Impaired Response Inhibition Research Articles

Significance of Beta-Band Oscillations in Autism Spectrum Disorders During Motor Response Inhibition Tasks: A MEG Study

In Autism Spectrum Disorders (ASD), impaired response inhibition and lack of adaptation are hypothesized to underlie core ASD symptoms, such as social communication and repetitive, stereotyped behavior. Thus, the aim of the present study was to compare neural correlates of inhibition, post-error adaptation, and reaction time variability in ASD and neuro-typical control (NTC) participants by investigating possible differences in error-related changes of oscillatory MEG activity. Twelve male NTC (mean age 20.3 ± 3.7) and fourteen male patients with ASD (mean age 17.8 ± 2.9) were included in the analysis. Subjects with ASD showed increased error-related reaction time variability. MEG analysis revealed decreased beta power in the ASD group in comparison to the NTC group over the centro-parietal channels in both, the pre-stimulus and post-response interval. In the ASD group, mean centro-parietal beta power negatively correlated with dimensional autism symptoms. In both groups, false alarms were followed by an early increase in temporo-frontal theta to alpha power; and by a later decrease in alpha to beta power at central and posterior sensors. Single trial correlations were additionally studied in the ASD group, who showed a positive correlation of pre-stimulus beta power with post-response theta, alpha, and beta power, particularly after hit trials. On a broader scale, the results deliver important insights into top-down control deficits that may relate to core symptoms observed in ASD.

Relations Between Acute Effects of Alcohol on Response Inhibition, Impaired Control over Alcohol Use, and Alcohol-Related Problems.

Alcohol consistently impairs response inhibition in the laboratory, and alcohol impairment of response inhibition may lead to excess consumption or increases in intoxicated risk behavior, both of which contribute to risk for alcohol-related problems. To our knowledge, no prior studies have examined relations between alcohol impairment of response inhibition and either impaired control over alcohol (i.e., inability to adhere to predetermined drinking limits) or real-world alcohol-related problems. The current study addressed this gap in the literature. Young adult social drinkers (N=215, 76% male) participated in a between-subjects, placebo-controlled alcohol challenge study and completed self-reports approximately 2weeks later. Multilevel models were used to examine the hypothesis that alcohol impairment of response inhibition would indirectly lead to alcohol-related problems through impaired control over alcohol use. Greater alcohol-induced impairment of response inhibition and impaired control over alcohol use were both significant predictors of alcohol-related problems. However, greater alcohol-induced response inhibition was not a significant predictor of impaired control over alcohol use. To our knowledge, this is the first study demonstrating relationships between alcohol impairment of response inhibition and real-world alcohol-related problems and the first to address relationships between alcohol impairment of response inhibition and impaired control over alcohol use. These results suggest that impaired control over alcohol use may result from deficits in the trait ability to control behavior rather than deficits in alcohol-induced response inhibition. Regardless, results suggest that alcohol impairment of response inhibition and impaired control over alcohol are both worthwhile intervention targets.

Emotional Response Inhibition: A Shared Neurocognitive Deficit in Eating Disorder Symptoms and Nonsuicidal Self-Injury.

Eating disorder (ED) symptoms often co-occur with non-suicidal self-injury (NSSI). This comorbidity is consistent with evidence that trait negative urgency increases risk for both of these phenomena. We previously found that impaired late-stage negative emotional response inhibition (i.e., negative emotional action termination or NEAT) might represent a neurocognitive mechanism for heightened negative urgency among people with NSSI history. The current study evaluated whether relations between negative urgency and ED symptoms similarly reflect deficits in this neurocognitive process. A total of 105 community adults completed an assessment of ED symptoms, negative urgency, and an emotional response inhibition task. Results indicated that, contrary to predictions, negative urgency and NEAT contributed independent variance to the prediction of ED symptoms, while controlling for demographic covariates and NSSI history. Worse NEAT was also uniquely associated with restrictive eating, after accounting for negative urgency. Our findings suggest that difficulty inhibiting ongoing motor responses triggered by negative emotional reactions (i.e., NEAT) may be a shared neurocognitive characteristic of ED symptoms and NSSI. However, negative urgency and NEAT dysfunction capture separate variance in the prediction of ED-related cognitions and behaviors, distinct from the pattern of results we previously observed in NSSI.

Acute Alcohol Effects on Response Inhibition Depend on Response Automatization, but not on GABA or Glutamate Levels in the ACC and Striatum.

Alcohol increases GABAergic signaling and decreases glutamatergic signaling in the brain. Variations in these neurotransmitter levels may modulate/predict executive functioning. Matching this, strong impairments of response inhibition are one of the most consistently reported cognitive/behavioral effects of acute alcohol intoxication. However, it has never been investigated whether baseline differences in these neurotransmitters allow to predict how much alcohol intoxication impairs response inhibition, and whether this is reflected in neurophysiological measures of cognitive control. We used MR spectroscopy to assess baseline (i.e., sober) GABA and glutamate levels in the anterior cingulate cortex (ACC) and striatum in n = 30 healthy young males, who were subsequently tested once sober and once intoxicated (1.01 permille). Inhibition was assessed with the sustained attention to response task (SART). This paradigm also allows to examine the effect of different degrees of response automatization, which is a known modulator for response inhibition, but does not seem to be substantially impaired during acute intoxication. As a neurophysiological correlate of response inhibition and control, we quantified EEG-derived theta band power and located its source using beamforming analyses. We found that alcohol-induced response inhibition deficits only occurred in the case of response automatization. This was reflected by decreased theta band activity in the left supplementary motor area (SMA), which may reflect modulations in the encoding of a surprise signal in response to inhibition cues. However, we did not find that differences in baseline (i.e., sober) GABA or glutamate levels significantly modulated differences in the size of alcohol-induced inhibition deficits.

Emotionally valenced stimuli impact response inhibition in those with substance use disorder and co-occurring anxiety and depression symptoms

BackgroundSubstance use disorder (SUD) is associated with impaired response inhibition. Given the deficits in emotion regulation associated with SUD, it is unclear if this impairment is exacerbated by emotionally valenced stimuli. Co-occurring conditions may further exacerbate these impairments as many co-occurring conditions further impact emotion regulation. It was hypothesized that negative stimuli may further impact response inhibition for this population. MethodsThe current study used the stop-signal task to examine response inhibition to negative, neutral and positive stimuli in a sample of those with a history of SUD and co-occurring depression and anxiety symptoms. ResultsResponse inhibition was poorer for negative stimuli relative to neutral stimuli. There was no difference between negative and positive stimuli. Depression severity moderated the difference between response inhibition for negative and neutral stimuli. At elevated depression, response inhibition was worse and there was no difference across emotional stimuli. At low depression, there was a significant difference between negative and neutral stimuli. This effect was not found for anxiety symptoms. LimitationsStudy participants presented with polysubstance use of varying duration and amount. It is unclear whether findings are attributed to specific substances, or substance use broadly. Additionally, happy, angry, and calm facial emotions were used to represent positive, negative, and neutral valences respectively. It is unclear whether these findings are generalizable to other emotional expressions. ConclusionResults suggested that emotionally valenced stimuli affected response inhibition among those with low symptom severity. At elevated symptom severity, response inhibition to all stimuli were impaired.

Motor cortex dysfunction in problem gamblers.

Impairments in response inhibition have been implicated in gambling psychopathology. This behavioral impairment may suggest that the neural mechanisms involved in response inhibition, such as GABAA -mediated neurotransmission in the primary motor cortex (M1), are also impaired. The present study obtained paired-pulse transcranial magnetic stimulation markers of GABAA and glutamate receptor activity from the left M1 of three groups-problem gamblers (n = 17, 12 males), at-risk gamblers (n = 29, 19 males), and controls (n = 23, six males)-with each group matched for alcohol use, substance use, and attention-deficit hyperactivity disorder (ADHD) symptomology. Response inhibition was measured using the stop signal task. Results showed that problem gamblers had weaker M1 GABAA receptor activity relative to controls and elevated M1 glutamate receptor activity relative to at-risk gamblers and controls. Although there were no differences in response inhibition between the groups, poorer response inhibition was correlated with weaker M1 GABAA receptor activity. These findings are the first to show that problem gambling is associated with alterations in M1 GABAA and glutamate-mediated neurotransmission.

Reduced response inhibition after exposure to drug-related cues in male heroin abstainers.

Deficits in response inhibition associated with heroin use could last several months after abstinence in heroin users, and their response inhibition can also be interfered with task-irrelevant drug-related cues. However, it is unclear whether exposure to drug-related cues affects subsequent response inhibition in heroin users following abstinence. The present study aimed to investigate how drug-related cues with different durations between stimulus presentations, referred to as stimulus onset asynchronies (SOAs), affect subsequent response inhibition in heroin abstainers (HAs) with different length of abstinence. Sixty-seven male HAs performed a modified Go/NoGo task in which a motor response to frequent Go targets and no response to rare NoGo targets were required and a Go or NoGo target was displayed after either a heroin-related or a neutral picture presented for the 200ms and 600ms SOAs. The HAs responded significantly faster to Go targets following the neutral pictures for the 600ms SOA compared to other conditions. They also made more commission errors following heroin-related pictures compared to neutral pictures regardless of the SOAs. The shorter-term HAs made more commission errors compared to the longer-term HAs following the 200ms SOA, and it was only a trend when the SOA was 600ms. Additionally, negative correlations between the duration of current abstinence and commission errors were observed following cues with the 200ms SOA. Impaired response inhibition in HAs can be improved through protracted drug abstinence. However, that effect can be reduced by exposure to drug-related cues, which may increase the risk of relapse.

Theta oscillations in prolactinomas: Neurocognitive deficits in executive controls

Impairment of cognitive functions has been reported in prolactinomas. However, the electrophysiological mechanisms of response activation and response inhibition in prolactinomas remain unclear. We recorded participants’ scalp electroencephalography (EEG) in a visual Go/Nogo task. Compared to the healthy controls (HCs), the patients demonstrated worse performance and their prolactin (PRL) levels negatively correlated with behavioral results. Meanwhile, patients’ P300 amplitudes in the Go and Nogo conditions were smaller than the HCs. The amplitudes of N200nogo in patients were smaller than the HCs as well. Lower frontal theta power was found in the patients than the HCs in both Go and Nogo conditions, which indicated a deficit in response activation and inhibition. Moreover, the PRL levels mediated the relationship between frontal theta power and behavior performance, implying that lower frontal theta power caused the dysfunction of response control by abnormally high PRL levels. Patients also showed lower occipital alpha power than the HCs, which suggested that the impaired response inhibition may arise from deficient attention control. Taken together, the present study revealed the neurocognitive discrepancies between prolactinomas and the HCs. The frontal theta oscillation was highlighted as the electrophysiological markers of the impaired response control in prolactinomas.

Fronto-parietal engagement in response inhibition is inversely scaled with attention-deficit/hyperactivity disorder symptom severity.

Impaired response inhibition is one of the most consistent findings in attention deficit hyperactivity disorder (ADHD). However, the underlying brain mechanisms are not clear. This study aimed to underpin atypical inhibition-related brain activation and connectivity patterns in ADHD using a novel Go/No-go task design, and to determine its association with clinical symptoms of the disorder. Forty-eight adults with ADHD performed a Go/No-go task in which target frequency was manipulated during functional MRI. Specific inhibition-related brain activation was correlated with ADHD symptom severity, to assess the relationship of individual differences in engagement of inhibition-related brain circuits with the magnitude of every-day functioning impairments. Finally, generalized psychophysical interaction analyses were carried out to examine whether not only engagement but also functional connectivity between regions implicated in response inhibition is related to symptom severity. We found no evidence for the expected parietal modulation by increased demand for inhibition at the group-level results. However, this lack of modulation was mediated by individual differences in ADHD symptom severity - increased engagement of the intraparietal sulcus (IPS) in inhibition-demanding events was evident in individuals with less severe symptoms but dissipated with increase in symptomatology. Similarly, functional connectivity between the IPS and the right inferior frontal gyrus (rIFG) was elevated under high inhibitory demand conditions, but this effect diminished with increased symptom severity. The results highlight the importance of IPS engagement in response inhibition and suggest that IPS modulation may be driven by top-down control from the IFG. Moreover, the current findings force the point of treating ADHD as a continuum whereby brain correlates are scaled with severity of the disorder, and point to the potential use of individual differences in the modulation of IPS activation and connectivity as a neuromarker of ADHD.

Effects of threat and sleep deprivation on action tendencies and response inhibition.

The ability to control action is crucial for adaptive responding, but may be compromised in situations involving strong emotions (e.g., threat) or when people are deprived of resources (e.g., sleep). As compromised action control can have large consequences in threatening situations, for example when police officers face a potentially armed suspect, we experimentally investigated how acute threat and partial sleep deprivation affect the ability to control impulsive responses, in 52 healthy young adults performing a simulated shooting task. The results showed that acute threat increased the tendency to act quickly (i.e., reduced response times; b = 9.46, SE = 2.90, 95% CI [3.49, 15.29], p = .001) and impaired response inhibition (i.e., increased stop signal reaction times; b = -4.91, SE = 2.31, 95% CI [-9.47, -0.44], p = .035). In addition, 3 nights of partial sleep deprivation (5 hr [n = 28] vs. 8 hr [n = 24] of sleep), led to a significant decrease in overall response accuracy (b = -0.22, SE = 0.09, 95% CI [-0.40, -0.05], p = .025). Contrary to expectations, our results did not show increased threat sensitivity in sleep-deprived individuals (all p > .13). Nevertheless, they may have important implications for professionals who are required to maintain behavioral control under high levels of threat and who experience disturbed sleep due to for example, shift work, as both factors negatively affected performance. (PsycINFO Database Record (c) 2019 APA, all rights reserved).

Familiality of behavioral flexibility and response inhibition deficits in autism spectrum disorder (ASD)

BackgroundDiminished cognitive control, including reduced behavioral flexibility and behavioral response inhibition, has been repeatedly documented in autism spectrum disorder (ASD). We evaluated behavioral flexibility and response inhibition in probands and their parents using a family trio design to determine the extent to which these cognitive control impairments represent familial traits associated with ASD.MethodsWe examined 66 individuals with ASD (probands), 135 unaffected biological parents, and 76 typically developing controls. Participants completed a probabilistic reversal learning task (PRL) and a stop-signal task (SST) to assess behavioral flexibility and response inhibition respectively. Rates of PRL and SST errors were examined across groups, within families, and in relation to clinical and subclinical traits of ASD. Based on prior findings that subclinical broader autism phenotypic (BAP) traits may co-segregate within families and reflect heritable risk factors, we also examined whether cognitive control deficits were more prominent in families in which parents showed BAP features (BAP+).ResultsProbands and parents each showed increased rates of PRL and SST errors relative to controls. Error rates across tasks were not related. SST error rates inter-correlated among probands and their parents. PRL errors were more severe in BAP+ parents and their children relative to BAP− parents and their children. For probands of BAP+ parents, PRL and SST error rates were associated with more severe social-communication abnormalities and repetitive behaviors, respectively.ConclusionReduced behavioral flexibility and response inhibition are present among probands and their unaffected parents, but represent unique familial deficits associated with ASD that track with separate clinical issues. Specifically, behavioral response inhibition impairments are familial in ASD and manifest independently from parental subclinical features. In contrast, behavioral flexibility deficits are selectively present in families with BAP characteristics, suggesting they co-segregate in families with parental subclinical social, communication, and rigid personality traits. Together, these findings provide evidence that behavioral flexibility and response inhibition impairments track differentially with ASD risk mechanisms and related behavioral traits.

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

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

Emotional Stop Cues Facilitate Inhibitory Control in Schizophrenia.

Inhibitory control is a key deficit in patients with schizophrenia. This study aims to test whether emotions can facilitate inhibition in patients with schizophrenia when they increase attention to inhibitory process. A total of 36 patients with schizophrenia and 36 healthy controls completed an emotional stop-signal task. The task involved selective responses to "Go" stimuli and stopped response when emotional or neutral stop cues occurred. In all conditions, patients with schizophrenia took longer time to inhibit response compared with healthy controls, indicating an overall impairment in response inhibition. Importantly, patients with schizophrenia and controls acquired similar size of benefit from the negative stop cues, showing as reduced reaction time to negative than neutral stop cues. However, the negative stop cues impaired subsequent Go performance only in patients with schizophrenia, indicating additional cost of the negative stop cues for patients with schizophrenia. In both groups, the positive stop cues did not have any significant influence on response inhibition. These findings provide novel evidence for the benefit of emotional stop cues on inhibitory control in patients with schizophrenia and reveal different after-effects of emotional enhancement effect in patients and healthy populations. The findings may help develop effective interventions for improving inhibitory control in patients with schizophrenia and other clinical populations.

Differential profiles of response inhibition deficit between male children with autism spectrum disorders and schizophrenia.

Autism spectrum disorders (ASD) and schizophrenia (SZ) are both associated with response inhibition impairment. However, the relative pattern of deficits in these two disorders remains unclear. Twenty-three male children with ASD, 23 male children with SZ, and 32 typically developing male controls were recruited to complete a set of tasks measuring response inhibition in the visual, auditory, and verbal domains. We found that visual, auditory, and verbal response inhibitions were impaired in both children with ASD and children with SZ. Compared with typically developing controls, children with ASD made more commission errors whereas children with SZ responded much slower in the visual response inhibition task. Both clinical groups showed comparable impairment in verbal response inhibition, but children with SZ were more impaired in auditory response inhibition than children with ASD. These different patterns of response inhibition deficit between male children with ASD and SZ may help to differentiate between these two disorders and may be potential targets for intervention. Autism Res 2020, 13: 591-602. © 2019 International Society for Autism Research, Wiley Periodicals, Inc. LAY SUMMARY: In this study, we found that male children with autism spectrum disorder (ASD) made more commission errors whereas male children with schizophrenia (SZ) responded much slower in the visual response inhibition task. Both clinical groups exhibited comparable impairments in verbal response inhibition, but male children with SZ were more impaired in auditory response inhibition than male children with ASD. Our findings provide potential targets for intervention.

Neural Basis of Response Bias on the Stop Signal Task in Misophonia.

Objective: Misophonia is a newly described condition in which specific ordinary sounds provoke disproportionately strong negative affect. Since evidence for psychobiological dysfunction underlying misophonia is scarce, we tested whether misophonia patients, like many patients with impulse control or obsessive-compulsive spectrum disorders, show impaired ability to inhibit an ongoing motor response.Methods: We collected functional magnetic resonance imaging data during a stop signal task in 22 misophonia patients and 21 matched healthy controls.Results: Compared to controls, patients tended to show longer stop signal delays, which is the time between stimuli signaling response initiation and inhibition. Additionally, patients tended to activate left dorsolateral prefrontal cortex more during responding rather than successful inhibition, as was seen in controls. Furthermore, patients lacked inhibition success-related activity in posterior cingulate cortices and activated the superior medial frontal gyri less during inhibition success compared to failure, a feature correlated with stop signal delays over the sample.Conclusions: Misophonia patients did not show impaired response inhibition. However, they tended to show a response bias on the stop signal task, favoring accuracy over speed. This implies perfectionism and compulsive, rather than impulsive, behavior. Moreover, brain activations were in line with patients, compared to controls, engaging more cognitive control for slowing responses, while employing more attentional resources for successful inhibition.

Do psychopathic traits predict impaired response inhibition to fearful expressions?: An investigation using facial expressions with direct and averted gazes

Do psychopathic traits predict impaired response inhibition to fearful expressions?: An investigation using facial expressions with direct and averted gazes

Impulsivity and relapse during treatment of methamphetamine use disorder

Abstract. Aims: The increasing prevalence of patients seeking treatment for methamphetamine use disorder (MUD) in some regions of Germany and the high relapse rates following common treatment interventions make more effective interventions highly needed. The aim of the present study was to enhance our understanding of the impact of impulsivity on relapse during treatment and thus to outline possible individual characteristics that make more tailored interventions necessary. Methodology: Forty-two patients with a diagnosis of MUD admitted to inpatient treatment and 21 matched healthy control participants (HC) completed the Barratt Impulsiveness Scale (BIS-11) as a self-reported measure of trait impulsivity and a go/no-go task with methamphetamine-associated and neutral stimuli to assess deficits of response inhibition. Relapse rates of patients during treatment were assessed. Results: Higher impairment of response inhibition, but not trait impulsivity, significantly predicted relapse during treatment. These findings were observed although patients with MUD compared to HC did not differ with regard to deficits of response inhibition. Conclusions: These findings suggest that patients with MUD who show enhanced deficits of response inhibition are more vulnerable to relapse during treatment and need more tailored treatment interventions.

Impulse control under emotion processing: an fMRI investigation in borderline personality disorder compared to non-patients and cluster-C personality disorder patients

Impulsivity is a characteristic syndromal and neurobehavioral feature of borderline personality disorder (BPD). Research suggests an important interaction between high negative emotions and low behavioral inhibition in BPD. However, knowledge about the generalizability across stimulus categories and diagnosis specificity is limited. We investigated neural correlates of hypothesized impaired response inhibition of BPD patients to negative, positive and erotic stimuli, by comparing them to non-patients and cluster-C personality disorder patients. During fMRI scanning, 53 BPD patients, 34 non-patients and 20 cluster-C personality disorder patients completed an affective go/no-go task, including social pictures. BPD patients showed more omission errors than non-patients, independent of the stimulus category. Furthermore, BPD patients showed higher activity in the inferior parietal lobule and frontal eye fields when inhibiting negative versus neutral stimuli. Activity of the inferior parietal lobule correlated positively with the BPD checklist subscale impulsivity. When inhibiting emotional stimuli, BPD patients showed an altered brain activity in the inferior parietal lobe and frontal eye fields, whereas previously shown dysfunctional prefrontal activity was not replicated. BPD patients showed a general responsivity across stimulus categories in the frontal eye fields, whereas effects in the inferior parietal lobe were specific for negative stimuli. Results of diagnosis specificity support a dimensional rather than a categorical differentiation between BPD and cluster-C patients during inhibition of social emotional stimuli. Supported by behavioral results, BPD patients showed no deficiencies in emotionally modulated response inhibition per se but the present findings rather hint at attentional difficulties for emotional information.

Freedom makes you lose control

PurposePast research suggests that heavy media multitaskers (HMMs) perform worse on tasks that require executive control, compared to light media multitaskers (LMMs). This paper aims to investigate whether individual differences between HMMs and LMMs make them respond differently to advertising in a media multitasking context and whether this stems from differences in the ability versus the motivation to regulate one’s attention. This is investigated by manipulating participants’ autonomy over attention allocation.Design/methodology/approachFor the first study (n = 85), a between subjects design with three conditions was used: sequential, multitasking under low autonomy over attention allocation and multitasking under high autonomy over attention allocation. This study investigated the inhibitory control of HMMs vs LMMs in a very controlled multitasking setting. The second study (n = 91) replicated the design of study one in a more naturalistic media multitasking setting and investigated the driving role of motivation vs ability for cognitive load differences between HMMs and LMMs and the consequent impact on advertising effectiveness.FindingsStudy I suggests that HMMs perform worse on a response inhibition task than LMMs after multitasking freely (in which case motivation to regulate attention determines the process), but not after their attention was guided externally by the experimenter (in which case their motivation could no longer determine the process). Study II argues that when motivation to switch attention is at play, cognitive load differences occur between HMMs and LMMs. This study additionally reveals that under these circumstances, HMMs are more persuaded by advertisements (report higher purchase intentions) compared to LMMs, while no differences appear when only ability is at play.Research limitations/implicationsExecutive control exists of different components (Miyake et al., 2000). The current study only focused on the impact of media multitasking frequency on response inhibition, but it would be interesting for future research to investigate whether media multitasking frequency equally affects the other sub-dimensions. Additionally, the impairment of response inhibition has been shown to predict a large number of other behavioral and impulse-control outcomes such as unhealthy food choices and alcohol and drug use (e.g. Friese et al., 2008). Future research should consider investigating other consequences of heavy media multitasking behavior, both advertising related and unrelated.Practical implicationsFrom a practical point of view, understanding the mechanisms that are driving the effects of media multitasking on advertising effectiveness for different groups of media-consumers could make it easier for practitioners to efficiently plan their media campaigns. Based on the findings of this study, the authors can derive that HMMs will be more depleted in cognitive resources and inhibitory control when media multitasking compared to LMMs. Consequently, this makes them more prone to advertising messages. This knowledge is of great importance for advertisers who could, based here on, aim to target HMMs more often than LMMs.Originality/valueTwo experimental studies by the authors confirm and add value to previous academic findings about the negative relation between media multitasking frequency and tasks that demand executive control. This study contributed to the previous by investigating whether individual differences between heavy and light media multitaskers make them respond differently toward advertising and whether the driving mechanism of these differences is a lack of motivation or ability to efficiently shift attention.

Effects of multisensory stop signals on alcohol-induced disinhibition in adults with ADHD.

Multisensory environments facilitate behavioral functioning in humans. The redundant signal effect (RSE) refers to the observation that individuals respond more quickly to stimuli when information is presented as multisensory, redundant stimuli (e.g., aurally and visually) rather than as a single stimulus presented to either modality alone. RSE appears to be because of specialized multisensory neurons in the superior colliculus and association cortex that allow intersensory coactivation between the visual and auditory channels. Our studies show that the disinhibiting effects of alcohol are attenuated when stop signals are multisensory (e.g., Visual + Auditory stop signals) versus unisensory (Roberts, Monem, & Fillmore, 2016). The present study expanded on this research to test the degree to which multisensory stop signals could also attenuate the disinhibiting effects of alcohol in those with attention-deficit hyperactivity disorder (ADHD), a clinical population characterized by poor impulse control. The study compared young adults with ADHD (n = 22) with healthy controls (n = 22) and examined the acute impairing effect of alcohol on response inhibition to stop signals that were presented as a unisensory (visual) stimulus or a multisensory (Visual + Auditory) stimulus. For controls, results showed alcohol impaired response inhibition to unisensory stop signals but not to multisensory stop signals. Response inhibition of those with ADHD was impaired by alcohol regardless of whether stop signals were unisensory or multisensory. The failure of multisensory stimuli to attenuate alcohol impairment in those with ADHD highlights a specific vulnerability that could account for heightened sensitivity to the disruptive effects of alcohol. (PsycINFO Database Record (c) 2019 APA, all rights reserved).