Successful Stop Trials Research Articles

Effects of fMRI neurofeedback of right inferior frontal cortex on inhibitory brain activation in children with ADHD.

We aimed to replicate previous effects of functional magnetic resonance imaging neurofeedback (fMRI-NF) in right inferior frontal cortex (rIFC) on IFC activation during a Stop Task in a larger group of boys with attention-deficit/hyperactivity disorder (ADHD). The present double-blind, randomized controlled trial tested the effects of 15 runs of active versus sham fMRI-NF of rIFC on performance and activation associated with successful and failed inhibition versus Go trials during a tracking Stop task in 88 boys with ADHD (44 active; 44 sham), controlling for age and medication status. No significant group-by-time interaction effects were observed for performance or brain activation during the successful stop trials, and post hoc analysis showed very low numbers of active fMRI-NF learners. Nevertheless, during error monitoring, there was a significant group-by-time interaction effect on post-error reaction time slowing and in left IFC activation, which were both increased after active compared to sham fMRI-NF. The findings are in line with our previous observation of left IFC upregulation after fMRI-NF of rIFC relative to active fMRI-NF of parahippocampal gyrus. This highlights the potentially wider regional effects that fMRI-NF of a particular self-control target region has on other self-regulatory regions in ADHD. This article is part of the theme issue 'Neurofeedback: new territories and neurocognitive mechanisms of endogenous neuromodulation'.

Early Rise and Persistent Inhibition of Electromyography during Failed Stopping.

Reactively canceling movements is a vital feature of the motor system to ensure safety. This behavior can be studied in the laboratory using the stop-signal task. There remains ambiguity about whether a "point-of-no-return" exists, after which a response cannot be aborted. A separate question concerns whether motor system inhibition associated with attempted stopping persists when stopping is unsuccessful. We address these two questions using electromyography (EMG) in two stop-signal task experiments. Experiment 1 (n = 24) involved simple right and left index finger responses in separate task blocks. Experiment 2 (n = 28) involved a response choice between the right index and pinky fingers. To evaluate the approximate point of no return, we measured EMG in responding fingers during the 100 msec preceding the stop signal and observed significantly greater EMG amplitudes during failed than successful stopping in both experiments. Thus, EMG before the stop signal differentiated success, regardless of whether there was a response choice. To address whether motor inhibition persists after failed stopping, we assessed EMG peak-to-offset durations and slopes (i.e., rate of EMG decline) for go, failed stop, and successful stop (partial response) trials. EMG peak-to-offset was shorter and steeper for failed stopping compared to go and successful stop partial response trials, suggesting motor inhibition persists even when failing to stop. These findings indicate EMG is sensitive to a "transition zone" at which the relative likelihood of stop failure versus success inverts and also suggest peak-to-offset time of response-related EMG activity during failed stopping reflects stopping-related inhibition.

Reduced inferior fronto-insular-thalamic activation during failed inhibition in young adults with combined ASD and ADHD compared to typically developing and pure disorder groups

Autism spectrum disorder (ASD) often co-occurs with attention-deficit/hyperactivity disorder (ADHD) and people with these conditions have frontostriatal functional atypicality during motor inhibition. We compared the neural and neurocognitive correlates of motor inhibition and performance monitoring in young adult males with “pure” and combined presentations with age-and sex-matched typically developing controls, to explore shared or disorder-specific atypicality. Males aged 20–27 years with typical development (TD; n = 22), ASD (n = 21), combined diagnoses ASD + ADHD (n = 23), and ADHD (n = 25) were compared using a modified tracking fMRI stop-signal task that measures motor inhibition and performance monitoring while controlling for selective attention. In addition, they performed a behavioural go/no-go task outside the scanner. While groups did not differ behaviourally during successful stop trials, the ASD + ADHD group relative to other groups had underactivation in typical performance monitoring regions of bilateral anterior insula/inferior frontal gyrus, right posterior thalamus, and right middle temporal gyrus/hippocampus during failed inhibition, which was associated with increased stop-signal reaction time. In the behavioural go/no-go task, both ADHD groups, with and without ASD, had significantly lower motor inhibition performance compared to TD controls. In conclusion, only young adult males with ASD + ADHD had neurofunctional atypicality in brain regions associated with performance monitoring, while inhibition difficulties on go/no-go task performance was shared with ADHD. The suggests that young people with ASD + ADHD are most severely impaired during motor inhibition tasks compared to ASD and ADHD but do not reflect a combination of the difficulties associated with the pure disorders.

Pre-saccadic attention relies more on suppression than does covert attention.

During covert and pre-saccadic attentional shifts, it is unclear how facilitation and suppression processes interact for target selection. A recent countermanding task pointed to greater suppression at unattended locations during trials with saccades compared to trials without saccades (i.e., fixation and successful stop trials), whereas target facilitation did not differ. It is unknown whether this finding is restricted to countermanding paradigms that involve inhibitory processes. To test this, we adapted Gaspelin and colleagues (2015)'s attention capture task where, within the same block, one location was primed with frequent line discrimination trials, and all locations were occasionally probed using letters report trials. Participants also performed a baseline condition without priming. We tested 15 participants and examined how performance at non-primed locations was affected by covert versus pre-saccadic attention in blocks of four or six items, as well as by position from the primed location and timing from saccade onset. For both attention conditions, letter report at non-primed locations was worse compared to baseline, demonstrating suppression, and letter report at primed location was better, demonstrating facilitation. In saccades trials, letter report was better at primed locations and worse at non-primed locations compared to fixation trials. The timing of this additional pre-saccadic suppression differed from saccadic suppression. In both attention conditions, suppression was greater when primed and non-primed locations were within the same hemifield or in diagonal opposite quadrants. These results confirmed that attention preceding saccade execution suppressed non-primed locations to a larger extent than covert attention, with the same spatial quadrant effect.

Repetitive transcranial magnetic stimulation promotes response inhibition in patients with major depression during the stop-signal task

BackgroundResponse inhibition (RI) deficit is an aspect of cognitive impairment in depressed individuals, but currently no effective treatment has been established. This study aimed to explore the effect of individualized repetitive transcranial magnetic stimulation (rTMS) targeting the left dorsolateral prefrontal cortex (lDLPFC)-nucleus accumbens (NAcc) network on RI in patients with major depressive disorder (MDD). MethodsFourty-four patients diagnosed with MDD were randomized to receive 15 once-daily sessions of active (10 Hz, 100% of resting motor threshold) or sham rTMS within a double-blind, sham-controlled trial. We measured the efficacy of rTMS by the improvements in behavioral and neurological manifestations during the stop-signal task. The Hamilton Depression Rating Scale-17 items (HAMD-17) was used to assess depressive symptoms. We analyzed the differences in RI performance between MDD patients and 30 healthy controls (HCs) at baseline and assessed whether MDD patients who completed rTMS treatment had comparable RI ability to HCs. ResultsAt baseline, the depressed patients showed longer stop-signal response time (SSRT), smaller P3 amplitudes, and weaker theta-band power in successful stop trials (SSTs) than HCs. The active group exhibited RI ability comparable to that of HCs after rTMS treatment, but the improvements were not significant in the sham group. The active group showed significant remission in depression symptoms post-treatment compared to the sham group, and the changes in P3 amplitudes and theta-band power during SSTs were negatively correlated with the decrease of HAMD-17 scores. ConclusionThe depressed patients have impaired RI and treatment with the individualized rTMS protocol may be an effective approach.

A method to assess response inhibition during a balance recovery step

BackgroundCorrelations between falls and individual differences in inhibitory control, suggest the ability to suppress automatic, but unwanted, action is important in fall prevention. Response inhibition has been a topic of considerable interest in the cognitive neuroscience community for many decades, bringing a wealth of techniques that could potentially inform assessment of reactive balance. For example, the stop signal task is a popular method to quantify inhibitory control ability. Research questionCan we apply the stop signal task to measure response inhibition in a balance recovery task? MethodsTwenty healthy, young adults completed a novel reactive balance test that required occasional suppression of a balance recovery step. Participants were released from a supported lean (‘Go’ cue) requiring them to quickly step forward to regain balance. On some trials, a tone (‘Stop’ cue) instructed participants to suppress a step and relax into a harness. Step trials were more frequent (80%) than stop trials (20%) to bias a rapid stepping response. The stop tone was presented at various delays following cable release, to manipulate task difficulty (i.e., longer delays make step suppression difficult). Individual differences in inhibitory control were determined using lift off times from force plates, and by contrasting muscle activation in failed compared to successful stop trials. ResultsMost participants were able to successfully suppress a balance recovery step on occasion, allowing for accurate estimation of individual differences in inhibitory control. The successful suppression of a balance recovery step was more likely in the group (n = 10) where shorter stop signal delays were used (i.e., the task was easier). SignificanceWhile balance assessments often stress reflexive action, there is a need for methods that evaluate response inhibition. The present study leveraged a well-established cognitive test of inhibitory control to develop a method to quantify stopping ability in a reactive balance context.

Cortico-subcortical β burst dynamics underlying movement cancellation in humans.

Dominant neuroanatomical models hold that humans regulate their movements via loop-like cortico-subcortical networks, which include the subthalamic nucleus (STN), motor thalamus, and sensorimotor cortex (SMC). Inhibitory commands across these networks are purportedly sent via transient, burst-like signals in the β frequency (15-29 Hz). However, since human depth-recording studies are typically limited to one recording site, direct evidence for this proposition is hitherto lacking. Here, we present simultaneous multi-site recordings from SMC and either STN or motor thalamus in humans performing the stop-signal task. In line with their purported function as inhibitory signals, subcortical β-bursts were increased on successful stop-trials. STN bursts in particular were followed within 50 ms by increased β-bursting over SMC. Moreover, between-site comparisons (including in a patient with simultaneous recordings from SMC, thalamus, and STN) confirmed that β-bursts in STN temporally precede thalamic β-bursts. This highly unique set of recordings provides empirical evidence for the role of β-bursts in conveying inhibitory commands along long-proposed cortico-subcortical networks underlying movement regulation in humans.

Neural correlates of inhibitory control are associated with stimulant-like effects of alcohol.

Poor inhibitory control and heightened feelings of stimulation after alcohol are two well-established risk factors for alcohol use disorder (AUD). Although these risk factors have traditionally been viewed as orthogonal, recent evidence suggests that the two are related and may share common neurobiological mechanisms. Here we examined the degree to which neural activity during inhibition was associated with subjective reports of stimulation following alcohol. To assess neural changes during inhibition, moderate alcohol drinkers performed a stop signal task during fMRI without drug. To assess subjective responses to alcohol they ingested alcohol (0.8 g/kg) or placebo beverages under double-blind conditions and provided subjective reports of stimulation and sedation. Feelings of stimulation following alcohol were inversely associated with activity in the supplementary motor area, insula, and middle frontal gyrus during inhibition (successful stop trials compared to go trials). Feelings of sedation did not correlate with brain activation. These results extend previous findings suggesting that poor inhibitory control is associated with more positive subjective responses to alcohol. These interrelated risk factors may contribute to susceptibility to future excessive alcohol use, and ultimately lead to neurobiological targets to prevent or treat AUD.

Dynamical EEG Indices of Progressive Motor Inhibition and Error-Monitoring.

Response inhibition has been widely explored using the stop signal paradigm in the laboratory setting. However, the mechanism that demarcates attentional capture from the motor inhibition process is still unclear. Error monitoring is also involved in the stop signal task. Error responses that do not complete, i.e., partial errors, may require different error monitoring mechanisms relative to an overt error. Thus, in this study, we included a “continue go” (Cont_Go) condition to the stop signal task to investigate the inhibitory control process. To establish the finer difference in error processing (partial vs. full unsuccessful stop (USST)), a grip-force device was used in tandem with electroencephalographic (EEG), and the time-frequency characteristics were computed with Hilbert–Huang transform (HHT). Relative to Cont_Go, HHT results reveal (1) an increased beta and low gamma power for successful stop trials, indicating an electrophysiological index of inhibitory control, (2) an enhanced theta and alpha power for full USST trials that may mirror error processing. Additionally, the higher theta and alpha power observed in partial over full USST trials around 100 ms before the response onset, indicating the early detection of error and the corresponding correction process. Together, this study extends our understanding of the finer motor inhibition control and its dynamic electrophysiological mechanisms.

The P300 as marker of inhibitory control – Fact or fiction?

Inhibitory control, i.e., the ability to stop or suppress actions, thoughts, or memories, represents a prevalent and popular concept in basic and clinical neuroscience as well as psychology. At the same time, it is notoriously difficult to study as successful inhibition is characterized by the absence of a continuously quantifiable direct behavioral marker. It has been suggested that the P3 latency, and here especially its onset latency, may serve as neurophysiological marker of inhibitory control as it correlates with the stop signal reaction time (SSRT). The SSRT estimates the average stopping latency, which itself is unobservable since no overt response is elicited in successful stop trials, based on differences in the distribution of go reaction times and the delay of the stop-relative to the go-signal in stop trials.In a meta-analysis and an independent electroencephalography (EEG) experiment, we found that correlations between the P3 latency and the SSRT are indeed replicable, but also unspecific. Not only does the SSRT also correlate with the N2 latency, but both P3 and N2 latency measures show similar or even higher correlations with other behavioral parameters such as the go reaction time or stopping accuracy. The missing specificity of P3–SSRT correlations, together with the general pattern of associations, suggests that these manifest effects are driven by underlying latent processes other than inhibition, such as behavioral adaptations in context of performance monitoring operations.

Neurocomputational Changes in Inhibitory Control Associated With Prolonged Exposure Therapy.

Posttraumatic stress disorder (PTSD) is associated with inhibitory control dysfunction that extends beyond difficulties inhibiting trauma-related intrusions. Inhibitory learning has been proposed as a potential mechanism of change underlying the effectiveness of extinction-based therapies such as prolonged exposure (PE), a first-line treatment for PTSD. To identify neurocognitive markers of change in inhibitory learning associated with PE, we applied a Bayesian learning model to the analysis of neuroimaging data collected during an inhibitory control task, both before and after PE treatment. Veterans (N = 20) with combat-related PTSD completed a stop-signal task (SST) while undergoing fMRI at time points immediately before and after PE treatment. Participants exhibited a small, significant improvement in performance on the SST, as demonstrated by longer reaction times and improved inhibition accuracy. Amplitude of neural activation associated with a signed prediction error (SPE; i.e., the discrepancy between actual outcome and model-based expectation of needing to stop) in the right caudate decreased from baseline to posttreatment assessment. Change in model-based activation was modulated by performance accuracy, with a decrease in positive SPE activation observed on successful trials, d = 0.79, and a reduction in negative SPE activation on error trials, d = 0.74. The decrease in SPE-related activation on successful stop trials was correlated with PTSD symptom reduction. These results are consistent with the notion that PE may help broadly strengthen inhibitory learning and the development of more accurate model-based predictions, which may thus facilitate change in cognitions in response to trauma-related cues and help reduce PTSD symptoms.

Shared Response Inhibition Deficits but Distinct Error Processing Capacities Between Schizophrenia and Obsessive-Compulsive Disorder Patients Revealed by Event-Related Potentials and Oscillations During a Stop Signal Task.

Background: Schizophrenia (SCH) patients are at high risk for obsessive-compulsive syndrome, which can lead to difficulty in differential diagnosis between SCH and obsessive-compulsive disorder (OCD). It would be of great clinical value to identify objective markers for these diseases based on behavioral or neurological manifestations. Deficient response inhibition has been reported in both SCH and OCD; however, it is unclear if common or distinct neural abnormalities underlie this impairment. Methods: To address this question, we compared Stop signal task performance and associated event-related potentials (ERPs) and event-related oscillation (ERO) among 24 SCH patients, 25 OCD patients, and 27 healthy controls (HCs). Results: In successful Stop trials, both SCH and OCD patients showed prolonged Stop signal response time, reduced ERP-P3 component amplitude, and weaker theta-band synchronization compared to HCs, while there were no significant differences between patient groups. In unsuccessful Stop trials, however, SCH patients demonstrated significantly lower P3 amplitudes and weaker theta-band activity than OCD patients. In addition, Stop accuracy rate in SCH patients was negatively correlated with Positive subscale score of the Positive and Negative Syndrome Scale. Conclusions: These results provide evidence that impaired response inhibition in SCH and OCD arises from common underlying neural processing abnormalities. However, the lower P3 amplitude and weaker theta-band activity in SCH patients in unsuccessful Stop trials suggest distinct neural activity patterns related to error processing. These differences in ERPs and ERO may provide clues to unique neurological abnormalities in SCH and provide objective measures for differential diagnosis.

Brain event-related potentials predict individual differences in inhibitory control

Stop-signal reaction time (SSRT), the time needed to cancel an already-initiated motor response, quantifies individual differences in inhibitory control. Electrophysiological correlates of SSRT have primarily focused on late event-related potential (ERP) components over midline scalp regions from successfully inhibited stop trials. SSRT is robustly associated with the P300, there is mixed evidence for N200 involvement, and there is little information on the role of early ERP components. Here, machine learning was first used to interrogate ERPs during both successful and failed stop trials from 64 scalp electrodes at 4 ms resolution (n = 148). The most predictive model included data from both successful and failed stop trials, with a cross-validated Pearson's r of 0.32 between measured and predicted SSRT, significantly higher than null models. From successful stop trials, spatio-temporal features overlapping the N200 in right frontal areas and the P300 in frontocentral areas predicted SSRT, as did early ERP activity (<200 ms). As a demonstration of the reproducibility of these findings, the application of this model to a separate dataset of 97 participants was also significant (r = 0.29). These results show that ERPs during failed stops are relevant to SSRT, and that both early and late ERP activity contribute to individual differences in SSRT. Notably, the right lateralized N200, which predicted SSRT here, is not often observed in neurotypical adults. Both the ascending slope and peak of the P300 component predicted SSRT. These results were replicable, both within the training sample and when applied to ERPs from a separate dataset.

Individual differences in intracortical inhibition during behavioural inhibition

The time required to abort an initiated response can be measured as the Stop Signal Reaction Time (SSRT). We determined whether GABAergic activity in the primary motor cortex (M1), measured using paired-pulse Transcranial Magnetic Stimulation (TMS) was related to SSRT. GABAergic activity in M1 was assessed by measuring Short-Interval Intracortical Inhibition (SICI). In two experiments, participants (males and females) completed the Stop Signal Task while we measured SICI from the first dorsal interosseous muscle. In Experiment 1, SICI was measured at fixed time points after Stop signal onset on Stop trials (50ms, 100ms, 150ms, 200ms), and at corresponding time points for Go trials. In Experiment 2 SICI was measured at fixed time points before the end of the SSRT interval (125ms, 75ms, 25ms) on Stop trials, and at corresponding time points for Go trials. In each experiment, 30 participants were classified as fast stoppers or slow stoppers based on a median split of their SSRTs. Fast stoppers had more SICI than slow stoppers, both when executing a response (Go trials) and when inhibiting a response (Stop trials). Indeed, the correlation between mean SICI and SSRT on successful Stop trials was 0.81. Experiment 2 showed that for fast stoppers (relative to baseline) there was reduced SICI on Go trials and recovery of SICI on Stop trials. Slow stoppers however, showed reduced SICI on Stop and Go trials relative to baseline. Our results show that individuals who are faster at stopping not only show more GABAergic activity in M1, but can more effectively control M1 GABAergic activity to inhibit motor cortical excitability when stopping a response and disinhibit excitability when executing a response.

Subthalamic Nucleus Activation Occurs Early during Stopping and Is Associated with Trait Impulsivity.

The subthalamic nucleus (STN) is thought to be a central regulator of behavioral inhibition, which is thought to be a major determinant of impulsivity. Thus, it would be reasonable to hypothesize that STN function is related to impulsivity. However, it has been difficult to test this hypothesis because of the challenges in noninvasively and accurately measuring this structure's signal in humans. We utilized a novel approach for STN signal localization that entails identifying this structure directly on fMRI images for each individual participant in native space. Using this approach, we measured STN responses during the stop signal task in a sample of healthy adult participants. We confirmed that the STN exhibited selective activation during "Stop" trials. Furthermore, the magnitude of STN activation during successful Stop trials inversely correlated with individual differences in trait impulsivity as measured by a personality inventory. Time course analysis revealed that early STN activation differentiated successful from unsuccessful Stop trials, and individual differences in the magnitude of STN activation inversely correlated with stop signal RT, an estimate of time required to stop. These results are consistent with the STN playing a central role in inhibition and related behavioral proclivities, with implications for both normal range function and clinical syndromes of inhibitory dyscontrol. Moreover, the methods utilized in this study for measuring STN fMRI signal in humans may be gainfully applied in future studies to further our understanding of the role of the STN in regulating behavior and neuropsychiatric conditions.

Response Inhibition Deficits in Insomnia Disorder: An Event-Related Potential Study With the Stop-Signal Task.

Background: Response inhibition is a hallmark of executive function, which was detected impaired in various psychiatric disorders. However, whether insomnia disorder (ID) impairs response inhibition has caused great controversy.Methods: Using the auditory stop-signal paradigm coupled with event-related potentials (ERPs), we carried out this study to examine whether individuals with ID presented response inhibition deficits and further investigated the neural mechanism correlated to these deficits. Twelve individuals with ID and 13 matched good sleepers (GSs) had participated in this study, and then they performed an auditory stop-signal task (SST) in the laboratory setting with high density EEG recordings.Results: The behavioral results revealed that compared to GSs, patients with ID presented significantly longer stop-signal reaction time (SSRT), suggesting the impairment of motor inhibition among insomniacs. Their reaction time in go trials, however, showed no significant between-group difference. Considering the electrophysiological correlate underlying the longer SSRT, we found reduced P3 amplitude in patients with insomnia in the successful stop trials, which might reflect their poor efficiency of response inhibition. Finally, when we performed exploratory analyses in the failed stop and go trials, patients with ID presented reduced Pe and N1 amplitude in the failed sop trials and go trials respectively.Discussion: Taken together, these findings indicate that individuals with ID would present response inhibition deficits. Moreover, the electrophysiological correlate underlying these deficits mainly revolves around the successful stop P3 component. The present study is the first to investigate the electrophysiological correlate underlying the impaired response inhibition among insomniacs.

Response Time Adjustment in the Stop Signal Task: Development in Children and Adolescents.

Adjusting speed to maintain fast and accurate performance is critical to goal-directed behavior. This study examined development of response time adjustments in the stop signal task in 13,709 individuals aged 6-17years (49.0% Caucasian) across four trial types: correct and incorrect go, successful (stop-inhibit), and failed (stop-respond) trials. People sped more after correct than incorrect go responses and slowed more after failed than successful stop trials. Greater slowing after stop-respond but less slowing after stop-inhibit trials was associated with better response inhibition. Response time adjustments were evident in children as young as age 6, developed throughout childhood, and plateaued by age 10. Results were consistent with the predictions of the error detection and shifting goal priority hypotheses for adjustments.

Sensory and cross-network contributions to response inhibition in patients with schizophrenia.

Patients with schizophrenia show response inhibition deficits equal to or greater than those seen in impulse-control disorders, and these deficits contribute to poor outcome. However, little is known about the circuit abnormalities underlying this impairment. To address this, we examined stop signal task performance in 21 patients with schizophrenia and 21 healthy controls using event related potential (ERP) and resting state functional connectivity. Patients showed prolonged stop signal reaction time (SSRT) and reduced N1, N2, and P3 amplitudes compared to controls. Across groups, P3 amplitudes were maximal after SSRT (i.e., after the time associated with the decision to stop occurred), suggesting that this component indexed response monitoring. Multiple regression analyses showed that longer SSRTs were independently related to 1) patient status, 2) reduced N1 amplitude on successful stop trials and 3) reduced anticorrelated resting state functional connectivity between visual and frontoparietal cortical networks. This study used a combined multimodal imaging approach to better understand the network abnormalities that underlie response inhibition in schizophrenia. It is the first of its kind to specifically assess the brain's resting state functional architecture in combination with behavioral and ERP methods to investigate response inhibition in schizophrenia.

The Temporal Dynamics of Response Inhibition and their Modulation by Cognitive Control.

Behavioral adjustments require interactions between distinct modes of cognitive control and response inhibition. Hypothetically, fast and global inhibition is exerted in the reactive control mode, whereas proactive control enables the preparation of inhibitory pathways in advance while relying on the slower selective inhibitory system. We compared the temporal progression of inhibition in the reactive and proactive control modes using simultaneous electroencephalography (EEG) and electromyography (EMG) recordings. A selective stop signal task was used where go stimuli required bimanual responses, but only one hand's response had to be suppressed in stop trials. Reactive and proactive conditions were incorporated by non-informative and informative cues, respectively. In 47% of successful stop trials, subthreshold EMG activity was detected that was interrupted as early as 150ms after stop stimulus presentation, indicating that inhibition occurs much earlier than previously thought. Inhibition latencies were similar across the reactive and proactive control modes. The EMG of the responding hand in successful selective stop trials indicated a global suppression of ongoing motor actions in the reactive condition, and less inhibitory interference on the ongoing actions in the proactive condition. Group-level second order blind separation (SOBI) was applied to the EEG to dissociate temporally overlapping event-related potentials. The components capturing the N1 and N2 were larger in the reactive than the proactive condition. P3 activity was distributed across four components, three of which were augmented in the proactive condition. Thus, although EEG indices were modulated by the control mode, the inhibition latency remained unaffected.

Comparing functional MRI protocols for small, iron-rich basal ganglia nuclei such as the subthalamic nucleus at 7 T and 3 T.

The basal ganglia (BG) form a network of subcortical nuclei. Functional magnetic resonance imaging (fMRI) in the BG could provide insight in its functioning and the underlying mechanisms of Deep Brain Stimulation (DBS). However, fMRI of the BG with high specificity is challenging, because the nuclei are small and variable in their anatomical location. High resolution fMRI at field strengths of 7 Tesla (T) could help resolve these challenges to some extent. A set of MR protocols was developed for functional imaging of the BG nuclei at 3 T and 7 T. The protocols were validated using a stop-signal reaction task (Logan et al. []: J Exp Psychol: Human Percept Perform 10:276-291). Compared with sub-millimeter 7 T fMRI protocols aimed at cortex, a reduction of echo time and spatial resolution was strictly necessary to obtain robust Blood Oxygen Level Dependent (BOLD) sensitivity in the BG. An fMRI protocol at 3 T with identical resolution to the 7 T showed no robust BOLD sensitivity in any of the BG nuclei. The results suggest that the subthalamic nucleus, as well as the substantia nigra, red nucleus, and the internal and external parts of the globus pallidus show increased activation in failed stop trials compared with successful stop and go trials. Hum Brain Mapp 38:3226-3248, 2017. © 2017 Wiley Periodicals, Inc.