Cognitive Control In Individuals Research Articles

A Diet that is Gone too Far

Anorexia nervosa is a serious eating disorder characterized by extreme food restriction, intense fear of gaining weight, and a distorted body image. This literature review synthesizes key research on the psychological, neurobiological, and genetic factors associated with anorexia nervosa. The disorder predominantly affects adolescent girls and young women and can have severe medical and psychological consequences. Research shows that psychological factors like perfectionism, body dissatisfaction, and low self-esteem contribute to the development and maintenance of anorexia. Neuroimaging studies reveal differences in brain regions related to reward processing and cognitive control in individuals with anorexia compared to healthy controls. These neural patterns may underlie the rigid, ritualistic eating behaviors and difficulties in changing thought patterns associated with the disorder. There is also evidence for a genetic component, with studies identifying associations between anorexia and variations in genes related to serotonin regulation, anxiety, obsessive-compulsive behaviors, and other psychiatric disorders. Integrating psychological, neurobiological, and genetic research provides greater insight into the multifaceted origins of anorexia nervosa. Understanding the complex factors that lead to and perpetuate the disorder can inform more effective, evidence-based treatments. Family-based therapy and cognitive-behavioral approaches focused on normalizing eating, addressing thought distortions, and building coping skills show promise. With comprehensive treatment, recovery from anorexia is possible, but early intervention is critical.

Neural Correlates of Impaired Cognitive Control in Individuals with Methamphetamine Dependence: An fMRI Study

Impaired cognitive and behavioral control has often been observed in people who use methamphetamine (MA). However, a comprehensive understanding of the neural substrates underlying these impairments is still lacking. The goal of the present study was to study the neural correlates of impaired cognitive control in individuals with MA dependence according to DSM-IV criteria. Eighteen individuals with MA dependence and 21 healthy controls were investigated using Stroop task, fMRI, and an impulsivity questionnaire. Overall, patients were found to have significantly poorer accuracy on the Stroop task and higher self-rated impulsivity. Comparing brain activations during the task, decreased activation in the dorsolateral prefrontal cortex (DLPFC), anterior midcingulate cortex (aMCC), and dorsal striatum was observed in individuals with MA dependence, compared to healthy controls. Altered fMRI signal in DLPFC and aMCC significantly correlated with impaired behavioral task performance in individuals with MA dependence. Furthermore, significantly lower and pronounced brain activations in the MA group were additionally detected in several sensory cortical regions, i.e., in the visual, auditory, and somatosensory cortices. The results of the current study provide evidence for the negative impact of chronic crystal meth consumption on the proper functioning of the fronto-cingulate and striatal brain regions, presumably underlying the often-observed deficits in executive functions in individuals with MA use disorder. As a new finding, we also revealed abnormal activation in several sensory brain regions, suggesting the negative effect of MA use on the proper neural activity of these regions. This blunted activation could be the cause of the observed deficits in executive functions and the associated altered brain activation in higher-level brain networks.

The use of the Eriksen Flanker Task as training instrument for cognitive control in inhibition disorder

A frequently used cognitive task to measure participants’ cognitive performance is the so-called Eriksen Flanker task (1974). This task requires a response where you have to indicate the direction of a central arrow, which is flanked with (un)corresponding arrows at its side. The Flanker task has many modified versions, adjusted to the different ways you can use the task to measure different aspects of executive cognitive functions. Such cognitive tasks, although often too simple and straightforward to represent daily life, tell us a lot about one’s executive cognitive functioning. Executive functions are very important for human behavior because they help us to engage with our surroundings and to participate in society. Problems of inhibition may have neural causes and may lead to negative behavioral consequences. Inhibitory problems can be determined by the Flanker task which might also be useful to practice cognitive control in individuals suffering from inhibitory disorders.

Relationship between Resting-State Alpha Coherence and Cognitive Control in Individuals with Internet Gaming Disorder: A Multimodal Approach Based on Resting-State Electroencephalography and Event-Related Potentials.

The human brain is constantly active, even at rest. Alpha coherence is an electroencephalography (EEG) rhythm that regulates functional connectivity between different brain regions. However, the relationships between resting-state alpha coherence and N2/P3 components associated with response inhibition and cognitive processes have not been investigated in addictive disorders. The present study investigated the relationships between alpha coherence during the resting state and N2/P3 components of event-related potentials during the Go/Nogo task in healthy controls (HCs) and patients with Internet gaming disorder (IGD). A total of 64 young adults (HC: n = 31; IGD: n = 33) participated in this study. Alpha coherence values at left fronto-central and bilateral centro-temporal electrode sites were significantly correlated with P3 latency in HCs, whereas inverse correlations were observed in patients with IGD. Furthermore, significant differences were observed in the correlation values between the groups. Our results suggest that patients with IGD lack dynamic interactions of functional connectivity between the fronto-centro-temporal regions during the resting state and the event-related potential (ERP) index during cognitive tasks. The findings of this study may have important implications for understanding the neurophysiological mechanisms linking resting-state EEG and task-related ERPs underlying IGD.

Dissociation of Proactive and Reactive Cognitive Control in Individuals with Schizotypy: An Event-Related Potential Study.

Patients with schizophrenia and individuals with schizotypy, a subclinical group at risk for schizophrenia, have been found to have impairments in cognitive control. The Dual Mechanisms of Cognitive Control (DMC) framework hypothesises that cognitive control can be divided into proactive and reactive control. However, it is unclear whether individuals with schizotypy have differential behavioural impairments and neural correlates underlying these two types of cognitive control. Twenty-five individuals with schizotypy and 26 matched healthy controls (HCs) completed both reactive and proactive control tasks with electroencephalographic data recorded. The proportion of congruent and incongruent trials was manipulated in a classic colour-word Stroop task to induce proactive or reactive control. Proactive control was induced in a context with mostly incongruent (MI) trials and reactive control in a context with mostly congruent (MC) trials. Two event-related potential (ERP) components, medial frontal negativity (MFN, associated with conflict detection) and conflict sustained potential (conflict SP, associated with conflict resolution) were examined. There was no significant difference between the two groups in terms of behavioural results. In terms of ERP results, in the MC context, HC exhibited significantly larger MFN (360-530 ms) and conflict SP (600-1000 ms) amplitudes than individuals with schizotypy. The two groups did not show any significant difference in MFN or conflict SP in the MI context. The present findings provide initial evidence for dissociation of neural activation between proactive and reactive cognitive control in individuals with schizotypy. These findings help us understand cognitive control deficits in the schizophrenia spectrum.

Neural substrates of deficient cognitive control in individuals with severe internet gaming disorder

Background and aimsInternet gaming disorder (IGD) is rapidly becoming a worldwide health concern. The prefrontal-subcortical model of self-regulation emphasizes that an impaired prefrontal cognitive control system and an overwhelming subcortical reward-seeking system are both crucial factors in health problems, including addiction. This study focused on the cognitive control system of IGD, aiming to investigate whether cognitive control is altered and the underlying neural correlates in college students with IGD. Methods: Thirty college students with IGD and twenty-five matched healthy controls were asked to complete a stop-signal task that measures cognitive control while being monitored by functional magnetic resonance imaging (fMRI). Results: Compared to the controls, only the college students with severe IGD, rather than those with mild IGD, had deficient brain activity involved in inhibitory control and response execution (specifically, the inferior frontal gyrus, anterior cingulate cortex and primary motor cortex); this result implies that cognitive control deficits are closely linked to addiction severity in individuals with IGD. Regarding performance monitoring function, college students with IGD exhibited unabated behavioral and brain activity, as did the control group. Conclusions: Combined with our previous finding that the subcortical reward system was enhanced in individuals with IGD, the present findings extend the prefrontal-subcortical model of self-regulation from the perspective of IGD in a college student population and thus provide useful insight for the effective prevention and treatment of IGD.

Chapter 7 - Dopamine and the motivation of cognitive control

The major ascending neuromodulator dopamine has long been implicated in cognitive control. Effects of dopamine-related disorders and the treatment of the cognitive control deficits associated with these disorders are commonly attributed to modulation of the prefrontal cortex. However, many disorders that are accompanied by cognitive control deficits also implicate abnormal dopamine transmission in the striatum, which has been associated more readily with value-based learning, choice, and motivation. We put forward the hypothesis that effects of dopamine on cognitive control reflect, in part, indirect modulation of value-based learning and choice computations that alter the motivation to exert control. This hypothesis is grounded in accumulating evidence from work with experimental animals as well as neurochemical PET, pharmacologic fMRI, and computational modeling work with healthy volunteers and patients with addictive disorders, ADHD, and Parkinson's disease. Consistent with an "inverted-U"-shaped relationship between dopamine and value-based learning, this evidence suggests that dopaminergic drugs might paradoxically increase our drive away from cognitive control in individuals with high baseline levels of dopamine, perhaps by "overdosing" dopamine levels, and thus reducing the value of cognitive control. The hypothesis has implications for the many dopamine-related disorders, which are often accompanied by either apathy or problems with impulse control, and their pharmacotreatment with dopaminergic drugs. For example, the cognitive deficits that are commonly associated with prefrontal cortex dysfunctioning might instead reflect modulation of striatal dopamine and its role in the willingness rather than the ability to exert control.

Monitor yourself! Deficient error-related brain activity predicts real-life self-control failures.

Despite their immense relevance, the neurocognitive mechanisms underlying real-life self-control failures (SCFs) are insufficiently understood. Whereas previous studies have shown that SCFs were associated with decreased activity in the right inferior frontal gyrus (rIFG; a region involved in cognitive control), here we consider the possibility that the reduced implementation of cognitive control in individuals with low self-control may be due to impaired performance monitoring. Following a brain-as-predictor approach, we combined experience sampling of daily SCFs with functional magnetic resonance imaging (fMRI) in a Stroop task. In our sample of 118 participants, proneness to SCF was reliably predicted by low error-related activation of a performance-monitoring network (comprising anterior mid-cingulate cortex, presupplementary motor area, and anterior insula), low posterror rIFG activation, and reduced posterror slowing. Remarkably, these neural and behavioral measures predicted variability in SCFs beyond what was predicted by self-reported trait self-control. These results suggest that real-life SCFs may result from deficient performance monitoring, leading to reduced recruitment of cognitive control after responses that conflict with superordinate goals.

Neuroplasticity of cognitive control networks following cognitive training for chronic traumatic brain injury.

Cognitive control is the ability to coordinate thoughts and actions to achieve goals. Cognitive control impairments are one of the most persistent and devastating sequalae of traumatic brain injuries (TBI). There have been efforts to improve cognitive control in individuals with post-acute TBI. Several studies have reported changes in neuropsychological measures suggesting the efficacy of cognitive training in improving cognitive control. Yet, the neural substrates of improved cognitive control after training remains poorly understood. In the current study, we identified neural plasticity induced by cognitive control training for TBI using resting-state functional connectivity (rsFC). Fifty-six individuals with chronic mild TBI (9 years post-injury on average) were randomized into either a strategy-based cognitive training group (N = 26) or a knowledge-based training group (active control condition; N = 30) for 8 weeks. We acquired a total of 109 resting-state functional magnetic resonance imaging from 45 individuals before training, immediately post-training, and 3 months post-training. Relative to the controls, the strategy-based cognitive training group showed monotonic increases in connectivity in two cognitive control networks (i.e., cingulo-opercular and fronto-parietal networks) across time points in multiple brain regions (pvoxel < 0.001, pcluster < 0.05). Analyses of brain-behavior relationships revealed that fronto-parietal network connectivity over three time points within the strategy-based cognitive training group was positively associated with the trail making scores (pvoxel < 0.001, pcluster < 0.05). These findings suggest that training-induced neuroplasticity continues through chronic phases of TBI and that rsFC can serve as a neuroimaging biomarker of evaluating the efficacy of cognitive training for TBI.

Drug abusers have impaired cerebral oxygenation and cognition during exercise.

BackgroundIndividuals with Substance Use Disorder (SUD) have lower baseline metabolic activity of the prefrontal cortex (PFC) associated with impairment of cognitive functions in decision-making and inhibitory control. Aerobic exercise has shown to improve PFC function and cognitive performance, however, its effects on SUD individuals remain unclear.PurposeTo verify the cognitive performance and oxygenation of the PFC during an incremental exercise in SUD individuals.MethodsFourteen individuals under SUD treatment performed a maximum graded exercise test on a cycle ergometer with continuous measurements of oxygen consumption, PFC oxygenation, and inhibitory control (Stroop test) every two minutes of exercise at different intensities. Fifteen non-SUD individuals performed the same protocol and were used as control group.ResultsExercise increased oxyhemoglobin (O2Hb) and total hemoglobin (tHb) by 9% and 7%, respectively. However, when compared to a non-SUD group, this increase was lower at high intensities (p<0.001), and the inhibitory cognitive control was lower at rest and during exercise (p<0.007). In addition, PFC hemodynamics during exercise was inversely correlated with inhibitory cognitive performance (reaction time) (r = -0.62, p = 0.001), and a lower craving perception for the specific abused substance (p = 0.0189) was reported immediately after exercise.ConclusionDespite SUD individuals having their PFC cerebral oxygenation increased during exercise, they presented lower cognition and oxygenation when compared to controls, especially at elevated intensities. These results may reinforce the role of exercise as an adjuvant treatment to improve PFC function and cognitive control in individuals with SUD.

Effects of An 8-Week Moderate-Intensity Aerobic Exercise Intervention on Episodic Memory and Cognitive Control

Although the effects of exercise on global cognitive function are well documented, there have been few randomized trials of aerobic exercise that focus specifically on select aspects of cognition, including episodic memory and cognitive control processes. Understanding these cognitive processes may be particularly important for individuals with major depressive disorder (MDD), as deficits in both memory and cognitive control are well recognized in MDD. PURPOSE: The primary aim was to assess the effects of an aerobic exercise intervention on episodic memory and cognitive control in individuals with and without MDD. METHODS: 48 participants (24 healthy, 24 MDD) were randomly assigned to either 8-weeks of aerobic exercise (AE) or a control group of time-matched light stretching. AE and stretching groups consisted of three weekly 30-45-min sessions per week. Depressive symptoms (BDI), peak aerobic fitness (VO2 peak), episodic memory, and cognitive control were assessed at baseline and follow-up. Episodic memory and cognitive control were assessed using behavioral and event-related brain potential (ERP) measures during old/new and modified flanker tasks. RESULTS: After 8-weeks of AE, there were significant reductions in depressive symptoms, despite no change in aerobic fitness. No significant behavioral findings were observed for the old/new task; however, ERP analyses indicated significant increases in the parietal late positive component (LPC) from pre-to-post intervention, p < .05. Improvements were observed for reaction time during the flanker task, F(1,17)=16.89, p < .001, but not accuracy. Significant increases in flanker N2 and P3 component amplitudes were observed, ps < .05. CONCLUSION: These findings suggest that 8-weeks of moderate-intensity AE has a significant influence on both episodic (recognition) memory and cognitive control processes, particularly among individuals with MDD. However, the effects were larger for cognitive control relative to recognition memory. The 8-week AE program improved select aspects of cognitive function, in addition to reducing depressive symptoms. These benefits occurred without a change in fitness, suggesting other psychobiological mechanisms of action.

A randomized trial of aerobic exercise on cognitive control in major depression.

The aim of this study was to examine the effects of an 8-week moderate-intensity aerobic exercise training intervention on cognitive control in individuals with major depressive disorder (MDD). Participants with a current diagnosis of MDD (n=30; 21.1±2.0years) were stratified by depressive symptoms and randomized to an 8-week intervention of aerobic exercise (AE) or placebo exercise (PE). AE consisted of three sessions/week of moderate-intensity exercise training while PE consisted of three sessions/week of light-intensity stretching. Cognitive control was assessed pre- and post-treatment using behavioral performance (i.e., reaction time and accuracy) and event-related potentials (i.e., N2 amplitude). Depressive symptoms and rumination were also assessed before and after the intervention. Compared with PE, the AE treatment arm was associated with an increase in N2 amplitude to incongruent flanker task trials, reflecting an increase in cognitive control processes. Symptoms of depression also decreased after AE although the treatments did not differ in their effects on rumination. Exploratory mediation analysis indicated that changes in N2 amplitude did not mediate pre-to-post treatment reductions in depressive symptoms. An 8-week moderate-intensity AE program is associated with improved neural indices of conflict monitoring and reduced depressive symptoms among individuals with MDD. Future research examining the influence of exercise in combination with behavioral and pharmacological treatments for neurocognitive function in MDD is warranted.

Anodal tDCS over the right dorsolateral prefrontal cortex modulates cognitive processing of emotional information as a function of trait rumination in healthy volunteers

Healthy individuals reporting higher (as compared to lower) levels of trait rumination recruit more neural activity in dorso-cortical regions (mostly in the right hemisphere) when inhibiting negative information, possibly to compensate their difficulty to disengage from it. In the present study, we investigated whether these latter neural correlates are causally implicated in cognitive control in these individuals. We administered the Cued Emotional Control Task, a measure of cognitive control indexed by cognitive costs for inhibiting versus providing a habitual response for emotional information, in thirty-five healthy volunteers reporting a broad range of trait rumination levels. Participants completed the task after receiving both real and sham-placebo (counterbalanced order) anodal transcranial Direct Current Stimulation (tDCS) over the right dorsolateral prefrontal cortex (DLPFC). Results reveal that the tDCS induced effects on cognitive costs for emotional information were associated with individual differences in trait rumination: the higher the trait rumination level, the less cognitive costs following real neuromodulation of the right DLPFC. Interestingly, these effects were observed for both positive and negative stimuli, and not only negative information as hypothesized. Overall, the data suggest that the right DLPFC is causally involved in the alteration of cognitive control in healthy individuals who tend to ruminate, possibly by helping them to disengage from emotional material.

Ventral striatal hyperconnectivity during rewarded interference control in adolescents with ADHD

ObjectiveAttention-deficit/hyperactivity disorder (ADHD) is characterized by cognitive deficits (e.g., interference control) and altered reward processing. Cognitive control is influenced by incentive motivation and according to current theoretical models, ADHD is associated with abnormal interactions between incentive motivation and cognitive control. However, the neural mechanisms by which reward modulates cognitive control in individuals with ADHD are unknown. MethodWe used event-related functional resonance imaging (fMRI) to study neural responses during a rewarded Stroop color-word task in adolescents (14–17 years) with ADHD (n = 25; 19 boys) and healthy controls (n = 33; 22 boys). ResultsAdolescents with ADHD showed increased reward signaling within the superior frontal gyrus and ventral striatum (VS) relative to controls. Importantly, functional connectivity analyses revealed a hyperconnectivity between VS and motor control regions in the ADHD group, as a function of reward-cognitive control integration. Connectivity was associated with performance improvement in controls but not in the ADHD group, suggesting inefficient connectivity. ConclusionAdolescents with ADHD show increased neural sensitivity to rewards and its interactions with interference control in VS and motor regions, respectively. The findings support theoretical models of altered reward-cognitive control integration in individuals with ADHD.

Neural Dysfunction in Cognitive Control Circuits in Persons at Clinical High-Risk for Psychosis.

Cognitive control, a set of functions that develop throughout adolescence, is important in the pathogenesis of psychotic disorders. Whether cognitive control has a role in conferring vulnerability for the development of psychotic illness is still unknown. The aim of this study was to investigate the neural systems supporting cognitive control in individuals deemed to be potentially prodromal for psychotic illness. We recruited 56 participants at clinical high-risk (CHR) for psychosis based on the Structured Interview for Psychosis-Risk Syndromes (SIPS) and 49 healthy controls. Twelve of the CHR participants eventually developed psychosis. We compared functional magnetic resonance imaging (fMRI) BOLD signal during the performance of the Simon task. We tested for differences between CHR individuals and controls in conflict-related functional activity. In the CHR group when compared with controls, we detected smaller conflict-related activations in several cortical areas, including the Dorsolateral Prefrontal Cortex (DLPFC). Furthermore, conflict-related activations in the DLPFC of those CHR individuals who ultimately developed psychosis (CHR converters) were smaller than in non-converters (CHR non-converters). Higher levels of conflict-related activation were associated with better social and role outcome. Risk for psychosis was associated at the neural level with reduced conflict-related brain activity. This neural phenotype appears correlated within the DLPFC with the development of psychosis and with functional outcome.

Conflict anticipation in alcohol dependence - A model-based fMRI study of stop signal task.

BackgroundOur previous work characterized altered cerebral activations during cognitive control in individuals with alcohol dependence (AD). A hallmark of cognitive control is the ability to anticipate changes and adjust behavior accordingly. Here, we employed a Bayesian model to describe trial-by-trial anticipation of the stop signal and modeled fMRI signals of conflict anticipation in a stop signal task. Our goal is to characterize the neural correlates of conflict anticipation and its relationship to response inhibition and alcohol consumption in AD.MethodsTwenty-four AD and 70 age and gender matched healthy control individuals (HC) participated in the study. fMRI data were pre-processed and modeled with SPM8. We modeled fMRI signals at trial onset with individual events parametrically modulated by estimated probability of the stop signal, p(Stop), and compared regional responses to conflict anticipation between AD and HC. To address the link to response inhibition, we regressed whole-brain responses to conflict anticipation against the stop signal reaction time (SSRT).ResultsCompared to HC (54/70), fewer AD (11/24) showed a significant sequential effect — a correlation between p(Stop) and RT during go trials — and the magnitude of sequential effect is diminished, suggesting a deficit in proactive control. Parametric analyses showed decreased learning rate and over-estimated prior mean of the stop signal in AD. In fMRI, both HC and AD responded to p(Stop) in bilateral inferior parietal cortex and anterior pre-supplementary motor area, although the magnitude of response increased in AD. In contrast, HC but not AD showed deactivation of the perigenual anterior cingulate cortex (pgACC). Furthermore, deactivation of the pgACC to increasing p(Stop) is positively correlated with the SSRT in HC but not AD. Recent alcohol consumption is correlated with increased activation of the thalamus and cerebellum in AD during conflict anticipation.ConclusionsThe current results highlight altered proactive control that may serve as an additional behavioral and neural marker of alcohol dependence.

S.04.04 TAAR1: from endogenous to selective agonists for the treatment of schizophrenia

The major ascending neuromodulator dopamine has long been implicated in cognitive control. Effects of dopamine-related disorders and the treatment of the cognitive control deficits associated with these disorders are commonly attributed to modulation of the prefrontal cortex. However, many disorders that are accompanied by cognitive control deficits also implicate abnormal dopamine transmission in the striatum, which has been associated more readily with value-based learning, choice, and motivation. We put forward the hypothesis that effects of dopamine on cognitive control reflect, in part, indirect modulation of value-based learning and choice computations that alter the motivation to exert control. This hypothesis is grounded in accumulating evidence from work with experimental animals as well as neurochemical PET, pharmacologic fMRI, and computational modeling work with healthy volunteers and patients with addictive disorders, ADHD, and Parkinson's disease. Consistent with an “inverted-U”-shaped relationship between dopamine and value-based learning, this evidence suggests that dopaminergic drugs might paradoxically increase our drive away from cognitive control in individuals with high baseline levels of dopamine, perhaps by “overdosing” dopamine levels, and thus reducing the value of cognitive control. The hypothesis has implications for the many dopamine-related disorders, which are often accompanied by either apathy or problems with impulse control, and their pharmacotreatment with dopaminergic drugs. For example, the cognitive deficits that are commonly associated with prefrontal cortex dysfunctioning might instead reflect modulation of striatal dopamine and its role in the willingness rather than the ability to exert control.

A specific impairment in cognitive control in individuals with high-functioning autism

Although it is largely demonstrated that Autism Spectrum Disorders (ASDs) are characterized by executive dysfunctions, little is known about the fine-grained levels of this impairment. Here, we investigated the hierarchical architecture of control modules in autism using an experimental paradigm based upon a multistage model of executive functions. This model postulates that executive functions are hierarchically organized as a cascade of three different control processes, which are implemented according to information conveyed by sensory signals (sensory control), the immediate perceptual context (contextual control), and the temporal episode in which stimuli occur (episodic control). Sixteen high-functioning adults with autism or Asperger Syndrome (HFA/AS) and sixteen matched comparison participants took part in two distinct visuo–motor association experiments designed to separately vary the demands of sensory and episodic controls (first experiment) and contextual and episodic controls (second experiment). Participants with HFA/AS demonstrated no significant differences in performances with comparison participants when they had to control sensory or contextual information. However, they showed decreased accuracy when having to control information related to episodic signals. Remarkably, performances in episodic control were associated to the autism spectrum quotient in both groups, suggesting that this episodic control impairment might be at the core of ASDs. Those results plead for a specific, rather than generalised, deficit in executive functions in autism. Our study contributes to a better understanding of the impaired cognitive processes that are unique to autism and warrants confirmation using other models of executive functions.

Cognitive control in opioid dependence and methadone maintenance treatment.

BackgroundSubstance misuse is associated with cognitive dysfunction. We used a stop signal task to examine deficits in cognitive control in individuals with opioid dependence (OD). We examined how response inhibition and post-error slowing are compromised and whether methadone maintenance treatment (MMT), abstinence duration, and psychiatric comorbidity are related to these measures in individuals with OD.MethodsTwo-hundred-and-sixty-four men with OD who were incarcerated at a detention center and abstinent for up to 2 months (n = 108) or at a correctional facility and abstinent for approximately 6 months (n = 156), 65 OD men under MMT at a psychiatric clinic, and 64 age and education matched healthy control (HC) participants were assessed. We computed the stop signal reaction time (SSRT) to index the capacity of response inhibition and post-error slowing (PES) to represent error-related behavioral adjustment, as in our previous work. We examined group effects with analyses of variance and covariance analyses, followed by planned comparisons. Specifically, we compared OD and HC participants to examine the effects of opioid dependence and MMT and compared OD sub-groups to examine the effects of abstinence duration and psychiatric comorbidity.ResultsThe SSRT was significantly prolonged in OD but not MMT individuals, as compared to HC. The extent of post-error slowing diminished in OD and MMT, as compared to HC (trend; p = 0.061), and there was no difference between the OD and MMT groups. Individuals in longer abstinence were no less impaired in these measures. Furthermore, these results remained when psychiatric comorbidities including misuse of other substances were accounted for.ConclusionsMethadone treatment appears to be associated with relatively intact cognitive control in opioid dependent individuals. MMT may facilitate public health by augmenting cognitive control and thereby mitigating risky behaviors in heroin addicts.

Performance Monitoring and Cognitive Control in Individuals with Mild Traumatic Brain Injury

Literature suggests that individuals with mild traumatic brain injury (mTBI) show subtle abnormalities in the cognitive control process of performance monitoring. The neural bases of performance monitoring can be measured using the error-related negaitivity (ERN) and post-error positivity (Pe) components of the scalp-recorded event-related potential (ERP). Thirty-six individuals with mTBI and 46 demographically similar controls completed a modified color-naming Stroop task while ERPs were recorded. Separate repeated-measures analyses of variance were used to examine the behavioral (response times [RT] and error rates) and ERP (ERN and Pe amplitudes) indices of performance monitoring. Both groups showed slower RTs and increased error rates on incongruent trials relative to congruent trials. Likewise, both groups showed more negative ERN and more positive Pe amplitude to error trials relative to correct trials. Notably, there were no significant main effects or interactions of group for behavioral and ERP measures. Subgroup and correlational analyses with post-concussive symptoms and indices of injury severity were also not significant. Findings suggest comparable performance to non-injured individuals in some aspects of cognitive control in this sample. Neuropsychological implications and comparison with other cognitive control component processes in individuals with TBI are provided.