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 461 publications

(362 citation statements)

References 45 publications

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“…These findings do not replicate previous studies showing either increased (e.g., Phan et al, 2006) or decreased (Lorberbaum et al, 2004) magnitude of dorsal anterior cingulate activation in socially anxious individuals in response to threat. One possibility is that increasing dorsal anterior cingulate activity in this context reflects an adaptive increase in cognitive control and preparation for the upcoming speech in healthy controls as the end of the task nears (Aarts et al, 2008), though more evidence is needed.…”

Section: Discussioncontrasting

confidence: 99%

“…In addition to amygdala and insula, anterior cingulate cortex and medial prefrontal cortex regions are also implicated in fear and anxiety neural circuitry (Etkin, 2012), and SAD individuals exhibit altered functioning in these areas in response to threatening or negative stimuli (Brühl et al, 2014). Specifically, studies largely show increased activity in anterior cingulate regions (e.g., Amir et al, 2005; Labuschagne et al, 2012; Phan et al, 2006; but see Pujol et al, 2013) and medial prefrontal cortex areas (e.g., Stein et al, 2002; Straube et al, 2004; Labuschagne et al, 2012) compared to controls, consistent with evidence for these regions in identifying and expressing negative emotion (Etkin et al, 2011). …”

Section: Introductionmentioning

confidence: 58%

“…For other ROIs, we hypothesized that SAD individuals would show heightened insula activity and reduced ventral striatum activity compared to controls. We also examined whether dACC activation in SAD was reduced (replicating Lorberbaum et al [2004] results) or elevated (e.g., Phan et al, 2006) compared to controls. Beyond main effects of group, hypotheses regarding the time course of activity in non-amygdala regions were largely exploratory.…”

Section: Introductionmentioning

confidence: 76%

“…Studies of the functional neuroanatomy of anxiety and emotional reactivity in SAD have revealed altered neural activity in response to social stimuli, including heightened amygdala responses to harsh (e.g., angry, disgusted) faces compared to happy faces (Phan et al, 2006; Stein et al, 2002), exaggerated amygdala reactivity to harsh faces compared to healthy controls (e.g., Klumpp et al, 2010), and greater amygdala and insula activity in response to faces with angry expressions compared to neutral ones (Straube et al, 2004). Indeed, amygdala and insula regions frequently show hyperactivation across provocation and affective processing study designs in individuals with anxiety disorders, including SAD (Etkin and Wager, 2007; Miskovic and Schmidt, 2012).…”

Section: Introductionmentioning

confidence: 99%

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Altered time course of amygdala activation during speech anticipation in social anxiety disorder

Davies

Young

Torre

et al. 2017

Journal of Affective Disorders

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Background Exaggerated anticipatory anxiety is common in social anxiety disorder (SAD). Neuroimaging studies have revealed altered neural activity in response to social stimuli in SAD, but fewer studies have examined neural activity during anticipation of feared social stimuli in SAD. The current study examined the time course and magnitude of activity in threat processing brain regions during speech anticipation in socially anxious individuals and healthy controls (HC). Method Participants (SAD n = 58; HC n = 16) underwent functional magnetic resonance imaging (fMRI) during which they completed a 90s control anticipation task and 90s speech anticipation task. Repeated measures multi-level modeling analyses were used to examine group differences in time course activity during speech vs. control anticipation for regions of interest, including bilateral amygdala, insula, ventral striatum, and dorsal anterior cingulate cortex. Results The time course of amygdala activity was more prolonged and less variable throughout speech anticipation in SAD participants compared to HCs, whereas the overall magnitude of amygdala response did not differ between groups. Magnitude and time course of activity was largely similar between groups across other regions of interest. Limitations Analyses were restricted to regions of interest and task order was the same across participants due to the nature of deception instructions. Conclusions Sustained amygdala time course during anticipation may uniquely reflect heightened detection of threat or deficits in emotion regulation in socially anxious individuals. Findings highlight the importance of examining temporal dynamics of amygdala responding.

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“…We found that anxiety disorders displayed increased activation in the bilateral amygdala, anterior cingulate gyrus, parahippocampal gyrus, and common decreased activation mainly in the posterior cingulate, lingual gyrus, and precuneus. These conclusions are consistent with the previous studies [14,[20][21][22][23][24][25][26][27][28][29][30].…”

Section: Discussionsupporting

confidence: 94%

“…Although activations in the amygdala always appear in anxiety disorders involving emotional stimulations, there was a divergence in the activation of the left and right amygdala. For instance, some studies have highlighted the hyperactivity of the two-sided amygdala in anxiety disorders [23,24,27,29,[31][32][33], while other studies have only found it in the unilateral amygdala. This may be related to the different functions of the left and right amygdala [34].…”

Section: Discussionmentioning

confidence: 99%

The Brain Activation of Anxiety Disorders During Emotional Stimulations: A Coordinate-Based Activation Likelihood Estimation Meta-Analysis

Liu

Wang²,

et al. 2021

Preprint

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Many studies have been analyzed the state of brain activation about anxiety under neuroimaging experiments with emotional stimuli. However, there is no meta-analysis to assess the commonality and specificity activation of different anxiety subtypes. Here, we used the activation likelihood estimation (ALE) to define the common and different activation between different subtypes of anxiety. A total of 29 functional magnetic resonance imaging (fMRI) studies revealed significantly increased bilateral amygdala, anterior cingulate gyrus, and parahippocampal gyrus activation in anxiety during emotional stimuli. Moreover, we observed the decreased activations in the posterior cingulate, lingual gyrus, and precuneus. In subanalyses of anxiety disorders, the increased activation of generalized anxiety and specific phobias are present in the left hippocampus and thalamus, respectively. Social anxiety and panic disorders showed increased activation in the parahippocampal gyrus, amygdala, thalamus, and insula. Social anxiety, generalized anxiety, and panic disorders displayed decreased activations in the fusiform gyrus, posterior cingulate, and specific phobias exhibited in the medial frontal gyrus. Although different anxiety showed dissimilar activations, the principal activations were observed in the limbic lobe, which might indicate the limbic circuit was a neural reflection of anxiety symptoms.

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“…Of note, only right amygdala connectivity was found to be associated with LOC in the present study. This is consistent with previous studies which reported that only the right amygdala was involved in anxiety and borderline personality disorders (Minzenberg, Fan, New, Tang, & Siever, 2007; Phan, Fitzgerald, Nathan, & Tancer, 2006). However, the lateralized effects of amygdala connectivity require further replication, considering the smaller sample size in the current study.…”

Section: Discussionsupporting

confidence: 93%

Amygdala functional connectivity is associated with locus of control in the context of cognitive aging

et al. 2017

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Locus of control (LOC) measures the extent to which individuals perceive control over their lives. Those with a more “internal” LOC feel self-sufficient and able to determine important aspects of their own future, while those with a more “external” LOC feel that their lives are governed by events beyond their control. Reduced internal LOC and increased external LOC have been found in cognitive disorders, but the neural substrates of these control perceptions are yet unknown. In the present study, we explored the relationship between amygdala functional connectivity and LOC in 18 amnestic mild cognitive impairment (MCI) and age-, sex-, and education-matched, 22 cognitively healthy controls (HC). Participants completed cognitive challenge tasks (Stroop Word Color task and Dual 1-back) for 20 minutes, and underwent resting-state functional magnetic resonance imaging immediately before and after the tasks. We found significantly lower internal LOC and higher external LOC in the MCI group than the HC group. Compared to HC, MCI group showed significantly stronger positive associations between internal LOC and baseline right amygdala connections (including right middle frontal gyrus and anterior cingulate cortex), and stronger negative associations between internal LOC and change of these right amygdala connections. Across all participants, external LOC explained the relationships between associations of another set of right amygdala connections (including middle cingulate cortex and right superior frontal gyrus), both at baseline and for change, and performance in the cognitive challenge tasks. Our findings indicate that the right amygdala networks might be critical in understanding the neural mechanisms underlying LOC’s role in cognitive aging.

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“…Study 2 also revealed that participants with higher SPAI scores were more accurate than participants with lower SPAI scores when the target faces were negative and the distractors were positive. This result is consistent with previous work showing that socially anxious individuals show a deeper neural processing of negative versus positive emotional faces [ 50 ] which could lead these individuals to attend more to negative than positive emotions. Taken together, these results demonstrate that participants high in traits related to social anxiety show different patterns of responses to emotional faces varying in emotion complexity and emotion valence.…”

Section: Discussionsupporting

confidence: 93%

“…That is, socially anxious individuals are impaired in understanding complex emotions [ 49 ], although less research has examined emotion identification. Socially anxious individuals also tend to show differences in processing emotions based on valence, such that they demonstrate more amygdala activation from negative than positive emotions [ 50 ], which may lead to greater attention to negative emotions. The social components of ASD and the symptoms of social anxiety are correlated yet distinguishable constructs that yield unique electrophysiological activation during social cognitive tasks [ 51 ] and each construct contributes unique variance to the success of certain social interventions [ 52 ].…”

Section: Introductionmentioning

confidence: 99%

“…To investigate this possibility, we manipulated the number of faces displayed (i.e., 8 or 16) and predicted that high anxiety participants would be less accurate on trials depicting faces with complex emotions but only on trials with a large number (i.e., 16) of faces. Regarding valence, fMRI research has demonstrated that socially anxious participants show increased amygdala activation to emotions with negative valence compared to positive valence [ 50 ]. This suggests that greater attention to negative emotions may lead high SPAI participants to have a higher accuracy identifying target faces depicting negative emotions when the distractors are positive.…”

Section: Introductionmentioning

confidence: 99%

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Autistic traits and social anxiety predict differential performance on social cognitive tasks in typically developing young adults

et al. 2018

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The current work examined the unique contribution that autistic traits and social anxiety have on tasks examining attention and emotion processing. In Study 1, 119 typically-developing college students completed a flanker task assessing the control of attention to target faces and away from distracting faces during emotion identification. In Study 2, 208 typically-developing college students performed a visual search task which required identification of whether a series of 8 or 16 emotional faces depicted the same or different emotions. Participants with more self-reported autistic traits performed more slowly on the flanker task in Study 1 than those with fewer autistic traits when stimuli depicted complex emotions. In Study 2, participants higher in social anxiety performed less accurately on trials showing all complex faces; participants with autistic traits showed no differences. These studies suggest that traits related to autism and to social anxiety differentially impact social cognitive processing.

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“…In terms of imaging, individuals with multiple disorders activated more fear encoding and expression regions (amygdala, insular cortex, and dACC) during conditioning. This finding is consistent with studies that have shown hyperactivation of fear-promoting regions during emotional tasks. During early conditioning, the vmPFC was less activated in the anxiety group compared with healthy controls.…”

Section: Discussionsupporting

confidence: 93%

Skin Conductance Responses and Neural Activations During Fear Conditioning and Extinction Recall Across Anxiety Disorders

et al. 2017

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IMPORTANCEThe fear conditioning and extinction neurocircuitry has been extensively studied in healthy and clinical populations, with a particular focus on posttraumatic stress disorder. Despite significant overlap of symptoms between posttraumatic stress disorder and anxiety disorders, the latter has received less attention. Given that dysregulated fear levels characterize anxiety disorders, examining the neural correlates of fear and extinction learning may shed light on the pathogenesis of underlying anxiety disorders.OBJECTIVES To investigate the psychophysiological and neural correlates of fear conditioning and extinction recall in anxiety disorders and to document how these features differ as a function of multiple diagnoses or anxiety severity. DESIGN, SETTING, AND PARTICIPANTSThis investigation was a cross-sectional, case-control, functional magnetic resonance imaging study at an academic medical center. Participants were healthy controls and individuals with at least 1 of the following anxiety disorders: generalized anxiety disorder, social anxiety disorder, specific phobia, and panic disorder. The study dates were between March 2013 and May 2015.EXPOSURES Two-day fear conditioning and extinction paradigm. CONCLUSIONS AND RELEVANCE Despite no skin conductance response group differences during extinction recall, brain activation patterns between anxious and healthy individuals differed. These findings encourage future studies to examine the conditions longitudinally and in the context of treatment trials to improve and guide therapeutics via advanced neurobiological understanding of each disorder.

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“…This is also in accord with previous results that showed an involvement of the amygdala in threat processing in SAD patients (e.g. Stein et al, 2002;Tillfors et al, 2002;Lorberbaum et al, 2004;Straube et al, 2004;Phan et al, 2006;Yoon et al, 2007;Schmidt et al, 2010).…”

Section: Discussionsupporting

confidence: 93%

Brain activation during anticipatory anxiety in social anxiety disorder

Boehme¹,

Ritter²,

Tefikow³

et al. 2013

Soc Cogn Affect Neurosci

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Exaggerated anticipatory anxiety during expectation of performance-related situations is an important feature of the psychopathology of social anxiety disorder (SAD). The neural basis of anticipatory anxiety in SAD has not been investigated in controlled studies. The current study used functional magnetic resonance imaging (fMRI) to investigate the neural correlates during the anticipation of public and evaluated speaking vs a control condition in 17 SAD patients and 17 healthy control subjects. FMRI results show increased activation of the insula and decreased activation of the ventral striatum in SAD patients, compared to control subjects during anticipation of a speech vs the control condition. In addition, an activation of the amygdala in SAD patients during the first half of the anticipation phase in the speech condition was observed. Finally, the amount of anticipatory anxiety of SAD patients was negatively correlated to the activation of the ventral striatum. This suggests an association between incentive function, motivation and anticipatory anxiety when SAD patients expect a performance situation.

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“…The fearrelated hyperactivity is consistent with a number of previous studies in GSAD where exaggerated amygdala reactivity has been reported to aversive social cues including fearful faces and to 'harsh' (fearful, angry, and contemptuous) faces ; Oxytocin and social anxiety disorder I Labuschagne et al Stein et al, 2002). However, we did not observe similar amygdala hyperactivity to angry faces, which has previously been reported in a number of studies (Evans et al, 2008;Phan et al, 2006;Stein et al, 2002;Straube et al, 2004). While we expected amygdala hyperactivity to 'harsh' (angry and fearful) faces, as each convey social signals of threat, the lack of hyperactivity to angry faces and the apparent inconsistency may be explained by a number of factors.…”

Section: Discussioncontrasting

(Expert classified)

“…Notably, patients with GSAD have deficits in emotion processing, and specifically exhibit attentional bias for critical/aversive faces and threatening social signals (Amir et al, 2003;Clark and McManus, 2002;Foa et al, 2000;Mogg et al, 2004), and tend to avert their gaze from salient facial features such as the eyes (Bogels and Mansell, 2004;Garner et al, 2006;Horley et al, 2004) to reduce excessive anxiety during social interactions. These deficits have been strongly linked to areas in the limbic system including the amygdala (Birbaumer et al, 1998;Blair et al, 2008;Etkin and Wager, 2007;Evans et al, 2008;Phan et al, 2006;Stein et al, 2002;Straube et al, 2004Straube et al, , 2005Veit et al, 2002;Yoon et al, 2006), where threat-related hyperactivity is a cardinal pathophysiological feature in patients with GSAD (Etkin and Wager, 2007;Shin and Liberzon, 2010).…”

Section: Introductionmentioning

confidence: 99%

“…Several functional magnetic resonance imaging (fMRI) studies have shown that GSAD subjects exhibit heightened activation of the amygdala in response to social cues conveying threat (eg, fearful or angry faces) (Evans et al, 2008;Goldin et al, 2009;Phan et al, 2006;Stein et al, 2002;Straube et al, 2004). Selective-serotonin reuptake-inhibitors, often used to treat GSAD, can attenuate amygdala reactivity to fearful faces in healthy volunteers (Harmer et al, 2006) and in GSAD patients (Phan et al, unpublished data), and to public speaking in GSAD patients (Furmark et al, 2002), suggesting that the amygdala could serve as a brain target to test the underlying neural substrate of social behaviors and social anxiety.…”

Section: Introductionmentioning

confidence: 99%

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Oxytocin Attenuates Amygdala Reactivity to Fear in Generalized Social Anxiety Disorder

Labuschagne

Phan

Wood

et al. 2010

Neuropsychopharmacol

437

300

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Patients with generalized social anxiety disorder (GSAD) exhibit heightened activation of the amygdala in response to social cues conveying threat (eg, fearful/angry faces). The neuropeptide oxytocin (OXT) decreases anxiety and stress, facilitates social encounters, and attenuates amygdala reactivity to threatening faces in healthy subjects. The goal of this study was to examine the effects of OXT on fear-related amygdala reactivity in GSAD and matched healthy control (CON) subjects. In a functional magnetic resonance imaging study utilizing a double-blind placebo-controlled within-subjects design, we measured amygdala activation to an emotional face matching task of fearful, angry, and happy faces following acute intranasal administration of OXT (24 IU or 40.32 μg) and placebo in 18 GSAD and 18 CON subjects. Both the CON and GSAD groups activated bilateral amygdala to all emotional faces during placebo, with the GSAD group exhibiting hyperactivity specifically to fearful faces in bilateral amygdala compared with the CON group. OXT had no effect on amygdala activity to emotional faces in the CON group, but attenuated the heightened amygdala reactivity to fearful faces in the GSAD group, such that the hyperactivity observed during the placebo session was no longer evident following OXT (ie, normalization). These findings suggest that OXT has a specific effect on fear-related amygdala activity, particularly when the amygdala is hyperactive, such as in GSAD, thereby providing a brain-based mechanism of the impact of OXT in modulating the exaggerated processing of social signals of threat in patients with pathological anxiety.

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“…Moreover, in accord with our current results, Phan et al [2006] showed that the magnitude of right amygdala activation to harsh faces in the SAD group was significantly positively correlated with severity of SAD as measured by the LSAS. Although exaggerated left amygdalar activation in SAD was reported by Stein et al [2002], the right amygdalar findings from this study and those by Phan et al [2006] parallel earlier imaging studies of other anxiety disorders, where the magnitude of right amygdala activation to emotional faces [Armony et al, 2005;Rauch et al, 2000] or symptom provocation [Fredrikson and Furmark, 2003] have been found to be correlated with symptom severity.…”

Section: Discussionsupporting

confidence: 92%

“…Given the ACCs known role in emotional information processing [Whalen et al, 1998b], its reciprocal connections with the amygdala and its hypothesized dysfunction within a prevailing model of cortico-limbic dysfunction in anxiety disorders , we speculate that the observed relative deactivation may represent insufficient cortical regulation of the exaggerated amygdalar responses. We hesitate to further emphasize our post hoc dACC finding as there are many inconsistencies among prefrontal findings in the SAD neuroimaging literature with regard to identified regions of interest, laterality and direction of change in brain activity [see, Van Ameringen et al, 2004;Amir et al, 2005;Phan et al, 2006]. Moreover, the study by Straube et al [2004], which also employed schematic (and photographic face) stimuli, found no between-group differences within the prefrontal cortex.…”

Section: Discussionmentioning

confidence: 91%

“…Although these findings appear to parallel those of this study, caution should be taken on making such comparisons as the reported findings of Straube et al [2005] were (1) based on photographic face stimuli (not schematic stimuli), (2) limited to group comparisons of the individual specific facial expressions (n.b., in contrast to this study no group by expression interactions were reported). Lastly, using fMRI at 4-Telsa, the laboratory of Phan et al [2006] has shown significantly greater amygdala activation in SAD compared with HC subjects in contrasts that compared ''harsh'' (i.e., angry, disgusted, and fearful) with either happy or neutral photographic faces as well as in contrasts that compared varying facial stimulus intensity [e.g., arousal; Yoon et al, 2007]. Moreover, in accord with our current results, Phan et al [2006] showed that the magnitude of right amygdala activation to harsh faces in the SAD group was significantly positively correlated with severity of SAD as measured by the LSAS.…”

Section: Discussionmentioning

confidence: 99%

“…Lastly, using fMRI at 4-Telsa, the laboratory of Phan et al [2006] has shown significantly greater amygdala activation in SAD compared with HC subjects in contrasts that compared ''harsh'' (i.e., angry, disgusted, and fearful) with either happy or neutral photographic faces as well as in contrasts that compared varying facial stimulus intensity [e.g., arousal; Yoon et al, 2007]. Moreover, in accord with our current results, Phan et al [2006] showed that the magnitude of right amygdala activation to harsh faces in the SAD group was significantly positively correlated with severity of SAD as measured by the LSAS. Although exaggerated left amygdalar activation in SAD was reported by Stein et al [2002], the right amygdalar findings from this study and those by Phan et al [2006] parallel earlier imaging studies of other anxiety disorders, where the magnitude of right amygdala activation to emotional faces [Armony et al, 2005;Rauch et al, 2000] or symptom provocation [Fredrikson and Furmark, 2003] have been found to be correlated with symptom severity.…”

Section: Discussionmentioning

confidence: 99%

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A functional MRI study of amygdala responses to angry schematic faces in social anxiety disorder

et al. 2008

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Neuroimaging studies using angry or contemptuous human facial photographic stimuli have suggested amygdala hyper-responsivity in social anxiety disorder (SAD). We sought to determine if an angry "schematic face" (simple line drawing) would evoke exaggerated amygdalar responses in SAD patients compared with healthy control (HC) subjects. Angry, happy, and neutral schematic faces were overtly presented to matched cohorts of 11 SAD and 11 HC subjects for passive viewing, whereas brain functional magnetic resonance imaging signal was measured at 1.5 Tesla. Voxel-wise analyses were performed using a random effects model in SPM99. Compared with HC subjects, SAD patients exhibited exaggerated responses in the right amygdala for the Angry versus Neutral contrast. The findings of exaggerated amygdala responses to angry schematic faces in SAD converge with results from earlier neuroimaging studies and illustrate the potential utility of schematic faces for probing amygdala function in psychiatric disorders. One prospective advantage of schematic faces is that they may minimize confounds related to gender, age, or race effects. However, extending earlier findings in healthy subjects, schematic faces appear more effective for probing amygdala responses to arousal-based (Angry versus Neutral) as opposed to valence-based (Angry versus Happy) contrasts.

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“…The finding of a hypersensitive amygdala in patients and a positive association between amygdala activation and disorder severity concur with several other studies [8] , [9] , [12] , [14] , [17] , [19] , [23] , [32] . In accordance with the results from Schmidt and colleagues [22] , our data underline the appropriateness of linguistic stimuli in clinical research.…”

Section: Discussionsupporting

(Expert classified)

“…The socially relevant stimuli are frequently operationalized as faces with aversive expressions [8] – [16] , for review see [7] . Studies reporting correlations between amygdala activation and symptom severity underlined the crucial role of this brain region [12] , [17] – [19] .…”

Section: Introductionmentioning

confidence: 99%

Of ‘Disgrace’ and ‘Pain’ – Corticolimbic Interaction Patterns for Disorder-Relevant and Emotional Words in Social Phobia

et al. 2014

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Limbic hyperactivation and an impaired functional interplay between the amygdala and the prefrontal cortex are discussed to go along with, or even cause, pathological anxiety. Within the multi-faceted group of anxiety disorders, the highly prevalent social phobia (SP) is characterized by excessive fear of being negatively evaluated. Although there is widespread evidence for amygdala hypersensitivity to emotional faces in SP, verbal material has rarely been used in imaging studies, in particular with an eye on disorder-specificity. Using functional magnetic resonance imaging (fMRI) and a block design consisting of (1) overall negative, (2) social-phobia related, (3) positive, and (4) neutral words, we studied 25 female patients with social phobia and 25 healthy female control subjects (HC). Results demonstrated amygdala hyperactivation to disorder-relevant but not to generally negative words in SP patients, with a positive correlation to symptom severity. A functional connectivity analysis revealed a weaker coupling between the amygdala and the left middle frontal gyrus in patients. Symptom severity was negatively related to connectivity strength between the amygdala and the ventromedial prefrontal and orbitofrontal cortex (Brodmann Area 10 and 11). The findings clearly support the view of a hypersensitive threat-detection system, combined with disorder-related alterations in amygdala-prefrontal cortex connectivity in pathological anxiety.

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“…Our findings replicate previous studies that reported an association of social anxiety symptoms and amygdala response in adults 33 and adolescents 32 with SAD. Furthermore, recent neural models demonstrate that fear-related amygdala activity can directly modulate attentional process 68 .…”

Section: Discussionsupporting

confidence: 92%

“…These results converge with prior findings of recognition bias and negative emotion reactivity to harsh faces in SAD 28, 33, 57–59 , and neural bases of emotion processing in primates 60–62 . Medial PFC and parahippocampal activations have been observed in a previous study of reactivity to harsh faces 28 and may be related to higher-order neural representations of self-focused attention, perspective taking 63 , and greater emotion intensity 26 that may be exaggerated in SAD.…”

Section: Discussionsupporting

confidence: 90%

“…While several prior studies of harsh facial expression have found greater amygdala response in SAD versus HC 28, 29, 33–35 , the present study utilized a face displaying a mixed emotion (anger+contempt), and included longer stimulus presentation times. These stimulus parameters differentiate this study from prior studies, and may increase the likelihood that HC will, like SAD, evaluate the stimuli as threatening.…”

Section: Discussionmentioning

(Expert classified)

“…Prior fMRI studies have shown that direct-facing angry and contemptuous facial expressions produce strong neural responses in SAD 28, 33 . We thus trained actors to produce harsh expressions that combined angry and contempt facial expressions according to the Facial Action Coding System (FACS) 50 .…”

Section: Methodsmentioning

confidence: 99%

“…Such expressions can serve as a potent signal communicating social disapproval for individuals with SAD. Viewing harsh faces has been shown to reliably activate negative emotions and amygdala response in adults 28–30 and adolescents 31, 32 with SAD, with greater SAD symptom severity predicting stronger amygdala response 33, 34 . Evidence also suggests abnormal neural response in regions interconnected with the amygdala in SAD, including increased activity in insular cortex in response to angry faces 30, 35 , in ACC in response to disgust faces 36 , and in parahippocampal gyrus, left ventrolateral and medial PFC in response to harsh faces 28 .…”

Section: Neuroanatomical Model Of Emotional Reactivity and Regulationmentioning

confidence: 99%

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Neural Bases of Social Anxiety Disorder

Goldin

Manber

Hakimi

et al. 2009

Arch Gen Psychiatry

405

168

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Context Social anxiety disorder is thought to involve emotional hyper-reactivity, 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. Objective This study investigated behavioral and neural correlates of emotional reactivity and cognitive regulation in patients and controls during processing of social and physical threat stimuli. Design 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. Setting Academic psychology department. Participants 15 adults with social anxiety disorder and 17 demographically-matched healthy controls. Main Outcome Measures Blood oxygen level dependent signal and negative emotion ratings. Results 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 to patients. Regulation during physical threat produced greater cognitive control-related response (i.e., right DLPFC) in patients compared to controls. Conclusions Compared to 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.

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

Cited by 461 publications

References 45 publications

Altered time course of amygdala activation during speech anticipation in social anxiety disorder

The Brain Activation of Anxiety Disorders During Emotional Stimulations: A Coordinate-Based Activation Likelihood Estimation Meta-Analysis

Amygdala functional connectivity is associated with locus of control in the context of cognitive aging

Autistic traits and social anxiety predict differential performance on social cognitive tasks in typically developing young adults

Skin Conductance Responses and Neural Activations During Fear Conditioning and Extinction Recall Across Anxiety Disorders

Brain activation during anticipatory anxiety in social anxiety disorder

Oxytocin Attenuates Amygdala Reactivity to Fear in Generalized Social Anxiety Disorder

A functional MRI study of amygdala responses to angry schematic faces in social anxiety disorder

Of ‘Disgrace’ and ‘Pain’ – Corticolimbic Interaction Patterns for Disorder-Relevant and Emotional Words in Social Phobia

Neural Bases of Social Anxiety Disorder

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