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.

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.

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.

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.

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.

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.

State dependency of inhibitory control performance: an electrical neuroimaging study.

Behavioral and brain responses to stimuli not only depend on their physical features but also on the individuals' neurocognitive states before stimuli onsets. While the influence of pre-stimulus fluctuations in brain activity on low-level perceptive processes is well established, the state dependency of high-order executive processes remains unclear. Using a classical inhibitory control Go/NoGo task, we examined whether and how fluctuations in the brain activity during the period preceding the stimuli triggering inhibition influenced inhibitory control performance. Seventeen participants completed the Go/NoGo task while 64-channel electroencephalogram was recorded. We compared the event-related potentials preceding the onset of the NoGo stimuli associated with inhibition failures false alarms (FA) vs. successful inhibition correct rejections (CR) with data-driven statistical analyses of global measures of the topography and strength of the scalp electric field. Distributed electrical source estimations were used to localize the origin of the event-related potentials modulations. We observed differences in the global field power of the event-related potentials (FA > CR) without concomitant topographic modulations over the 40 ms period immediately preceding NoGo stimuli. This result indicates that the same brain networks were engaged in the two conditions, but more strongly before FA than CR. Source estimations revealed that this effect followed from a higher activity before FA than CR within bilateral inferior frontal gyri and the right inferior parietal lobule. These findings suggest that uncontrolled quantitative variations in pre-stimulus activity within attentional and control brain networks influence inhibition performance. The present data thereby demonstrate the state dependency of cognitive processes of up to high-order executive levels.

Language specificity of lexical-phonological therapy in bilingual aphasia: A clinical and electrophysiological study.

Based on findings for overlapping representations of bilingual people's first (L1) and second (L2) languages, unilingual therapies of bilingual aphasia have been proposed to benefit the untrained language. However, the generalisation patterns of intra- and cross-language and phonological therapy and their neural bases remain unclear. We tested whether the effects of an intensive lexical-phonological training (LPT) in L2 transferred to L1 word production in a Persian-French bilingual stroke patient with Broca's aphasia. Language performance was assessed using the Bilingual Aphasia Test, a 144-item picture naming (PN) task and a word-picture verification (WPV) task. Electroencephalography (EEG) was recorded during PN and WPV in both languages before and after an LPT in French on a wordlist from the PN task. After the therapy, naming improved only for the treated L2 items. The naming performance improved neither in the untrained L2 items nor in the corresponding items in L1. EEG analyses revealed a Language x Session topographic interaction at 540 ms post-stimulus, driven by a modification of the electrophysiological response to the treated L2 but not L1 items. These results indicate that LPT modified the brain networks engaged in the phonological-phonetic processing during naming only in the trained language for the trained items.

Experience-based Auditory Predictions Modulate Brain Activity to Silence as do Real Sounds.

Interactions between stimuli's acoustic features and experience-based internal models of the environment enable listeners to compensate for the disruptions in auditory streams that are regularly encountered in noisy environments. However, whether auditory gaps are filled in predictively or restored a posteriori remains unclear. The current lack of positive statistical evidence that internal models can actually shape brain activity as would real sounds precludes accepting predictive accounts of filling-in phenomenon. We investigated the neurophysiological effects of internal models by testing whether single-trial electrophysiological responses to omitted sounds in a rule-based sequence of tones with varying pitch could be decoded from the responses to real sounds and by analyzing the ERPs to the omissions with data-driven electrical neuroimaging methods. The decoding of the brain responses to different expected, but omitted, tones in both passive and active listening conditions was above chance based on the responses to the real sound in active listening conditions. Topographic ERP analyses and electrical source estimations revealed that, in the absence of any stimulation, experience-based internal models elicit an electrophysiological activity different from noise and that the temporal dynamics of this activity depend on attention. We further found that the expected change in pitch direction of omitted tones modulated the activity of left posterior temporal areas 140-200 msec after the onset of omissions. Collectively, our results indicate that, even in the absence of any stimulation, internal models modulate brain activity as do real sounds, indicating that auditory filling in can be accounted for by predictive activity.

Submillisecond unmasked subliminal visual stimuli evoke electrical brain responses.

Subliminal perception is strongly associated to the processing of meaningful or emotional information and has mostly been studied using visual masking. In this study, we used high density 256-channel EEG coupled with an liquid crystal display (LCD) tachistoscope to characterize the spatio-temporal dynamics of the brain response to visual checkerboard stimuli (Experiment 1) or blank stimuli (Experiment 2) presented without a mask for 1 ms (visible), 500 µs (partially visible), and 250 µs (subliminal) by applying time-wise, assumption-free nonparametric randomization statistics on the strength and on the topography of high-density scalp-recorded electric field. Stimulus visibility was assessed in a third separate behavioral experiment. Results revealed that unmasked checkerboards presented subliminally for 250 µs evoked weak but detectable visual evoked potential (VEP) responses. When the checkerboards were replaced by blank stimuli, there was no evidence for the presence of an evoked response anymore. Furthermore, the checkerboard VEPs were modulated topographically between 243 and 296 ms post-stimulus onset as a function of stimulus duration, indicative of the engagement of distinct configuration of active brain networks. A distributed electrical source analysis localized this modulation within the right superior parietal lobule near the precuneus. These results show the presence of a brain response to submillisecond unmasked subliminal visual stimuli independently of their emotional saliency or meaningfulness and opens an avenue for new investigations of subliminal stimulation without using visual masking.

Differential patterns of functional and structural plasticity within and between inferior frontal gyri support training-induced improvements in inhibitory control proficiency.

Ample evidence indicates that inhibitory control (IC), a key executive component referring to the ability to suppress cognitive or motor processes, relies on a right-lateralized fronto-basal brain network. However, whether and how IC can be improved with training and the underlying neuroplastic mechanisms remains largely unresolved. We used functional and structural magnetic resonance imaging to measure the effects of 2 weeks of training with a Go/NoGo task specifically designed to improve frontal top-down IC mechanisms. The training-induced behavioral improvements were accompanied by a decrease in neural activity to inhibition trials within the right pars opercularis and triangularis, and in the left pars orbitalis of the inferior frontal gyri. Analyses of changes in brain anatomy induced by the IC training revealed increases in grey matter volume in the right pars orbitalis and modulations of white matter microstructure in the right pars triangularis. The task-specificity of the effects of training was confirmed by an absence of change in neural activity to a control working memory task. Our combined anatomical and functional findings indicate that differential patterns of functional and structural plasticity between and within inferior frontal gyri enhanced the speed of top-down inhibition processes and in turn IC proficiency. The results suggest that training-based interventions might help overcoming the anatomic and functional deficits of inferior frontal gyri manifesting in inhibition-related clinical conditions. More generally, we demonstrate how multimodal neuroimaging investigations of training-induced neuroplasticity enable revealing novel anatomo-functional dissociations within frontal executive brain networks.

Early attentional processes distinguish selective from global motor inhibitory control: an electrical neuroimaging study.

The rapid stopping of specific parts of movements is frequently required in daily life. Yet, whether selective inhibitory control of movements is mediated by a specific neural pathway or by the combination between a global stopping of all ongoing motor activity followed by the re-initiation of task-relevant movements remains unclear. To address this question, we applied time-wise statistical analyses of the topography, global field power and electrical sources of the event-related potentials to the global vs selective inhibition stimuli presented during a Go/NoGo task. Participants (n=18) had to respond as fast as possible with their two hands to Go stimuli and to withhold the response from the two hands (global inhibition condition, GNG) or from only one hand (selective inhibition condition, SNG) when specific NoGo stimuli were presented. Behaviorally, we replicated previous evidence for slower response times in the SNG than in the Go condition. Electrophysiologically, there were two distinct phases of event-related potentials modulations between the GNG and the SNG conditions. At 110-150 ms post-stimulus onset, there was a difference in the strength of the electric field without concomitant topographic modulation, indicating the differential engagement of statistically indistinguishable configurations of neural generators for selective and global inhibitory control. At 150-200 ms, there was topographic modulation, indicating the engagement of distinct brain networks. Source estimations localized these effects within bilateral temporo-parieto-occipital and within parieto-central networks, respectively. Our results suggest that while both types of motor inhibitory control depend on global stopping mechanisms, selective and global inhibition still differ quantitatively at early attention-related processing phases.

Age-related changes in the bimanual advantage and in brain oscillatory activity during tapping movements suggest a decline in processing sensory reafference.

Deficits in the processing of sensory reafferences have been suggested as accounting for age-related decline in motor coordination. Whether sensory reafferences are accurately processed can be assessed based on the bimanual advantage in tapping: because of tapping with an additional hand increases kinesthetic reafferences, bimanual tapping is characterized by a reduced inter-tap interval variability than unimanual tapping. A suppression of the bimanual advantage would thus indicate a deficit in sensory reafference. We tested whether elderly indeed show a reduced bimanual advantage by measuring unimanual (UM) and bimanual (BM) self-paced tapping performance in groups of young (n = 29) and old (n = 27) healthy adults. Electroencephalogram was recorded to assess the underlying patterns of oscillatory activity, a neurophysiological mechanism advanced to support the integration of sensory reafferences. Behaviorally, there was a significant interaction between the factors tapping condition and age group at the level of the inter-tap interval variability, driven by a lower variability in BM than UM tapping in the young, but not in the elderly group. This result indicates that in self-paced tapping, the bimanual advantage is absent in elderly. Electrophysiological results revealed an interaction between tapping condition and age group on low beta band (14-20 Hz) activity. Beta activity varied depending on the tapping condition in the elderly but not in the young group. Source estimations localized this effect within left superior parietal and left occipital areas. We interpret our results in terms of engagement of different mechanisms in the elderly depending on the tapping mode: a 'kinesthetic' mechanism for UM and a 'visual imagery' mechanism for BM tapping movement.

Progression of auditory discrimination based on neural decoding predicts awakening from coma.

Auditory evoked potentials are informative of intact cortical functions of comatose patients. The integrity of auditory functions evaluated using mismatch negativity paradigms has been associated with their chances of survival. However, because auditory discrimination is assessed at various delays after coma onset, it is still unclear whether this impairment depends on the time of the recording. We hypothesized that impairment in auditory discrimination capabilities is indicative of coma progression, rather than of the comatose state itself and that rudimentary auditory discrimination remains intact during acute stages of coma. We studied 30 post-anoxic comatose patients resuscitated from cardiac arrest and five healthy, age-matched controls. Using a mismatch negativity paradigm, we performed two electroencephalography recordings with a standard 19-channel clinical montage: the first within 24 h after coma onset and under mild therapeutic hypothermia, and the second after 1 day and under normothermic conditions. We analysed electroencephalography responses based on a multivariate decoding algorithm that automatically quantifies neural discrimination at the single patient level. Results showed high average decoding accuracy in discriminating sounds both for control subjects and comatose patients. Importantly, accurate decoding was largely independent of patients' chance of survival. However, the progression of auditory discrimination between the first and second recordings was informative of a patient's chance of survival. A deterioration of auditory discrimination was observed in all non-survivors (equivalent to 100% positive predictive value for survivors). We show, for the first time, evidence of intact auditory processing even in comatose patients who do not survive and that progression of sound discrimination over time is informative of a patient's chance of survival. Tracking auditory discrimination in comatose patients could provide new insight to the chance of awakening in a quantitative and automatic fashion during early stages of coma.

High and low stimulus-driven conflict engage segregated brain networks, not quantitatively different resources.

Task-irrelevant information is constantly present in our environment and may interfere with the processing of the information necessary to achieve goal-directed behavior. While task goals determine which information must be suppressed, the demand for inhibitory control depends on the strength of the interference induced by incoming, task-irrelevant information. Whether the same or distinct inhibitory processes are engaged to suppress various degrees of interference from task-irrelevant information remains largely unresolved. We investigated this question by manipulating the strength of the conflict induced by automatic word reading in a classical color Stroop task. High conflict was induced by presenting words in participant's native language and low conflict by presenting words in a less familiar language. Behavioral performance and electrical neuroimaging analyses of event-related potentials to the words were analyzed following a two-by-two within-subject design with factors conflict strength (high; low) and color word/word ink congruency (congruent; incongruent). Behaviorally, we observed a significant conflict strength × congruency driven by a smaller Stroop effect in the low- than high conflict condition. Electrophysiologically, we observed a significant conflict strength × congruency interaction at the topographic level during the period of the N450 components, indicative of the engagement of distinct configurations of brain networks. No such interaction was found at the level of response strength. Electrical sources analyses localized the topographic effect within the anterior cingulate cortex and basal ganglia, left middle frontal and occipital areas. We interpret our results in terms of qualitatively distinct executive mechanisms for reactive inhibitory control in conditions of high versus low stimulus-driven conflict.

Inter- and intrahemispheric dissociations in ideomotor apraxia: a large-scale lesion-symptom mapping study in subacute brain-damaged patients.

Pantomimes of object use require accurate representations of movements and a selection of the most task-relevant gestures. Prominent models of praxis, corroborated by functional neuroimaging studies, predict a critical role for left parietal cortices in pantomime and advance that these areas store representations of tool use. In contrast, lesion data points to the involvement of left inferior frontal areas, suggesting that defective selection of movement features is the cause of pantomime errors. We conducted a large-scale voxel-based lesion-symptom mapping analyses with configural/spatial (CS) and body-part-as-object (BPO) pantomime errors of 150 left and right brain-damaged patients. Our results confirm the left hemisphere dominance in pantomime. Both types of error were associated with damage to left inferior frontal regions in tumor and stroke patients. While CS pantomime errors were associated with left temporoparietal lesions in both stroke and tumor patients, these errors appeared less associated with parietal areas in stroke than in tumor patients and less associated with temporal in tumor than stroke patients. BPO errors were associated with left inferior frontal lesions in both tumor and stroke patients. Collectively, our results reveal a left intrahemispheric dissociation for various aspects of pantomime, but with an unspecific role for inferior frontal regions.

Electrical neuroimaging during auditory motion aftereffects reveals that auditory motion processing is motion sensitive but not direction selective.

Following prolonged exposure to adaptor sounds moving in a single direction, participants may perceive stationary-probe sounds as moving in the opposite direction [direction-selective auditory motion aftereffect (aMAE)] and be less sensitive to motion of any probe sounds that are actually moving (motion-sensitive aMAE). The neural mechanisms of aMAEs, and notably whether they are due to adaptation of direction-selective motion detectors, as found in vision, is presently unknown and would provide critical insight into auditory motion processing. We measured human behavioral responses and auditory evoked potentials to probe sounds following four types of moving-adaptor sounds: leftward and rightward unidirectional, bidirectional, and stationary. Behavioral data replicated both direction-selective and motion-sensitive aMAEs. Electrical neuroimaging analyses of auditory evoked potentials to stationary probes revealed no significant difference in either global field power (GFP) or scalp topography between leftward and rightward conditions, suggesting that aMAEs are not based on adaptation of direction-selective motion detectors. By contrast, the bidirectional and stationary conditions differed significantly in the stationary-probe GFP at 200 ms poststimulus onset without concomitant topographic modulation, indicative of a difference in the response strength between statistically indistinguishable intracranial generators. The magnitude of this GFP difference was positively correlated with the magnitude of the motion-sensitive aMAE, supporting the functional relevance of the neurophysiological measures. Electrical source estimations revealed that the GFP difference followed from a modulation of activity in predominantly right hemisphere frontal-temporal-parietal brain regions previously implicated in auditory motion processing. Our collective results suggest that auditory motion processing relies on motion-sensitive, but, in contrast to vision, non-direction-selective mechanisms.

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.