Enhanced reactive inhibition in adolescents with non-suicidal self-injury disorder.

AIM: To investigate whether the core of the pathophysiology underlying non-suicidal self-injury (NSSI) relates to poor impulse control due to impaired motor inhibition (i.e. the ability to inhibit a preplanned motor response). METHOD: We conducted a case-control study to compare the proficiency of two domains of motor inhibition, that is, reactive and proactive inhibition, by giving the reaching arm version of the stop-signal task and a go-only task to 28 drug-naive adolescents with NSSI disorder (NSSID) (mean age [SD] 15 years 8 months [1 year 4 months]; three males and 25 females) and 28 typically developing adolescents (mean age 15 years 8 months [1 year 5 months]; three males and 25 females). RESULTS: Reactive inhibition, as determined by the duration of the stop-signal reaction time, was enhanced in adolescents with NSSID compared to typically developing controls (194.2 [22.5 ms] vs 217.5 [17.3 ms], p < 0.001). By contrast, proactive inhibition was similar in both groups. Lastly, the level of impulsivity, assessed using the Barratt Impulsiveness Scale Version 11, did not differ between typically developing adolescents and adolescents with NSSID. However, adolescents with NSSID were more impulsive than controls in a subscale of the UPPS-P Impulsive Behavior Scale. INTERPRETATION: NSSID is not driven by heightened motor impulsivity. Instead, adolescents with NSSID exhibited greater proficiency in reactive inhibition, a proxy for motor impulsivity. We suggest that the enhancement of reactive inhibition strengthens action control, allowing adolescents to suppress their self-protection instinct and perform NSSI behaviours.

Prefrontal Responses during Proactive and Reactive Inhibition Are Differentially Impacted by Stress in Anorexia and Bulimia Nervosa.

Binge eating is a distressing, transdiagnostic eating disorder symptom associated with impulsivity, particularly in negative mood states. Neuroimaging studies of bulimia nervosa (BN) report reduced activity in frontostriatal regions implicated in self-regulatory control, and an influential theory posits that binge eating results from self-regulation failures under stress. However, there is no direct evidence that psychological stress impairs self-regulation in binge-eating disorders, or that any such self-regulatory deficits generalize to binge eating in underweight individuals (i.e., anorexia nervosa bingeing/purging subtype; AN-BP). We therefore determined the effect of acute stress on inhibitory control in 85 women (BN, 33 women; AN-BP, 22 women; 30 control participants). Participants underwent repeated functional MRI scanning during performance of the Stop-signal anticipation task, a validated measure of proactive (i.e., anticipation of stopping) and reactive (outright stopping) inhibition. Neural and behavioral responses to induced stress and a control task were evaluated on 2 consecutive days. Women with BN had reduced proactive inhibition, while prefrontal responses were increased in both AN-BP and BN. Reactive inhibition was neurally and behaviorally intact in both diagnostic groups. Both AN-BP and BN groups showed distinct stress-induced changes in inferior and superior frontal activity during both proactive and reactive inhibition. However, task performance was unaffected by stress. These results offer novel evidence of reduced proactive inhibition in BN, yet inhibitory control deficits did not generalize to AN-BP. Our findings identify intriguing alterations of stress responses and inhibitory function associated with binge eating, but they counsel against stress-induced failures of inhibitory control as a comprehensive explanation for loss-of-control eating.SIGNIFICANCE STATEMENT Binge eating is a common psychiatric syndrome that feels uncontrollable to the sufferer. Theoretically, it has been related to reduced self-regulation under stress, but there remains no direct evidence for this link in binge-eating disorders. Here, we examined how experimentally induced stress affected response inhibition in control participants and women with anorexia nervosa and bulimia nervosa. Participants underwent repeated brain scanning under stressful and neutral conditions. Although patient groups had intact action cancellation, the slowing of motor responses was impaired in bulimia nervosa, even when the likelihood of having to stop increased. Stress altered brain responses for both forms of inhibition in both groups, yet performance remained unimpaired. These findings counsel against a simple model of stress-induced disinhibition as an adequate explanation for binge eating.

Intact Proactive Motor Inhibition after Unilateral Prefrontal Cortex or Basal Ganglia Lesions.

Previous research provided evidence for the critical importance of the PFC and BG for reactive motor inhibition, that is, when actions are cancelled in response to external signals. Less is known about the role of the PFC and BG in proactive motor inhibition, referring to preparation for an upcoming stop signal. In this study, patients with unilateral lesions to the BG or lateral PFC performed in a cued go/no-go task, whereas their EEG was recorded. The paradigm called for cue-based preparation for upcoming, lateralized no-go signals. Based on previous findings, we focused on EEG indices of cognitive control (prefrontal beta), motor preparation (sensorimotor mu/beta, contingent negative variation [CNV]), and preparatory attention (occipital alpha, CNV). On a behavioral level, no differences between patients and controls were found, suggesting an intact ability to proactively prepare for motor inhibition. Patients showed an altered preparatory CNV effect, but no other differences in electrophysiological activity related to proactive and reactive motor inhibition. Our results suggest a context-dependent role of BG and PFC structures in motor inhibition, being critical in reactive, unpredictable contexts, but less so in situations where one can prepare for stopping on a short timescale.

Association between lack of functional connectivity of the frontal brain region and poor response inhibition in children with frontal lobe epilepsy.

PURPOSE: We investigated the relationship between electroencephalographic (EEG) functional connectivity and executive function in children with frontal lobe epilepsy (FLE). METHODS: We enrolled 24 children with FLE (mean age, 11.0 years; 13 boys) and 22 sex-, age-, and intelligence-matched typically developing children (TDC) to undergo 19-channel EEG during light sleep. We estimated functional connectivity using the phase lag index (PLI) that captures the synchronization of EEG. We also performed continuous performance tests (CPTs) on the children and obtained questionnaire responses on attention deficit hyperactivity disorder and oppositional defiant disorder (ODD). RESULTS: The average gamma PLI was lower in the FLE group than in the TDC group, especially between long-distance frontoparietal pairs, between interhemispheric frontal pairs, and between interhemispheric parietotemporal pairs. Gamma PLIs with long-distance frontoparietal and interhemispheric frontal pairs were positively associated with inattention, ODD scores, omission error, and reaction time in the FLE group but not in the TDC group. Conversely, they were negatively associated with age, hyperactivity score, and commission error. CONCLUSIONS: A lack of functional connectivity of the frontal brain regions in children with FLE was associated with poor response inhibition.

Enhanced facilitation and diminished inhibition characterizes the pronociceptive endogenous pain modulatory balance of persons living with HIV and chronic pain.

Chronic pain in persons living with HIV (PLWH) may be related to alterations in endogenous pain modulatory processes (e.g., high facilitation and low inhibition of nociception) that promote exaggerated pain responses, known as hyperalgesia, and central nervous system (CNS) sensitization. This observational study examined differences in endogenous pain modulatory processes between 59 PLWH with chronic pain, 51 PLWH without chronic pain, and 50 controls without HIV or chronic pain. Quantitative sensory testing for temporal summation (TS) of mechanical and heat pain as well as conditioned pain modulation (CPM) were used to assess endogenous pain facilitatory and inhibitory processes, respectively. Associations among TS, CPM, and self-reported clinical pain severity were also examined in PLWH with chronic pain. Findings demonstrated significantly greater TS of mechanical and heat pain for PLWH with chronic pain compared to PLWH without chronic pain and controls. CPM effects were present in controls, but not in either PLWH with or without chronic pain. Among PLWH with chronic pain, greater TS of mechanical pain was significantly associated with greater average clinical pain severity. Results of this study suggest that enhanced facilitation and diminished inhibition characterizes the pronociceptive endogenous pain modulatory balance of persons living with HIV and chronic pain.

Children with ADHD symptoms show deficits in reactive but not proactive inhibition, irrespective of their formal diagnosis.

BACKGROUND: Attenuated inhibitory control is one of the most robust findings in the neuropsychology of attention-deficit/hyperactivity disorder (ADHD). However, it is unclear whether this represents a deficit in outright stopping (reactive inhibition), whether it relates to a deficit in anticipatory response slowing (proactive inhibition), or both. In addition, children with other development disorders, such as autism spectrum disorder (ASD), often have symptoms of inattention, impulsivity, and hyperactivity similar to children with ADHD. These may relate to similar underlying changes in inhibitory processing. METHODS: In this study, we used a modified stop-signal task to dissociate reactive and proactive inhibition. We included not only children with ADHD, but also children primarily diagnosed with an ASD and high parent-rated levels of ADHD symptoms. RESULTS: We replicated the well-documented finding of attenuated reactive inhibition in children with ADHD. In addition, we found a similar deficit in children with ASD and a similar level of ADHD symptoms. In contrast, we found no evidence for deficits in proactive inhibition in either clinical group. CONCLUSIONS: These findings re-emphasize the role of reactive inhibition in children with ADHD and ADHD symptoms. Moreover, our findings stress the importance of a trans-diagnostic approach to the relationship between behavior and neuropsychology.

Competing Motivations: Proactive Response Inhibition Toward Addiction-Related Stimuli in Quitting-Motivated Individuals.

We examined whether addiction-related cues impact proactive inhibition (the restraint of actions in preparation for stopping) in individuals who are motivated to quit gambling or cannabis use. In Study 1, treatment-seeking individuals with cannabis use disorder and matched controls performed a stop-signal task that required them to inhibit categorizing cannabis or neutral pictures, and within varying levels of stop-signal probability. In Study 2, two groups of individuals, who applied to a voluntary self-exclusion program toward gambling, performed the stop-task following relaxation or gambling craving induction, with results compared to non-gamblers. Study 1 showed that despite being less efficient in proactive inhibition, individuals with cannabis use disorder exhibited heightened proactive inhibition toward cannabis cues. In Study 2, proactive inhibition toward gambling cues was heightened in gamblers after craving, but the degree of proactive adjustment decreased as a function of induced changes in gambling-related motivation. Present findings demonstrate that exposure to addiction-related cues can modulate proactive inhibition in individuals who are motivated to restrict their addictive behaviors.

Neural and behavioral mechanisms of proactive and reactive inhibition.

Response inhibition is an important component of adaptive behavior. Substantial prior research has focused on reactive inhibition, which refers to the cessation of a motor response that is already in progress. More recently, a growing number of studies have begun to examine mechanisms underlying proactive inhibition, whereby preparatory processes result in a response being withheld before it is initiated. It has become apparent that proactive inhibition is an essential component of the overall ability to regulate behavior and has implications for the success of reactive inhibition. Moreover, successful inhibition relies on learning the meaning of specific environmental cues that signal when a behavioral response should be withheld. Proactive inhibitory control is mediated by stopping goals, which reflect the desired outcome of inhibition and include information about how and when inhibition should be implemented. However, little is known about the circuits and cellular processes that encode and represent features in the environment that indicate the necessity for proactive inhibition or how these representations are implemented in response inhibition. In this article, we will review the brain circuits and systems involved in implementing inhibitory control through both reactive and proactive mechanisms. We also comment on possible cellular mechanisms that may contribute to inhibitory control processes, noting that substantial further research is necessary in this regard. Furthermore, we will outline a number of ways in which the temporal dynamics underlying the generation of the proactive inhibitory signal may be particularly important for parsing out the neurobiological correlates that contribute to the learning processes underlying various aspects of inhibitory control.

The Role of the Frontal and Parietal Cortex in Proactive and Reactive Inhibitory Control: A Transcranial Direct Current Stimulation Study.

Mounting evidence suggests that response inhibition involves both proactive and reactive inhibitory control, yet its underlying neural mechanisms remain elusive. In particular, the roles of the right inferior frontal gyrus (IFG) and inferior parietal lobe (IPL) in proactive and reactive inhibitory control are still under debate. This study aimed at examining the causal role of the right IFG and IPL in proactive and reactive inhibitory control, using transcranial direct current stimulation (tDCS) and the stop signal task. Twenty-two participants completed three sessions of the stop signal task, under anodal tDCS in the right IFG, the right IPL, or the primary visual cortex (VC; 1.5 mA for 15 min), respectively. The VC stimulation served as the active control condition. The tDCS effect for each condition was calculated as the difference between pre- and post-tDCS performance. Proactive control was indexed by the RT increase for go trials (or preparatory cost), and reactive control by the stop signal RT. Compared to the VC stimulation, anodal stimulation of the right IFG, but not that of the IPL, facilitated both proactive and reactive control. However, the facilitation of reactive control was not mediated by the facilitation of proactive control. Furthermore, tDCS did not affect the intraindividual variability in go RT. These results suggest a causal role of the right IFG, but not the right IPL, in both reactive and proactive inhibitory control.

Dissociable Effects of Dopamine on the Initial Capture and the Reactive Inhibition of Impulsive Actions in Parkinson's Disease.

Dopamine plays a key role in a range of action control processes. Here, we investigate how dopamine depletion caused by Parkinson disease (PD) and how dopamine restoring medication modulate the expression and suppression of unintended action impulses. Fifty-five PD patients and 56 healthy controls (HCs) performed an action control task (Simon task). PD patients completed the task twice, once withdrawn from dopamine medications and once while taking their medications. PD patients experienced similar susceptibility to making fast errors in conflict trials as HCs, but PD patients were less proficient compared with HCs at suppressing incorrect responses. Administration of dopaminergic medications had no effect on impulsive error rates but significantly improved the proficiency of inhibitory control in PD patients. We found no evidence that dopamine precursors and agonists affected action control in PD differently. Additionally, there was no clear evidence that individual differences in baseline action control (off dopamine medications) differentially responded to dopamine medications (i.e., no evidence for an inverted U-shaped performance curve). Together, these results indicate that dopamine depletion and restoration therapies directly modulate the reactive inhibitory control processes engaged to suppress interference from the spontaneously activated response impulses but exert no effect on an individual's susceptibility to act on impulses.

Backward Semantic Inhibition in Toddlers.

Attention switching is a crucial ability required in everyday life, from toddlerhood to adulthood. In adults, shifting attention from one word (e.g., dog) to another (e.g., sea) results in backward semantic inhibition, that is, the inhibition of the initial word ( dog). In this study, we used the preferential-looking paradigm to examine whether attention switching is accompanied by backward semantic inhibition in toddlers. We found that 24-month-olds can indeed refocus their attention to a new item by selectively inhibiting attention to the old item. The consequence of backward inhibition is that subsequent attention to a word semantically related to the old item is impaired. These findings have important implications for understanding the underlying mechanism of backward semantic inhibition and the development of lexical-semantic inhibition in early childhood.

Vocal response inhibition is enhanced by anodal tDCS over the right prefrontal cortex.

Stopping outright (reactive inhibition) and slowing down (proactive inhibition) are types of response inhibition which have mainly been investigated in the manual effector system. This study compared reactive inhibition across manual and vocal effector systems, examined the effects of excitatory anodal transcranial direct current stimulation (anodal tDCS) over the right prefrontal cortex (right-PFC) and looked at the relationship between reactive and proactive inhibition. We hypothesised (1) that vocal reactive inhibition would be less effective than manual reactive inhibition as evidenced by longer stop signal reaction times; (2) that anodal tDCS would enhance both vocal and manual reactive inhibitions and (3) that proactive and reactive inhibitions would be positively related. We tested 14 participants over two sessions (one session with anodal tDCS and one session with sham stimulation) and applied stimulation protocol in the middle of the session, i.e. only during the second of three phases. We used a stop signal task across two stop conditions: relevant and irrelevant stop conditions in which stopping was required or ignored, respectively. We found that reactive inhibition was faster during and immediately after anodal tDCS relative to sham. We also found that greater level of proactive inhibition enhanced reactive inhibition (indexed by shorter stop signal reaction times). These results support the hypothesis that the right-PFC is part of a core network for reactive inhibition and supports previous contention that proactive inhibition is possibly modulated via preactivating the reactive inhibition network.

Common and unique neural networks for proactive and reactive response inhibition revealed by independent component analysis of functional MRI data.

Response inhibition involves proactive and reactive modes. Proactive inhibition is goal-directed, triggered by warning cues, and serves to restrain actions. Reactive inhibition is stimulus-driven, triggered by salient stop-signals, and used to stop actions completely. Functional MRI studies have identified brain regions that activate during proactive and reactive inhibition. It remains unclear how these brain regions operate in functional networks, and whether proactive and reactive inhibition depend on common networks, unique networks, or a combination. To address this we analyzed a large fMRI dataset (N=65) of a stop-signal task designed to measure proactive and reactive inhibition, using independent component analysis (ICA). We found 1) three frontal networks that were associated with both proactive and reactive inhibition, 2) one network in the superior parietal lobe, which also included dorsal premotor cortex and left putamen, that was specifically associated with proactive inhibition, and 3) two right-lateralized frontal and fronto-parietal networks, including the right inferior frontal gyrus and temporoparietal junction as well as a bilateral fronto-temporal network that were uniquely associated with reactive inhibition. Overlap between networks was observed in dorsolateral prefrontal and parietal cortices. Taken together, we offer a new perspective on the neural underpinnings of inhibitory control, by showing that proactive inhibition and reactive inhibition are supported by a group of common and unique networks that appear to integrate and interact in frontoparietal areas.

Subthalamic nucleus activity dissociates proactive and reactive inhibition in patients with Parkinson's disease.

Models of action selection postulate the critical involvement of the subthalamic nucleus (STN), especially in reactive inhibition processes when inappropriate responses to a sudden stimulus must be overridden. The STN could also play a key role during proactive inhibition, when subjects prepare to potentially suppress their actions. Here, we hypothesized that STN responses to reactive and proactive inhibitory control might be driven by different underlying mechanisms with specific temporal profiles. Direct neural recordings in twelve Parkinson's disease patients during a modified stop signal task (SST) revealed a decrease of beta band activity (ßA, 13-35Hz) in the STN during reactive inhibition of smaller amplitude and shorter duration than during motor execution. Crucially, the onset latency of this relative increase of ßA took place before the stop signal reaction time. It could thus be thought of as a "stop" signal inhibiting thalamo-cortical activity that would have supported motor execution. Finally, results also revealed a higher level of ßA in the STN during proactive inhibition, which correlated with patient's inhibitory performances. We propose that ßA in the STN would here participate in the implementation of a "hold your horse" signal to delay motor responses, thus prioritizing accuracy as compared to speed. In brief, our results provide strong electrophysiological support for the hypothesized role of the STN during executive control underlying proactive and reactive response suppression.

Comparison of online, offline, and hybrid hypotheses of motor sequence learning using a quantitative model that incorporate reactive inhibition.

Two hypotheses have been advanced for when motor sequence learning occurs: offline between bouts of practice or online concurrently with practice. A third possibility is that learning occurs both online and offline. A complication for differentiating between those hypotheses is a process known as reactive inhibition, whereby performance worsens over consecutively executed sequences, but dissipates during breaks. We advance a new quantitative modeling framework that incorporates reactive inhibition and in which the three learning accounts can be implemented. Our results show that reactive inhibition plays a far larger role in performance than is appreciated in the literature. Across four groups of participants in which break times and correct sequences per trial were varied, the best overall fits were provided by a hybrid model. The version of the offline model that does not account for reactive inhibition, which is widely assumed in the literature, had the worst fits. We discuss implications for extant hypotheses and directions for future research.

Impaired Reactive Control But Preserved Proactive Control in Hyperactive Children.

OBJECTIVE: To examine the manifestation of cognitive control deficit of children with different levels of hyperactivity, an "at risk" dimension for ADHD. METHOD: A group of children with high hyperactivity (N = 40) and another group of children with low levels of hyperactivity (N = 38) performed a modified stop-signal anticipation task, a revised Go/NoGo task, and the AX-continuous performance test (AX-CPT). RESULTS: Children with higher levels of hyperactivity displayed: (1) significantly prolonged stop signal reaction time (SSRT) in the modified stop-signal anticipation task; (2) no notable differences in commission errors in the revised Go/NoGo task; (3) increased reaction time (RT) in stop-signal task and Go/NoGo task with increased probabilities of stop or NoGo signal; and (4) positive proactive behavioral index scores in AX-CPT. CONCLUSION: The results suggested that children with heightened hyperactivity exhibited impaired reactive control, especially for responses already underway, but preserved proactive control. Further studies concerning these children are warranted.

Bilateral stimulation of the subthalamic nucleus has differential effects on reactive and proactive inhibition and conflict-induced slowing in Parkinson's disease.

It has been proposed that the subthalamic nucleus (STN) mediates response inhibition and conflict resolution through the fronto-basal ganglia pathways. Our aim was to compare the effects of deep brain stimulation (DBS) of the STN on reactive and proactive inhibition and conflict resolution in Parkinson's disease using a single task. We used the conditional Stop signal reaction time task that provides the Stop signal reaction time (SSRT) as a measure of reactive inhibition, the response delay effect (RDE) as a measure of proactive inhibition and conflict-induced slowing (CIS) as a measure of conflict resolution. DBS of the STN significantly prolonged SSRT relative to stimulation off. However, while the RDE measure of proactive inhibition was not significantly altered by DBS of the STN, relative to healthy controls, RDE was significantly lower with DBS off but not DBS on. DBS of the STN did not alter the mean CIS but produced a significant differential effect on the slowest and fastest RTs on conflict trials, further prolonging the slowest RTs on the conflict trials relative to DBS off and to controls. These results are the first demonstration, using a single task in the same patient sample, that DBS of the STN produces differential effects on reactive and proactive inhibition and on conflict resolution, suggesting that these effects are likely to be mediated through the impact of STN stimulation on different fronto-basal ganglia pathways: hyperdirect, direct and indirect.

Imbalanced weighting of proactive and reactive control as a marker of risk-taking propensity.

According to the dual mechanisms of control (DMC), reactive and proactive control are involved in adjusting behaviors when maladapted to the environment. However, both contextual and inter-individual factors increase the weight of one control mechanism over the other, by influencing their cognitive costs. According to one of the DMC postulates, limited reactive control capacities should be counterbalanced by greater proactive control to ensure control efficiency. Moreover, as the flexible weighting between reactive and proactive control is key for adaptive behaviors, we expected that maladaptive behaviors, such as risk-taking, would be characterized by an absence of such counterbalance. However, to our knowledge, no studies have yet investigated this postulate. In the current study, we analyzed the performances of 176 participants on two reaction time tasks (Simon and Stop Signal tasks) and a risk-taking assessment (Balloon Analog Risk Taking, BART). The post-error slowing in the Simon task was used to reflect the spontaneous individuals' tendency to proactively adjust behaviors after an error. The Stop Signal Reaction Time was used to assess reactive inhibition capacities and the duration of the button press in the BART was used as an index of risk-taking propensity. Results showed that poorer reactive inhibition capacities predicted greater proactive adjustments after an error. Furthermore, the higher the risk-taking propensity, the less reactive inhibition capacities predicted proactive behavioral adjustments. The reported results suggest that higher risk-taking is associated with a smaller weighting of proactive control in response to limited reactive inhibition capacities. These findings highlight the importance of considering the imbalanced weighting of reactive and proactive control in the analysis of risk-taking, and in a broader sense, maladaptive behaviors.

Prepared and reactive inhibition in smokers and non-smokers.

INTRODUCTION: Models of addiction have identified deficits in inhibitory control, or the ability to inhibit inappropriate or unwanted behaviors, as one factor in the development and maintenance of addictive behaviors. Current literature supports disruption of the prefrontal circuits that mediate reactive inhibitory control processes (i.e., inhibition in response to sudden, unplanned changes in environmental demands) in substance use disorders. However, the relationship between disorders of addiction, such as nicotine dependence, and planned inhibitory processes (i.e., inhibition that occurs after advance warning) is unclear. The goal of the present study was to examine the extent to which reactive and planned inhibitory processes are differentially disrupted in nicotine dependent individuals. METHOD: We employed an internet-based novel stop signal task wherein participants were instructed to stop a continuous movement at either a predictable or unpredictable time. This task explicitly separated planned and reactive inhibitory processes and assessed group differences in task performance between smokers (N = 281) and non-smokers (N = 164). The smoker group was defined as any participant that identified as a smoker and reported an average daily nicotine consumption of at least 2 mg. The non-smoker group was defined as any participant that identified as a non-smoker and had not been a former smoker that quit within the last year. The smoker group also completed a questionnaire regarding smoking behaviors which included the Fägerstrom Test of Nicotine Dependence (FTND). We used these data to assess the continuous relation between planned stopping, unplanned stopping, and smoking behaviors. RESULTS: We found significant differences in stop times for both reactive and planned stopping between groups as well as within the smoker group. Additionally, in the smoker group, dependence as measured by the FTND was associated with longer stop times on planned stop trials. Surprisingly, greater daily average consumption of nicotine was related to faster stopping for both trial types. CONCLUSION: These results indicate the relevance of measuring both reactive and planned inhibitory processes for elucidating the relationship between nicotine addiction and mechanisms of inhibitory control.

Proactive and reactive response inhibition of individuals with high schizotypy viewing different facial expressions: An ERP study using an emotional stop-signal task.

The present study aimed to examine whether impairments in reactive (outright stopping) and proactive (preparation for stopping) response inhibition are affected by negative emotions in individuals with high schizotypy, a subclinical group at risk for schizophrenia, as well as the neural mechanisms underlying these processes. Twenty-seven participants with high schizotypy and 28 matched low-schizotypy individuals completed an emotional stop-signal task in which they responded to facial emotions (neutral or angry) or inhibited their responses (when the frame of the picture turned red). Electroencephalogram (EEG) data were also recorded during the task. At the neural level, analysis of go trials revealed that viewing angry faces impaired proactive inhibition. In addition, the high-schizotypy group exhibited a greater P3 amplitude in go trials in the neutral condition than the low-schizotypy group; however, no group difference was found in the angry condition. For stop trials (reactive inhibition), a smaller P3 amplitude was found in the angry condition than in the neutral condition. Moreover, high-schizotypy individuals showed smaller P3 amplitudes than low-schizotypy individuals. The current findings suggest that, at the neural level, viewing negative emotions impaired both proactive and reactive response inhibition. Individuals with high schizotypy exhibited impairments in proactive response inhibition in the neutral condition but not in the angry condition; they exhibited impaired reactive response inhibition in both emotion conditions. The present findings deepen our understanding of emotional response inhibition in individuals on the schizophrenia spectrum.