at the level of language control and production networks, but within domain-general executive areas. They further call for including multi-tasking and interference suppression as key processes in models of unrecognizable speech production. Our results also concur with current demonstrations that measures of brain structural remodeling may help identifying whether cognitive skills depend on networks specialization or on a recycling of already existing processes.

Acute alcohol intoxication and expectations reshape the spatiotemporal functional architecture of executive control.

While the deleterious effects of acute ethyl alcohol intoxication on executive control are well-established, the underlying spatiotemporal brain mechanisms remain largely unresolved. In addition, since the effects of alcohol are noticeable to participants, isolating the effects of the substance from those related to expectations represents a major challenge. We addressed these issues using a double-blind, randomized, parallel, placebo-controlled experimental design comparing the behavioral and electrical neuroimaging acute effects of 0.6 vs 0.02 â€‹g/kg alcohol intake recorded in 65 healthy adults during an inhibitory control Go/NoGo task. Topographic ERP analyses of covariance with self-reported dose expectations allowed to dissociate their neurophysiological effects from those of the substance. While alcohol intoxication increased response time variability and post-error slowing, bayesian analyses indicated that it did not modify commission error rates. Functionally, alcohol induced topographic ERP modulations over the periods of the stimulus-locked N2 and P3 components, arising from pre-supplementary motor and anterior cingulate areas. In contrast, alcohol decreased the strength of the response-locked anterior cingulate error-related component but not its topography. This pattern indicates that alcohol had a locally specific influence within the executive control network, but disrupted performance monitoring processes via global strength-based mechanisms. We further revealed that alcohol-related expectations induced temporally specific functional modulations of the early N2 stimulus-locked medio-lateral prefrontal activity, a processing phase preceding those influenced by the actual alcohol intake. Our collective findings thus not only reveal the mechanisms underlying alcohol-induced impairments in impulse control and error processing, but also dissociate substance- from expectations- related functional effects.

Stimulus Reward Value Interacts with Training-induced Plasticity in Inhibitory Control.

Training inhibitory control, the ability to suppress motor or cognitive processes, not only enhances inhibition processes, but also reduces the perceived value and behaviors toward the stimuli associated with the inhibition goals during the practice. While these findings suggest that inhibitory control training interacts with the aversive and reward systems, the underlying spatio-temporal brain mechanisms remain unclear. We used electrical neuroimaging analyses of event-related potentials to examine the plastic brain modulations induced by training healthy participants to inhibit their responses to rewarding (pleasant chocolate) versus aversive food pictures (unpleasant vegetables) with Go/NoGo tasks. Behaviorally, the training resulted in a larger improvement in the aversive than in the rewarding NoGo stimuli condition, suggesting that reward responses impede inhibitory control learning. The electrophysiological results also revealed an interaction between reward responses and inhibitory control plasticity: we observed different effects of practice on the rewarding vs. aversive NoGo stimuli at 200 ms post-stimulus onset, when the conflicts between automatic response tendency and task demands for response inhibition are processed. Electrical source analyses revealed that this effect was driven by an increase in right orbito-cingulate and a decrease in temporo-parietal activity to the rewarding NoGo stimuli and the reverse pattern to the aversive stimuli. Our collective results provide direct neurophysiological evidence for interactions between stimulus reward value and executive control training, and suggest that changes in the assessment of stimuli with repeated motoric inhibition likely follow from associative learning and behavior-stimulus conflicts reduction mechanisms.

Executive control training does not generalize, even when associated with plastic changes in domain-general prefrontal areas.

How executive function training paradigms can be effectively designed to promote a transfer of the effects of interventions to untrained tasks remains unclear. Here, we tested the hypothesis that training with a complex task involving motor, perceptual and task-set control components would result in more transfer than training with a simple motor control task, because the Complex training would lead to more involvement-and in turn modification-of domain-general executive control networks. We compared performance and electrophysiological activity before and after 10 days of executive control training with the complex (n = 18) versus the simple task (n = 17). We further assessed the effect of the two training regimens on untrained executive tasks involving or not one of the trained control components. A passive control group (n = 19) was used to assess retest effects. Both training groups improved at the trained task but exhibited different plastic changes within left-lateralized and medial frontal areas at 200-250 ms post-stimulus onset. However, contrary to our hypotheses, they showed equivalent improvement to the passive group to the transfer tasks. Our collective results reveal that the effect of training with a task involving multiple executive control components is highly specific to the trained task, even when the training modifies the functional networks underlying the trained executive components. Our findings corroborate current evidence that general cognitive enhancement cannot be achieved with training, even when the interventions modify domain-general brain areas.

Practice-induced functional plasticity in inhibitory control interacts with aging.

Inhibitory control deficits represent a key aspect of the cognitive declines associated with aging. Practicing inhibitory control has thus been advanced as a potential approach to compensate for age-induced neurocognitive impairments. Yet, the functional brain changes associated with practicing inhibitory control tasks in older adults and whether they differ from those observed in young populations remains unresolved. We compared electrical neuroimaging analyses of ERPs recorded during a Go/NoGo practice session with a Group (Young; Older adults) by Session (Beginning; End of the practice) design to identify whether the practice of an inhibition task in older adults reinforces already implemented compensatory activity or reduce it by enhancing the functioning of the brain networks primarily involved in the tasks. We observed an equivalent small effect of practice on performance in the two age-groups. The topographic ERP analyses and source estimations revealed qualitatively different effects of the practice over the N2 and P3 ERP components, respectively driven by a decrease in supplementary motor area activity and an increase in left ventrolateral prefrontal activity in the older but not in the young adults with practice. Our results thus indicate that inhibition task practice in older adults increases age-related divergences in the underlying functional processes.

Effects of Prefrontal Transcranial Direct Current Stimulation on Lexical Access in Chronic Poststroke Aphasia.

BACKGROUND: A successful interplay between prefrontal and domain-specific language areas is critical for language processing. Previous studies involving people with aphasia have shown that executive control processes might act on lexical-semantic representations during retrieval. Modulating the prefrontal control network by means of noninvasive brain stimulation might, therefore, improve lexical access in people with aphasia. OBJECTIVE: The present study investigates the effects of prefrontal transcranial direct current stimulation (tDCS) on lexical access in chronic poststroke aphasia. METHODS: We report data of 14 participants with chronic poststroke aphasia. We used a sham-tDCS (S-tDCS) controlled and double-blind within-subjects design. Performances in picture naming, verbal fluency, and word repetition were assessed immediately after stimulation. RESULTS: As compared with S-tDCS, anodal tDCS (A-tDCS) improved verbal fluency as well as the speed of naming high frequency words, but not word repetition. CONCLUSION: The results of our study suggest that the brain network dedicated to lexical retrieval processing can be facilitated by A-tDCS over the left dorsolateral prefrontal cortex. This finding supports the notion that strengthening executive control functions after stroke could complement speech and language-focused therapy.

Dorsolateral Prefrontal Transcranial Direct Current Stimulation Modulates Language Processing but Does Not Facilitate Overt Second Language Word Production.

Word retrieval in bilingual speakers partly depends on executive control systems in the left prefrontal cortex - including dorsolateral prefrontal cortex (DLPFC). We tested the hypothesis that DLPFC modulates word production of words specifically in a second language (L2) by measuring the effects of anodal transcranial direct current stimulation (anodal-tDCS) over the DLPFC on picture naming and word translation and on event-related potentials (ERPs) and their sources. Twenty-six bilingual participants with "unbalanced" proficiency in two languages were given 20 min of 1.5 mA anodal or sham tDCS (double-blind stimulation design, counterbalanced stimulation order, 1-week intersession delay). The participants then performed the following tasks: verbal and non-verbal fluency during anodal-tDCS stimulation and first and second language (L1 and L2) picture naming and translation [forward (L1 → L2) and backward (L2 → L1)] immediately after stimulation. The electroencephalogram (EEG) was recorded during picture naming and translation. On the behavioral level, anodal-tDCS had an influence on non-verbal fluency but neither on verbal fluency, nor on picture naming and translation. EEG measures revealed significant interactions between Language and Stimulation on picture naming around 380 ms post-stimulus onset and Translation direction and Stimulation on translation around 530 ms post-stimulus onset. These effects suggest that L2 phonological retrieval and phoneme encoding are spatially and temporally segregated in the brain. We conclude that anodal-tDCS stimulation has an effect at a neural level on phonological processes and, critically, that DLPFC-mediated activation is a constraint on language production specifically in L2.

Spatiotemporal brain dynamics underlying attentional bias modifications.

Exaggerated attentional biases toward specific elements of the environment contribute to the maintenance of several psychiatric conditions, such as biases to threatening faces in social anxiety. Although recent literature indicates that attentional bias modification may constitute an effective approach for psychiatric remediation, the underlying neurophysiological mechanisms remain unclear. We addressed this question by recording EEG in 24 healthy participants performing a modified dot-probe task in which pairs of neutral cues (colored shapes) were replaced by probe stimuli requiring a discrimination judgment. To induce an attentional bias toward or away from the cues, the probes were systematically presented either at the same or at the opposite position of a specific cue color. This paradigm enabled participants to spontaneously develop biases to initially unbiased, neutral cues, as measured by the response speed to the probe presented after the cues. Behavioral result indicated that the ABM procedure induced approach and avoidance biases. The influence of ABM on inhibitory control was assessed in a separated Go/NoGo task: changes in AB did not influence participants' capacity to inhibit their responses to the cues. Attentional bias modification was associated with a topographic modulation of event-related potentials already 50-84 ms following the onset of the cues. Statistical analyses of distributed electrical source estimations revealed that the development of attentional biases was associated with decreased activity in the left temporo-parieto-occipital junction. These findings suggest that attentional bias modification affects early sensory processing phases related to the extraction of information based on stimulus saliency.

Modulation of inhibitory control by prefrontal anodal tDCS: A crossover double-blind sham-controlled fMRI study.

Prefrontal anodal transcranial direct current stimulation (tDCS) has been proposed as a potential approach to improve inhibitory control performance. The functional consequences of tDCS during inhibition tasks remain, however, largely unresolved. We addressed this question by analyzing functional magnetic resonance imaging (fMRI) recorded while participants completed a Go/NoGo task after right-lateralized prefrontal anodal tDCS with a crossover, sham-controlled, double-blind experimental design. We replicated previous evidence for an absence of offline effect of anodal stimulation on Go/NoGo performance. The fMRI results revealed a larger increase in right ventrolateral prefrontal activity for Go than NoGo trials in the anodal than sham condition. This pattern suggests that tDCS-induced increases in cortical excitability have larger effects on fMRI activity in regions with a lower task-related engagement. This was the case for the right prefrontal cortex in the Go condition in our task because while reactive inhibition was not engaged during execution trials, the unpredictability of the demand for inhibitory control still incited an engagement of proactive inhibition. Exploratory analyses further revealed that right prefrontal stimulation interacted with task-related functional demands in the supplementary motor area and the thalamus. Our collective results emphasize the dependency of offline tDCS functional effects on the task-related engagement of the stimulated areas and suggest that this factor might partly account for the discrepancies in the functional effects of tDCS observed in previous studies.

Spatiotemporal brain dynamics supporting the immediate automatization of inhibitory control by implementation intentions.

While cognitive interventions aiming at reinforcing intentional executive control of unwanted response showed only modest effects on impulse control disorders, the establishment of fast automatic, stimulus-driven inhibition of responses to specific events with implementation intention self-regulation strategies has proven to be an effective remediation approach. However, the neurocognitive mechanisms underlying implementation intentions remain largely unresolved. We addressed this question by comparing electrical neuroimaging analyses of event-related potentials recorded during a Go/NoGo task between groups of healthy participants receiving either standard or implementation intentions instructions on the inhibition stimuli. Inhibition performance improvements with implementation intentions were associated with a Group by Stimulus interaction 200-250 ms post-stimulus onset driven by a selective decrease in response to the inhibition stimuli within the left superior temporal gyrus, the right precuneus and the right temporo-parietal junction. We further observed that the implementation intentions group showed already at the beginning of the task the pattern of task-related functional activity reached after practice in the group having received standard instructions. We interpret our results in terms of an immediate establishment of an automatic, bottom-up form of inhibitory control by implementation intentions, supported by stimulus-driven retrieval of verbally encoded stimulus-response mapping rules, which in turn triggered inhibitory processes.