Association between Amygdala Hyperactivity to Harsh Faces and Severity of Social Anxiety in Generalized Social Phobia

Phan, K. Luan; Fitzgerald, Daniel A.; Nathan, Pradeep J.; Tancer, Manuel E.

doi:10.1016/j.biopsych.2005.08.012

Cited by 462 publications

(363 citation statements)

References 45 publications

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“…Most of these parameters correlated positively with symptom severity. These results also fit in well with other recent imaging studies, suggesting that threat processing in anxiety disorders is associated with increased activity in amygdala, hippocampus 21 , 25 , 26 , 60 , 61 , 62 and occipital cortex, 27 , 62 or in dorsal ACC and mPFC, 17 , 18 , 19 , 20 , 21 , 22 areas that have been implicated in selective attention, threat bias and monitoring. 56 , 63 , 64 , 65 , 66 , 67 , 68 …”

Section: Discussionsupporting

confidence: 91%

“…However, a number of novel findings suggest that while decreased allocation of lateral and ventral prefrontal resources seems to be an important characteristic of participants with non-clinical high trait anxiety or worry, 15 , 16 activation in these areas is more likely to be increased in clinical anxiety disorders during threat processing. In particular, studies have reported increased activation in the dorsal anterior cingulate cortex (ACC) and dorsomedial PFC (dmPFC) in specific phobia, 17 social anxiety disorder, 18 , 19 panic disorder 20 , 21 and generalised anxiety disorder. 22 Similarly, anxiety-specific threat processing has increasingly been associated with heightened activation in dorsolateral (dlPFC), 23 , 24 ventrolateral (vlPFC) 20 , 21 , 25 and ventromedial PFC (vmPFC).…”

Section: Introductionmentioning

confidence: 99%

Effective emotion regulation strategies improve fMRI and ECG markers of psychopathology in panic disorder: implications for psychological treatment action

et al. 2015

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Impairments in emotion regulation are thought to have a key role in the pathogenesis of anxiety disorders, but the neurobiological underpinnings contributing to vulnerability remain poorly understood. It has been a long-held view that exaggerated fear is linked to hyperresponsivity of limbic brain areas and impaired recruitment of prefrontal control. However, increasing evidence suggests that prefrontal–cortical networks are hyperactive during threat processing in anxiety disorders. This study directly explored limbic–prefrontal neural response, connectivity and heart-rate variability (HRV) in patients with a severe anxiety disorder during incidental versus intentional emotion regulation. During 3 Tesla functional magnetic resonance imaging, 18 participants with panic disorder and 18 healthy controls performed an emotion regulation task. They either viewed negative images naturally (Maintain), or they were instructed to intentionally downregulate negative affect using previously taught strategies of cognitive reappraisal (Reappraisal). Electrocardiograms were recorded throughout to provide a functional measure of regulation and emotional processing. Compared with controls, patients showed increased neural activation in limbic–prefrontal areas and reduced HRV during incidental emotion regulation (Maintain). During intentional regulation (Reappraisal), group differences were significantly attenuated. These findings emphasize patients' ability to regulate negative affect if provided with adaptive strategies. They also bring prefrontal hyperactivation forward as a potential mechanism of psychopathology in anxiety disorders. Although these results challenge models proposing impaired allocation of prefrontal resources as a key characteristic of anxiety disorders, they are in line with more recent neurobiological frameworks suggesting that prefrontal hyperactivation might reflect increased utilisation of maladaptive regulation strategies quintessential for anxiety disorders.

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“…However, in another study, when angry faces were presented for 500 ms, youth with generalized anxiety disorder relative to comparisons showed greater ventrolateral prefrontal cortex activation to angry faces (Monk et al, 2006). In contrast to several studies in anxious adults that examined amygdala activation to angry faces when awareness was not restricted (Phan, Fitzgerald, Nathan, & Tancer, 2006; Stein, Goldin, Sareen, Zorrilla, & Brown, 2002; Stein, Simmons, Feinstein, & Paulus, 2007), we found no group differences in amygdala activation. Indeed, the amygdala was not particularly responsive.…”

Section: Anxietycontrasting

confidence: 99%

The development of emotion-related neural circuitry in health and psychopathology

2008

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Disturbances in the detection of, response to, and interpretation of emotion are common in many forms of psychopathology. The amygdala, striatum, and structures within the prefrontal cortex are highly involved in mediating these stages of emotion processing, and evidence indicates that these regions show structural and functional alterations in different types of psychopathology, including anxiety, depression, and autism spectrum disorders. However, we do not know how genes and the environment interact to alter development of these brain regions in ways that give rise to emotion-related psychopathology. This review discusses the current understanding of brain regions that are involved in emotional functioning, how they develop, and how they are altered in three forms of psychopathology: anxiety, depression, and autism spectrum disorders. Following this, a framework is described that may facilitate the integration of investigations of genetic variation and brain function with symptom and diagnostic measures. The framework involves three components: (a) a greater emphasis on simultaneously analyzing multiple levels (genes, brain function, behavior, symptoms, and diagnoses); (b) further integration of developmental considerations, including timing of environmental events, adaptations (or maladaptations), and disorder-related trajectories that guide some children toward atypical experiences; and (c) greater cross-talk between animal and human investigations to take advantage of biological measures that cannot be acquired in humans.

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“…Supporting "In agreement with previous work" indicates support, while "the trisomic clones showed similar aberrations, albeit to a lesser degree (Supplemental Figure S2B)" provides evidence for this supporting statement. "In contrast to several studies in anxious adults that examined amygdala activation to angry faces when awareness was not restricted (Phan, Fitzgerald, Nathan, & Tancer, 2006;Stein, Goldin, Sareen, Zorrilla, & Brown, 2002;Stein, Simmons, Feinstein, & Paulus, 2007), we found no group differences in amygdala activation. "…”

Section: Citation Statement Classification Explanationcontrasting

confidence: 99%

“…This citation statement refers to Phan et al 2006 without providing evidence that supports or contrasts the claims made in the cited study.…”

Section: Mentioningmentioning

confidence: 93%

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scite: A smart citation index that displays the context of citations and classifies their intent using deep learning

Nicholson¹,

Mordaunt²,

Lopez³

et al. 2021

Quantitative Science Studies

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Citation indices are tools used by the academic community for research and research evaluation which aggregate scientific literature output and measure impact by collating citation counts. Citation indices help measure the interconnections between scientific papers but fall short because they fail to communicate contextual information about a citation. The usage of citations in research evaluation without consideration of context can be problematic, because a citation that presents contrasting evidence to a paper is treated the same as a citation that presents supporting evidence. To solve this problem, we have used machine learning, traditional document ingestion methods, and a network of researchers to develop a “smart citation index” called scite, which categorizes citations based on context. Scite shows how a citation was used by displaying the surrounding textual context from the citing paper and a classification from our deep learning model that indicates whether the statement provides supporting or contrasting evidence for a referenced work, or simply mentions it. Scite has been developed by analyzing over 25 million full-text scientific articles and currently has a database of more than 880 million classified citation statements. Here we describe how scite works and how it can be used to further research and research evaluation. Peer Review https://publons.com/publon/10.1162/qss_a_00146

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“…Given that subcallosal frontal regions, such as the OFC, serve important roles in top-down regulation of amygdala reactivity to control negative affect (i.e., anxiety) and mediate threat perception (6), this UF white matter tract is suggested to play a key role in emotional responding (24). This is consistent with evidence from functional neuroimaging studies implicating aberrant reactivity in amygdala to social threat and scrutiny in GSAD (2-4), and thus abnormalities in UF which carries the most prominent fibers between these two regions may explain why differential reactivity exists. This finding is consistent with recent functional neuroimaging studies have implicated the OFC in social anxiety disorder (25,26).…”

Section: Discussionsupporting

confidence: 89%

Preliminary Evidence of White Matter Abnormality in the Uncinate Fasciculus in Generalized Social Anxiety Disorder

Phan

Orlichenko

Boyd

et al. 2009

Biological Psychiatry

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208

157

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Background-Individuals with generalized social anxiety disorder (GSAD) exhibit exaggerated amygdala reactivity to aversive social stimuli. These findings could be explained by microstructural abnormalities in white matter (WM) tracts that connect the amygdala and prefrontal cortex, which is known to modulate the amygdala's response to threat. The goal of this study was to investigate brain frontal WM abnormalities by using diffusion tensor imaging (DTI) in patients with social anxiety disorder.

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“…The current results also fit with the neuroscientific literature on amygdala hyperactivity for emotional faces in social phobia ( Lira Yoon, Fitzgerald, Angstadt, McCarron, & Phan, 2007 ; Phan, Fitzgerald, Nathan, & Tancer, 2006 ; Straube, Mentzel, & Miltner, 2005 ; Veit et al, 2002 ). Recent studies on the functional role of amygdala responses to facial expressions suggest that activity in this brain region is implicated in triggering reflexive gaze shifts towards the eyes ( Gamer and Büchel, 2009 , Gamer et al, 2013 ).…”

Section: Discussionsupporting

confidence: 89%

Attentional mechanisms of social perception are biased in social phobia

Boll

Bartholomaeus

Peter³

et al. 2016

Journal of Anxiety Disorders

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“…Of note, our meta-analysis highlighted for the first time also areas that are more active in HC as compared to SAD during face perception, namely in a cluster of the occipital visual cortex (lingual gyrus) and in the posterior cingulate, Finally, consistently with the other available meta-analyses and with the vast majority of functional brain imaging studies, we identified an abnormal activation in the amygdalae of SAD patients as compared to HCs in response to face stimuli (e.g. in the literature 8,11,12,14,35,45 ).…”

Section: Discussionsupporting

confidence: 88%

“…in the literature 11,13,14,31,33,35,37,38 ), while others found a lateralized greater amygdala response. For instance, several works identified an altered response in the right amygdala only, 13,14,31,37 while others reported an opposite pattern (e.g. Gentili et al…”

Section: Discussionmentioning

confidence: 99%

“…13,23,24,27,31,32,40 Table 1 reports the characteristics of each study of the present meta-analysis including type of faces, type of contrasts, and type of task used. 8,11,13–15,23–27,29–41 Table 2 reports the 20 studies excluded in the second step of the selection and the main reason why they were not included in the final analysis.…”

Section: Methodsmentioning

confidence: 99%

“…While a hyperreactivity in the amygdala has been a consistent finding across most studies on face perception in SAD (e.g. in the literature 8,11–14 ), results diverged regarding the potential role of other structures that are involved in face perception (e.g. in the literature 8,12,15 ).…”

Section: Introductionmentioning

confidence: 96%

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Beyond emotions: A meta-analysis of neural response within face processing system in social anxiety

Gentili

Cristea

Angstadt

et al. 2015

Exp Biol Med (Maywood)

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Patients with social anxiety disorder (SAD) experience anxiety and avoidance in face-to-face interactions. We performed a metaanalysis of functional magnetic resonance imaging (fMRI) studies in SAD to provide a comprehensive understanding of the neural underpinnings of face perception in this disorder. To this purpose, we adopted an innovative approach, asking authors for unpublished data. This is a common procedure for behavioral meta-analyses, which, however has never been used in neuroimaging studies. We searched Pubmed with the key words ''Social Anxiety AND faces'' and ''Social Phobia AND faces.'' Then, we selected those fMRI studies for which we were able to obtain data for the comparison between SAD and healthy controls (HC) in a face perception task, either from the published papers or from the authors themselves. In this way, we obtained 23 studies (totaling 449 SAD and 424 HC individuals). We identified significant clusters in which faces evoked a higher response in SAD in bilateral amygdala, globus pallidus, superior temporal sulcus, visual cortex, and prefrontal cortex. We also found a higher activity for HC in the lingual gyrus and in the posterior cingulate. Our findings show that altered neural response to face in SAD is not limited to emotional structures but involves a complex network. These results may have implications for the understanding of SAD pathophysiology, as they suggest that a dysfunctional face perception process may bias patient person-to-person interactions.

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“…The current findings extend the existing literature and show that socially anxious individuals have a processing bias (Hirsch and Clark, 2004) not only toward visual social signals of threat (Merckelbach et al, 1989; Stein et al, 2002; Straube et al, 2004; Kolassa and Miltner, 2006; Phan et al, 2006; Blair et al, 2008; Moser et al, 2008; Mühlberger et al, 2009), but also in response to social chemosensory signals of anxiety. This processing bias involves both early attentional, as well as late behaviorally relevant information processing.…”

Section: Discussionsupporting

confidence: 87%

“…This is reflected in enhanced early (N170) and late (LPP) ERPs in HSA participants. Previous studies have shown enhanced automatic guidance of motivated attention (Schupp et al, 2004) toward fearful faces in social anxiety (Mühlberger et al, 2009), and socially anxious individuals have been shown to respond to angry or fearful faces with increased amygdala activation (Straube et al, 2004; Phan et al, 2006). …”

Section: Discussionmentioning

confidence: 98%

Context counts! social anxiety modulates the processing of fearful faces in the context of chemosensory anxiety signals

Adolph¹,

Meister²,

Pause³

2013

Front. Hum. Neurosci.

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During emotion perception, context is an important source of information. Whether contextual cues from modalities other than vision or audition influence the perception of social emotional information has not been investigated. Thus, the present study aimed at testing emotion perception and regulation in response to fearful facial expressions presented in the context of chemosensory stimuli derived from sweat of anxious individuals. In groups of high (HSA) and low socially anxious (LSA) participants we recorded the startle reflex (Experiment I), and analysed event-related potentials (ERPs; Experiment II) while they viewed anxious facial expressions in the context of chemosensory anxiety signals and chemosensory control stimuli. Results revealed that N1/P1 and N170 amplitudes were larger while late positive potential (LPP) activity was smaller for facial expressions presented in the context of the anxiety and the chemosensory control stimulus as compared to facial expressions without a chemosensory context. Furthermore, HSA participants were highly sensitive to the contextual anxiety signals. They showed enhanced motivated attention allocation (LPP, Study II), as well as larger startle responses toward faces in the context of chemosensory anxiety signals than did LSA participants (Study I). Chemosensory context had no effect on emotion regulation, and both LSA and HSA participants showed effective emotion regulation (Study I and II). In conclusion, both anxiety and chemosensory sport context stimuli enhanced early attention allocation and structural encoding, but diminished motivated attention allocation to the facial expressions. The current results show that visual and chemosensory information is integrated on virtually all levels of stimulus processing and that socially anxious individuals might be especially sensitive to chemosensory contextual social information.

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“…The response pattern of anterior dorsal ACC supports previous findings of increased activation in medial prefrontal cortex areas in response to threatening stimuli or situations in patients with anxiety disorders [32], including SAD patients (for example, [6,8,66], but see [19,37,62]). Our results suggest a time-independent, constant affective-cognitive processing of threat in SAD due to the assumed role of midline regions of prefrontal cortex.…”

Section: Discussionsupporting

confidence: 87%

“…Especially the anterior insula has been shown to play an important role in the processing of visceral and autonomic responses to emotional stimuli (for example, [30,74]) and the integration of affective arousal responses with the perception of current physiological states [75]. Although several studies found a differential activation between SAD patients and controls in the insula (for example, [5,8,10,63,66]) others did not (for example, [3,6,13,60,61]). The delayed emergence of insula hyperactivation in SAD patients in the present study might indicate an increased monitoring of bodily states that follows after an initial phase of arousal and hypervigilance during the confrontation with disorder-related video clips.…”

Section: Discussionmentioning

confidence: 99%

Area-dependent time courses of brain activation during video-induced symptom provocation in social anxiety disorder

Boehme

Mohr

Becker

et al. 2014

Biology of Mood & Anxiety Disorders

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BackgroundPrevious functional imaging studies using symptom provocation in patients with social anxiety disorder (SAD) reported inconsistent findings, which might be at least partially related to different time-dependent activation profiles in different brain areas. In the present functional magnetic resonance imaging study, we used a novel video-based symptom provocation design in order to investigate the magnitude and time course of activation in different brain areas in 20 SAD patients and 20 healthy controls.ResultsThe disorder-related videos induced increased anxiety in patients with SAD as compared to healthy controls. Analyses of brain activation to disorder-related versus neutral video clips revealed amygdala activation during the first but not during the second half of the clips in patients as compared to controls. In contrast, the activation in the insula showed a reversed pattern with increased activation during the second but not during the first half of the video clips. Furthermore, a cluster in the anterior dorsal anterior cingulate cortex showed a sustained response for the entire duration of the videos.ConclusionsThe present findings suggest that different regions of the fear network show differential temporal response patterns during video-induced symptom provocation in SAD. While the amygdala is involved during initial threat processing, the insula seems to be more involved during subsequent anxiety responses. In accordance with cognitive models of SAD, a medial prefrontal region engaged in emotional-cognitive interactions is generally hyperactivated.

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“…13, 14 Earlier, studies of functional alterations in the fusiform gyrus to emotional faces have been inconsistent in SAD with reports of hypo- 25 and hyper-reactivity, 18 as well as null findings. 14, 17 In line with our results, a meta-analysis by Etkin and Wager 6 showed that SAD was associated with fusiform hyper-reactivity to negative emotional stimuli. In contrast to the study by Gentili et al 25 that showed fusiform hypoactivation in response to both emotional and neutral faces in combination compared with scrambled pictures, we studied the difference in activation between fearful and neutral faces including only the emotional component of face processing.…”

Section: Discussionsupporting

confidence: 86%

“…LSAS-SR was included as predictor in the second-level, group analysis. The amygdala was chosen as seed region, because reactivity here was associated with SAD severity, in accordance with earlier studies 15, 16, 17 and because the amygdala is a core component of the fear network that is proposed to be crucially involved in SAD neuropathology. 6, 8 …”

Section: Methodssupporting

(Expert classified)

“…These findings are in line with previous reports on amygdala hyper-reactivity to emotional faces in anxiety disorders, 8, 13 as well as a positive association between amygdala activity and social anxiety symptom severity. 15, 16, 17 The amygdala may in turn drive fusiform activity, which would be consistent with cognitive therories of increased attentional bias to negative social stimuli in SAD. 37 Interestingly, Prater et al 21 recently showed decreased connectivity between the amygdala and frontal cortex during processing of fearful vs happy faces in SAD.…”

Section: Discussionsupporting

(Expert classified)

“…The most consistent finding from neuroimaging studies of negative emotional face stimuli in SAD is amygdala hyper-reactivity. 13, 14 Amygdala reactivity to threatening face stimuli has further been shown to be positively correlated with clinical ratings of SAD severity, 15, 16, 17 suggesting a central role for this brain region in the neuropathology of SAD. Altered responses to emotional faces, both in medial prefrontal and insular regions, have also been found in SAD.…”

Section: Introductionmentioning

confidence: 99%

“…23, 27 This posterior cortical region has been found to be functionally related to SAD, 18, 25 but null findings have also been reported. 14, 17 Moreover, in a recent study, Danti and colleagues 24 examined functional connectivity between regions in the face perception network in patients with SAD, in comparison with healthy control (HC) participants. The authors used three seed regions involved in face perception, that is, the fusiform gyrus, superior temporal sulcus (STS) and amygdala.…”

Section: Introductionmentioning

confidence: 99%

“…Specifically, the aim of the study was to investigate neural responses to fearful vs neutral faces and the connectivity between the implicated brain regions. Furthermore, following previous reports of association between social anxiety severity and amygdala reactivity, 15, 16, 17 we sought to examine the relationship between SAD symptom severity, brain reactivity and brain connectivity during the face processing task.…”

Section: Introductionmentioning

(Expert classified)

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Altered fusiform connectivity during processing of fearful faces in social anxiety disorder

et al. 2013

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Social anxiety disorder (SAD) has been associated with hyper-reactivity in limbic brain regions like the amygdala, both during symptom provocation and emotional face processing tasks. In this functional magnetic resonance imaging study we sought to examine brain regions implicated in emotional face processing, and the connectivity between them, in patients with SAD (n=14) compared with healthy controls (n=12). We furthermore aimed to relate brain reactivity and connectivity to self-reported social anxiety symptom severity. SAD patients exhibited hyper-reactivity in the bilateral fusiform gyrus in response to fearful faces, as well as greater connectivity between the fusiform gyrus and amygdala, and decreased connectivity between the fusiform gyrus and ventromedial prefrontal cortex. Within the SAD group, social anxiety severity correlated positively with amygdala reactivity to emotional faces, amygdala-fusiform connectivity and connectivity between the amygdala and superior temporal sulcus (STS). These findings point to a pivotal role for the fusiform gyrus in SAD neuropathology, and further suggest that altered amygdala-fusiform and amygdala-STS connectivity could underlie previous findings of aberrant socio-emotional information processing in this anxiety disorder.

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“…Complementing these investigations, here we show that similar effects are obtained with task-irrelevant distracters inducing specific emotions (i.e., anxiety). These findings are also in line with evidence linking hyperactivity of the ventral system during processing of threat-related cues, both in non-clinically anxious but anxiety-prone participants [9], [10] and in clinically anxious patients [1], [2], [3], [4], [5], [42], [43]. Fewer studies, however, also reported deficient recruitment of activity in the dorsal regions (e.g.…”

Section: Discussionsupporting

confidence: 85%

“…However, further investigation of the emotion impact on WM performance according to the level of confidence (LOC; 1 = lowest, 3 = highest) identified a significant detrimental effect of angry face distracters on the responses associated with the highest level of confidence (i.e., LOC3) (Figure 2). A two-way ANOVA on items correctly identified as old yielded a significant level of confidence (LOC1, LOC2, LOC3) x distracter type (emotional, neutral, scrambled) interaction (F [4], [60] = 6.24; p<0.0003). Second, post-hoc analyses showed that the emotional distraction had an impairing effect only on LOC3, with the emotional distracters being associated with lower level of performance compared to both neutral (p<0.005) and scrambled distracters (p<0.0002).…”

Section: Resultsmentioning

confidence: 93%

“…A two-way ANOVA on corrected recognition scores (% Hits – % FAs) yielded a significant level of confidence (LOC1, LOC2, LOC3) x distracter type (emotional, neutral, scrambled) interaction (F [4], [60] = 8.57; p<0.00002), and post-hoc analyses showed that the emotional distraction had an impairing effect only on LOC3, with the emotional distracters being associated with lower level of performance compared to both neutral (p<0.02) and scrambled distracters (p<0.0005). Emo = Emotional Distracter; Neu = Neutral Distracters; Scr = Scrambled Distracters; FAs = False Alarms; WM = Working Memory.…”

Section: Resultsmentioning

confidence: 99%

“…General trait anxiety was measured using the trait scale of the State Trait Anxiety Inventory (STAI-T) [32], and the specific trait anxiety linked to social behaviour was measured using the Liebowitz Social Anxiety Scale (LSAS) [33], [34]. Given the specific nature of the transient emotional distracters used in the present study (i.e., angry faces expected to induce social anxiety) and previous evidence showing that the neural response to angry and fearful faces may be specifically influenced by trait social anxiety [4], we decided to also specifically assess social trait anxiety, in addition to assessing general trait anxiety. By using these two measures of anxiety, one indexing the level of general (non-specific) anxiety and the other indexing the level of specific (social) anxiety, the present study sought to investigate potential dissociable effects linked to emotion-cognition interactions in the presence of anxiety-inducing distraction.…”

Section: Methodsmentioning

confidence: 99%

“…Investigations of the role of anxiety-related individual differences showed that increased reactivity to potential threat conveyed by socially relevant stimuli (e.g., angry faces) is associated with exacerbated activity in AMY in both clinical patients with social anxiety disorder (SAD) (linked to individual variations in the severity of the symptoms) [2], [3], [4], [5], and in non-clinical individuals (linked to variations in the level of anxiety) [6], [7], [8], [9]. This suggests that altered functioning of AMY is not only disorder specific, but could also be observed in individuals who may be prone to develop anxiety disorders [9], [10].…”

Section: Introductionmentioning

confidence: 99%

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The Impact of Anxiety-Inducing Distraction on Cognitive Performance: A Combined Brain Imaging and Personality Investigation

et al. 2010

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BackgroundPrevious investigations revealed that the impact of task-irrelevant emotional distraction on ongoing goal-oriented cognitive processing is linked to opposite patterns of activation in emotional and perceptual vs. cognitive control/executive brain regions. However, little is known about the role of individual variations in these responses. The present study investigated the effect of trait anxiety on the neural responses mediating the impact of transient anxiety-inducing task-irrelevant distraction on cognitive performance, and on the neural correlates of coping with such distraction. We investigated whether activity in the brain regions sensitive to emotional distraction would show dissociable patterns of co-variation with measures indexing individual variations in trait anxiety and cognitive performance.Methodology/Principal FindingsEvent-related fMRI data, recorded while healthy female participants performed a delayed-response working memory (WM) task with distraction, were investigated in conjunction with behavioural measures that assessed individual variations in both trait anxiety and WM performance. Consistent with increased sensitivity to emotional cues in high anxiety, specific perceptual areas (fusiform gyrus - FG) exhibited increased activity that was positively correlated with trait anxiety and negatively correlated with WM performance, whereas specific executive regions (right lateral prefrontal cortex - PFC) exhibited decreased activity that was negatively correlated with trait anxiety. The study also identified a role of the medial and left lateral PFC in coping with distraction, as opposed to reflecting a detrimental impact of emotional distraction.ConclusionsThese findings provide initial evidence concerning the neural mechanisms sensitive to individual variations in trait anxiety and WM performance, which dissociate the detrimental impact of emotion distraction and the engagement of mechanisms to cope with distracting emotions. Our study sheds light on the neural correlates of emotion-cognition interactions in normal behaviour, which has implications for understanding factors that may influence susceptibility to affective disorders, in general, and to anxiety disorders, in particular.

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123 4 5 6 7 8 9 10

Association between Amygdala Hyperactivity to Harsh Faces and Severity of Social Anxiety in Generalized Social Phobia

Cited by 462 publications

References 45 publications

Effective emotion regulation strategies improve fMRI and ECG markers of psychopathology in panic disorder: implications for psychological treatment action

The development of emotion-related neural circuitry in health and psychopathology

scite: A smart citation index that displays the context of citations and classifies their intent using deep learning

Preliminary Evidence of White Matter Abnormality in the Uncinate Fasciculus in Generalized Social Anxiety Disorder

Attentional mechanisms of social perception are biased in social phobia

Beyond emotions: A meta-analysis of neural response within face processing system in social anxiety

Context counts! social anxiety modulates the processing of fearful faces in the context of chemosensory anxiety signals

Area-dependent time courses of brain activation during video-induced symptom provocation in social anxiety disorder

Altered fusiform connectivity during processing of fearful faces in social anxiety disorder

The Impact of Anxiety-Inducing Distraction on Cognitive Performance: A Combined Brain Imaging and Personality Investigation

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