Neural Mechanisms Of Emotion Regulation Research Articles

Effects of nonsocial and circumscribed interest images on neural mechanisms of emotion regulation in autistic adults.

Emotion dysregulation is commonly reported among autistic individuals. Prior work investigating the neurofunctional mechanisms of emotion regulation (ER) in autistic adults has illustrated alterations in dorsolateral prefrontal cortex (dlPFC) activity, as well as concurrent atypical patterns of activation in subcortical regions related to affect during cognitive reappraisal of social images. Whereas most research examining ER in autism has focused on regulation of negative emotions, the effects of regulating positive emotions has been generally understudied. This is surprising given the relevance of positive motivational states to understanding circumscribed interests (CI) in autism. Accordingly, the purpose of this study was to use fMRI with simultaneous eye-tracking and pupillometry to investigate the neural mechanisms of ER during passive viewing and cognitive reappraisal of a standardized set of nonsocial images and personalized (self-selected) CI images. The autistic group demonstrated comparatively reduced modulation of posterior cingulate cortex (PCC) activation during cognitive reappraisal of CI images compared to viewing of CI, although no eye-tracking/pupillometry differences emerged between-groups. Further, the autistic group demonstrated increased PCC connectivity with left lateral occipital and right supramarginal areas when engaging in cognitive reappraisal vs. viewing CI. In autistic adults, CI may be differentially modulated via PCC. Considering the documented role of the PCC as a core hub of the default mode network, we further postulate that ER of CI could potentially be related to self-referential cognition.

A Pilot Study of Cognitive Training Effects on Neural Mechanisms of Emotion Regulation

Abnormalities within neural regions implicated in cognitive control and social-emotional appraisal contribute to impaired emotion regulation in schizophrenia patients with a history of aggression. The current study examined the effect of cognitive training on circuits implicated in emotion regulation.

Neural characteristics of cognitive reappraisal success and failure: An ERP study.

IntroductionCognitive reappraisal, an important strategy of emotion regulation, can change emotional experience and attention to emotional information. However, not all individuals can deploy reappraisal strategies successfully. In the current study, we investigated event‐related potential (ERP) characteristics of reappraisal success and of reappraisal failure.MethodsTwenty‐six participants were divided into the success group or the failure group based on self‐report ratings of how successful they were in reducing their response to negative images using cognitive reappraisal strategy. All participants viewed 30 neutral images and 30 negative images which they were asked to just watch, and 30 negative stimuli that they were asked to reappraise, while electroencephalogram (EEG) was recorded.ResultsThe success group reported a significant reduction in the unpleasantness of negative images than the failure group in the negative‐reappraisal condition. The ERP data indicated that two time windows differentiated between the success and failure groups. In 200–300 ms, P200 was significantly more positive to the negative‐watch condition relative to both negative‐reappraisal and neutral conditions in the failure group, while no difference was observed in the success group. In 300–5,000 ms, cognitive reappraisal led to increased late positive potential (LPP) relative to negative‐watch in the early and middle latency windows (300–3,100 ms) in both groups; in the late latency window (3,100–5,000 ms), the reappraisal success group showed the LPP amplitude to the negative‐reappraisal stimuli to be more positive than to the negative‐watch stimuli, while no difference was found in the reappraisal failure group.ConclusionOur study provided direct evidence that different neurophysiological features were associated with reappraisal success and failure while engaging in the reappraisal of negative stimuli. This result will contribute to better understanding of the neural mechanism of emotion regulation in emotional disorders (i.e., depression and anxiety).

Altered neural processing of negative stimuli in people with internet gaming disorder: fMRI evidence from the comparison with recreational game users

BackgroundAbundant clinical studies have suggested that emotion dysregulation seems to be the essential pathogenesis for Internet gaming disorder (IGD). However, the neural mechanism of emotion regulation for IGD is still unclear. MethodsSubjective evaluation and fMRI data were collected from 50 subjects (IGD: 24; recreational game user (RGU): 26) while they were performing an emotion reappraisal task. We collected and compared their brain features during emotion processing of different visual stimuli. ResultsHigher activation in the left dorsal anterior cingulate cortex (dACC), right ventral ACC, left claustrum and bilateral insula was observed in participants with IGD during emotion reappraisal relative to that of the RGU participants. In addition, generalized psychophysiological interaction analysis also showed that IGD participants had stronger functional connectivity between the right insula and bilateral dorsolateral prefrontal cortex (DLPFC) than the RGU participants. ConclusionsThe results suggest that IGD participants could not down-regulate their negative emotional experiences as efficiently as the RGU participants, although they engaged more cognitive resources. These results reveal the special neural circuits of emotion dysregulation in IGD individuals and provide new neural perspective for the intervention of IGD.

Brain-machine interfaces from motor to mood.

Brain-machine interfaces (BMIs) create closed-loop control systems that interact with the brain by recording and modulating neural activity and aim to restore lost function, most commonly motor function in paralyzed patients. Moreover, by precisely manipulating the elements within the control loop, motor BMIs have emerged as new scientific tools for investigating the neural mechanisms underlying control and learning. Beyond motor BMIs, recent work highlights the opportunity to develop closed-loop mood BMIs for restoring lost emotional function in neuropsychiatric disorders and for probing the neural mechanisms of emotion regulation. Here we review significant advances toward functional restoration and scientific discovery in motor BMIs that have been guided by a closed-loop control view. By focusing on this unifying view of BMIs and reviewing recent work, we then provide a perspective on how BMIs could extend to the neuropsychiatric domain.

Neural Mechanisms of Emotion Regulation Moderate the Predictive Value of Affective and Value-Related Brain Responses to Persuasive Messages.

Emotionally evocative messages can be an effective way to change behavior, but the neural pathways that translate messages into effects on individuals and populations are not fully understood. We used a human functional neuroimaging approach to ask how affect-, value-, and regulation-related brain systems interact to predict effects of graphic anti-smoking messages for individual smokers (both males and females) and within a population-level messaging campaign. Results indicated that increased activity in the amygdala, a region involved in affective reactivity, predicted both personal quit intentions and population-level information-seeking and this was mediated by activity in ventromedial prefrontal cortex (vmPFC), a region involved in computing an integrative value signal. Further, the predictive value of these regions was moderated by expression of a meta-analytically defined brain pattern indexing emotion regulation. That is, amygdala and vmPFC activity strongly tracked with population behavior only when participants showed low recruitment of this brain pattern, which consists of regions involved in goal-driven regulation of affective responses. Overall, these findings suggest that affective and value-related brain responses can predict the success of persuasive messages and that neural mechanisms of emotion regulation can shape these responses, moderating the extent to which they track with population-level message impact.SIGNIFICANCE STATEMENT People and organizations often appeal to our emotions to persuade us, but how these appeals engage the brain to drive behavior is not fully understood. We present an fMRI-based model that integrates affect-, control-, and value-related brain responses to predict the impact of graphic anti-smoking stimuli within a small group of smokers and a larger-scale public messaging campaign. This model indicated that amygdala activity predicted the impact of the anti-smoking messages, but that this relationship was mediated by ventromedial prefrontal cortex and moderated by expression of a distributed brain pattern associated with regulating emotion. These results suggest that neural mechanisms of emotion regulation can shape the extent to which affect and value-related brain responses track with population behavioral effects.

情绪调节的神经机制研究

情绪调节的神经机制研究

Neural mechanisms of emotion regulation: A neuroimaing approach

Neural mechanisms of emotion regulation: A neuroimaing approach

Basis of Inability to Regulate Emotions in Autism Identified

Back to table of contents Previous article Next article Clinical and Research NewsFull AccessBasis of Inability to Regulate Emotions in Autism IdentifiedNick ZagorskiNick ZagorskiSearch for more papers by this authorPublished Online:20 Mar 2015https://doi.org/10.1176/appi.pn.2015.3a6AbstractYoung adults with autism spectrum disorder show differing brain activity from controls when trying to change their emotional perceptions of facial images.While impaired social skills, communication difficulties, and repetitive behaviors are the core features used to diagnose someone as having an autism spectrum disorder (ASD), many parents and clinicians would say that emotional deficits such as irritability, tantrums, and aggressive behavior are also real elements of concern.Emotional outbursts like tantrums are the leading contributors to stress among parents of ASD children and are the most common reason parents seek professional treatment. The only two Food and Drug Administration–approved drugs for autism—risperidone and aripiprazole—are prescribed to treat irritability.The question at large is how two areas of deficiency—sociocommunication and emotion—overlap. Do children with ASD throw a tantrum as a result of frustrations at being unable to adequately express themselves?New findings using functional magnetic resonance imaging (fMRI) suggest that the problems with emotional regulation in ASD lie deeper. When comparing fMRI scans of 15 young adults with ASD and 15 matched controls, the study found that the brain activity of the ASD subjects was different when trying to change their emotional perception of an image.The tests carried out are known as cognitive reappraisals; after seeing an image of a face, the participants were given instructions to either “think positive” or “think negative,” which may or may not be in tune with the facial expression. As lead author Gabriel Dichter, Ph.D., an associate professor of psychiatry and psychology at the University of North Carolina School of Medicine, told Psychiatric News, “Cognitive reappraisal measures one’s ability to take a deep breath following an emotional stimulus, as it were, and refrain from reacting inappropriately.“With fMRI, we’ve now seen that the difficulties in emotion regulation observed in people with autism have a biological basis.”Specifically, the images revealed that subjects in the ASD group had a decreased capacity to upregulate activity in the nucleus accumbens brain region when instructed to think more positively and had a decreased ability to downregulate activity in the amygdala when asked to think negatively. There were also deficits in activity in the prefrontal cortex during both regulatory conditions.Moreover, the degree to which brain activity was deficient correlated with the severity of the individual’s autism, Dichter noted.These differences were evident only in the imaging data. The ASD participants had the same subjective ratings of the faces as controls did—they could distinguish “happy,” and both groups spent the same amount of time looking at and thinking about the faces, as measured by eye trackers and pupil dilation.“This is a very good pilot study that arrives at an opportune time as clinicians have become more cognizant of how strongly emotional regulation can determine long-term independence and well-being in people with ASD,” said Antonio Hardan, M.D., a professor of psychiatry and behavioral sciences at Stanford University Medical Center and director of the center’s Autism and Developmental Disorders Clinic. “The participants were all high-functioning adults with ASD, though, and it is important to test if these results are generalizable to the larger spectrum, especially those who have more severe autism.” As for the possibility that emotional regulation problems might be a core deficiency in ASD, Hardan noted these findings were intriguing. Nonetheless, “we need to determine if the same pathophysiology that leads to the social and communication deficits also leads to the emotional deficits, and the science is not there yet.”On a practical level, identifiable brain changes do provide a target for examining the emotional state of someone with ASD, which could be very useful in future clinical work.“A big issue in autism clinical studies is obtaining personal insight,” Dichter explained. “Unlike a depression study, where you can ask people about their mood, people with autism often have difficulty reporting how they feel. Now with fMRI we have a way to bypass those communication difficulties and look at emotional activity right at the source.”This study was published online in the Journal of Autism and Developmental Disorders as part of a special issue on emotion regulation. Funding was provided by grants from the National Institute of Mental Health and the Eunice Kennedy Shriver National Institute of Child Health and Human Development. ■An abstract of “Neural Mechanisms of Emotion Regulation in Autism Spectrum Disorder” can be accessed here. ISSUES NewArchived

Neural emotion regulation circuitry underlying anxiolytic effects of perceived control over pain.

Anxiolytic effects of perceived control have been observed across species. In humans, neuroimaging studies have suggested that perceived control and cognitive reappraisal reduce negative affect through similar mechanisms. An important limitation of extant neuroimaging studies of perceived control in terms of directly testing this hypothesis, however, is the use of within-subject designs, which confound participants' affective response to controllable and uncontrollable stress. To compare neural and affective responses when participants were exposed to either uncontrollable or controllable stress, two groups of participants received an identical series of stressors (thermal pain stimuli). One group ("controllable") was led to believe they had behavioral control over the pain stimuli, whereas another ("uncontrollable") believed they had no control. Controllable pain was associated with decreased state anxiety, decreased activation in amygdala, and increased activation in nucleus accumbens. In participants who perceived control over the pain, reduced state anxiety was associated with increased functional connectivity between each of these regions and ventral lateral/ventral medial pFC. The location of pFC findings is consistent with regions found to be critical for the anxiolytic effects of perceived control in rodents. Furthermore, interactions observed between pFC and both amygdala and nucleus accumbens are remarkably similar to neural mechanisms of emotion regulation through reappraisal in humans. These results suggest that perceived control reduces negative affect through a general mechanism involved in the cognitive regulation of emotion.

Neural Mechanisms of Emotion Regulation in Autism Spectrum Disorder.

Autism spectrum disorder (ASD) is characterized by high rates of comorbid internalizing and externalizing disorders. One mechanistic account of these comorbidities is that ASD is characterized by impaired emotion regulation (ER) that results in deficits modulating emotional responses. We assessed neural activation during cognitive reappraisal of faces in high functioning adults with ASD. Groups did not differ in looking time, pupilometry, or subjective ratings of faces during reappraisal. However, instructions to increase positive and negative emotional responses resulted in less increase in nucleus accumbens and amygdala activations (respectively) in the ASD group, and both regulation instructions resulted in less change in dorsolateral prefrontal cortex activation in the ASD group. Results suggest a potential mechanistic account of impaired ER in ASD.

Neural Mechanisms of Emotion Regulation in Autism Spectrum Disorder

Neural Mechanisms of Emotion Regulation in Autism Spectrum Disorder

Negative Emotion Regulation in Patients with Posttraumatic Stress Disorder

ObjectiveTo explore the neural mechanisms of negative emotion regulation in patients with post-traumatic stress disorder (PTSD).MethodsTwenty PTSD patients and 20 healthy subjects were recruited. Event-related functional magnetic resonance imaging (fMRI) was used to investigate the modification of emotional responses to negative stimuli. Participants were required to regulate their emotional reactions according to the auditory regulation instructions via headphones, to maintain, enhance or diminish responses to negative stimuli during fMRI scans.ResultsThe PTSD group showed poorer modification performance than the control group when diminishing responses to negative stimuli. On fMRI, the PTSD group showed decreased activation in the inferior frontal cortex, inferior parietal lobule, insula and putamen, and increased activation in posterior cingulate cortex and amygdala during up-regulation of negative emotion. Similar decreased activation regions were found during down-regulation of negative emotion, but no increased activation was found.ConclusionTrauma exposure might impair the ability to down-regulate negative emotion. The present findings will improve our understanding of the neural mechanisms of emotion regulation underlying PTSD.

Neural mechanisms of cognitive reappraisal in remitted major depressive disorder

BackgroundDown-regulation of negative emotions by cognitive strategies relies on prefrontal cortical modulation of limbic brain regions, and impaired frontolimbic functioning during cognitive reappraisal has been observed in affective disorders. However, no study to date has examined cognitive reappraisal in unmedicated euthymic individuals with a history of major depressive disorder relative to symptom-matched controls. Given that a history of depression is a critical risk factor for future depressive episodes, investigating the neural mechanisms of emotion regulation in remitted major depressive disorder (rMDD) may yield novel insights into depression risk. MethodWe assessed 37 individuals (18 rMDD, 19 controls) with functional magnetic resonance imaging (fMRI) during a task requiring cognitive reappraisal of sad images. ResultsBoth groups demonstrated decreased self-reported negative affect after cognitive reappraisal and no group differences in the effects of cognitive reappraisal on mood were evident. Functional MRI results indicated greater paracingulate gyrus (rostral anterior cingulate cortex, Brodmann area 32) activation and decreased right midfrontal gyrus (Brodmann area 6) activation during the reappraisal of sad images. LimitationsTrial-by-trial ratings of pre-regulation affect were not collected, limiting the interpretation of post-regulation negative affect scores. ConclusionsResults suggest that activation of rostral anterior cingulate cortex, a region linked to the prediction of antidepressant treatment response, and of the right midfrontal gyrus, a region involved in cognitive control in the context of cognitive reappraisal, may represent endophenotypic markers of future depression risk. Future prospective studies will be needed to validate the predictive utility of these neural markers.

Neural mechanisms of emotion regulation in childhood anxiety

The present study was designed to examine the cortical processes that mediate cognitive regulation in response to emotion-eliciting stimuli in anxious children. Electroencephalographic (EEG) activity was recorded from clinically anxious children (n = 29) and typically developing children (n = 34). Event-related potential components were recorded while children performed a go/no-go task using facial stimuli depicting angry, calm, and happy expressions. Anxious children had significantly greater posterior P1 and frontal N2 amplitudes, components associated with attention/arousal and cognitive control, respectively, than typically developing children. Anxious children also had significantly greater error-related negativities and correct-response negativities relative to typically developing children. For the anxious group only, there were no differences in neural activation between face (emotion) types or trial (Go vs. No-go) types. A regression analysis revealed that No-go N2 amplitudes for calm faces predicted self-reported anxiety levels. Anxious children appeared to show increased cortical activation regardless of the emotional content of the stimuli. Anxious children also showed greater medial-frontal activity regardless of task demands and response accuracy. Taken together, these findings suggest indiscriminate cortical processes that may underlie the hypervigilant regulatory style seen in clinically anxious individuals.

Amygdala–orbitofrontal resting-state functional connectivity is associated with trait anger

An important distinction in research on the neural mechanisms of emotion regulation involves the relatively limited duration of emotional states versus emotional traits that are defined as the stable tendency to experience particular emotions in daily life. Neuroimaging investigations of the regulation of anger states point to the involvement of reciprocal changes in the prefrontal cortex and amygdala activity, but the neural substrate of trait anger has received less attention. We used resting-state functional MRI to determine whether the variation in the strength of functional connectivity between the amygdala and the orbitofrontal cortex is associated with trait anger. Sixteen healthy men completed the Spielberger State-Trait Anger Expression Inventory. Correlational analysis for resting-state functional connectivity (RSFC) was carried out with the left and the right amygdala as separate seed regions. Anger measures were correlated to RSFC involving the right and the left amygdala on a voxel-by-voxel basis across all individuals. We found that Trait Anger was inversely associated with the strength of RSFC between the amygdala and the contralateral middle orbitofrontal cortex. The association was stronger for the right amygdala-left orbitofrontal connection. Anger Control, the tendency to try to control expressions of anger, showed the opposite pattern of being positively correlated with amygdala-orbitofrontal connectivity. The present study provides evidence that RSFC in a corticolimbic circuit might subserve stable differences in anger regulation. Our findings also suggest that RSFC may prove valuable as a trait marker for disorders characterized by emotional dysregulation such as depression, anxiety, and personality disorders.

Magnitude and chronometry of neural mechanisms of emotion regulation in subtypes of aggressive children

Emotion regulation is a key social skill and children who fail to master it are at risk for clinical disorders. Specific styles of emotion regulation have been associated with particular patterns of prefrontal activation. We investigated whether anxious aggressive children would reveal a different pattern of cortical activation than non-anxious aggressive children and normally-developing children. We examined the magnitude and timing of source activation underlying the N2—an ERP associated with inhibitory control—during a go/nogo task with a negative emotion induction component (loss of earned points). We estimated cortical activation for two regions of interest—a ventral prefrontal and a dorsomedial prefrontal region—for three 100-ms windows over the range of the N2 (200–500 ms). Anxious aggressive children showed high ventral prefrontal activation in the early window; non-anxious aggressive children showed high ventral prefrontal activation in the late window, but only for the duration of the emotion induction; and normally-developing children showed low ventral prefrontal activation throughout. There were no group differences in dorsomedial prefrontal activation. These results suggest that anxious aggressive children recruit ventral prefrontal activation quickly and indiscriminately, possibly giving rise to their rigid, threat-oriented approach to conflict. The late ventral prefrontal activation seen for non-anxious aggressive children may underlie a more delayed, situation-specific, but ineffective response to frustration.

Brain Imaging Investigation of the Neural Correlates of Emotion Regulation

The ability to control/regulate emotions is an important coping mechanism in the face of emotionally stressful situations. Although significant progress has been made in understanding conscious/deliberate emotion regulation (ER), less is known about non-conscious/automatic ER and the associated neural correlates. This is in part due to the problems inherent in the unitary concepts of automatic and conscious processing. Here, we present a protocol that allows investigation of the neural correlates of both deliberate and automatic ER using functional magnetic resonance imaging (fMRI). This protocol allows new avenues of inquiry into various aspects of ER. For instance, the experimental design allows manipulation of the goal to regulate emotion (conscious vs. non-conscious), as well as the intensity of the emotional challenge (high vs. low). Moreover, it allows investigation of both immediate (emotion perception) and long-term effects (emotional memory) of ER strategies on emotion processing. Therefore, this protocol may contribute to better understanding of the neural mechanisms of emotion regulation in healthy behaviour, and to gaining insight into possible causes of deficits in depression and anxiety disorders in which emotion dysregulation is often among the core debilitating features.

Neural correlates of regulation of positive and negative emotions: An fMRI study

Regulation of emotion is important for adaptive social functioning and mental well-being. This functional magnetic resonance imaging study identified neural correlates of regulation of positive or negative emotion. Twelve healthy female Chinese participants performed the experimental task that required them to simply view emotional pictures or to regulate their emotions induced by these pictures while their brain activities were monitored by a 1.5T MRI scanner. The neuroimaging findings indicate that the left superior and lateral frontal regions (BA8/9) are common neural correlates of regulation of both emotions. For regulation of positive or negative emotion, changes of BOLD responses in the prefrontal regions and the left insula are associated with regulation of positive emotion; whereas activity of the left orbitofrontal gyrus, the left superior frontal gyrus, and the anterior cingulate gyrus appears to be involved in regulation of negative emotion. According to the participants’ self-report, they appeared to be more effective in regulating positive than negative emotions, which may relate to the distinct patterns of neural activity associated with regulation of the specific emotion. As a conclusion, our findings suggest that there are shared as well as valence-specific neurocognitive mechanisms underlying regulation of positive and negative emotions. Enhanced knowledge about the neural mechanisms of emotion regulation helps improve understanding of the complex interplay of emotion and cognition underlying human behaviors.

Neural Bases of Social Anxiety Disorder

Social anxiety disorder is thought to involve emotional hyperreactivity, cognitive distortions, and ineffective emotion regulation. While the neural bases of emotional reactivity to social stimuli have been described, the neural bases of emotional reactivity and cognitive regulation during social and physical threat, and their relationship to social anxiety symptom severity, have yet to be investigated. To investigate behavioral and neural correlates of emotional reactivity and cognitive regulation in patients and controls during processing of social and physical threat stimuli. Participants were trained to implement cognitive-linguistic regulation of emotional reactivity induced by social (harsh facial expressions) and physical (violent scenes) threat while undergoing functional magnetic resonance imaging and providing behavioral ratings of negative emotion experience. Academic psychology department. Fifteen adults with social anxiety disorder and 17 demographically matched healthy controls. Blood oxygen level-dependent signal and negative emotion ratings. Behaviorally, patients reported greater negative emotion than controls during social and physical threat but showed equivalent reduction in negative emotion following cognitive regulation. Neurally, viewing social threat resulted in greater emotion-related neural responses in patients than controls, with social anxiety symptom severity related to activity in a network of emotion- and attention-processing regions in patients only. Viewing physical threat produced no between-group differences. Regulation during social threat resulted in greater cognitive and attention regulation-related brain activation in controls compared with patients. Regulation during physical threat produced greater cognitive control-related response (ie, right dorsolateral prefrontal cortex) in patients compared with controls. Compared with controls, patients demonstrated exaggerated negative emotion reactivity and reduced cognitive regulation-related neural activation, specifically for social threat stimuli. These findings help to elucidate potential neural mechanisms of emotion regulation that might serve as biomarkers for interventions for social anxiety disorder.