Response Inhibition Performance Research Articles

Contextuality of cognitive control deficits in alcohol dependence — pro et contra

Cognitive impairment, including cognitive control, mediates the negative social consequences of alcohol-related behavior, but few studies have examined these processes in the Russian speaking population using modern and standardized assessment methods. Thus, the aim of the study was to examine the features of cognitive control (inhibition of automatic response) and the general level of cognitive functioning in a Russianspeaking sample of alcohol-dependent individuals (AD) using quantitative assessment methods. Materials and Methods. 111 individuals diagnosed with alcohol dependence (F10.30) and 27 healthy participants were examined by using the Brief Assessment of Cognitive Functioning in Affective Disorders Battery (BAC-A) and additional tests of cognitive control (Stroop test with incongruent stimuli, Stroop test with alcohol-associated stimuli). The statistical methods were U-Mann-Whitney test, Spearman correlation coefficient, two-stage least squares regression. Results. In the AD group the indices of cognitive functioning were significantly lower in all parameters except for the subtests of verbal memory and digit sequence (p<0,05). The model of the relationship between the parameters of general cognitive functioning and cognitive control reveals that the index of incongruence to alcohol-related stimuli was a significant predictor of sampe affiliation. Discussion. The obtained results may indicate the presence of impairments of speed of mental processes, planning , verbal fluency and response inhibition function in the group of individuals with AD. In the studied group, the automatic response inhibition function mediates the general cognitive functioning only within the relevant contextual stimuli.

Neuroimaging Biomarkers in Addiction.

As a neurobiological process, addiction involves pathological patterns of engagement with substances and a range of behaviors with a chronic and relapsing course. Neuroimaging technologies assess brain activity, structure, physiology, and metabolism at scales ranging from neurotransmitter receptors to large-scale brain networks, providing unique windows into the core neural processes implicated in substance use disorders. Identified aberrations in the neural substrates of reward and salience processing, response inhibition, interoception, and executive functions with neuroimaging can inform the development of pharmacological, neuromodulatory, and psychotherapeutic interventions to modulate the disordered neurobiology. Based on our systematic search, 409 protocols registered on ClinicalTrials.gov include the use of one or more neuroimaging paradigms as an outcome measure in addiction, with the majority (N=268) employing functional magnetic resonance imaging (fMRI), followed by positron emission tomography (PET) (N=71), electroencephalography (EEG) (N=50), structural magnetic resonance imaging (MRI) (N=35) and magnetic resonance spectroscopy (MRS) (N=35). Furthermore, in a PubMed systematic review, we identified 61 meta-analyses including 30 fMRI, 22 structural MRI, 8 EEG, 7 PET, and 3 MRS meta-analyses suggesting potential biomarkers in addictions. These studies can facilitate the development of a range of biomarkers that may prove useful in the arsenal of addiction treatments in the coming years. There is evidence that these markers of large-scale brain structure and activity may indicate vulnerability or separate disease subtypes, predict response to treatment, or provide objective measures of treatment response or recovery. Neuroimaging biomarkers can also suggest novel targets for interventions. Closed or open loop interventions can integrate these biomarkers with neuromodulation in real-time or offline to personalize stimulation parameters and deliver the precise intervention. This review provides an overview of neuroimaging modalities in addiction, potential neuroimaging biomarkers, and their physiologic and clinical relevance. Future directions and challenges in bringing these putative biomarkers from the bench to the bedside are also discussed.

Brain Endurance Training Improves Dynamic Calisthenic Exercise and Benefits Novel Exercise and Cognitive Performance: Evidence of Performance Enhancement and Near Transfer of Training.

Dallaway, N, Mortimer, H, Gore, A, and Ring, C. Brain endurance training improves dynamic calisthenic exercise and benefits novel exercise and cognitive performance: Evidence of performance enhancement and near transfer of training. J Strength Cond Res XX(X): 000-000, 2024-The purpose of this dual study was to evaluate whether brain endurance training (BET)-a mental fatigue countermeasure involving physical and cognitive training-enhanced exercise compared with physical training alone. Two studies (N = 29) used a pretest/training/posttest design, with participants randomized to BET or control groups. During testing, participants performed calisthenic exercises (study 1: press-ups, wall sit, and plank; study 2: burpees, jump squats, leg raises, press-ups, and plank) to failure before and after completing 20-minute cognitive tasks (study 1: memory updating; study 2: memory updating, response inhibition, and nonexecutive functions). Training comprised 3 sessions per week for 4 weeks. In study 1 training sessions, participants completed 2 submaximal exercise sets; each exercise was followed by a 3-minute cognitive task with high (BET) or low (control) cognitive loads. In study 2 training sessions, participants completed 1 submaximal exercise set; after 12-minute cognitive tasks (BET) or rest (control), each exercise was preceded by a 3-minute cognitive task (BET) or rest (control). These cognitive tasks involved response inhibition and memory updating. Performance (exercise repetitions/duration), perceived exertion, and mental fatigue were assessed. In pretesting, exercise performance was matched between groups. In posttesting, BET groups performed more dynamic exercises than control groups but the same number of static exercises. Cognitive task performance was either greater for BET or not different between groups. Neither perceived exertion nor mental fatigue differed between groups and tests. Brain endurance training enhanced dynamic but not static calisthenic exercise performance compared with physical training alongside near transfer of training benefits for novel physical and cognitive task performance.

Investigation of Siblings of Patients Diagnosed with Substance-Induced Psychotic Disorder in terms of Cognitive Functions and Clinical High-Risk State for Psychosis

Objective: This study aimed to investigate the influence of familial predisposition on substance-induced psychosis among healthy siblings of patients diagnosed with substance-induced psychotic disorder, who themselves lack any family history of psychotic disorders. Additionally, the study aimed to explore clinical high-risk states for psychosis, schizotypal features, and neurocognitive functions in comparison to a healthy control group. Method: The study compared healthy siblings of 41 patients diagnosed with substance-induced psychotic disorder with 41 healthy volunteers without a family history of psychotic disorders, matching age, gender, and education. Sociodemographic and clinical characteristics of participants were obtained using data collection forms. The Comprehensive Assessment of At-Risk Mental States (CAARMS) and the Structured Interview for Schizotypy-Revised Form (SIS-R) scales were utilized to assess clinical high risk for psychosis. Neurocognitive functions were evaluated with digit span test (DST), trail making test part A-B (TMT), verbal fluency test (VFT), and Stroop test (ST). Results: Analysis using the CAARMS scale revealed that 39% of siblings and 7.3% of the control group were at clinically high risk for psychosis, indicating a significant difference in rates of psychotic vulnerability. Comparison between siblings and the control group showed significant differences in mean SIS-R subscale scores, including social behavior, hypersensitivity, referential thinking, suspiciousness, illusions, and overall oddness, as well as in mean neurocognitive function scores, including errors in TMT-A, TMT-B, and VFT out-of-category errors, with siblings exhibiting poorer performance. Conclusion: Our study suggests that healthy siblings of patients with substance-induced psychosis exhibit more schizotypal features and have a higher risk of developing psychosis compared to healthy controls. Additionally, siblings demonstrate greater impairment in attention, response inhibition, and executive functions compared to healthy controls, indicating the potential role of genetic predisposition in the development of substance-induced psychotic disorder.

The Neural Correlates of Response Inhibition across the Transition from Infancy to Toddlerhood: An fNIRS study

Abstract The transition from late infancy into toddlerhood represents a fundamental period in early development. During this time, the prefrontal cortex (PFC) is undergoing structural and functional maturation processes that parallel the emergence and improvement of executive function skills, such as inhibitory control. Despite the importance of this developmental period, relatively little is known about the emergence and development of response inhibition, a form of inhibitory control, and the associated neural substrates across this key transition. Using functional near-infrared spectroscopy (fNIRS), an optical imaging technique suitable for imaging the developing brain, and an age-appropriate response inhibition task, we investigated the brain regions associated with response inhibition in 16-month-old toddlers. This pre-registered study extends our previous work with 10-month-old infants (Fiske et al., 2022) as it follows the same cohort of participants, now at 16-months of age. Whilst our previous work demonstrated that 10-month-old infants recruited right-lateralised regions of the PFC and parietal cortex when inhibition was required, the current study suggests that by 16-months, toddlers recruit the left superior parietal gyrus, the right inferior frontal gyrus, and bilateral regions of the dorsolateral PFC and orbital frontal cortex. Although there was no longitudinal change in response inhibition performance, more widespread, bilateral regions of the PFC were recruited during response inhibition at 16-months compared to 10 months. We acknowledge the need for replication of these results. Nevertheless, our findings suggest that the transition from infancy to toddlerhood may constitute an important period of reorganisation of the PFC that might support the development of early inhibitory control processes.

Neurocognitive functioning in adults with trichotillomania: Predictors of treatment response and symptom severity in a randomized control trial

Trichotillomania (TTM) is associated with impairments in response inhibition and cognitive flexibility, but it is unclear how such impairments relate to treatment outcome. The present study examined pre-treatment response inhibition and cognitive flexibility as predictors of treatment outcome, change in these domains from pre-to post-treatment, and associations with TTM severity. Participants were drawn from a randomized controlled trial comparing acceptance-enhanced behavior therapy (AEBT) to psychoeducation and supportive therapy (PST) for TTM. Adults completed assessments at pre-treatment (n = 88) and following 12 weeks of treatment (n = 68). Response inhibition and cognitive flexibility were assessed using the Stop Signal Task and Object Alternation Task, respectively. Participants completed the MGH-Hairpulling Scale. Independent evaluators administered the NIMH-Trichotillomania Severity Scale and Clinical Global Impressions-Improvement Scale. Higher pre-treatment TTM severity was associated with poorer pre-treatment cognitive flexibility, but not response inhibition. Better pre-treatment response inhibition performance predicted positive treatment response and lower post-treatment TTM symptom severity, irrespective of treatment assignment. Cognitive flexibility did not predict treatment response. After controlling for age, neither neurocognitive variable changed during treatment. Response inhibition and cognitive flexibility appear uniquely related to hair pulling severity and treatment response in adults with TTM. Implications for treatment delivery and development are discussed.

A differential impact of action–effect temporal contiguity on different measures of response inhibition in the Go\\No-Go and Stop-signal paradigms

Response inhibition refers to suppressing a prepotent motor response and is often studied and discussed as an act of cognitive control. Much less attention was given to the potential contribution of motor control processes to response inhibition. Accumulated empirical findings show that a perceptual effect temporally contiguous with a response improves motor control performance. In the current study, we followed this work by manipulating action–effect temporal contiguity to enhance motor performance and investigated its impact on response selection and inhibition. In two experiments, we integrated a Go/No-Go (GNGT; Experiment 1) and a Stop-signal (SST; Experiment 2) task with the Effect–Motivation task, previously used to capture the facilitating impact of action–effect temporal contiguity on response times (RTs). Replicating previous findings, RTs were shorter following temporally contiguous compared to Lagged action–effect in Go trials in both the GNGT (Experiment 1) and SST (Experiment 2). Notably, an Immediate action–effect improved response inhibition in the GNGT (Experiment 1) but did not modulate Stop-signal reaction time (SSRT) in the SST (Experiment 2). Unexpectedly, the error rate on Go trials was higher in the Immediate effect condition in Experiment 2. We interpret the findings to suggest that an action’s (Immediate) perceptual effect may promote response inhibition performance by enhancing selective association between the Go stimuli and the Go response and not by improving cognitive control ability. The findings also imply that an Immediate action–effect may hamper action control (e.g., by increasing general readiness to respond), at least when action control does not benefit from automatic stimulus–response association.

Reduced sleep quality defines a subtype of obsessive-compulsive disorder with lower Glx levels in the resting thalamus and worse response inhibition

BackgroundThe aim of this study was to investigate the differences between resting and active thalamic neurometabolite levels and inhibitory function in obsessive compulsive disorder (OCD) patients with poor sleep quality (PSQ was defined as Pittsburgh Sleep Quality Index >5 and sleep efficiency ≤85%) compared to OCD patients with good sleep quality (GSQ) and healthy controls (HCs), as well as the relationship of these indices to obsessive compulsive symptoms. MethodsFunctional magnetic resonance spectroscopy (fMRS) was used to measure resting and active thalamic neurometabolite levels in 72 subjects (20 HCs and 38 OCD patients included in study analysis). Response inhibition function was measured by the Go-Nogo task before and during MRS recording. Subjective sleep quality was assessed using the Pittsburgh Sleep Quality Index (PSQI). The symptoms of OCD, anxiety and depression were evaluated using relevant clinical scales. ResultsOCD patients exhibited significantly reduced Glx/Cr levels in the resting thalamus. The levels of resting thalamic Glu/Cr and Glx/Cr in OCD patients with PSQ were significantly lowest. OCD patients had significantly lower correct rates on Go tasks, higher error rates on Nogo tasks, and longer error average response times (EART) to the Nogo task. OCD patients with PSQ demonstrated the highest Nogo task error rate and the longest EART to Nogo task. Furthermore, PSQI scores exhibited negative correlations with Glu/Cr and Glx/Cr in the resting thalamus. ConclusionOCD patients with PSQ demonstrated reduced levels of thalamic resting Glx and more pronounced response inhibitory function impairment. Aberrant neurometabolite levels in critical brain regions, coupled with heightened response inhibition function deficits, may be a neurobiological basis for the PSQ that OCD patients generally exhibit.

The effects of cocaine use severity and abstinence on behavioral performance and neural processes of response inhibition

Previous studies identified cerebral markers of response inhibition dysfunction in cocaine dependence. However, whether deficits in response inhibition vary with the severity of cocaine use or ameliorate during abstinence remain unclear. This study aimed to address these issues and the neural mechanisms supporting the individual variation. We examined the data of 67 individuals with cocaine dependence (CD) and 84 healthy controls (HC) who underwent functional magnetic resonance imaging during a stop-signal task (SST). The stop-signal reaction time (SSRT) was computed using the integration method, with a longer SSRT indicating poorer response inhibition. The results showed that, while CD and HC did not differ significantly in SSRT, years of cocaine use (YOC) and days of abstinence (DOA) were each positively and negatively correlated with the SSRT in CD. Whole-brain regressions of stop minus go success trials on SSRT revealed correlates in bilateral superior temporal gyrus (STG) in response inhibition across CD and HC. Further, mediation and path analyses revealed that YOC and DOA affected SSRT through the STG activities in CD. Together, the findings characterized the contrasting effects of cocaine use severity and abstinence on response inhibition as well as the neural processes that support these effects in cocaine dependence.

Dual-site beta tACS over rIFG and M1 enhances response inhibition: A parallel multiple control and replication study

Response inhibition is a core component of cognitive control. Past electrophysiology and neuroimaging studies have identified beta oscillations and inhibitory control cortical regions correlated with response inhibition, including the right inferior frontal gyrus (rIFG) and primary motor cortex (M1). Hence, increasing beta activity in multiple brain regions is a potential way to enhance response inhibition. Here, a novel dual-site transcranial alternating current stimulation (tACS) method was used to modulate beta activity over the rIFG-M1 network in a sample of 115 (excluding 2 participants) with multiple control groups and a replicated experimental design. In Experiment 1, 70 healthy participants were randomly assigned to three dual-site beta-tACS groups, including in-phase, anti-phase or sham stimulation. During and after stimulation, participants were required to complete the stop-signal task, and electroencephalography (EEG) was collected before and after stimulation. The Barratt Impulsiveness Scale was completed before the experiment to evaluate participants' impulsiveness. In addition, we conducted an active control experiment with a sample size of 20 to exclude the potential effects of the dual-site tACS “return” electrode. To validate the behavioural findings of Experiment 1, 25 healthy participants took part in Experiment 2 and were randomized into two groups, including in-phase and sham stimulation groups. We found that compared to the sham group, in-phase but not anti-phase beta-tACS significantly improved both response inhibition performance and beta synchronization of the inhibitory control network in Experiment 1. Furthermore, the increased beta synchronization was correlated with enhanced response inhibition. In an independent sample of Experiment 2, the enhanced response inhibition performance observed in the in-phase group was replicated. After combining the data from the above two experiments, the time dynamics analysis revealed that the in-phase beta-tACS effect occurred in the post-stimulation period but not the stimulation period. The state-dependence analysis showed that individuals with poorer baseline response inhibition or higher attentional impulsiveness had greater improvement in response inhibition for the in-phase group. These findings strongly support that response inhibition in healthy adults can be improved by in-phase dual-site beta-tACS of the rIFG-M1 network, and provide a new potential treatment targets of synchronized cortical network activity for patients with clinically deficient response inhibition.

Prefrontal oxygenation varies as a function of response inhibition performance in healthy participants but not in youth with non-suicidal self-injury.

Non-suicidal self-injury (NSSI), a highly prevalent symptom in adolescence, has been associated with impulsivity. Behavioral measures of response inhibition in combination with the recording of brain activity potentially improve the understanding of the etiology of the behavior. We therefore investigated prefrontal cortex (PFC) oxygenation during a response inhibition task using functional near-infrared spectroscopy (fNIRS) in n=152 adolescents with NSSI and n=47 healthy controls. We compared groups regarding behavioral performance and PFC oxygenation and tested whether the association between task performance and PFC oxygenation differed between groups. PFC oxygenation was slightly higher in adolescents with NSSI than in controls. Further, there was evidence for a group by performance interaction: In healthy controls, higher oxygenated hemoglobin was associated with better task performance, which was not the case in the NSSI group. We did not find evidence of associations between PFC oxygenation and clinical measures. Our study provides preliminary evidence of altered brain functional correlates of response inhibition in adolescents with NSSI potentially reflecting deficient top-down regulation of limbic regions through prefrontal regions. Due to methodological limitations of the current study, findings must be interpreted with caution and future studies should optimize task designs for fNIRS processing.

Brain tissue iron neurophysiology and its relationship with the cognitive effects of dopaminergic modulation in children with and without ADHD

Children with attention-deficit/hyperactivity disorder (ADHD) exhibit impairments in response inhibition. These impairments are ameliorated by modulating dopamine (DA) via the administration of rewards or stimulant medication like methylphenidate (MPH). It is currently unclear whether intrinsic DA availability impacts these effects of dopaminergic modulation on response inhibition. Thus, we estimated intrinsic DA availability using magnetic resonance-based assessments of basal ganglia and thalamic tissue iron in 36 medication-naïve children with ADHD and 29 typically developing (TD) children (8–12 y) who underwent fMRI scans and completed standard and rewarded go/no-go tasks. Children with ADHD additionally participated in a double-blind, randomized, placebo-controlled, crossover MPH challenge. Using linear regressions covarying for age and sex, we determined there were no group differences in brain tissue iron. We additionally found that higher putamen tissue iron was associated with worse response inhibition performance in all participants. Crucially, we observed that higher putamen and caudate tissue iron was associated with greater responsivity to MPH, as measured by improved task performance, in participants with ADHD. These results begin to clarify the role of subcortical brain tissue iron, a measure associated with intrinsic DA availability, in the cognitive effects of reward- and MPH-related dopaminergic modulation in children with ADHD and TD children.

Neurophysiological mechanisms underlying the differential effect of reward prospect on response selection and inhibition

Reward and cognitive control play crucial roles in shaping goal-directed behavior. Yet, the behavioral and neural underpinnings of interactive effects of both processes in driving our actions towards a particular goal have remained rather unclear. Given the importance of inhibitory control, we investigated the effect of reward prospect on the modulatory influence of automatic versus controlled processes during response inhibition. For this, a performance-contingent monetary reward for both correct response selection and response inhibition was added to a Simon NoGo task, which manipulates the relationship of automatic and controlled processes in Go and NoGo trials. A neurophysiological approach was used by combining EEG temporal signal decomposition and source localization methods. Compared to a non-rewarded control group, rewarded participants showed faster response execution, as well as overall lower response selection and inhibition accuracy (shifted speed-accuracy tradeoff). Interestingly, the reward group displayed a larger interference of the interactive effects of automatic versus controlled processes during response inhibition (i.e., a larger Simon NoGo effect), but not during response selection. The reward-specific behavioral effect was mirrored by the P3 amplitude, underlining the importance of stimulus–response association processes in explaining variability in response inhibition performance. The selective reward-induced neurophysiological modulation was associated with lower activation differences in relevant structures spanning the inferior frontal and parietal cortex, as well as higher activation differences in the somatosensory cortex. Taken together, this study highlights relevant neuroanatomical structures underlying selective reward effects on response inhibition and extends previous reports on the possible detrimental effect of reward-triggered performance trade-offs on cognitive control processes.

Baseline cognitive function predicts full remission of suicidal symptoms among patients with treatment-resistant depression and strong suicidal ideation after low-dose ketamine infusion.

Whether pretreatment working memory and response inhibition function are associated with the rapid and sustained antisuicidal effect of low-dose ketamine among patients with treatment-resistant depression (TRD) and strong suicidal ideation is unclear. We enrolled 65 patients with TRD, comprising 33 who received a single infusion of 0.5 mg/kg ketamine and 32 who received a placebo infusion. The participants performed working memory and go/no-go tasks prior to infusion. We assessed suicidal symptoms at baseline and on postinfusion Days 2, 3, 5, and 7. The full remission of suicidal symptoms persisted for 3 days after a single ketamine infusion and the ketamine-related antisuicidal effect persisted for 1 week. Lower cognitive impairment at baseline (indicated by a higher rate of correct responses on a working memory task) was associated with the rapid and sustained antisuicidal effect of low-dose ketamine in patients with TRD and strong suicidal ideation. Patients with TRD and strong suicidal ideation but low cognitive impairment may benefit the most from the antisuicidal effect of low-dose ketamine.

Mania and Hemiballismus: A rare presentation of subthalamic stroke (P12-5.008)

<h3>Objective:</h3> Mania and hemiballismus are rare presenting features of acute ischemic stroke. We present a unique case of acute subthalamic stroke presenting with mania preceding hyperkinetic movements by several days making the diagnosis challenging and precluding the patient from acute stroke care. <h3>Background:</h3> 66 year old patient presented with abnormal movements. The patient’s symptoms began with sudden onset of increased activity levels, pressured speech, and insomnia. Four days later he presented to the hospital with acute onset of uncontrolled flailing and pain in the left arm and leg. MRI brain revealed an acute right subthalamic infarct. He was diagnosed with post stroke mania and hemiballismus. <h3>Design/Methods:</h3> NA <h3>Results:</h3> NA <h3>Conclusions:</h3> Hemiballismus is a rare presenting symptom of acute stroke. Widely accepted pathophysiology behind hemiballismus is a structural lesion in the subthalamic nucleus. The subthalamic nucleus contains glutaminergic neurons with projections to the globus pallidus interna. The glutaminergic neurons increase the activity of the globus pallidus interna, which contains GABAergic neurons that, in turn, decrease the activity of the thalamus and inhibit movement. Lesions of the subthalamic nucleus can disrupt the inhibition of movement by the globus pallidus interna and results in hyperkinetic movements like hemiballismus. The subthalamic nucleus has a role is mood, memory and behavior. Studies have shown to have variable effects of subthalamic deep brain stimulation on working memory and response inhibition performance and some reported cases with aggressive impulsive episodes, suicide and suicidal attempts, apathy, severe depression, psychosis, and hypomania following bilateral sub thalamic nucleus DBS. Our patient presented with acute onset of mania preceding development of hemiballismus by several days making the case diagnostically challenging. On literature review, we could not find a case with this presentation. With this case, we add to the multitude of presentation of acute stroke since acute stroke is a medical emergency and requires prompt management. <b>Disclosure:</b> Dr. Mann has nothing to disclose. Dr. Kelly has nothing to disclose. Dr. Leichliter has received personal compensation in the range of $500-$4,999 for serving on a Speakers Bureau for Neurocrine.

Inhibitory control in children with agenesis of the corpus callosum compared with typically developing children.

The developmental absence (agenesis) of the corpus callosum (AgCC) is a congenital brain malformation associated with risk for a range of neuropsychological difficulties. Inhibitory control outcomes, including interference control and response inhibition, in children with AgCC are unclear. This study examined interference control and response inhibition: 1) in children with AgCC compared with typically developing (TD) children, 2) in children with different anatomical features of AgCC (complete vs. partial, isolated vs. complex), and 3) associations with white matter volume and microstructure of the anterior (AC) and posterior commissures (PC) and any remnant corpus callosum (CC). Participants were 27 children with AgCC and 32 TD children 8-16 years who completed inhibitory control assessments and brain MRI to define AgCC anatomical features and measure white matter volume and microstructure. The AgCC cohort had poorer performance and higher rates of below average performance on inhibitory control measures than TD children. Children with complex AgCC had poorer response inhibition performance than children with isolated AgCC. While not statistically significant, there were select medium to large effect sizes for better inhibitory control associated with greater volume and microstructure of the AC and PC, and with reduced volume and microstructure of the remnant CC in partial AgCC. This study provides evidence of inhibitory control difficulties in children with AgCC. While the sample was small, the study found preliminary evidence that the AC (f2=.18) and PC (f2=.30) may play a compensatory role for inhibitory control outcomes in the absence of the CC.

Response inhibition in children with different subtypes/presentations of attention deficit hyperactivity disorder: A near-infrared spectroscopy study.

Executive dysfunction in children with attention deficit hyperactivity disorder (ADHD) is thought to be closely related to the prefrontal cortex (PFC). However, there is controversy over the activation of the PFC in children with ADHD. Differences could be related to the subtype. Meanwhile, no study to date has used functional near-infrared spectroscopy (fNIRS) to explore the differences between subtypes. Thus, this study aimed to explore the activation of the PFC in children with different subtypes of ADHD during executive function task. Participants in this study include typically developing (TD) children (n = 28), ADHD-predominantly inattentive (ADHD-PI) (n = 39) and ADHD-combined (ADHD-C) (n = 24). To examine the executive function of ADHD, the Go/No-go task is chosen to assess the response inhibition function. The activation of PFC in all participants during the Go/No-go task was recorded by fNIRS. Meanwhile, behavioral data were also recorded. Both TD and ADHD children activated the right PFC [middle frontal gyrus (MFG) and inferior frontal gyrus (IFG)] during response inhibition. However, the range and degree of activation differed among these groups. Compared with TD children, those with ADHD-PI had a smaller extent of activation in the right PFC, and those with ADHD-C only had a tendency to enhance activation. In addition, children with ADHD-PI and ADHD-C had impaired activation of the temporal gyrus. Besides, compared with ADHD-C and TD, those with ADHD-PI also had impaired activation of the right precentral gyrus (PG), and the supplementary motor area (SMA). Compared with ADHD-PI, ADHD-C showed decreased activation of the right MFG. The activation of Ch34 (BA44, rPFC) in children with ADHD-PI and ADHD-C was negatively correlated with their clinical symptoms. The activation of the PFC in children with different subtypes of ADHD has both commonalities and differences. The degree of activation of the right PFC Ch34 in children with ADHD is negatively correlated with clinical symptoms. fNIRS could be served as a candidate hemodynamic biomarker for the diagnosis of ADHD.

The clinical, neuropsychological, and brain functional characteristics of the ADHD restrictive inattentive presentation.

There is an ongoing debate about the restrictive inattentive (RI) presentation of attention deficit hyperactivity disorder (ADHD). The current study aimed to systematically investigate the clinical, neuropsychological, and brain functional characteristics of children with ADHD restrictive inattentive presentation. A clinical sample of 789 children with or without ADHD participated in the current study and finished clinical interviews, questionnaires, and neuropsychological tests. Those individuals with a diagnosis of ADHD were further divided into three subgroups according to the presentation of inattentive and/or hyperactive/impulsive symptoms, the ADHD-RI, the ADHD-I (inattentive), and the ADHD-C (combined) groups. Between-group comparisons were carried out on each clinical and neuropsychological measure using ANCOVA, with age and sex as covariates. Bonferroni corrections were applied to correct for multiple comparisons. Two hundred twenty-seven of the subjects also went through resting-state functional magnetic resonance imaging scans. Five ADHD-related brain functional networks, including the default mode network (DMN), the dorsal attention network (DAN), the ventral attention network, the executive control network, and the salience network, were built using predefined regions of interest (ROIs). Voxel-based group-wise comparisons were performed. Compared with healthy controls, all ADHD groups presented more clinical problems and weaker cognitive function. Among the ADHD groups, the ADHD-C group had the most clinical problems, especially delinquent and aggressive behaviors. Regarding cognitive function, the ADHD-RI group displayed the most impaired sustained attention, and the ADHD-C group had the worst response inhibition function. In terms of brain functional connectivity (FC), reduced FC in the DMN was identified in the ADHD-C and the ADHD-I groups but not the ADHD-RI group, compared to the healthy controls. Subjects with ADHD-I also presented decreased FC in the DAN in contrast to the control group. The ADHD-RI displayed marginally significantly lower FC in the salience network compared to the ADHD-I and the control groups. The ADHD-RI group is distinguishable from the ADHD-I and the ADHD-C groups. It is characterized by fewer externalizing behaviors, worse sustained attention, and better response inhibition function. The absence of abnormally high hyperactive/impulsive symptoms in ADHD-RI might be related to less impaired brain function in DMN, but potentially more impairment in the salience network.

Physical Activity Level Moderates the Association Between Response Inhibition and Anterior Cingulate Cortex Volume in Older Adults

AbstractBackgroundAging is generally associated with a decline in executive function, a cognitive domain that is critical to functional independence. Response inhibition is an executive process that contributes to anticipation, planning, and goal setting. The anterior cingulate cortex (ACC) is a key brain structure that supports response inhibition and shows gray matter loss with age. Evidence suggests that both response inhibition performance and the Anterior Cingulate Cortex (ACC) are responsive to exercise training. Whether physical activity moderates the relationship between response inhibition and the ACC in older adults is unknown.MethodA cross‐sectional analysis of a subset of community‐dwelling older adults enrolled in a 3‐arm, 8‐week proof of concept randomized control trial of computerized cognitive training, with or without exercise, who completed T1 magnetic resonance imaging (MRI) at baseline. Of the 68 MRI participants, 11 were removed from this analysis due to poor scan quality. Response inhibition was measured using the Flanker Task from the NIH Toolbox Cognitive Battery. Participants were split into either a high or low physical activity groups determined by their median Physical Activity Scale for the Elderly (PASE) score. Caudal and rostral ACC volumes were segmented and quantified using FreeSurfer. To assess for moderation, we performed linear regressions with age‐adjusted Flanker Task score as the dependent variable, and ACC volume, high/low PASE, and the interaction of ACC volume * high/low PASE as independent variables.ResultPhysical activity level significantly moderated the association between left caudal anterior cingulate cortex (LCACC) volume and age‐adjusted Flanker Task score, (β = –6.428, t(53) = ‐2.075, p &lt; .05). Among those with low physical activity levels (n = 30), greater LCACC volume was associated with better response inhibition (r = 0.44, p = .01) while there was no association among those with high physical activity levels (n = 27; r = ‐0.13; p = .52).ConclusionHigher physical activity may mitigate the negative effects of age‐related gray matter loss in the ACC on response inhibition performance in community‐dwelling older adults.

On the Role of Stimulus-Response Context in Inhibitory Control in Alcohol Use Disorder

The behavioral and neural dynamics of response inhibition deficits in alcohol use disorder (AUD) are still largely unclear, despite them possibly being key to the mechanistic understanding of the disorder. Our study investigated the effect of automatic vs. controlled processing during response inhibition in participants with mild-to-moderate AUD and matched healthy controls. For this, a Simon Nogo task was combined with EEG signal decomposition, multivariate pattern analysis (MVPA), and source localization methods. The final sample comprised n = 59 (32♂) AUD participants and n = 64 (28♂) control participants. Compared with the control group, AUD participants showed overall better response inhibition performance. Furthermore, the AUD group was less influenced by the modulatory effect of automatic vs. controlled processes during response inhibition (i.e., had a smaller Simon Nogo effect). The neurophysiological data revealed that the reduced Simon Nogo effect in the AUD group was associated with reduced activation differences between congruent and incongruent Nogo trials in the inferior and middle frontal gyrus. Notably, the drinking frequency (but not the number of AUD criteria we had used to distinguish groups) predicted the extent of the Simon Nogo effect. We suggest that the counterintuitive advantage of participants with mild-to-moderate AUD over those in the control group could be explained by the allostatic model of drinking effects.